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A SYSTEM OF MEDICINE
/
.j2^^
SYSTEM OF MEDICINE
BY MANY WRITERS
EDITED BY
THOMAS CLIFFORD ALLBUTT
M.A., M.D., I,L.D., F.B.C.F., F.R.S., F.I..S., F.S.A.
BBeiUS PROFESSOR OF PHTSIC IN THE UMIVEESITT OF CAJUBBIDQB,'
FELLOW OF OONYILLE AST} OAIUB COLLBOS
NEW AND CHEAPMR EDITION
VOLUME V.
THE MACMILLAN COMPANY
LONDON: MACMIIXAN & CO., Ltd.
1905
All rights reserved
Copyright, 1898,
By the MACMILLAN COMPANY.
f-
J. S. Gushing & Co. — Berwick & Smith.
Norwood Maas. U.S.A.
CONTENTS
DISEASES OF THE RESPIRATORY ORGANS
Diseases of the Ltjngs — paoe
1
53
Bronchitis. Dr. Wm. Ewart .....
Bronchiectasis. Dr. Wm. Ewart .....
Pneumonia [including Cirrhosis and other Indurations, and
Broncho-pneumonia of Children]. Dr. P. H. Pye-Smitli . 91
Phthisis Pulmonalis. Dr. Percy Kidd ..... 156
Pneumoconiosis. Dr. J. T. Arlidge ..... 242
Pulmonary Aspeeoillosis. Dr. Rolleston .... 257
Emphysema of the Lunos. Dr. Kingston Fowler . . .263
Asthma and Hay Fever. Dr. James F. Goodhart . . . 286
Syphilitic Disease of the Lungs. Dr. Kingston Fowler . . 311
DISEASES OF THE PLEURA
Intrapleural Tension. Dr. Samuel West ..... 335
Pleurisy. Dr. Gee and Dr. Herringham ..... 346
Pneumothorax. Dr. D. W. Finlay . ..... 378
DISEASES OF THE CIRCULATORY SYSTEM
General Features of the Blood. Prof. Michael Foster . . . 391
Methods of Clinical Examination of the Blood. Dr. Monokton Cope-
man ......... 408
Cardiac Physios. Prof. Sherrington ...... 464
Chlorosis. Prof. AUbutt ....... 479
Pernicious ANa;MiA. Dr. Sidney Coupland ..... 519
Splenic Anaemia. Dr. Samuel West ...... 539
SYSTEM OF MEDICINE
HEMOPHILIA. Dr. Wiokham Legg
HiEMOKRHAGEs IN New-bokn ChildPlEN. Dr. John Thomson
PtTEPFRA. Dr. Stephen Mackenzie
Scurvy. Mr. W. Johnson Smith
Infantile Scurvy. Dr. Cheadle .
HaiMOGLOBlNTTRlA, Dr. S. Monckton Copeman
LEUCOOYTHiBMiA. Dr. Robert Muir
Dropsy. Dr. Dickinson .
Heart Diseases —
CoNOBNiTAL MALFORMATION OF THE Hbart. Dp. Laurence Humphry
Diseases os the Pericardium. Dr. F. T. Roberts
Functional Disorders of the Heart. Prof. AUbutt .
Mechanical Strain of the Heart. Prof. AUbutt
Injuries by Electric Currents of High Pressure. Dr. Thomas
Oliver ........
Endocarditis. Prof. Dresohfeld .....
Diseases of the Myocardium. Sir R. Douglas Powell .
Chronic Valvular Diseases —
Disease of the Aortic Area of the Heart. Prof. AUbutt
Diseases of the Mitral Valve. Dr. Ernest Sansom
PAGE
548
556
568
586
604
621
635
666
697
726
807
841
855
860
885
907
INDEXES
1041
TABLE
To face page 668
ILLUSTKATIONS
no. PAGE
1. Casts expectorated by two Patients suffering from Plastic Bronchitis . 28
2. External Surface of the Lung dotted with Vesicles in Acute Bronchiectasis 56
3. Vertical Section of the same Lung showing dilated Bronchioles . . 57
4. Alleged Mechanism of Dilatation, according to the Inspiratory Theory . 68
5. Some of the Effects of Cough in Bronchiectasis , . . .60
6. Composite Photograph illustrating the Development of the Tubercular
Process ......... 177
7. Diagram illustrating the Localisation of Tuberculous Lesions in the Lungs 189
8. Photograph of a Section of the Lung from a Case of Acute Miliary Tuber-
culosis ......... 191
9. Sputum showing Pus Corpuscles and Tubercle Bacilli . . . 194
10. Elastic Tissue from the Lung, with well-marked Alveolar Arrangement . 195
11. Specific Colour-curve of Blood, Daylight ..... 431
12. Specific Colour-curve of Blood, Candlelight ..... 432
13. Oliver's Hsemoglobinometer ....... 434
14. Camera Tube for use with Oliver's Hsemoglobinometer . . . 436
15. Gowers' Haemoglobinometer ....... 437
16. Gowers' Hgemoglobinometer, Improved Form .... 438
17. Von Eleischl's Haemometer . . . . . . .439
18. Gowers' Haemoeytometer ....... 442
19. Capillary Tube . . . . . . . .444
20. 21, 22. Thoma-Zeiss Apparatus for counting Blood Corpuscles . . 455
23. "Wright's Coagulometer ....... 452
24. Brodie and Russell's Coagulometer ...... 453
25. Browning's Micro-Spectroscope ...... 455
26. Chart of Blood Spectra ....... 456
27. Area of Pulmonary Artery and Conns ..... 505
28. Area of Right Ventricle and Conns ...... 505
29. Area of Aorta ......... 505
30. Systolic Murmurs in Pulmonary Artery and at Apex coexisting . . 505
31. Systolic Apex Murmur only ....... 505
32. Spectra of Haemoglobin and its Derivatives ..... 623
33. Pericardium not distended ....... 728
34. Pericardium artificially distended with fifteen ounces of Fluid 7 28
35. Case of Pericarditis in which the Sac contained 3^ lbs. of Fluid . . 740
36-43. Illustrations of the Morbid Conditions in Pericarditis and the Physical
Signs associated therewith ...... 760, 761
44. Illustrating " Rotch's Sign " in Disease of the Pericardium . . . 764
45. Outline of a large Effusion in Disease of the Pericardium . . . 764
SYSTEM OF MEDICINE
FAOE
765
765
FIG.
46. Outlines of the total and absolute Areas of Pericardial Dulnesa
47. The " Posterior Pericardial Patch of Dulness " . . . •
48. 49. Figures showing Position of Internal Organs in Cases of Adherent Peri-
cardium ,.....••• 785
50. Dilatation of Arch of Aorta ....... 922
51. Loud Systolic Murmur in Aortic Area ..... 928
52-59. Tracings illustrating the Anacrotic and Bisferiens Pulse . . 930-932
60. Typical Pulse of Aortic Incompetence ..... 937
61. Aortic Incompetence with Bigeminal Pulse ..... 961
62. Sites of Systolic Murmurs at or near the Apex of the Heart . . . 978
63. Portion of Heart and Pericardium uncovered by Lungs . . . 979
64. Cardiogram and Sphygmogram from a Case of free Mitral Regurgitation . 983
65. Cardiograms in Mitral Insufficiency ...... 983
66. Schema of a Cardiac Eevolution ...... 1014
67. Cardiogram in a Case of Mitral Stenosis ..... 1015
68. Cardiogram in a Case of Hypertrophy of the Left Ventricle . . . 1022
69. Cardiogram in a Case of Mitral Stenosis with Presystolic Murmur and
Thrill 1022
70. Trace in Mitral Stenosis ....... 1022
71. Sphygmograma in Mitral Stenosis ...... 1023
CHARTS
1. Influence of the Creasote Inhalation Treatment upon the Pyrexia of
Bronchiectasis ........ 86
2. Besults of Observations in the Specific Gravity of the Blood of Healthy
Males of Dififerent Ages ....... 493
3. Results of Observations on the Specific Gravity of the Blood of Healthy
Females of Different Ages ....... 494
4. Variations in the Specific Gravity of the Blood in Healthy Women from 2
to 42 years of Age ........ 495
5. Temperature Chart in Splenic Anaemia ..... 544
6. Range of Temperature during a Typical Attack of Paroxysmal Hsemoglobinuria 628
7. Temperature Curve in a Case of Paroxysmal Hsemoglobinuria , . 631
PLATES
I. Fig. 1. Case of Infantile Scurvy. Drawn from life . . To fcKC pcige &Qi
II. Figs. 2, 3. Illustrations of same Case . . . . „ 609
III. Fig. 1. Spleno-medullary Leucocythaemia. Fig. 2. Lym-
phatic Leucocythaemia or Lymphocythsemia . , , , 637
LIST OF AUTHOKS
Allbutt, Thomas CUfiford, M.D., LL.D., F.R.C.P., T.E.S., Regius Professor of Physic
in the University of Cambridge, Fellow of Gonville and Caius College, Consulting
Physician to the Leeds General Infirmary.
Arlidge, John T., M.D., F.E.C.P., Consulting Physician to the North Staffordshire
Infirmary.
Cheadle, W. B., M.D., F.E.C.P., Physician and Lecturer on Clinical Medicine, St.
Mary's Hospital ; Consulting Physician, Hospital for Sick Children.
Copeman, Sydney Monckton, M.D., M.E.C.P., D.P.H., Medical Inspector to H.M.
Local GoTernment Board, Whitehall ; Lecturer on Hygiene and Public Health
in the Westminster Hospital School of Medicine.
Coupland, Sidney, M.D., F.K.C.P., Physician and Lecturer on the Practice of
Medicine to the Middlesex Hospital.
Dickinson, W. Howship, M.D., F.E.C.P., Consulting Physician, St. George's Hospital
and Hospital for Sick Children ; Honorary Fellow of Gonville and Caius College,
Cambridge.
Dresohfeld, Julius, M.D., B.Sc, F.E.C.P., Physician to the Manchester Eoyal
Infirmary, and Professor of Medicine in the Owens College, Victoria University.
Ewart, William, M.D., F.E.C.P., Physician to St. George's Hospital, and to the
Belgrave Hospital for Children ; Joint Lecturer on Medicine, St. George's
Hospital.
Finlay, David W., M.D., F.E.C.P., Eegius Professor of Practice of Medicine in the
University of Aberdeen ; Physician to the Aberdeen Koyal Infirmary ; Consulting
Physician to the Eoyal Hospital for Diseases of the Chest, London.
Foster, Michael, M.D., D.Sc, D.C.L., LL.D., Sec. E.S., Professor of Physiology in
the University of Cambridge.
Powler, J. K., M.D., F.E.C.P., Physiciaii and late Lecturer on Pathology to the
Middlesex Hospital, Physician to the Brompton Hospital for Consumption.
Gee, Samuel Jones, M.D., F.R.C.P., Physician to St. Bartholomew's Hospital.
XU SYSTEM OF MEDICINE
Goodhart, James Frederick, M.D., F.R.C.P., Physician to Guy's Hospital, and Con-
sulting Physician to the Evelina Hospital.
Herringham, W.P., M.D., r.R.C.P., Assistant Physician St. Bartholomew's Hospital,
Physician to the Paddington Green Children's Hospital.
Humphry, Laurence, M.D., M.R.C.P., Assistant Physician to the Addenbrooke's
Hospital, Examiner in Medicine in the University of Cambridge.
Kidd, Percy, M.D., F.R.C.P., Physician and Joint Lecturer on Pathology to the
London Hospital, Physician to the Brompton Hospital for Consumption.
Legg, J. Wickham, M.D., F.R.C.P., late Assistant Physician to St. Bartholomew's
Hospital, and Lecturer on Pathological Anatomy in the Medical School.
Mackenzie, Stephen, M.D., F.R.C.P., Physician and Lecturer on Medicine to the
London Hospital.
Muir, Robert, M.D., F.R. C.P.Ed., Senior PathoWgist to the Royal Infirmary,
Edinburgh ; Senior Demonstrator of Pathology and Lecturer on Pathological
Bacteriology, University of Edinburgh.
Oliver, Thomas, M.D., F.R.C.P., Physician to the Newcastle-upon-Tyne Infirmary,
and Professor of Physiology in the University of Durham.
Powell, Sir R. Douglas, Bart., M.D., F.R.C.P., Physician Extraordinary to H.M. the
Queen ; Physician, Middlesex Hospital ; Consulting Physician, Brompton Hospital
for Diseases of the Chest.
Pye-Smith, Philip H., M.D., F.R.C.P., F.R.S., Physician and Lecturer on Medicine
to Guy's Hospital.
Roberts, Frederick T., M.D., F.R.C.P., Professor of Medicine, and of Clinical Medi-
cine, University College, London, and Physician to the University College
Hospital ; Consulting Physician to the Brompton Hospital for Consumption.
Rolleston, Humphry Davy, M.D., F.R.C.P., late Fellow of St. John's College, Cam-
bridge ; Senior Assistant Physician and Lecturer on Pathology to St. George's
Hospital ; Physician to Out-patients, Victoria Hospital for Children.
Sansom, A. Ernest, M.D., F.R.C.P., Fellow of King's CoUege, London; Physician to
the London Hospital ; Consulting Physician N.E. Hospital for Children.
Sherrington, C. S., M.D., F.R.S., Holt Professor of Physiology in University College,
Liverpool.
Smith, W. Johnson, F.R.C.S., Surgeon to the Branch Seamen's Hospital.
Thomson, John, M.D., F.R.C.P.Ed., Extra Physician to the Royal Hospital for Sick
Children ; Lecturer on Diseases of Children, School of Medicine, Edinburgh.
"West, S., M.D., F.R.C.P., Assistant Physician to St. Bartholomew's Hospital, Senior
Physician to the Royal Free Hospital.
In order to avoid frequent mterrwption of the text, the Editor has only inserted
the nvmibers indicative of items in the lists of " References " in cases of emphasis,
where two or more references to one author are in the list, where an author is
quoted from a work published under another name, or where an authoritative state-
ment is made without mention of the author's name. In ordinary cases an author's
name is a sufficient indication of the corresponding item in the list.
DISEASES OF THE EESPIKATOKY OEGANS
{CONTINUED)
BRONCHITIS
BRONCHIECTASIS
PNEUMONIA
PHTHISIS PULMONALIS
PNEUMOCONIOSIS
PULMONARY ASPERGILLOSIS
EMPHYSEMA OF THE LUNGS
ASTHMA AND HAY FEVER
SYPHILITIC DISEASE Ot THE
LUNGS
BEONCHITIS
We owe to Badham the introduction of the name bronchitis. Before
him and Laennec the disease was confounded with the catarrhs, and more
or less with phthisis and pneumonia ; from the latter, however, in its
broncho-pneumonic form it was distinguished by the name " peripneu-
monia notha." The name " peribronchitis " is reserved for an affection
which chiefly implicates the outer coat ; but the distinction is rather one
of degree than of kind, the three coats being more or less involved in all
cases. The clinical type of the disease is apt to vary with its distribu-
tion in the chest, with the degree of its severity, with its course and
duration, and with its kind ; and additional sub-varieties arise from its
manifold associations with other diseases and from the multiplicity of
its causes. The size and calibre of the bronchi concerned are also
important factors. The patency of the smaller, and especially of the non-
cartilaginous tubes, largely depends on a free transmission of the mechan-
ical forces of respiration ; that is, on the even and symmetrical play of
the siirrounding pulmonary tissue. Tubes of minute diameter, whilst
easily blocked by tenacious secretion, have little expulsive force for its
removal ; their inflammation is thus fraught with special consequences.
The pathological results of bronchitis are not, however, limited to an
interference with the air-conducting function, nor to changes in the
mucous membrane ; collateral changes may be set up. Bronchitis and
bronchiectasis cannot, therefore, be satisfactorily studied in their vari-
ous aspects without a brief preliminary reference to the anatomy and
relations of the bronchial system.
The normal structure and relations of the bronchial tubes. — The
distribution of the air-tubes in relation to the pulmonary substance is
such that the lobules, which may be regarded as the pulmonary periph-
ery, occupy not only the surface but also the centre of the organ.
The perfect and even respiratory movements of the lung, associated with
a minimum of pleural friction, are essentially dependent upon a uniform
patency of the air-tubes. If the central lobules should fail to expand,
compensating stress will fall upon the outer periphery — a result clearly
seen in emphysema. The bronchi distributed to the more central parts
of the lung being shorter and narrower than those proceeding to the
SYSTEM OF MEDICINE
surface may perhaps be more easily obstructed ; and in any portion of
the lung structural conditions may place some of the tubes at a relative
disadvantage. The part which these easily obstructed bronchioles may
play in the genesis of bronchiectasis will be explained under that head-
ing. Their temporary obstruction in bronchitis would tend to increase
any pre-existing hyperinflation of collateral lobules.
The relation of the bronchi to the pulmonary parenchyma is not
merely one of direct continuity ; close vascular connections establish a
functional relationship between the respiratory surface of the air-cells
and that of the intralobular bronchioles. With the pulmonary stroma
the connection is also intimate. In each lobule the peribronchial tissue
(as well as the periarterial) is continuous with the perilobular tissue, and
therefore also with the interlobular connective tissue which binds to-
gether all the lobules. Lastly, with the visceral pleura the bronchi
present a definite, though more distant, relation. The deep layer of the
visceral pleura is nothing more than the perilobular investment of the
superficial lobules ; and the interlobular septa throughout the lung may
be regarded as a continuous prolongation of this subpleural layer. The
structure of the bronchi is as follows : — The epithelial lining, consist-
ing of three layers of cells, (a) columnar ciliated, (6) pyriform, and (c)
flattened (Debove's membrane), rests, according to Professor Hamilton,
on a tough, homogeneous, elastic membrane, the basement membrane,
which is pierced only by the wide orifices of the mucous glands. An
inner fibrous coat underlies this membrane, and is separated by the
muscular coat from the outer fibrous coat in which are embedded the
cartilages and the mucous glands.
The adventitia or outer fibrous coat is in intimate relation with the
perilobular, and therefore with the intralobular tissue of each lobule.
In the case of the larger bronchi the connection is also direct with the
interlobular stroma. The adventitia is thus the medium of extensive
communications, chiefly lymphatic, between the air-tubes and the rest
of the lung ; and in disease it shares in all those processes to which the
term " interstitial " is applied.
The muscular coat, in addition to those functions which are obvious,
may also discharge other physiological duties, a knowledge of which
might throw light on pulmonary pathology. Hitherto we have heard more
of the perversion of the function of the bronchial muscles than of their
natural uses. It is generally admitted that they are liable to tonic spasm,
and that this spasm and the resulting partial closure of the smaller air-
tubes enter largely into the causation of asthma, and in varying degrees
complicate the respiratory diflaculties special to bronchitis.
The vascular system of the bronchi consists of the posterior or main
bronchial arteries originating from the descending aorta, the anterior
bronchial arteries supplied by the internal mammaries, and the small
branches contributed by the oesophageal, mediastinal, and pericardial
arteries ; these vessels accompany the bronchi, supplying not them alone,
but the entire pulmonary stroma with nutrient blood, the pulmonary
BRONCHITIS 3
artery being exclusively subservient to respiration. The capillaries of
both sets of arteries anastomose freely in the alveolar district, and
probably also in the mucous membrane of the air-tubes. According to
Zuckerkandl, " only the larger bronchi are irrigated by the bronchial
arteries, the terminal tubes being vascularised by the pulmonary artery,
and the intermediate bronchi by both."
A similar intercommunication exists between the bronchial veins of
the smaller air-tubes (and even, according to Zuckerkandl, of the larger
ones) and the pulmonary veins. The bronchial veins also anastomose
in the posterior mediastinum with the venous plexus formed by branches
from the oesophageal and from the diaphragmatic veins (Hamilton).
The bronchial lymphatics take their origin in the inner fibrous layer,
which is in lymphatic communication with the tunica muscularis and,
through the thickness of the latter, with the abundant plexus of the
outer fibrous layer, where probably they are chiefly discharged into
the periarterial channels. Both fibrous layers contain lymphatics in
abundance ; but since, according to Hamilton, these do not traverse the
basement membrane, no absorption would take place from the epithelial
lining, and the emunction of the latter would be effected directly into
the bronchial lumen.
Before and at its entrance into the lobule the lobular bronchiole is
in lymphatic connection with the perilobular and with the interlobular
network.
Within the lobule the lymphoid tissue described by Arnold (which
also occurs under the pleura) is distributed around the alveolar passage
and in the bronchial wall, as well as along the blood-vessels. The peri-
bronchial masses are said to occur on the side of the bronchus opposite
to that occupied by the accompanying pulmonary artery.
The activity of the intra-alveolar lymphatics is shown by the rapid
absorption of the products of pneumonia. The interepithelial spaces
and their connective tissue corpuscles communicate with interalveolar
plasmatic spaces or lymph capillaries, which converge either into the
superficial or into the deep lymphatic network of the lobule. The
larger vessels which arise from both these networks accompany the
pulmonary arteries and veins to the hilus ; whilst another set reaches
the latter from the superficial subpleural lymphatic network. Accord-
ing to Hamilton, the subpleural lymphatics have but little intercom-
munication with the lobular.
In the carbon-injected miner's lung (which usually is not fibrosed)
the entire lymphatic scheme is displayed ; and this may be studied in
Hamilton's beautiful illustrations. According to Hamilton, the soot
particles lie in the perilobular and interlobular tissue, around the
pulmonary artery and bronchi, in the lymphadenoid bodies of the lung
and of the bronchial glands, in the alveolar walls (sparsely), in their
epithelial interspaces, and in their desquamated epithelial cells.
The absence of pigment from the visceral pleura might have been
expected; its absence from the bronchial mucous membrane (which
SYSTEM OF MEDICINE
retains in the miner's lung the pink hue of bronchitis) is explained by
Hamilton and others in connection with the impermeability of its epi-
thelium and basement membrane, the injection of the lymphatics taking
place through the alveoli only, which but few of the inhaled particles
would reach. The isolating property of the basement membrane thus
demonstrated has much significance from a pathological as well as
from a physiological standpoint.
Classifications of bronchitis. — The anatomical nomenclature. — Although
a separation of the air-tubes, according to their size, into (a) the large
bronchi, (6) the middle-sized bronchi, (c) the small bronchi and sub-
lobular bronchioles, and (d) the intralobular or capillary bronchioles, is
in great part conventional, still this supplies a convenient anatomical
classification for the varieties of simple bronchitis, among which we
may describe the following : —
i. Trachear-bronchitis, or bronchitis ]
of the large tubes. J
ii. Simple or mild acute bronchitis,
or bronchitis of the middle-sized
tubes.
iii. Severe acute bronchitis of the adult, -i
or acute suffocative bronchitis, or I
bronchitis of the smaller tubes. \
iv. Capillary bronchitis of infancy and i
of old age, or "peripneumonia [
notha."
-{
\
An inflammation of the trachea and
larger cartilaginous tubes.
{An inflammation of the tubes of medium
size, and of the smaller cartilagi-
nous tubes.
r An inflammation of the smallest carti-
i laginous, and of the non-cartilag-
1 inous tubes down to the lobular
I. bronchioles.
An inflammation of the sublobular and
lobular bronchioles, extendinginto
the intralobular bronchioles and
air-passages.
These groups are not rigidly isolated but frequently combine.
Whilst trachea-bronchitis and bronchitis of the middle-sized tubes most
often occur independently of the later members of the series, and often
indeed independently of each other, the most important of the mixed
forms are those involving some of the small tubes in addition to the
larger ones.
There is also a clinical nomenclature based upon the severity and
duration of the attack. Although usually acute in their onset, trachea-
bronchitis and bronchitis of the middle-sized tubes are, in themselves,
seldom severe or dangerous. Bronchitis of the fine tubes is always a
severe as well as an acute affection, and its termination in death or in
recovery is usually not long delayed. This special feature of acuteness
and of gravity explains, and to a certain extent justifies, the use of the
term "acute bronchitis," which has been applied to it by rule of custom,
but which is neither exclusive nor explicit. " Chronic bronchitis " is
also a general name which has become specialised, without, however,
involving much ambiguity ; for, neither capillary bronchitis nor bron-
chitis of the small tubes being susceptible of a chronic development,
this name can only apply to group ii., which is exceedingly prone to
BRONCHITIS
chronicity, in contrast with trachea-bronchitis which is apt to be re-
current rather than lasting.
The occasional severity of the acute stage of a primary bronchitis of
the middle-sized tubes shows the disadvantage of monopolising the name
" Acute Bronchitis " as a name for the affection of the smaller tubes ;
and secondary varieties will be described, which may also run through
acute and subacute stages.
Lastly, a pathological nomenclature recognises a bronchitis pure and
simple — not hitherto traceable, as in the diphtheritic, the tuberculous,
and some other forms, to parasitic influences — which presents the
following well-marked varieties : —
i. Catarrhal bronchitis: (a) simple mucous catarrh; (&) chronic or
muco-purulent catarrh.
ii. Plastic bronchitis.
iii. Putrid bronchitis.
The immense majority of cases belong to the catarrhal group. The
putrid purulent form is seldom met with. The plastic variety is so rare
as to be little more than a clinical curiosity.
I. Simple Bronchitis
Causation. — A. Remote causes. — (i.) No age is exempt ; but during
early adult life the disease is much less prevalent, in spite of greater ex-
posure. Infants and the aged are particularly liable to it, and the periods
of dentition favour its onset, (ii.) Except during the working periods
of life, when men are more exposed, sex makes little difference, (iii.)
Many occupations involve direct exposure to the extremes of temperature ;
others are indirect causes, through relaxing influences or confined air.
Some trades lead to inhalation of fumes or particles which mechanically
set up bronchitis, such as particles of steel, granite, chalk, charcoal,
or cotton, (iv.) Luxurious habits both in diet and in clothing, and
the overheating of rooms, induce a liability which is especially re-
grettable in childhood, when the individual tendencies are capable of
some measure of control, (v.) Heredity and temperament constitute
distinct factors ; a delicate bronchial membrane may be inherited as a
delicate skin or any other outward peculiarity may be. Again, acquired
constitutional weakness from any cause (poverty, overwork, prolonged
illness, or intemperance) has an unfavourable effect, (vi.) Certain blood
diseases favour the production of bronchitis in a special degree ; such are
Bright's disease, gout, diabetes, enteric fever, and, particularly, measles
and rickets, (vii.) Heart disease is a potent factor, more especially
those forms of it which lead to pulmonary and bronchial congestion,
(viii.) Pre-existing chest affections — thoracic, pleural, and pulmonary
— also dispose to bronchitis ; but none in so well marked a degree as
emphysema, (ix.) Relative impurity of air renders the inhabitants of
large towns more liable to bronchitis than country folk ; but the depriva-
tion of an open-air life, and long sedentary hours in crowded dwellings,
SYSTEM OF MEDICINE
are probably more potent influences ; and those whose lives are chiefly-
spent out of doors, even if they perpetually breathe town air, probably
do not suffer in the same degree. Dr. Frederick Roberts, in Reynolds'
System of Medicine, states that in Cheshire and Lancashire, during the
year 1868, the ratio of mortality from bronchitis to the number of
inhabitants was 1 in 379-5; whilst in London it was only 1 in 442-3.
It is suggested that this striking mortality is due to the sedentary lives
led by so many mill-hands, to the high temperature of the factories, and
perhaps to the efiluvia which pervade the manufacturing districts,
(x.) The climate of this country, by its humidity and variability, favours
the prevalence of bronchitis. Variations occur in the mortality year
by year as the weather oscillates more or less. In 1867 it reached
1902 to every million living ; but the mean rate for fifteen years, from
1860 to 1864, was 1344-4.
Although sudden changes to cold winds, and particularly to the north-
easterly winds, are marked by a large increase of bronchitis, it does not
appear that mere bleakness or habitual exposure to strong winds, par-
ticularly to the north and to the east winds, so largely tend to set up
bronchitis as might be supposed. This is shown, in the figures for 1868,
in the relatively favourable return from the eastern counties, which head
the list with a mortality of 1 in 987-5 inhabitants, and of the north
midland counties (1 in 876-2), as against the south-western counties
(1 in 844-8), and all the other districts which have yet higher rates of
mortality. We notice, however, that Monmouthshire and Wales (1 in
955-4) closely approach the position taken by the eastern counties.
The difference between the seasons is that which might be expected.
Bronchitis is greatly more prevalent during the winter months than in
summer, and the liability to it extends into early spring. Thus, whereas
the greatest prevalence of pneumonia occurs during March and April,
that of bronchitis belongs to the colder months.
(xi.) Aerial impurities may be solid, fluid, or gaseous. Strongly
irritating particles or vapours may act as direct exciters of bronchitis,
as for instance the vapour of ammonia, of iodine, of bromine; finely
powdered ipecacuanha, pepper, or tobacco; and, in the case of those
specially liable, the pollen of certain varieties of flowering grass.
B. Immediate causes. — The most usual proximate cause is a chill.
The patient is said to have "caught cold." The precise meaning of this
phrase is obscure. So long as the adaptive mechanisms are in full
efftciency, mere extremes of temperature do not constitute a danger to
the mucous membrane, and a strong man may pass unscathed from one
extreme to the other. Even infants and old people may breathe cold air
with impunity, especially if it be dry, so long as they are adequately clad
and in perfect health. The liability to "catch cold" is sometimes an
individual peculiarity ; more often it is acquired, but it is usually inten-
sified by sundry debilitating causes and by faulty hygiene.
Very little is known concerning any functions of the aerial mucous
membrane analogous to the regulating mechanisms of the skin for tem-
BRONCHITIS 7
perature. Their existence is rendered probable not only by the notice"
able differences in individual susceptibility, but by the interdependence
of the cutaneous and of the bronchial system in the process of " chill."
There are two kinds of chill — that directly applied to the air-passages
by cold and damp air, the body being at the time warm and well covered ;
and that which is due mainly to exposure of the cutaneous surface. In
both cases the sensation experienced at the time is apt to be referred
partly to the skin, the patient " feeling chilly all over," and partly to
the air-passages ; often to the pharynx or down the trachea. A nervous
link is indicated by these paired sensations. Eossbach's experiments
show that application of cold to the skin is followed in one or two
minutes by a reflex contraction of the tracheal vessels, and a little later
by venous congestion and an increased flow of mucus. Any fault in the
regulating mechanism, and particularly in its nervous factor, would leave
the mucous membrane unprotected against the physical results of con-
tinued exposure to extremes ; or incapable of that rapid adaptation which
is our safeguard against sudden transition from one extreme to another.
Smoke is a powerful irritant, whether by its scorching effect when
inhaled hot, by the mechanical action of the suspended carbon or ash, or
by the irritating nature of the volatile products of combustion.
Steam, when inhaled from the spout of a kettle by the children of the
poor, usually checks inspiration, and its irritating effects are limited to
the upper air-passages ; but when there is no escape from the inhalation
the damage to the air-tubes may be extensive.
Suspended cold moisture, as in ordinary mist, seems capable of irri-
tating very sensitive bronchi, but it is difiicult to eliminate the chilling
effect of the mist on the body surface ; and it is noteworthy that when an
equivalent amount of moisture is inhaled in crystalline form, as in a
severe frost, its mere cooling effect is not as a rule resented. The nasal
passages, of course, exercise some warming influence.
Town fogs are directly responsible for a great deal of bronchitis.
Consisting as they do of a mixture of suspended moisture with varying
proportions of the products of combustion, fogs differ greatly in their
irritating qualities. The fog is acid, and each droplet of water is coated
not only with a minute proportion of some tar-like body, but with an
equally minute quantity of sulphuric acid ; a combination most likely to
excite inflammation of the respiratory passages in delicate persons.
Irritant gases have been classified as non-respirable and respirable.
To the first group belong chlorine, ammonia, sulphurous anhydride, and
the vapours of iodine and bromine. The danger of their continuous
inhalation is obviated by the intensity of the irritation causing spas-
modic arrest of respiration. A single whiff of ammonia is commonly
followed by a transient watery flow from the mucous membrane.
Among the mildly irritating vapours ether, so largely used for surgical
purposes, deserves special mention. In the case of small children, in
the aged, and in those with limited respiratory surface, its use is to be
avoided ; even though a proportion of the instances of so-called " ether
SYSTEM OF MEDICINE
bronchitis " may be regarded as due to exposure of the surface during
the operation, or to the cold produced by the evaporation of the ether,
rather than to any direct irritation of the membrane.
As regards temperature, we know that standing in a cold draught,
staying out at sunset with insufficient wraps, keeping on wet clothing
after severe fatigue, or sitting long with wet or cold feet are so many
modes of causation of bronchitis by cutaneous chill. When the impres-
sion of chill is confined to the mucous membrane itself, the mischief is
usually due less to the intensity of the cold than to previous exposure
of the membrane to hot and impure air.
Intolerance of any but the milder kinds of atmosphere is most com-
monly the artificial result of injudicious physical education. It also
belongs to states of debility and to the extremes of age.
The popular belief in the contagious character of common catarrh has
received from time to time considerable support from the prevalence of
epidemic catarrh and influenza. Although the latter disease does not
exclusively attack the respiratory passages, still the almost universal co-
incidence with it of more or less inflammation of the air-passages must
give it a place among the causes of bronchitis. In many instances the
irritation, whatever be its mechanism, is severe, the cough being of a
harassing type which resembles that due to mechanical irritants, and not
infrequently inveterate. Ordinary bronchitis has never been attributed
to a specific contagium, so far as I am aware.
Lastly, the possibility of a penetration, through any mucous abrasions,
of the micro-organisms of disease, and particularly of the staphylococcus
pyogenes, of the streptococcus pyogenes, or of the pneumococcus — not
to mention numerous less harmful microbes found in normal air-passages
(8 different streptococci, 21 bacilli, 10 micrococci, and several sarcinee,
according to Panzieri) — should not be forgotten. Bronchitis might, it
has been suggested, be brought about by a combination of influences, the
micro-organisms finding access through an epithelial layer previously
loosened or damaged by undue exposure.
Pathological anatomy. — Professor Hamilton's researches,^ from which
the present account is largely derived, furnish us with the most recent
data.
(i.) Acute catarrhal bronchitis begins with a relaxation and distension
of the blood-vessels of the inner fibrous coat; a few hours after this the
basement membrane becomes cedematous, much swollen, and folded:
twenty to thirty hours afterwards it loses its ciliated cells in patches, and
some of these may be inhaled into the smaller bronchial tubes. Immature
cells are supplied in great number by the proliferation of Debove's cells,
and they constitute the cellular element of the bronchitic secretion.
Absolute denudation of the basement membrane may occur, but only tem-
porarily, and over limited areas. Desquamation and active secretion of
mucus take place at the same time in the mucous glands. The entire
thickness of the bronchial wall is swollen, congested, and infiltrated with
iCf. loc.cit.
BRONCHITIS 9
leucocytes. Eeparative changes are initiated by a diminution in the
congestion, and in the dilatation of the vessels ; and the cells gradually
resume their normal development and functions. Throughout the
attack the normal gray colour of the mucosa is replaced by a dull red.
(ii.) Chronic bronchitis. — (o) The common form, the result of a series
of acute attacks, is usually associated with much permanent emphysema
with intervening congested areas. The lower part of the trachea and
the bronchial surface in general are congested and purple, and yellowish
muco-pus can be squeezed out of the middle-sized and small air-tubes.
The characteristic smooth and shiny aspect of the mucosa is due to
the basement membrane being laid bare, only a few ill-shapen cells
adhering to it ; it is not always much swollen. Some dilatations may
occur in the smaller tubes ; the larger ones on the contrary may be
slightly narrowed by the great thickening of their coats. The coats are
densely infiltrated with cells, among which are seen many dilated
capillaries — some of which may project into the thickness of the base-
ment membrane — ^many thickened arterioles, and over-distended lym-
phatics ; these are especially abundant close to the cartilages which
are vacuolated, and in various stages of absorption. The muscular coat
may be hypertrophied, or on the contrary greatly atrophied ; or even
absent. The mucous glands also may be destroyed by cell infiltration,
or on the other hand much enlarged, with active mucous transformation
of the glandular and duct cells. Atheroma is frequently observed in the
middle-sized pulmonary arteries in the subjects of chronic bronchitis.
(b) A separate form of chronic bronchitis is characterised by a
peribronchitis fibrosa chronica (Virchow), and in some cases the fibrosis
extends along the pulmonary lymphatics to the entire interlobular stroma.
Instead of the common atrophic, rarefying emphysema, the lung tissue
then presents diffuse condensing fibrotic changes.
Physical signs. — ^The physical signs common to all forms of bronchitis
are so familiar that little more than a cursory review of them is necessary.
In shape and in size the chest tends to assume the inspiratory type,
without deformity, but with marked elevation of the clavicles and
shoulders, deepening the suprasternal and supraclavicular fossae. In
consequence of this and of the hyperinflation of the lungs, the diaphragm,
liver, and heart are more or less depressed.
The thorax moves at an increased rate, but to a diminished extent.
In severe bronchitis the inspiratory efforts fail to expand the chest,
except in its upper part ; and there may be inspiratory recession of the
lower interspaces, and in children of the lower ribs and sternum. The
abdominal muscles are thrown into strong and prolonged contraction
during expiration.
Bronchial fremitus is felt on palpation during the entire respiratory
act, or may be confined to inspiration or to expiration. Vocal and
tussive fremitus are not materially altered.
Percussion in most cases elicits an increased resonance, which may,
however, be masked by the strong contraction of the inspiratory muscles,
SYSTEM OF MEDICINE
to which is also due the peculiar tenderness of the chest. In small
children the occurrence of broncho-pneumonia or of collapse may detract
from the resonance, or may even cause an imperfect dulness.
Auscultation. — Except at the upper part of the thorax, where they
are often exaggerated, the respiratory sounds are much diminished or
may be inaudible. Their coarse and harsh character is indirectly due to
the feebleness of the alveolar murmur, which no longer veils the sounds
produced in the bronchioles ; a condition also observed in emphysema.
The adventitious sounds arising in the chest in the course of a simple
bronchitis include the two great classes of the dry and of the moist
sounds. To the first belong the large or sonorous, the small or sibilant,
and the intermediate or subsibilant rhonchi. The jEolian harmony
often audible seems to be specially frequent where some emphysema is
kept up under the joint influence of bronchitis and of muscular spasm.
Another musical sound is the rhythmic sibilus which may be set up in
the neighbourhood of the heart by each cardiac systole. Considerable
extension and loudness of the bronchitic sounds, although indicating the
implication of rather small tubes, and compatible with severe symptoms,
are not usually of anxious import in themselves, since they indicate that
air passes, though not freely, through a large number of tubes. Clicks
are sounds of sudden and snapping character, lacking musical quality
and difficult to interpret ; being occasionally suggestive of a parched, at
other times of a moist, condition of the tubes. Hence they are described
in different instances as moist clicks or as dry clicks, thus occupying an
intermediate position between the rhonchi and the mucous r§,les. The
moist sounds of bronchitis have a gurgling or bubbling quality. Nomen-
clature and description are much simplified by calling them mucous
rdles (large, medium-sized, or small), in contrast with the hard or metallic
rattles, crackles, or crepitations which may occur in the same chest if
broncho-pneumonia, or lobar pneumonia, or phthisis should complicate
the bronchial catarrh. The fine crepitations which may become audible
over limited patches in capillary bronchitis, in association with abundant
mucous r§,les elsewhere, illustrate this distinction.
Cardiac signs. — In fully established bronchitis a more or less distinct
epigastric beat is felt, the heart being not only depressed but enlarged
also. The enlargement is mainly due to an over-filling of the right
auricle and ventricle, evidenced by the distended jugulars ; whilst the
left ventricle presents little change. At the same time the absolute
dulness of the heart is lessened in its size, and the heart sounds in their
loudness by the inflation and encroachment of the sternal fringes of the
lung. A relative increase in the loudness of the second pulmonary
sound also belongs to uncomplicated bronchitis.
BRONCHITIS
A. SIMPLE BEONCHITIS LIMITED TO THE LARGE AND MIDDLE-
SIZED TUBES
Symptoms and course. — At the onset the attack may make itself
felt as a severe cold in the chest, with deep-seated rawness, soreness, and
parching ; or it may begin in the larynx, or in the pharyngeal or nasal
region, implicating also the ocular conJTinctivse, the frontal sinuses, and
the upper nasal cavities. Again, there may be more or less gastric and
hepatic disturbance. Individual peculiarity and local susceptibility may
help in each ease to determine the site of invasion. That these are not,
however, the only factors is shown by the regularity with which special
forms, such as the bronchitis of measles, begin in special situations.
In acute cases much continued or intermittent chilliness, and in
children slight delirium, or even convulsions (especially during the first
dentition), may open the scene.
With every variety of onset there is a uniformity in the general
symptoms. The pulse and respiration are moderately quickened, and
the temperature is raised two or three degrees. The patient complains
of respiratory discomfort, malaise, aching pains, headache, mental and
physical languor, drowsiness during waking hours, and restless sleep —
the results of the sudden check to the secreting and exhaling functions
of a large section of the respiratory membrane. Almost invariably the
alimentary mucous membrane is involved : the appetite fails, the tongue
is heavily coated, the liver inactive, and the bowels torpid.
The symptoms of the disease when in progress may be classed as
general, local, and respiratory. The local pain is seldom acute. The
sensation is almost always retrosternal ; it is variously described as
" sore," " raw," or " burning," and the cough as " tearing." Tenderness
on pressure is also felt at the sternum, but greater tenderness arises later
from the constant strain of cough, and is then felt over the entire chest,
but particularly over the pectoral muscles and at the base of the thorax.
The general symptoms are those of slight feverishness. The dry heat
of the skin which follows the stage of invasion in most cases soon gives
way to moisture. The temperature oscillates in the usual manner
between a morning minimum and a maximum at night, but does not
often rise very high. The pulse is moderately quickened and full ; at
first it is excited in action and almost bounding, but subsequently, with
the advent of diaphoresis, large, soft, and undulating. The tongue is
furred but moist, and the appetite bad ; vomiting is unusual, constipation
almost the rule. The urine is of the febrile type, with rather high
specific gravity ; in healthy subjects it is free from albumin, but loaded
with lithates, pigment, and urea ; sometimes it contains less than the
usual amount of sodium chloride.
Respiratory symptoms. — The patient's complaint is of tightness and
oppression at the chest, rather than of dyspnoea, though this would be
brought out on any exertion. Even in the position of rest the respira-
SYSTEM OF MEDICINE
tions are markedly quickened and proportionately more so than the
pulse ; they are shallow, and ultimately become laboured. Cough sets
in early, especially in the laryngeal, tracheal, and bronchial forms of
onset ; rather later when the pharynx is affected first, and sometimes not
for a day or two when the attack begins with coryza, in which cases
sneezing is more common. At first the cough is dry and irritating, and
usually associated with a tickling sensation in the larynx or trachea ;
when these structures are involved it is much altered in tone. It is
easily set up by slight irritation, and is difftcult to check. At a later
date the paroxysmal character is no longer due to simple irritation of the
nerve-endings over a dry and parched surface, or to a congested uvula
and epiglottis, but to the difiBculty in expelling the viscid and frothy
secretion.
The expectoration, in all cases of bronchitis, furnishes us with indica-
tions as to the stage and progress of the affection. From the healthy
state of simple moisture, free from any perceptible excess of fluid or of
miicus, the inflamed membrane, after a preliminary phase of checked
secretion and of dryness, quickly passes through a stage of excessive
hydration, during which the mucin of the cells is matured ; though but
little of it finds its way into the saline watery flux. After a very few
hours mucus is poured out more freely, and renders the fluid ropy ; but
it is still as transparent as glass, and free from bubbles other than those
produced in the mouth or in the larger tubes. The next stage is that
of purely mucous catarrh. The secretion stiffens, and, in the smaller
tubes, soon offers considerable resistance to the respiratory current. This
is clearly seen in the amount of air-bubbles held in the mucus, which,
although in itself hyaline and colourless, forms with them a white opaque
froth. This is the " crude stage " described in ancient books. In cases
of rapid resolution the mucus may soon undergo a secondary hydration,
losing its bubbles, and coming up with less effort and in rapidly lessening
quantities.
More commonly in the ordinary case of bronchitis the sputum passes
through some degree of "coction " (to use again an obsolete term), losing
together with its extreme viscidity and frothiness the hyaline colourless
quality, and becoming either streaked or uniformly tinged with light
yellow pus, whilst continuing to form as before a confluent mass in the
receiver. In more protracted cases the admixture of pus gradually
increases, and imparts a greater opacity and a greenish tinge to the
sputum, which becomes less hydrated, quite free from bubbles, and ulti-
mately nummular. This is a sign that the catarrhal process is lingering
in the larger tubes. There is much analogy and yet a distinction between
this expectoration and the more purulent and fluid discharge which from
its quantity and inveterate character has received the name of purulent
bronchorrhoea, and in which the individual sputa fuse into a mawkish
yellowish semi-fluid mass. In the later stage of bronchitis the sputa
remain distinct.
Haemoptysis, in simple uncomplicated bronchitis, is of exceptional
BRONCHITIS 13
occurrence ; but a few streaks of blood may be seen in the earlier and
drier stage. Tbey are probably due to the sudden detachment of super-
ficial layers of the membrane under the effort of cough.
Prognosis. — As to the duration of the attack prognosis is of necessity
somewhat uncertain, and is partly governed by atmospheric conditions.
In healthy children, youths, and adults, especially if not previously
affected, complete recovery under appropriate treatment niay be looked
for within one or two weeks, according to the severity and extent of the
inflammation. Any antecedent bronchial trouble would modify and
unsettle the estimate. In infants and the aged it is wise not to fix any
date.
As to danger to life, it is only at the two extremes of age, and in
albuminuria, or diabetes, or heart disease, or cachexia, that doubt is
likely to arise. However much they may ultimately tend to shorten
life, even repeated attacks of this mild form of bronchitis are never
directly fatal in subjects otherwise sound. If the respiratory muscles be
feeble, as in infancy, old age, or obesity, there is risk of bronciio-pneumonia
a retentis, the termination of which cannot be foretold ; the other risk,
peculiar to the same group of patients, arises from weakness of the heart,
and especially of the right heart, which may undergo dilatation and
eventually paralysis; or the bronchitis, especially in the aged, may
become chronic, and prove at length a fatal drain on an exhausted
vitality.
B. ACUTE SUFFOCATIVE BRONCHITIS OF ADULTS, OR BRONCHITIS
OF THE SMALL TUBES
Symptoms. — The following sketch of the clinical history of suffocative
bronchitis may justify our attempt to deal with it as a separate study.
Walshe, who obviously appreciated the essential differences between it
and capillary bronchitis, nevertheless included their description under
one heading, — " General and capillary bronchitis — olim peripneumonia
notha " ; and subsequent authors have followed him.
A first distinctive feature of simple asphyxial bronchitis is the
exceedingly rapid and general implication of the small tubes throughout
the lung. Walshe says: "I have known life destroyed in forty-six
hours, reckoning from the first moment of seizure, in a middle-aged adult,
who, in previous years, had had more than one seizure." In the adult
(and it is noteworthy that young adults are rarely attacked) orthopncea is
the rule, and, as observed by Walshe, "Maintenance of the head on a low
level from the first, in a case otherwise grave, is of evil augury." It is
hard to say to what extent superadded muscular spasm of the bronchioles
may increase the constriction due to inflammatory swelling.
More air is at first drawn into the lung by the strenuous breathing
than can be expelled by expiration. Subsequently, in spite of the
powerful contractions of the muscles of extraordinary respiration-, the chest
moves comparatively little, and vdtimately the character of the respiration
14 SYSTEM OF MEDICINE
tends more and more to become expiratory and abdominal. The lower
intercostal spaces are drawn in with each inspiration, but the ribs do not
usually recede. The whole chest is enlarged, and the lungs OTer-distended
by the powerful muscular forces applied to sufficiently rigid bones and
cartilages. An excess of air is, as it were, locked in by the obstruction of
the bronchioles : henceforth little passes through them into the lobules,
whether in the shape of air or of secretion ; and the direction taken by
the latter is outwards, not inwards as in capillary bronchitis. The
oxygen of the imprisoned air becomes exhausted, and the turgid veins and
the asphyxial complexion of the patient warn us of the degree of the
obstruction to the pulmonary circulation, and of the congestion of the
overloaded right heart.
Expectoration is not suppressed as often occurs in capillary bronchitis.
A fine white foam resembling " whipped egg " gives in the minute size of
its bubbles the gauge of the tubes affected. An analogous " whipped egg "
sputum (not, however, quite so fine) is sometimes observed in the sud-
den pulmonary congestion apt to complicate an anginal attack. In the
absence of angina this sputum is diagnostic of suffocative bronchitis. A
change to a coarser froth with the admixture of watery, hyaline, and
subsequently of purulent mucus gradually occurs in the later stages of the
more favourable cases.
Asphyxiating bronchitis of the adult is not complicated with any
parenchymatous inflammation of the lung. Pneumonia is perhaps
mechanically obviated by the intra^alveolar pressure of gas, and by the
stretching of the alveolar vessels. At any rate this immunity is attested
by the pulmonary appearances after death and by the observations of
every clinical observer. Walshe says : " True pneumonia, lobular or
diffused, is of purely exceptional occurrence ; the parenchyma is often
even unusually pale " ; and again, "but, without meaning to deny the
possibility of the fact, I must observe I have never yet seen local collapse
of lobules on an extensive enough scale in simple adult bronchitis
(antagonised as it is by the distending influence of the disease on the
alveoli) to justify me in looking upon it as a sufficing cause of deficiency
of tone " ; once more he says, "Bleeding is useless for the prevention of
pneumonia, seeing that, in the adult, idiopathic inflammation of the tubes
does not pass on to the parenchyma."
The later course of the disease need not be detailed at full length.
The symptoms are those of a progressive asphyxia — a prolonged
struggle for breath, the duration of which is measxtred by the patient's
cardiac energy. In Walshe's unsurpassed description : —
"As long as his strength permits, the patient sits erect or bends for-
ward ; but the body gradually yields ; and it is not uncommon to find
patients, while still perfectly conscious, lying sidewards or forwards with
the head lower than the shoulders. In rare cases, a posture of this kind
is adopted from the very onset.
" The sputa gradually diminish in quantity from failure of power to
expectorate ; the skin, generally livid or cyanotic in tint, falls in tempera-
BRONCHITIS IS
ture, becomes covered ■with cold, clammy perspiration. — sometimes
copious, rarely attended with, formation of sudamina; the expired air
grows cool, the feet and hands swell, in protracted cases the anasarca
rising to the trunk, unaided by coexistent disease of the heart, or of any
other organ promotive of dropsy ; fitful dozes lapse into a state of som-
nolescence, constant, except from momentary interruptions by the cough ;
muttering delirium, associated in some instances with slight convulsions,
precedes a comatose state which is the immediate forerunner of death."
The pulse gains in frequency as it loses in power, ranging from 120 to
150 or more. The respirations, varying from 36 to 60, may ultimately
recede from the maximum rate they had attained.
The temperature is moderately elevated. Dyspnoea, oppression,
retrosternal pain, restlessness, and cough are the chief symptoms com-
plained of.
The urine is scanty and concentrated. There is occasionally a tran-
sient albuminuria, but, in spite of the great diminution in the oxygen
supply, there is no sugar, and usually no excess of urates.
The physical signs are those of emphysema, as regards increased bulk
of the chest and of the lung, depression of the diaphragm and of the heart,
and pulmonary hyperresonance, coupled with bronchitic rales in the
larger tubes owing to the ascent within them of the frothy secretion.
The prognosis is anxious even in the best subjects. The worst cases
are those of pre-existing emphysema with incipient or advanced dilatation
of the right heart; these subjects seldom long survive the onset of a genu-
ine bronchitis of the small tubes. Cardiac defects, or inherent debility,
whether from exhaustion or atheroma, chronic albuminuria and the
various cachexies greatly reduce the chances of recovery.
The duration of a fatal attack may be reckoned in hours, or may
" drag on to the tenth or twelfth day " (Walshe). The same authority
has recorded unexpected recovery after long periods of an apparently
hopeless condition, with cold clammy sweat and almost complete loss of
conjunctival reflex. Such cases are rare ; they seem to suggest that
spasm of the bronchioles had contributed to the bronchial stoppage.
Morbid anatomy. — The post-mortem appearances are almost invari-
ably those of an over-distended, non-collapsing lung, the pale pink colour
of which contrasts strangely with the deep cyanosis of the body surface,
and is readily explained by the influence of the residual oxygen of the
distended air-cells on the reduced quantity of blood which their over-
stretched capillaries accommodate. The small bronchi present, on the
contrary, a swollen and deep red surface of section. Their contents vary
with the duration of the cases : in early deaths they consist chiefly of
mucus ; they are semi-purulent in those who have survived for several
days. Exceptionally here and there a pulmonary lobule may be found
collapsed, but pneumonic consolidation is absent. In all cases the heart
presents the asphyxial condition, and the viscera are engorged.
l6 SYSTEM OF MEDICINE
c. capillary bronchitis of infancy and old age
(peripneumonia notha)
This name specially belongs to the inflammation which extends from
the small bronchial tubes into the lobules and into the alveoli. It is in
great part a pneumonia, and was originally observed and referred to as
such long before the existence of bronchitis as a disease was thought of.
Indeed the pneumonic changes, where they coexist with bronchitis, are
obvious enough ; whilst of all diseases, equally intense and clinically
definite, none leaves after death traces slighter in themselves, or more
easily overlooked by the inexperienced observer, than those of simple
acute bronchitis.
It is singular that this liability to the pneumonic complications should
be shared exclusively by the earliest and by the latest stages of life, in
spite of most opposite anatomical conditions ; the lung being atrophied
and rarefied in old age, with relatively large air-spaces and tubes, whilst in
the infant it is only partly developed, and is fully packed with relatively
narrow air-tubes and air-cells yet imperfectly expanded : the thorax in
the one case is roomy and almost rigid, in the other relatively smaller than
at a later date, and exceedingly yielding ; the morbid processes reflect-
ing in the first the sluggishness of age, in the second the activity of
budding life. It can hardly be doubted that the intimate changes in the
two conditions must present essential differences, and that the similarity
between them must reside mainly in the general lines of march of the
disease, and in the direction taken by its extension. At any rate in the
capillary bronchitis of infants we perceive a factor entirely foreign to
that of old age, the tendency to rapid proliferation of the tissue elements
under irritation, and to the choking of space by direct cell overgrowth.
One peculiarity is common to both extremes of life — feebleness of the
mechanisms of respiration, which allows the obstruction to tell in a degree
not witnessed in the adult. In other respects the processes differ.
Infantile 6»-oracMzs attacking the small tubes almost inevitably disables
some of them at an early date, owing to the very unequal local resistances
of the chest walls, and to the influence of decubitus. A!t given spots the
thorax fails to draw out the subjacent lung, and is dragged in instead.
The subjacent lobules quickly become airless and collapsed, and are
henceforth sealed against the entrance of gases, fluids, and solids alike ;
they are incapable of becoming pneumonic. Collateral emphysema
results from the increased respiratory stress thrown on other parts, and,
thanks to their early over-distension, these lobules also may remain free
from pneumonia. It is in the remaining portions of the lung, imperfectly
expanded and traversed by enfeebled respiratory currents, that the
changes occur. The secretion, failing to be expelled by its stagnation,
sets up intralobular irritation, and a tissue-reaction which is mainly
proliferative.
BRONCHITIS 17
Two forms are noticed — the strictly broncho-pneumonic with
prevailing proliferation of epithelia, infiltration of the bronchial and
alveolar walls, and consolidation of the alveoli by epithelial cells ; and
the purulent form in which loose, semi-fluid bronchial secretion accu-
mulates in the smaller divisions, dilating many of them and setting up
a form of acute generalised bronchiectasis ; ^ whilst a varying amount
of pneumonic change is also present.
hi old age rigidity of the thorax, degenerative changes in the lung,
such as widening of the alveoli and of the air-tubes, atheroma of the
pulmonary artery and relaxation of the pulmonary veins, loss of
inspiratory energy and considerable loss of general expiratory ppwer,
and especially of the expulsive power of individual districts the
expansibility of which may have been reduced by pleural adhesions
or by the reticular fibrosis left behind by former attacks, are some of
the factors determining the variety of capillary bronchitis. The minute
diameters of the tubes and the yielding of the thoracic parietes, to which
are due the pulmonary collapse and collateral emphysema distinctive of
the infantile form, are conditions conspicuously absent. The character
is that of passive retention rather than of primary bronchial obstruc-
tion, though this element is not entirely excluded. Gravitation has a
larger share in determining the locality of the changes ; and the basic
and posterior regions are affected with much greater regularity than
in the infant. For these and other reasons the ingravescent, slowly
developing form, beginning in the medium-sized tubes, is of special
frequency in senile bronchitis. Again, the tissue reaction is of a dif-
ferent quality. Peribronchitis and alveolar wall infiltrations are ill-
developed. The consolidations are more definitely broncho-pneumonic
or terminal, and, owing to the even operation of gravitation, tend to
be confluent. At the same time they are less dense and are usually
combined with passive congestion and with oedema, which are not
features of the infantile variety.
The preceding remarks must have made it clear that between
capillary bronchitis and broncho-pneumonia it is difiicult to draw a hard
and fast line : the one and the other are made up of bronchitis and of
pneumonia. Nevertheless, on clinical as well as on pathological grounds,
it is desirable to uphold both forms in our nomenclature. Capillary
bronchitis, as bronchitis, is always a general affection of the entire lung
leading to severe dyspnoea. It is quite true than broncho-pneumonia in
its worst forms often becomes generalised and leads to intense breathless-
ness, but these are results which need time for their manifestation ; their
evolution is comparatively gradual, in opposition to the early and often
rapid onset of the dyspnoea of capillary bronchitis. Again, although
capillary bronchitis, especially in infants, always tends to set up some
1 For two interesting cases ol this kind, and for excellent drawings of sections of the
lungs, see a paper by Dr. Sharkey in St. Thomas's Hospital Reports, 1894, and the writer's
article on "Bronchiectasis " in the present volume. Bronchiolectasis has also been sug-
gested by Dr. Tooth and Dr. T. H. Fisher. Vide Dr. Tooth, Path. Soc. Trans, vol. xlviii.
pp. 30-34.
VOL. V C
l8 SYSTEM OF MEDICINE
parenchymatous inflammation, the occurrence of a broncho-pneumonia
is not invariable, death may occur from the bronchitis before time is
given for the consolidation ; and in other cases the tendency is rather to
peribronchitis, to purulent infiltration of the bronchi, and to dilatation,
than to consolidation.
Symptoms and Diagnosis. — In the infant or young child the history
of the attack, combined with the physical signs about to be described,
generally suffices to establish the diagnosis.
The signs are those of pulmonary collapse at the anterior and lateral
base of the thorax with inspiratory inward suction of the costal arch, and
of emphysema of the upper part of the lung. The resonance due to the
latter disguises the dulness which otherwise might have arisen from any
pneumonic condensation. Nevertheless examination may reveal a lack
of freedom and fulness of the auditory and tactile vibrations. Little air
enters the chest in spite of the strenuous efforts of the upper inspiratory
muscles and of the diaphragm, the contractions of which drag the sides
of the chest inwards instead of expanding them. Sibili may be heard
at first, but they are soon replaced or silenced by rales, the loudness of
which, always great in the small chests of children, is intensified by
any existing collapse or consolidation, and precludes the distinct per-
ception of any bronchiolar or tubular breath sound. In reality these
rales, the only sounds audible, do not arise in the capillary bronchi, but
are produced by the to-and-fro movements of the secretion within the
imperfectly swept medium-sized and larger tubes.
Exhaustion is an early feature ; the patients, if not too young to be
able to sit up in orthopnoea, rapidly lose that power ; and lie pale, livid,
and helpless, with hurried respiration, distended nostrils, and extremely
rapid pulse. Expectoration does not occur in the younger children, or
but rarely, and from an early period in the disease cough may be
absent ; but both the cough and the dyspnoea are prone to paroxysmal
aggravations after remissions.
The temperature varies with the amount of pneumonic action, but
probably also with the susceptibility of the individual nervous system.
It may rapidly lessen with the advent of cardiac exhaustion and coma.
The disease is usually fatal, and the prognosis, except in relatively
robust constitutions, is practically hopeless. The duration of the urgent
symptoms varies, but, for obvious reasons, is on the average much shorter
than in ordinary broncho-pneumonia. The acute stage of the disease
does not often exceed five or six days ; it commonly destroys life at an
earlier date.
In the aged the affection is usually ushered in by a pharyngeal,
tracheal, or bronchial cold, which more or less gradually assumes the
character of general bronchitis ; or it may be grafted upon a chronic
catarrh. The extension of the inflammation to the bronchioles is marked
by moderate pyrexia, paroxysmal cough and dyspnoea, laboured expec-
toration, a dusky flush changing to pallor, a rise in the rate of pulse and
respiration, and great prostration. All appetite is lost, the tongue be-
BRONCHITIS 19
comes dry and brown, and muttering delirium sets in, to be followed by-
deepening coma. In tbe less rapid cases, evidence of a low form of
broncho-pneumonia, associated with oedema and with the signs of bron-
chitis, may be ultimately obtained at the bases; but, as a rule, the
exhausted state of the patient forbids any searching examination of the
posterior pulmonary regions. In extreme old age treatment is unavail-
ing, and the disease is almost invariably fatal.
D. CHRONIC BRONCHITIS, CHRONIC BRONCHIAL CATARRH, AND
BRONOHORRHGEA
In this brief review of a wide and important subject, Walshe's divi-
sion into four clinical groups will be adopted.
(a) The simple winter cough, moderate, not disabling, accompanied
with the easy expectoration of a yellowish white muco-pus, is merely an
expression of the bronchial irritation set up by atmospheric conditions ;
it is frequently observed in children and young adults, as well as in
older people.
(6) An aggravated form of the same winter cough is peculiar to
chronic bronchial catarrh. The health and strength suffer; and the
patients are invalids, though often struggling to pursue their avocations.
Decided functional and some organic change may be traced in the
organs of respiration, of circulation, and of alimentation ; such as short
breath, venous fulness both general and portal, and delicate digestion.
The winter is spent in a succession of slight pyrexial relapses, during
which the expectoration, habitually loose and muco-purulent, may, after
being frothy for a while and difficult to raise, become unduly abundant
and puriform. The feverish bouts may last a week or a fortnight,
during which the appetite is in abeyance, the tongue, stomach, and liver
are out of order, and considerable weight is lost. Between these attacks
the patient regains some of the previous health and strength, but never
shakes off the cough, which may even last, in a modified degree, through
the summer.
These patients are protected from graver risks by their general
delicacy and invalidism ; but the process is progressive and devitalising:
through the inevitable changes it causes in the lung and in the heart.
It induces premature senility and shortens life.
(c) Bronchorrhaea indicates a special group in which the constitu-
tional factor has probably no less a share than the pulmonary changes.
Two varieties need description : —
(i.) The thin mucous or thin watery bronchorrhaea is thus described
by Walshe : — " In this variety paroxysms of cough and dyspncBa, which
may be of almost daily occurrence, or even more frequent, are relieved
by copious expectoration of a thin, watery fluid, or of a ropy, gluey,
transparent substance, like raw white of egg mixed with water; a
quarter of a pint of this may be secreted in the course of half an hour
SYSTEM OF MEDICINE
on tte decline of a paroxysm." Though sometimes fatal in the aged, the
flux is regarded by Walshe as occasionally useful in relieving pulmonary
congestion due to mitral disease. This singular affection is well identified
by the name of " bronchorrhoea serosa " given to it by Biermer, by that
of " mucoid asthma," or by its original name " chronic pituitous catarrh,"
used by Laennec. The paroxysms of dyspnoea and mucorrhoea may be of
isolated occurrence in the morning after waking; and the chest, after
two hours, may be comparatively clear for the day : or the discharge
may be repeated once or twice, producing in extreme instances a daily
output of three or four pints ; and this may last for years (Laennec).
Lebert mentions a case of survival to the age of eighty-two, after thirty
years of bronchorrhoea ; but Wilson Fox regards gradual failure as being
the common tendency, together with increasing dyspnoea and delicacy
of digestion. Pulmonary and cardiac degeneracy progressively lead to
emaciation, anaemia, cyanosis, oedema, and exhaustion.
Much obscurity still attaches to the pathology of the affection ; and
it is still doubtful whether the disease is primarily associated with
emphysema and bronchiectasis, or whether these be merely secondary
changes.
(ii.) Purulent bronchorrhoea or bronchial catarrh is a severe, in-
veterate, and progressive affection refractory to all treatment except the
climatic. The bronchial discharge resembles in general character that
observed in the diflduent stage of chronic catarrhal bronchitis during the
exacerbations noted under (6) ; but generally exceeds it in quantity, and
in the semi-fluid, mucoid nature and mawkish odour of the pus. Patho-
logically the affection differs from simple chronic catarrh, chiefly in the
extent of the bronchial and pulmonary change. The mucous membrane
is thickened, the bronchial walls infiltrated, and the calibre of the smaller
tubes increased, though there need be no sacculation or extensive
cylindrical dilatations such as belong to bronchiectasis. Between these
two conditions there is, however, no strict demarcation, and mixed
forms are met with. Emphysema is a direct and never-failing result
of the loaded state of the bronchial system, and of the constant strain
of cough. The atrophy of the pulmonary parenchyma contributes the
progressive element in the disease, and renders it intractable after it
has lasted for considerable periods.
The amount of the expectoration, which may reach one, two, or even
three pints daily, is in itself a serious drain ; and the cough is a severe
tax on the strength. Night sweats, an habitually subpyrexial temperar
ture, and the recurring anorexia or dyspepsia are additional depressants.
In connection with the latter, or with disturbance in the function of the
liver, or with temporary retentions within, or inflammatory conditions of
some of the bronchi, the mawkish secretion may become fetid in odour,
sometimes almost gangrenous ; and this reacts most unfavourably on the
general state.
In spite of these distressing and wearing symptoms, the resistance of
some of the patients to the fatal tendency of the disease is remarkable,
BRONCHITIS 21
and should encourage every effort to procure for them the healing effect
of appropriate climate. Failing this, recurring winters bring with them
steady aggravation, and life may be cut short by intercurrent broncho-
pneumonia, or may lapse from gradual exhaustion and cardiac dilatation,
(d) In the fourth classical variety, that of dry clironic hronchitis, the
sputum presents characters exactly opposite to those which have just
been described. It is extremely scanty, and consists of semi-transparent,
tough, pearl-like, roundish, small masses, apparently a highly concentrated
and partly dehydrated form of hyaline mucus, in which Charcot-Leyden
crystals or Curschmann's spirals are usually contained. The peculiarity
of the sputum led Laennec to apply to the affection the name of " dry
catarrh," although at times a little watery fluid may be expectorated.
The distinctive clinical features are the distressing paroxysmal cough,
causing much soreness at the chest ; and the dyspnoea and oppression of
breathing, intensified by the cough, but in most cases kept up by the
emphysema, which almost invariably complicates these cases. Laennec
described this form as exceedingly prevalent ; but, as pointed out by
Wilson Pox, he included under " dry catarrh " not only the asthmatic
cases, but all forms of nervous and sympathetic cough (gastric, hepatic,
hysterical). Walshe regarded the symptoms as mainly due to active
congestion of the tubes. Bronchial spasm is doubtless largely associated
with the congestion. Indeed, bronchial susceptibility and bronchial
irritation are its unmistakable etiological factors. One of the forms of
chronic gouty bronchitis belongs to this type. Dry catarrh is also said
to be prevalent at seaside places, and to occur after the cure of chronic
cutaneous eruptions, and in those weakened by excesses (F. Roberts).
The physical signs are those of the dry stage of acute bronchitis.
II. The SECONDAEr and the Special Varieties oe Bkonchitis
A. INTEKOUKRENT BRONCHITIS
This malady is a complication common to many acute disorders ; it
will sufB.ce briefly to indicate the relation which the bronchial affection
bears to the several diseases.
(i.) The most important group is formed by prevalent affections such
as whooping-cough, influenza, summer catarrh, phthisis, and measles ; of
the last bronchitis is an essential and prominent feature.
(ii.) In some of the continued fevers, but especially in typhoid fever, a
varying degree of bronchitis is almost the rule ; but its importance is
rarely of the first order, and the same remark applies to cases of typhus
fever. In enteric fever the severity of the early bronchial catarrh may
occasionally mislead the physician for a day or two ; and in protracted
and exceptional cases the unabated persistence of bronchial r9,les may
arouse uneasy suspicions of general tuberculosis. A malarial bronchitis
has also been described.
22 SYSTEM OF MEDICINE
In scarlet fever and in small-pox bronchitis is not a regular symptom.
The occurrence of bronchitis in rheumatic fever, fortunately infrequent,
was, before the introduction of the salicylic treatment, a most painful and
dreaded complication; it still remains a serious trouble, in spite of the
earlier relief afforded to the articular pain.
(iii.) In other affections bronchitis is only an occasional complication.
Among them chronic disease of the kidney probably takes the chief place,
both as regards the occurrence and the gravity of secondary bronchitis.
Gout is also prominent for the frequency of bronchial symptoms. Refer-
ence has already been made to the " dry bronchial irritation " so often
observed in the gouty, independently of any articular seizure. In cases
of retrocedent gout bronchitis may assume alarming severity, and is then
probably characterised by extreme congestion. Severe bronchitis of a
congestive and catarrhal type may, however, also occur as a precursor of
the arthritic attack, usually subsiding with the onset of the latter. A
syphilitic bronchitis was described by Graves, by Stokes, and by Munck ;
and .Walshe bestows two pages upon its discussion. It was supposed to
occur prior to the cutaneous eruption, and to alternate in gravity with the
latter. Bronchitis was also described as complicating cases of syphilis
between the secondary and the tertiary stages ; and again during the
tertiary stage, when it might be unilateral, whereas in the secondary
stage it was said to be invariably bilateral. Nothing has been added to
Walshe's description, which is reproduced by Wilson Fox. Indeed,
syphilitic bronchitis does not now hold any independent place, and of
lateyears has obtained no recognition ; althoughconsiderable attention has
been given meanwhile to the study of pulmonary syphilis {vide p. 311).
The scrofulous bronchitis of Graves is another constitutional varietywhich
has failed to obtain a permanent footing in the practical nomenclature of the
disease. Among blood diseases, anaemia, chlorosis, and pernicious anaemia
do not especially favor the occurrence of bronchitis. In scurvy, however,
bronchitis is not an infrequent complication, and is often associated with
haemoptysis, which does not belong in a comparable degree to any of the
other forms, except the phthisical and the cardiac.
Walshe draws attention to the occasional admixture with the sputum
of substances derived from the blood; such as bile in icterus, sugar in
glycosuria and diabetes, u.rea or its products in uraemia.
(iv.) A special group may be made of those forms of bronchitis which
are dependent upon pre-existing pulmonary or intrathoracic disease.
Aneurysm, mediastinal growths, or cicatricial stricture of a bronchus
(usually syphilitic, vide pp. 71 and 326) may give rise below the seat of
stenosis to a localised bronchitis or bronchiectasis, and this may ultimately
lead to disorganisation of the pulmonary substance. This result, which is
very apt to follow in the rare instances of primary malignant disease of the
bronchial mucous membrane, is not often observed in that of the lung,
nor m secondary peribronchial malignant disease, whether generalised or
occurring m single or multiple deposits. I have observed that the presence
withm the lung of separate malignant masses of moderate size, even in large
BRONCHITIS 23
number, may, owing to the distension of the intervening puhnonary tissue,
give no signs of consolidation either auscultatory or percussive, and yield
only the common physical signs of bronchitis. Gangrenous ulceration into
the root of the lung or into a large bronchus is a frequent mode of death
in oesophageal cancer, and is preceded by the signs of severe bronchial
irritation. Emphysema stands in the most intimate relation to bronchitis,
both as cause and effect. This association is fully dealt with in another
article {vide p. 273). The close connection existing between pleurisy,
bronchitis, and catarrh is a matter of every-day clinical observation, and
it will be briefly studied under a special heading. Pulmonary phthisis is
invariably in part, and often to a great extent, a bronchitic process :
it is enough to indicate that, in addition to the general bronchitis which
is an intermittent complication of most cases, the local deposits and the
local pleurisies of early phthisis determine strictly localised bronchial
catarrhs which often raise the first alarm and suggest an examination of
the sputum. Lastly, acute pneumonia is sometimes associated with well-
marked bronchitis, and forms a most serious, though by no means
necessarily fatal, complication. I have observed bronchial haemorrhage
persisting for several days as a result of this combination. In the
pneumonia of influenza the association with bronchitis is the rule ; but
here the relation between the two diseases is reversed. Bronchitis begins
and pneumonia may follow. (Fide art. "Influenza," vol. i. p. 679.)
(v.) Another special place must be reserved for the truly secondary
bronchitis of mitral disease, in which clinically, as well as anatomically,
three stages may be indicated : (a) A passive congestion of the mucous
membrane, the mechanism of which has been described by every writer
on valvular disease of the heart as the chief cause of the well-known
"heart-cough" — short, slight, dry, and habitual, and especially common
in mitral stenosis. (&) A mild chronic catarrhal bronchitis, easily set up
and difficult to throw off, may occur in both kinds of mitral disease ; but
is most frequent in mitral regurgitation. It is not, or is but occasionally,
associated with streaking of the sputum, (c) A disabling acute bron-
chitis is the almost invariable agent in overthrowing the fine adjustment
previously maintained between the task and the strength of the ventricles.
The rest and the treatment necessitated by the cardiac breakdown may
subdue for a time the bronchial trouble ; but in both forms of valvular
disease the bronchial complication inevitably reappears with the relapsing
failure of energy of the right heart. At this final stage the process is
almost entirely passive and dependent upon the engorgement of the
bronchial circulation. In cases of pure mitral stenosis previous pulmonary
apoplexies may have cleared up ; but their aggravated recurrence often
has a direct share in hastening the fatal event. More commonly, in
mitral stenosis combined with regurgitation as well as in pure mitral
reflux, the expectoration becomes watery with the onset of hypostatic
pulmonary congestion and oedema ; and the final obstruction of the air-
tubes with frothy mucus is the immediate result of cardiac and of general
failure.
24 SYSTEM OF MEDICINE
B. MECHANICAL BRONCHITIS
Acute mechanical bronchitis. — Hay asthma is the most striking
instance of the production of acute symptoms from the mechanical
irritation of suspended particles. The stronger irritants, such as the
sternutatories, cannot be long tolerated, and their effect is momentary
and slight. No such safeguard limits the inhalation of the pollen of
AntJioxanthum odorahun, so noxious to a small class of sufferers. The
irritation may involve the entire respiratory tract, including its
diverticular, from the frontal sinuses to the small bronchi. Violent and
continued sneezing, dyspnoea occurring in paroxysms, oppression and
retrosternal soreness, and wearisome cough, which is at first dry but
ultimately may produce a varying amount of watery, mucoid, or faintly
opaque expectoration, are the main symptoms in cases involving the
bronchi. For a further account of this disease the reader is referred to
the article on Asthma in the present volume (p. 286).
Chronic mechanical bronchitis is the main clinical feature and the
pathological starting-point of all pulmonary diseases due to the inhalation
of dust ; whether this be vegetable, as in the case of unloaders of grain-
ships, grinders of cereals, hemp-spinners, cotton-batters, and coal-miners ;
or animal, as in that of wool-carders, bedding-makers, brush-makers, and
bristle-drawers ; or mineral, as in that of stone-cutters, quarrymen, glass-
cutters, and calico-weavers (from the china clay used in calico-making) ;
or lastly metallic, as in that of knife-grinders, metal-turners, and needle-
pointers (Walshe). In the early stages of all these varieties the symp-
toms and the physical signs are exclusively those of bronchitis — the
sputum alone yielding on examination the special clue to the nature of
the irritant. Sooner or later in all of them the mischief strikes deeper ;
and to the bronchial catarrh, which becomes permanent, are superadded
indurative or destructive parenchymatous changes, causing the affections
to be classed under the heading of interstitial pneumonia or of phthisis,
under which their description will be found. [^Vide art. "Pneumoconio-
sis," p. 242 in the present volume.]
C. PARASITIC AFFECTIONS OF BEONCHI
More closely allied in some of their aspects to mechanical bronchitis
than to any other affection are the parasitic pulmonary diseases affecting
the bronchi, — detailed descriptions of which belong to other sections of
this work ; namely, hydatid disease and pulmonary distomiasis in the
group of animal parasites (vol. ii. p. 1102), actinomycosis (vol. ii. p. 81)
and aspergillosis (p. 257) in the vegetable group.
The Endemic Parasitic Hmmoptysis of some parts of Japan, of Corea,
and of Formosa was, in 1880, simultaneously and independently traced by
Manson and by Balz to its cause, the settling of the Distoma Bingeri oi
BRONCHITIS 25
Westmanii near the root of the lung, and the periodical discharge of its
yellowish-brown ova into the bronchi. The rusty expectoration resembles
that of pneumonia rather than that of bronchitis, whilst the anaemia and
progressive wasting are analogous to those of phthisis but have a much
more protracted course. Cases of pulmonary distomiasis have not hitherto
been reported in this country.
Hydatid disease and the rupture of a hydatid into the bronchi may
result in considerable bronchial irritation ; but the clinical details of the
affection cannot be described here. The occurrence of the cysticercus in
the lung is exceedingly rare.
Lastly, we owe to Diesing the account of a unique case of the pres-
ence of Strongylus longevaginatus in the bronchus of a child.
Among the vegetable parasites the most important is the Actinomyces.
Pulmonary actinomycosis has long been mistaken for the catarrh of
phthisis, of bronchiectasis, and of putrid bronchitis. It can now be readi'ly
identified by the discovery in the sputum of the clubbed radiating threads
of the fungus, which were first described by Bollinger in 1870.
Pulmonary aspergillosis, relatively common in animals and rare in man,
still occupies a somewhat doubtful position in pathology. Originally
described by Virchow as a separate disease, the invasion of the fungus
had since then been regarded as a mere complication of phthisis and of
chronic bronchial affections. Latterly the tendency has been to ascribe
to the aspergilli, and particularly to the Aspergillus fumigatus, primary
pathogenetic effects. Eenon, the latest writer on this subject, considers
that in some cases the pulmonary and bronchial affections which had
been attributed to tubercle or to actinomycosis were really due to the
aspergillus (vide p. 257).
Glanders. — Although the bacillus mallei, like that of tubercle, is not
limited to the lung, it deserves to be mentioned in connection with the
bronchial catarrh to which it gives rise (vol. ii. p. 513).
D. BEONCHITIS AND BBONCHIAL CATAKEH IN THEIK EELATION TO
PLEURISY
(a) Acute pleurisy with bronchitis, or acute pleuro-bronchitis. — The
not infrequent association of acute plenrisy with an acute bronchitis of
the middle-sized tubes is the more worthy of attention, as there is not
between these affections that necessary nexus which exists between
pleurisy and acute pneumonia ; and their occasional combination may be
regarded as a definite clinical complex. This view finds support in the
etiology and mode of onset, the two affections often arising from one and
the same exciting cause and with a simultaneous invasion. I have long
been in the habit of using the name " pleuro-bronchitis " to suggest some-
thing more than an accidental coincidence ; some definite tendency in the
subject, and some definite relationship between the pathological processes.
Rheumatism seems to be the constitutional tendency, and a simultaneous
implication of the pleural and bronchial lymphatics the most plausible
26 SYSTEM OF MEDICINE
explanation of the process. The occasional occurrence of bronchitis in
conjunction with rheumatic fever makes it the more probable that the
rheumatic tendency, in itself so often answerable for attacks of pleurisy,
may be at the root of this association, even in the absence of any arthritic
manifestations ; in the same way as non-articular gout is a common and
fully recognised factor in the causation of bronchitis.
Cases of this kind are usually classed as " pleurisies with bronchitis
as a complication " — a description justified by the relative prominence
of the two sets of symptoms. When the pleurisy, as often happens, is
of the dry variety, the physical signs of the bronchitis are those most
easily obtained ; whilst the most urgent symptoms belong rather to the
pleural affection. In cases with considerable effasion this relation is
reversed ; extensive dulness is a prominent physical sign, but the urgency
of the symptoms is largely due to the bronchitis, and is often in excess
of the loudness of the auscultatory signs special to the latter. When
the diaphragm is implicated in the pleurisy, the combined affection
assumes unusually severe features, owing to the acutely painful dysp-
noea, and to the interference with the mechanical function of cough in
clearing the air-tubes.
(/8) Chronic bronchial catarrh associated with pleuritic adhesions. —
Strictly speaking, the affection which has been described has no chronic
form, since, although bronchitis may be chronic, the results of the
pleurisy, in opposition to the inflammatory process, are lasting. It is
unusual for the acute attack to be continued into a chronic bronchitis ;
on the other hand, an eventual agglutination of the pleural surfaces, and
especially a sealing up of the diaphragmatic groove, are fertile sources
of recurring and ultimately of permanent bronchial trouble, in the shape
of a localised basic catarrh. Of all local bronchial catarrhs the most
common is the apex-catarrh or phthisis, or the recurrent simple apex-
catarrh so often determined by the indurated and adherent scar of an
old tuberculous lesion. In both cases the same mechanical influence is
exerted by the adhesions in hampering the pulmonary movements and
in interfering with the systematic play of the expiratory currents.
At the base, and particularly at the lateral base, distinguished in
health by its active inspiratory movements, the local catarrh is apt to lead to
extensive tissue changes. It is customary to speak of the affection as a
" chronic pulmonary catarrh," and of the ultimate anatomical condition as
a " chronic interstitial pleuro-pneumonia." We should not lose sight,
however, of the essentially bronchitic origin of the mischief. The localisar
tion and the permanence of the catarrh are primarily due to the paralysing
influence of the adhesions. The combined irritations exerted within the
air-passages by the retained secretion, and without by the recurring
respiratory traction, may set up a purely secondary fibrosis ; and in some
cases the fibrosis is mainly perilobular. Sometimes, however, the affection
remains to the end essentially bronchitic with a tendency to rarefaction
rather than to condensation of the pulmonary substance. Purther con-
sideration will be given to this subject in the article on " Bronchiectasis."
BRONCHITIS 27
E. PLASTIC BRONCHITIS
This curious and rare disease, referred to by Galen and studied in
1697 by Clarke and Lister, has been repeatedly described since that time.
Biermer deals with a series of fifty-eight reported cases ; but Peacock had
previously given the first collection of cases on record. Lebert treats
exhaustively of the same subject. Dr. Samuel West has collected fifty-
two cases recorded since Lebert's article, and compiled a full bibliography.
Plastic bronchitis, according to Biermer, occurs twice as frequently in
the male as in the female sex, but is not confined to any age from early
infancy to advanced life ; though most commonly observed in the inter-
vening period. It is still a pathological enigma.
The membranous exudations sometimes occurring in the air-passages
form a large and varied group. False membranes may originate from
the action of strong fumes or irritating fluids. The inhalation of steam
(Parker), or of the fumes of ammonia, or of alcohol in the shape of
eau-de-Cologne, are well-known instances. Again, the introduction into
the air-passages of strong solutions, such as lactic acid, has been followed
by plastic exudation (cf. Hoffmann) ; and Fritzsche describes a case in
which he attributed the latter to the internal use of iodide of potassium.
As a result of disease, thin false membranes have been observed in
the bronchi not only in instances of diphtheria, phthisis, erysipelas,
variola, scarlet fever, measles, typhoid fever, and sewer infection (as in
the cases of Picchini, quoted by Magniaux), but also in ordinary bron-
chitis, or pneumonia (E. Koch), in various pulmonary and cardiac dis-
eases, in articular rheumatism (Degler), and in pemphigus (Mader).
From all these varieties of membrane;as well as from the rarer forms
which have been described as primary diphtheritic and primary pneumo-
cocCic (Magniaux), the membrane of plastic bronchitis differs in its
greater firmness, which allows it to be expectorated in considerable
arborescent masses. The casts occasionally brought up after haemop-
tysis could alone compare with the latter in size and in consistence,
but their origin and their composition are both sufficiently manifest.
Thus whilst presenting distant affinities with the minute bronchiolar and
sometimes the coarser bronchial plugs of pneumonia, with the tubular
casts of diphtheria and of membranous tracheitis, and even with the
occasional intratubal mucous inspissations of acute bronchitis seen
chiefly in children, the formation of a continuous arborescent mould
of a considerable portion of the bronchial tree stands by itself as a well-
defined, although hitherto unexplained pathological process.
Whether, this feature may be trusted as a sufficient indication of the
pathological individuality of the affections is doubtful. Plastic bron-
chitis may possibly be not always of the same kind ; it may be due to a
variety of causes, just as there are distinct varieties of pseudo-membra-
nous affections. Again, the fact that most of the latter have been traced
to a bacterial origin, suggests that a similar causation may at some future
28
SYSTEM OF MEDICINE
time be made out in plastic bronchitis. In spite of this uncertainty as
to the unity and as to the mode of origin of the latter, we note in the
cases a general agreement which binds them together into a distinct
nosological group characterised anatomically by the recurring exudation,
both rapid and extensive, of eoagulable material in the bronchial tubes,
coupled, it is said, with denudation of epithelium, and nosologically by
the mechanical results of the exudation, namely, paroxysmal dyspnoea
Fig. 1. — Casts expectorated by two patients suflFering from plastic bronchitis. For an account of the
cases see Catidogue of St. George's Hospital Museum, Series vii. 30a, 30b. (Size considerably reduced.)
and the partial or total expulsion of the casts ; or, in the more severe
cases, suifocation and death.
Clinically the disease is clearly distinct from any of the affections
enumerated, occurring rather in connection with some personal idiosyn-
crasy than under the influence of any recognised predisposing circum-
stance, diathesis, or disease, and affecting robust subjects as well as those
suspected of actual or of threatening tuberculosis. It was observed by
Oppolzer recurrently during menstrual periods, with intermittence during
pregnancy ; whilst Biermer records several cases occurring during preg-
BRONCHITIS 29
nancy (Wilson Pox). In its exciting causes — climatic, seasonal, and
others — ^it is closely analogous to common bronchitis, and is in its begin-
nings almost indistinguishable from the latter, the exudation supervening
upon an initial catarrh.
The symptoms are those which would ensue from any extensive
obstruction of air-tubes. The cough, which may have a peculiar tone,
varies in intensity with the extent and consistence of the recurring
thrombi; when they attain considerable size and extension their ex-
pulsion is preceded by hacking dry cough and dyspnoea lasting for hours,
and in the expiratory type of the spasms resembling that of asthma. The
cyanosis is usually moderate. Permanent dyspnoea is present in the pro-
portion of the existing obstruction : during the intervals of freedom from
membrane it is not complained of. Slight haemoptysis, more often
following than preceding the expulsion of the casts, is very frequent in
nearly one-third of all cases (Biermer) ; or in one-third of the acute cases
(Lebert). Sometimes it is considerable ; and this has given rise to an
opinion that the casts might consist merely of coagulated blood ; but they
contain no blood-discs, except in their outermost layers, which are fre-
quently streaked with blood (Wilson Fox, Biermer).
Ordinary mucous sputum is apt to alternate with the casts, or to
accompany them throughout when they are expectorated piecemeal ; and
a mucous expectoration precedes the expulsion of the larger masses, which
are commonly ejected balled up in a slimy investment. Five to ten days
is the most common period of retention of the casts ; but this may range
from one or two days to upwards of three weeks. The daily expectora/-
tion of casts may be considerable for long periods, or limited to a few
fragments for a few days (Wilson Fox).
The constitutional symptoms in average cases are slight ; including
little or no pyrexia, except in the early stage, but occasionally a re-
current pyrexia with rigors, little emaciation, and, in a few cases only,
dropsy, epistaxis, diarrhoea, or albuminuria, which may not exceed the
duration of the attack. The spleen is sometimes enlarged.
A convenient division has been made between a small group of cases
running an acute course (from one to four weeks or more), and a much
larger group of chronic course, extending over years with intermissions
and relapses of varying durations. Biermer again subdivides the acute
cases into a mild variety, of shorter duration, in which the ordinary
symptoms of a slight bronchitis are simply varied by the expectoration
of a few casts ; and a severe variety, pyrexial and suffocative, in which
death may occur (six cases fatal in a series of ten) before any of the casts
have been expelled. The chronic form may long simulate ordinary
bronchial catarrh; or it may declare itself early. It also resembles
bronchitis in its relapsing character.
The physical signs, ill-defined where the plugs are small and few, are
well marked in cases of extensive obstruction. Inspiratory retraction of
the chest may occur. At any rate the respiratory movement is locally
impaired ; and pulmonary collapse may give rise to dulness, whilst full or
30 SYSTEM OF MEDICINE
exaggerated resonance is elsewhere obtained. The respiratory murmur
is diminished or absent ; or it may be replaced by sibilant rales, by moist
rales of various sizes, and, on the coagula becoming loosened, by loud
whistling (Corrigan), by tubular breathing and coarse rales (Van Meer-
beck), by a peculiar valve sound (Earth and Cazeaux), or by various
flapping sounds described by German authors as schmetterend, schnarrend,
and. flatter-gerdusch (Hoffmann). On palpation a tactile fremitus may
also be felt, which has been attributed to the flapping of the bronchial
casts.
Prognosis. — The association of the disease with tuberculous phthisis in
a certain proportion of the cases somewhat artificially raises its mortality.
Putting aside this latter group, and the unusual instances with severe
onset and rapidly fatal tendency, in which grave dyspnoea coinciding with
scanty expectoration and with extensive collapse of the lung are the most
anxious features, the disease, as generally observed, " neither destroys
life nor does grave damage, general or local " (Walshe). The liability to
attacks may last for considerable periods. The case recorded by Kisch
extended over twenty-five years.
Morbid anatomy. — (i.) The casts may be expectorated in mere frag-
ments or in their unbroken state. When freed from mucus, by suspension
in water, undamaged specimens are found to reproduce the structure of
the bronchi, from the tubes of the diameter of a goose-quill (rarely of
much larger size) down to the finest ramifications, with such perfect
accuracy that the site of their formation can be readily identified by
comparing them with a cast of the bronchial tree obtained by artificial
injection and corrosion. They are, with the exception of the smaller
branchings, of firm consistence, and often perceptibly tubular ; their bore
beingcommonly plugged with mucus. " Their colour is whitish or pearly
gray. They are distinctly stratified, and consist of a structureless or
fibrillated basis in which are embedded inflammatory cells, mucous cor-
puscles, pus cells, pigmented cells, and altered gland cells, and, in their
outer layers only, blood cells. They are soluble in alkalies, and also in
lime-water" (Wilson Fox).
The expression " plastic bronchitis " does not define the nature of the
exudation ; and in this there is an advantage, since the casts are invariably
mixed products, and may consist largely of mucus, as shown by the action
of the solvents just mentioned. Nevertheless they are mainly fibrinous,
and owe to fibrin their characteristic consistence. Of this an indirect
proof is found in the great rapidity with which fresh casts may be formed
after the expectoration of previous ones. Waldenburg, and subsequently
P. Lucas-Championniere, had described the occasional presence of fat in
the casts. This observation has been confirmed by Model, who finds that
the fat occurs as a fine granular deposit, or in droplets between layers of
fibrin ; it is sometimes to be seen floating in the sputum, which may
contain so much of it as to suggest an escape of lymph or of chyle from
the bronchial membrane.
Among the formed elements detected by the microscope in the casts
BRONCHITIS 31
sbould be mentioned bacteria, and occasionally "hsematoidin crystals,
Curschmann's spirals, and particularly Charcot Leyden's crystals and
eosinophilic cells.^
■ (ii.) The bronchi after death may contain casts in place, or imperfectly
solidified curdy collections ; or they may be quite clear and present
catarrhal mucus only. The membrane may be injected, or pale, as in
Biermer's case, in which the epithelial lining persisted under the cast. In
Kretschy's instance of an exceedingly rapid reproduction of the casts, the
bronchi affected were deprived of their epithelium, and it was evident
that the casts were not due to desquamation and transformation of cells,
but to a genuine outpouring from the blood-vessels or lymphatics.
Emphysema is almost invariably present. Cases are sometimes cut
short by intercurrent acute bronchitis or pneumonia. Traces of pleurisy,
recent or antecedent, are sometimes found. Tubercle is present in a
small proportion of the fatal cases. Model has recorded its occurrence
in 10 cases in a series of 21 cases of the afEection. Dilatation of the
bronchi has been very rarely found. Mader attaches some etiological
importance tp the coincidence of pemphigus with plastic bronchitis.
The diagnosis can only be made after the expectoration of some of
the coagula. The characters special to the latter, when recognised on
examination, should enable us to distinguish the case from cases of
intrabronchial haemorrhage and clotting, of diphtheria, of acute bron-
chitis, and of asthma.
Treatment of an effectual kind has yet to be discovered. The solu-
bility of the easts in lime-water, originally discovered by Dixon, which
strongly suggests the presence within the casts of a large proportion of
mucin, led Biermer to recommend the inhalation of atomised lime-water,
and a case of its successful employment has been reported by Walden-
burg.
The only other rational treatment which has been specially recom-
mended is the use of emetics.
The natural process of catarrh by which the plugs are loosened tells
in favour of the emollient action of an atmosphere of vapour. This
measure, strongly advocated by Walshe, has the advantage of being harm-
less ; and Dr. Ogle suggested that the steam might be medicated with
tar or with other stimulating ingredients. Iodide of potassium, internally,
was favourably spoken of in 1854 by Thierf elder and Wunderlich. Crear
sote, tar, turpentine have also been advocated ; and Biermer recommends
the free administration of mercury in acute cases.
The ordinary treatment of bronchitis is suitable for the generality
of cases ; and this applies also to the climatic indication, in spite of the
disappointing results which have been reported.
An important precautionary measure in connection with the severe
dyspnoea to which such patients are liable, is to provide, in all ascer-
tained or suspected cases of the disease, a readily available, if small,
1 For references on these and on various other points the writer is indebted to Professor
Hoffmann's valnahle article, " Die fibrinose bronchitis."
32 SYSTEM OF MEDICINE
supply of oxygen for immediate use in the event of a sudden difficulty
of breathing ; whereby time may be afforded for procuring more abun-
dant supplies, and for the adoption of other measures of relief.
Among the latter I would also suggest in future cases the trial of
two other rational methods of treatment. The local treatment of the
mucous membrane and the removal of the casts are clearly our first indi-
cations ; and we are now in possession of a method by which they seem
likely to be fulfilled, namely, the cautious intratracheal injection of oil
or of some mild solvent. These forms of treatment have not yet, so far
as I am aware, been resorted to in plastic bronchitis ; but I believe that
they may ultimately be found more successful, in promoting the expul-
sion of the casts and in obviating their recurrence, than any legs direct
method hitherto adopted.
Had we a free choice, our preference would be for some safe means
of speedily and completely detaching the bronchial cast ; and on apply-
ing the remedy we should be aiding nature by following her own method.
We might even improve upon the latter if the agent employed could
exert some healing action upon the damaged mucous surface. Oil may
prove to fulfil both requirements. Its non-irritating character, its power
of penetration, and its property of rapidly spreading over, and of pro-
tecting moist surfaces, even when used in small quantities only, are im-
portant recommendations. The intratracheal method suffers from the
lack of any means of regulating the course taken by the injection and
of ascertaining whether the latter comes more into contact with the
healthy mucous membrane or with the casts. In the case of oil this
is happily an unimportant objection: we can trust it to find its way
wherever any space offers. At the same time there remains, even in
connection with its sparing use, the important reservation that the air
way is already greatly obstructed, and that any form of injection might
aggravate the dyspncea.
Some support is given to this suggestion by the happy result obtained
in a case of diphtheria, where obstruction of the trachea with membrane
was set up after a previous tracheotomy. Creasoted oil (1 in 20) dropped
at intervals through the tracheotomy tube excited the desired amount of
cough, and enabled the membrane to be expectorated with remarkable
facility, so that the case ended in recovery.^
The notion of breaking up the membrane agrees less closely with
rational principles and with the lines of the spontaneous process of cure.
Whichever be the solvents selected for injection, their concentration has
to be slight ; their action will therefore be slow, and their bulk must be
relatively large. Moreover, their influence upon the diseased mucous
membrane itself is an anxious question. Above all, we cannot forget
that our object is the removal of the plug rather than its destruc-
tion. Integrity of the bronchial casts is an important help towards its
1 Favourable results in obstruction of the trachea by diphtheritic membrane, from the
introduction of creasoted oil through the tracheotomy tube, by William Ewart, M.D.,
F.R.C.P., and W. A. Hubert, L.K.C.P., M.B.C.S. Srit. Med. Journal, Nov. 27 1897
BRONCHITIS Zi
complete expectoration : its solution piecemeal might be a doubtful gain,
if the smaller branches of the cast were to be left behind.
Among the solvents at our disposal, lime-water would probably be the
one least open to objection, putting aside the serious risk connected with
the bulkiness of the injection. Lactic acid and the digestive ferments,
which Dr. Kolleston has suggested to me as alternatives, are perhaps not
equally suitable. Lactic acid has been credited with setting up pseudo-
membranous bronchitis when accidentally dropped into the trachea, and
its employment even in dilute solutions might be open to question. The
digestive ferments have been tried in diphtheria of the fauces with very
unequal results. Trypsin is free from the chemical objection which
may be urged against pepsin, and to a slighter extent even against the
vegetable ferments papayotin and papain, which act best, though not
exclusively, as does pepsin, in acid solutions. The results obtained with
papayotin in diphtheria were not encouraging. The favourable opinion
entertained by Rossbach has not been shared by other observers, the
solution of the ferment having been either too dilute to be effective, or,
when of a strength sufficient to destroy the false membrane, not free
from damaging effects upon the mucous surface. Papain itself, the more
powerful product yielded by the fruit of Garica Papaya (papayotin being
derived from the milky sap), has been recommended; but the success of its
employment, even with the advantage of the relative accessibility of the
surface to be treated, has not been such as to bring it into general use.
The effects of the intratracheal injection would need to be studied ex-
perimentally before it could be confidently recommended, since any
advantage might be outweighed by the slightest irritation set up in the
mucous membrane.
In conclusion, the suggestion of a local treatment of the affection,
whilst opening up a promising therapeutic prospect, may prove in the
event impracticable. In any case the attempt to carry it out should be
made with the utmost caution. The local treatment by bactericidal
agents and the hypodermic treatment by antitoxins are possibilities
contingent upon the results of future pathological discovery.
F. PUTKID BRONCHITIS
In the course of an inveterate purulent bronchorrhoea the expectora-
tion occasionally becomes putrid ; and to this condition in its worst form
the name putrid bronchitis has been applied. Putrid expectoration
occurs in bronchiectasis, and is commonly associated with destructive
pulmonary lesions. Instances of the uncomplicated kind are compara-
tively rare, the majority of the cases occurring as a late complication
of long-established bronchial dilatation.
If foulness of the expectoration in itself constituted a putrid bron-
chitis, we might group under that name, together with many cases of
bronchiectasis, all cases of pulmonary gangrene, of gangrenous tubercu-
lous phthisis, and of putrid empyema discharging through the lung.
VOL. V T\
34 SYST£M OF MEDICINE
All these, however, are removed into other categories by reason of the
prevailing importance of their extra-bronchial lesions. It is to the re-
maining cases, in which the bronchial trouble either stands alone or
largely predominates, that the name strictly applies. Although even
here the affection is seldom, if ever, absolutely primary, the pre-existing
catarrh, emphysema, pleuro-pneumonia, interstitial pneumonia, or fibroid
degeneration, whilst they account for a delayed expectoration of the
bronchial contents, do not in themselves explain their putrid decom-
position. The cause of the latter is intra-bronchial ; and two views have
been taken of its etiology. According to some bacteriologists putridity
is mainly due to the influence of micro-organisms, and the bronchitis is
secondary to the microbian invasion — a view to which we shall presently
refer. Other pathologists have regarded the bronchitis as the primary
event, and have sought to trace the sceptic process to definite structural
changes in the bronchial mucous membrane.
The association of gangrene with bronchiectasis had been dwelt upon
by Laennec. It was more definitely described in 1841 by Briguet as
affecting the terminations of the dilated tubes. Marfan has recently en-
deavoured to apply the same explanation to putrid bronchitis. He
assumes the existence of a primary gangrene of the brmichi which, he
contends, attacks the middle-sized and smaller tubes independently of
any bronchiectasis, or in association with but small terminal dilatations.
Additional evidence will be needed before this view can be regarded as
proved. Meanwhile it is significant that lesions of this kind have not
been noticed by other observers ; and that in one ease in which they
were specially looked for after death they were reported, by See, to have
been absent.
The view more generally accepted is that an ordinary bronchitis may
degenerate into the putrid form, which may or may not be a merely
passing phase, but cannot persist for long periods without progressive
damage to the bronchial structures and serious risk to life.
That putridity may be set up within the air-tubes by the inhalation
of septic matter is a possibility suggested by cases such as that of Tiede-
mann, in which this was brought about by a leakage into a pulmonary
cavity from a traction diverticulum. The attempt to attach the blame to
any individual variety of micro-organism is rendered difficult not only by
the number of microbes gaining access to the bronchi, but also by the
necessity of explaining this occasional failure of the protective mech-
anisms which normally succeed in repressing them even in cases, for
instance those of phthisis, apparently most liable to infection.
The bacteriology of the sputum has already grown to considerable
proportions. Among the numerous micro-organisms discovered in putrid
expectoration, several of which have been cultivated, J. Lumniczer has
succeeded in isolating a bacillus which perhaps may be the same as that
isolated by Bernabei, giving, after a few days, the same odour as the
sputum. Bernabei is inclined to regard putrid bronchitis as directly due
to the growth of the specific bacillus which he has described. Hitzig has
BRONCHITIS
35
likewise described two bacilli not unlike the bacilli coli communis, also
yielding a fetid odour.
The inhalation of oidium albicans was regarded as the cause of the
afEection in an isolated case reported by Eosenstein ; and Canali has
reported a case in which actinomycosis was either a cause or a compli-
cation.
The sputum sometimes presents a brownish discoloration ; it is in-
tensely fetid, either of gangrenous or of foul, sweetish odour. It sepa-
rates into three layers — an upper muco-purulent and frothy layer, a
middle translucent opalescent layer, and a lowermost dirty, yellowish,
granular layer containing the solid constituents which have been deposited.
As far back as 1850 Dittrich had described the plugging of some of the
bronchial tubes by small friable masses, varying in size from that of a
millet seed to that of a bean, made up of cellular debris, pus cells, granules,
oil globules, hsematoidin crystals, and various micro-organisms, including
the monas and cercomonas described by Kannenberg and by Streng, and
leptothrix pulmonalis. These "Dittrich's plugs " make their appearance
in the expectoration and, together with the intensely fetid odour, settle
the diagnosis. Fatty crystals (palmitic and stearic), volatile fatty acids
(valerianic and butyric), leucin and tyrosin, methylamin, ammonia, and
sulphuretted hydrogen are also found. Leptothrix pulmonalis occasions
a purple, violet, or blue discoloration of the sputum when treated by
iodine, a reaction observed by Virchow and by Gamgee. JafEe's observa-
tions of the presence of minute quantities of leucin and of tyrosin are of
interest in connection with the ferment obtained from the sputum by
Filehne and by Stolnikow, which they regard as analogous to pancreatic
ferment. The same observers confirm the observation that Dittrich's
plugs contain a substance striking blue with iodine.
Morbid anatomy. — Pathological changes special to the affection are
comparatively few. The post-mortem appearances are those of an intense
bronchitis and peribronchitis with pneumonic infiltration of the surround-
ing tissue. Pneumonic consolidation may be found extending over more
or less extensive patches ; but the greater part of the lung is in a state
of congestive and puriform oedema, and the bronchial glands are swollen
and soft. Some of the bronchi may show ulceration, or the mucous mem-
brane is softened in places and deprived of its epithelium ; or it may
become involved with the adjoining pulmonary tissue into genuine
gangrene. Cases of this kind have doubtless supplied Marfan with the
basis for his separate description of a gangrene of the bronchi. The
collateral changes are varied according to the morbid antecedents of
each case.
The symptoms accurately given by Dittrich consist in a sudden onset
of feverishness soon assuming a typhoid character, intense depression,
collapse, coma, and death. The attack is accompanied or preceded by an
equally sudden change in the sputum, from the habitual muco-purulent
type of chronic bronchial catarrh to the putrid variety. At the approach
of death expectoration diminishes and finally ceases.
36 SYSTEM OF MEDICINE
The long paroxysmal coughs peculiar to advauced excavating disease,
and the gushes of sputum of bronchiectasis are not witnessed ; but the
frequency of the cough and of the expectoration is often severe, particu-
larly in the pleuro-pneumonic and fibroid cases, in which the thoracic
excursions are much restricted. Fever of a remittent type is usually
present throughout the putrid stage; and it may be regarded as a meas-
ure of the septic absorption.
The diagnosis is based upon the clinical history and upon the nega-
tive results of a physical examination for the lesions of bronchiectasis,
of phthisis, and of pulmonary gangrene.
The prognosis varies according as the putrid condition of the bronchial
contents is grafted upon a simple chronic catarrh, or is combined with
deep-seated tissue irritation and overgrowth. In the first group of cases
recovery may take place after a few weeks, but relapses will be apt to
occur. In the second group the fatal tendency may be hastened by
catarrhal pneumonia, acute bronchitis, pulmonary gangrene, pleurisy,
metastatic abscesses (including cerebral abscesses), or endocarditis.
Treatment or bronchitis. — Some account has been given of the
treatment of plastic bronchitis : that of putrid bronchitis will be dealt
with under the heading of Fetid Bronchiectasis. The other varieties of
bronchitis will now be considered in turn from the point of view of the
abortive, the curative, and the palliative treatment ; and of prophylaxis.
I. Trachea-bronchitis. — (a) The abortive treatment of simple chest
cold, at its preliminary stage of coryza, has probably been more often
attempted than in any other ailment, and with a greater variety of
methods, most of which are based on diaphoresis and diuresis. The
suppression of the coryza has, however, been sometimes attempted by a
direct local action on the mucous membrane of the upper air-passages, or
by way of the nervous and vaso-motor system. The direct application of
powders or snuffs variously compounded of quinine, camphor, subnitrate of
bismuth, morphine and astringents, and the inhalation of stimulant cam-
phorated vapours, in which ammonia, carbolic acid, iodine, and essential
oils are prominent ingredients, have often been prescribed; and remedies
of this kind have at times been advertised as specifics. Of internal
medication two methods have been used — the tonic and the sedative; on
the one hand, liberal doses of quinine or, as strongly advocated by my
friend Dr. Isambard Owen, of the tincture of perchloride of iron ; on the
other, large doses of potassium bromide or some of the antipyretic reme-
dies recently brought into use, especially phenacetin.
The diaphoretic methods do not need any detailed description : they
include the traditional help of a Dover's powder, of hot grog, of blankets, of
the hot air or Turkish bath, or of the vapor bath, a medicated modifica-
tion of which has enjoyed some reputation in country districts. In
practising this homely and doubtless efiicacious method the patient stoops
over a vessel of boiling water in which are infused a quantity of selected
herbs, while the body is entirely covered with a sheet or blankets ; after
BRONCHITIS 37
a few minutes' inhalation of the aromatic vapour profuse perspiration is
induced, and a cure may result. The late Sir Andrew Clark's favourite
diaphoretic treatment was the hourly administration of ammonium citrate
assisted by warm drinks and warm wraps.
(6) The curative treatment. — If in spite of all efforts trachea-bronchitis
should advance, its rapid relief can only be secured by rest in bed, fluid
diet, warm drinks, and assiduous treatment beginning with a quickly
acting purge and combining diuretic and sedative action with the all-
important diaphoresis. A hot foot-bath with the addition of mustard, a
mustard poultice to the front of the chest, and the inhalation of steam
medicated with terebene, eucalyptol, or the compound tincture of benzoin,
are valuable adjuncts to the treatment. As soon as decided improvement
becomes manifest, iron and quinine should be substituted for the saline
remedies, and the ordinary diet resumed.
II. Simple acute bronchitis of the middle-sized tubes. — This
affection, though not usually dangerous, calls for judicious and active
treatment. The preliminary measures are directed to the relief of
congestion of the liver and of the alimentary canal by two to four grains
of calomel followed in an hour or two by a black draught. Meanwhile
arrangements are to be made for the regulation of the temperature of the
room, at a mean of about 66° F. ; for the occasional supply of steam, and
for its medication with eucalyptus, thymol, or wool-fir oil. The delay
before purgation may afford time for a foot-bath or for the application of
mustard leaves to the calves, to the upper sternum, and to the shoulders,
— or of dry cups over the back. Blisters are unnecessary, and may be
inconvenient during the subsequent perspiration. The patient should be
kept in bed and allowed to assume the position of greatest comfort,
probably one of slight elevation of the head and shoulders.
The more quickly diaphoresis can be obtained the greater will be the
hope of checking the spread of the bronchitis. The wet-pack is some-
times used ; but more generally the vapour-bath will be preferred, some
form of which may easily be improvised. Internally the administration
of acetate of ammonium, spirits of nitrous ether and of chloroform, with
syrup of squills or of red poppies, and infusion of senega, will be found
useful together with other means of keeping up the perspiration. In
more active inflammation nothing will relieve the tightness at the chest
and the hardness of the cough, whilst reducing arterial tension and
keeping the skin moist, better than antimony. Eelatively small doses
(not exceeding 8 rn,) of antimonial wine, combined with small doses of
Dover's powder, or of bimeconate of morphiue, the tendency of which is
likewise to relax arterial and bronchial spasm and to reduce active conges-
tion, afford much relief. A fluid diet of beef tea, milk, gruel, and tea of
moderate strength, belongs to this stage ; and, when administered warm,
adds much to the action of the treatment.
Expectorants. — Antimony, used as indicated above, undoubtedly
loosens the phlegm and promotes its expectoration ; but a different com-
bination is called for as soon as the initial discomfort has been allayed,
38 SYSTEM OF MEDICINE
and the skin, kidneys, and liver have been thoroughly brought into action.
It is now time for the direct expectorants — squills, ipecacuanha, car-
bonate of ammonium, and especially potassium iodide, which, in cases
presenting much spasm of the air-tubes, may be successfully combined
with the ethereal tincture of lobelia and spirits of chloroform.
Belladonna, one of the early remedies for bronchitis, has not perma-
nently held the position repeatedly claimed for it. This suggests that
it may not be equally suitable to all cases, and that in some instances the
adjustment of the dose may be a matter of unusual importance, as might
well happen with a drug possessing several powerful phy siological actions.
Ea«h of the latter has in turn been credited with the remarkable results
reported by observers. As the element of bronchial spasm in varying
degrees enters into all cases of bronchitis, belladonna would be more useful
where this factor more largely prevails ; as in the bronchitis of asthma and
sometimes of emphysema. In cases of this kind the remedy has, in my
experience, occasionally afforded more relief when worn as a plaster over
the chest than in the form of internal medication. Recently Dr. Sydney
Ringer has recalled our attention to its efficacy in bronchitis in reliev-
ing the incessant cough and checking the flow of mucus, which, whether
viscid and scanty or profuse and watery, is regarded by him rather as an
increase of secretion than as an inflammatory product. He prescribes
10 iTL doses thrice daily or of tener. On the strength of the same property
of checking the secretion he suggests its employment in ether bronchitis,
and in those cases in which aspiration of the chest is followed by a
profuse and sometimes suffocating amount of expectoration. The value
of belladonna is also advocated by Dr. Murrell, who points out that the
same advantages may be obtained by a solution of homatropine. Lastly,
Mr. Davies of Sherborne has dwelt upon its " magic " effects as an in-
halation, not only in asthma bat in acute bronchitis. He recommends
the use of 1 grain of the extract in \ oz. of water with Siegel's inhaler,
which has the additional advantage of moistening the atmosphere.
Inhalations.— To allay the irritable cough conium or chloroforin may
be added, in the steam inhaler, to representatives of the turpentine
group, such as thymol or eucalyptol; but, for the relief of spasm of the
smaller tubes, the dry inhaler ^ is usually found more effectual. It con-
sists essentially of a Woolffe's bottle, provided with a long inhaling tube
and mouthpiece, and packed with tow or loose cotton-wool steeped in
volatile principles which impregnate the air inhaled through the bottle.
The chief sedative agent to be used in all the mixtures for inhalation is
undoubtedly spirits of chloroform ; the other constituents may be freely
varied according to indications and to suit the patient's taste.
_ Emetics and bleeding, formerly much in vogue and regarded as almost
indispensable, are still not infrequently resorted to in some European
countries ; but they have long been neglected in England. Against
this neglect Dr. C. J. Hare has raised an energetic protest. He has
Kec.^m ^"'^^'' 'i«=="P"°'i of ""s apparatus by the writer, vide Clinical Journal, 21st
BRONCHITIS 39
specially insisted on the great value of emesis in acute bronchitis. In
addition to its general and hepatic action, it not only removes the
existing accumulation, but^ by its mechanical effect, squeezes out of the
mucous membrane a large quantity of the effete cellular and mucous
material, thus warding off the danger of an implication of the smaller
tubes. Its early employment before the onset of this complication would
be free from the risk of overtaxing the heart at a time when recovery in
great measure depends upon the cardiac energy being fully sustained.
Bleeding was prescribed early in the attack in bygone days. At the
present time it is not systematically used as a prophylactic, but is
reserved for any more urgent symptoms which might supervene. The
treatment of the catarrhal muco-purulent stage of this milder form of
bronchitis is practically the same as that of chronic bronchial catarrh,
and to that section the reader is referred.
III. Acute suffocative bronchitis of the adult. — In all cases of
severe bronchitis, or in any case of mild bronchitis threatening to become
severe, the first and all-important indication is to provide a ready supply
of oxygen. In a dilute form oxygen cannot fail to be of use even before
the onset of urgent dyspnoea ; and it cannot do harm. When dyspnoea
has set in, the amount of relief its undiluted administration wUl afford is
limited only by the difficulties of respiration. The objection that the air-
distended chest and the choked bronchioles often refuse to inspire has
led some authors to regard the treatment by oxygen as useless ; but this
should not discourage our efforts, for we must bear in mind how relatively
small is the bulk of oxygen which corresponds to the ordinary intake of
air : during the stage of greatest severity the inhalation of oxygen in some
form or other- should be maintained continuously. This method tends
to fulfil two needs, the pulmonary and cardiac. The excellent results
of the local treatment of cutaneous ulcers by an atmosphere of oxygen
as originally prescribed and practised by Dr. George Stoker would
lead us to expect a like beneficial action upon the mucous membrane.
But the second is perhaps the more important function : final success
in a protracted and severe struggle for breath is directly dependent upon
the vigour of the heart and upon the endurance of the respiratory muscles.
Any improvement in their effectual working will tend to increase the
subsequent intake of oxygen, and with it the cardiac and thoracic
energy.
Another therapeutic agent of importance is moisture supplied as
steam. Its application, however, needs care. An excess of steam, or
still worse, of the heat directly due to it and to the lamp or fire used to
raise it, is injurious. Steam and oxygen work well together ; the dryness
of the oxygen is tempered by the steam, and the depressing effect of the
vapoiir is relieved by the stimulation of the gas.
In the medicinal treatment three objects must be kept steadily in view
from the first, all being urgent : — (i.) to keep up the patient's strength ;
(ii.) to relieve the bronchial spasm as much as possible ; (iii.) to mature,
that isj to loosen the catarrh. A preliminary dose of calomel, followed
40 SYSTEM OF MEDICINE
by a saline, will do good ia every way ; but this is the full extent to
which any depressing treatment or methods involving exertion on the
part of the patient can be countenanced. The question of an emetic
should, however, be considered, and will need much judgment. This
remedy is one exclusively for. early employment. A large jacket poultice,
made as light as it is possible in front, is of distinct advantage.
Alcoholic stimulation. — Whenever, as in this dangerous malady, the
patient's safety lies in the correctness of the estimate we can form of his
vital powers as a guide to treatment, the worst evil would be a delusive
aspect of strength : the early and over-zealous administration of alcohol
entails this risk. Although in certain cases a need for alcoholic stimular
tion may seem to exist from the first, let -us bear in mind that alcohol
is not curative in suffocative bronchitis ; it should not be our first resort,
but be brought in rather as a powerful reserve to carry a desperate
position or to ensure its being firmly held. It is impossible, of course,
to lay down any general rule as to the time for the employment of
alcohol. The physician's estimate of the actual and prospective store of
cardiac energy in the individual case is the best guide.
Cardiac stimulants. — Meanwhile, however, cardiac stimulants are to
be administered without any delay. A mixture containing carbonate of
ammonium in sufficient amount, liquid extract of cinchona, iodide of
potassium (3 grains), and antimonial wine (3 %), with syrup of squills
and senega, may be administered every two or three hours at first. A few
doses of the following mixture may also be at hand for separate adminis-
tration : 15 to 20 drops of tincture of digitalis, 5 ni, of liq. strychninae,
20 WL of sulphuric ether or of aromatic spirits of ammonia, with compound
tincture of lavender or some other excipient. A dose or .two should be
prescribed against the risks of the night, and may be given at suitable
intervals or under special indications in the day.
The frequency of the administration of the expectorant is modified
according to the progress of the case ; and an occasional intermission of
it, with some cooling acid draught as a substitute, may be welcome to
the patient. Perceptible amendment should be noticeable within the
first twenty-four hours. In the worst cases it will not be a discouraging
result if the patient has done no more than maintain his strength.
Mechanically aided expiration.— As previously stated, the existence of
emphysema is a specially dangerous factor, and may call for something
more than medicinal treatment. I have found decidedly good results
from mechanical assistance to expiration; this may be carried out by the
attendant, who places his hands, well spread out, over the axillary bases
of the patient's lungs, and exerts very carefully timed pressures,
judiciously adapted to the phase of spontaneous expiration The
special appropriateness of this method rests on the fact that in emphy-
sematous cases an important part of the dyspncsa and impeded expiration
IS dependent upon the inherent weakness of the elastic fibre of the air-
sacs, over and above the mechanical obstacle produced within the small
tubes by the viscid secretion. The larger the share of the first of these
BRONCHITIS 41
two factors in tlie individual case, the greater will be the relief obtained.
The method may be tried in all cases, but requires to be used with
considerable discretion, and with due regard to the patient's feelings,
and the effect produced upon the depth and frequency of breathing.
A case cannot remain stationary at this stage ; if it do not improve
it is rapidly deteriorating, and at any moment, owing to progressive
congestion of the right heart, exhaustion may set in. Our duty is to
apply the only adequate remedy, venesection, without waiting for the
manifestations of extreme cyanosis, cold sweats, jactitation, and flutter-
ing pulse. Direct puncture of the right auricle is for obvious reasons
impracticable ; but the next best means to a sudden and ample depletion
of the cavity is to open the external jugular vein, from which 8 to 10 oz.
should be boldly abstracted. The benefit obtained is immediate and
considerable ; the duration of it will depend upon the degree of remaining
cardiac energy.
At this moment alcoholic stimulation, if not previously pushed with
improvidence, should prove a boon. This is also the time to bring every
cardiac tonic to bear, and to inject, if necessary, under the skin -j^th to
^ij5^th grain of strychnine. Oxygen, if it had been discontinued, should
again be inhaled. Any resulting rally in the cardiac and general energy
will afford a fresh opportunity for clearing the chest of loose mucus.
After a series of mechanically aided expirations the patient should be
encouraged to cough up the accumulations ; and, by repeating this
process, a good deal may be got rid of.
Very shortly after the bleeding — as soon as the respiration has been
attended to — the treatment of the right heart should be resumed. It is
all-important to save it from a return of its previous engorgement. A
liberal supply of india-rubber cups (six to eight) should be applied to the
chest simultaneously, utilising any positioi;! accessible without undue
disturbance to the patient ; and each of them should be reapplied in
rotation, so that the depleting action may be kept up for a relatively
considerable period. At the same time mustard leaves may be used to
the calves.
Good results may be obtained from this alternation of the cardiac and
of the respiratory treatment, and from the continued administration of
digitalis, bark, and ammonia. If all these fail, no other measures, such as
electricity in its various forms, will succeed.
The treatment to be followed in favourable cases, after recovery from
the asphyxial stage, is analogous to that which has been described under
a previous heading.
IV. Capillary bronchitis. — In infants and small children the same
dangers have to be reckoned with, but they are complicated with that of
pulmonary collapse, which is practically beyond our power of control, and
with the yet more uncontrollable pneumonic changes. Fortunately
the onset is often less rapid than in the acute suffocative bronchitis
of the adult, and affords a somewhat wider opportunity for treatment.
We are acquainted with three measures of primary importance:
42 SYSTEM OF MEDICINE
poulticing, emetics, and the combined inlialation of steam and of oxygen.
Poultices frequently renewed are specially useful in the small chests of
children, but it is essential that they should be light. The old practice
of the early induction of vomiting is probably the most effectual means
of saving life, and is not in itself a source of danger, the act being
relatively easy in small children. If the case be seen before the onset of
marked respiratory distress the strength will be quite equal to this
treatment ; and any sign of respiratory retraction of the thoracic base
should call for its immediate employment. For threatening pulmonary
collapse vomiting is probably the best, if not the only cure. It tends
to fulfil two essential needs, namely, the dislodgment of the mucus from
the bronchioles, and the inflation of the lobules by the deep inspirations
connected with vomiting. This is indeed the safest way of carrying out
the method briefly described in the treatment of the adult ; namely,
that of affording somemechanical assistance to the thoracicandpulmonary
movements. Tartar emetic is generally considered to be unnecessarily
depressing. A dose of sulphate of zinc, followed by relays of ipecacuanha
wine and of lukewarm drinks, is a prompt and effectual agent. Dr.
EoUeston has found good results from the hypodermic injection of apo-
morphine -^-^ gr. with liq. strychninse ni |. to prevent collapse.
Steam is readily supplied in sufficient quantity with the help of the
steam-tent. The latter should never form a complete investment, but
be limited only to the head of the bed, or to three of its sides. It is
dangerous to render the atmosphere oppressive. The inhalation of
oxygen needs special management in children. No attempt should ever
be made to place the tube into the mouth ; it is quite enough to direct
the stream of gas towards the nostrils. The first tendency to resist the
apparent interference is easily got over, and even infants take kindly to
the gas when they have experienced the relief it gives. The administra-
tion need not exceed more than' a few minutes at a time.
Medicinally the lines to be followed are, with some minor differences,
almost identical with those indicated for the adult. Belladonna is a
remedy not to be lost sight of in the capillary bronchitis of infants and
of young children. Dr. March, who is loud in its. praise, administers it
in minim doses every four hours for infants of six months old, but
reduces the dose on the slightest indication of improvement. He ascribes
its value to its stimulant action on the respiratory centres ; and this is to
be set against the objection sometimes made that it checks the action of
the skin and the bronchial secretion, both of which we have been taught
to promote.
In the capillary bronchitis of old persons neither emetics nor bleeding
are admissible undfer ordinary circumstances. In them treatment must
consist in careful feeding and 'stimulation, the saving of energy, the
promotion of expectoration, and constant and judicious nursing. Oxygen
is indispensable; andthe regulation of the temperature and of themoist-
ure of the atmosphere is also a point of much nicety.
Theoretically, mechanically aided expiration would seem to be
BRONCHITIS 43
specially indieated ; but the rigidity of the senile cartilages, although
not always so great as might be expected, is an apparent objection to
the method. Moreover, the other conditions are not quite simple, and
aged patients are often intolerant of any mechanical interference with
the thorax.
Among internal medicines the stimulant and balsamic expectorants
are specially appropriate, and, up to a certain point, successful. Quinine
or caffeine may have to be associated with carbonate of ammonia, although
they are not in themselves remedies for the cough. Digitalis and
strychnine must also be thought of, and called to aid if necessary.
Strong counter-irritation cannot be recommended without reservation,
and blisters are not advisable. A milder form of stimulation of the
skin may, however, be obtained from the application to the front of the
chest of flannel sprinkled with a drachm or two of terebene, which also
serves the purpose of an insensible inhalation.
As previously explained, capillary bronchitis at an advanced age is
a most fatal affection, and the chief aim and result of treatment may be
but a short prolongation of life.
V. Acute gouty bronchitis. — The special form of acute bronchitis
occurring in gouty subjects, sometimes as a precursor, at other times as
a phenomenon of recession of the arthritic trouble, is apt to be alarming
in its onset, and sometimes fatal. The special features are the degree of
the pulmonary congestion and the irregularity of the heart. The sudden
subsidence of these grave symptoms on the reappearance of the arthritis
has suggested the old treatment of applying mechanical irritation to the
great toe or other joints with a view to calling back the local inflam-
mation. If this attempt should succeed, pulmonary relief will frequently
follow ; but the remedy is an uncertain one. Moreover, the bronchitis
does not always stand in this relation to the articular paroxysms ; it may
be independent of them ; and it should be borne in mind that its gravity
is sometimes the expression of a complicating renal difficulty. The
indications in the more urgent stage are stimulation and derivation.
Among derivatives the most convenient are mustard foot-baths and dry
cups freely applied ; whilst a rapidly acting purge, such as calomel and
senna, should be followed up by mild doses of colchicum and of an
alkali, if no special contra-indication should exist.
VI. Symptomatic bronchitis. — The treatment of the bronchitis
associated with the infectious fevers, sometimes, as originally observed
by Laennec, throughout their course, does not often call for separate
attention. The management of the bronchitis of asthma and of hay-
fever, of mechanically induced bronchitis, of the bronchitis of phthisis,
and of that incidental to other parasitic diseases, will be considered in
other sections of 'this work.
VII. Chronic bronchitis. — The varieties of chronic bronchitis call for
some detail in their several treatment ; but for all of them our therapeutic
agents may be arranged under four main indications : (i.) the atmospheric
treatment, including the climatic; (ii.) the topical, including counter-
44 SYSTEM OF MEDICINE
irritation ; (iii.) the medicinal, and (iv.) the constitutional, including the
balnear treatment.
(i.) The value of climatic treatment is . demonstrated by the rarity of
chronic bronchitis aiiiong inhabitants of more temperate zones, and by
the improvement of invalids from the north whilst under the warmer
influences. For the larger number distant journeys are impracticable ;
artificial atmospheric conditions must therefore be devised. The essentials
in an artificial atmosphere are purity of the air-supply, freedom from
suspended particles, and due regulation of temperature and moisture.
A constant renewal of air without oscillations in the temperature, and a
proper supply of moisture — the dryness of artificially-heated air being
specially noxious in chronic bronchitis — are problems claiming earnest
attention in practical hygiene. Evenness of temperature and of moisture,
if they can be secured, will enable the chronic bronchitic to spend indoors
the periods of more wintry weather, whilst occasionally enjoying exercise
in the open during warmer spells. But this after all is merely protective
treatment, rather devised for safety than for cure.
(ii.) Topical treatment. — Atmospheric therapeutics aim at something
more than mere prophylaxis, and are needed in the more active stages.
Strictly, the term should be limited to the volatile agents, which can be
used to impregnate the air at the normal temperature. Members of the
turpentine group — terebene, pinol, cresol, eucalyptol, creasote, tar, car-
bolic acid, iodine, and the like — are all in some slight degree volatile ;
though not to the extent observed in the case of chloroform, alcohol, and
ether. Chloride of ammonium vapour, supplied by means of a special
inhaler, may be combined with some of the vapours enumerated. All
these substances may be inhaled in greater concentration when combined
with steam, and this method has the most beneficial effect. The prac-
tical means of volatilising carbolic acid and other agents at varying
temperatures have received much attention from Dr. Eobert Lee.
Reference has already been made to the dry inhaler by means of
which the more volatile, as well as a slight proportion of the less volatile,
substances can be directly inhaled with the inspiratory current. Lastly,
the fine atomising or nebulising sprays, for which some excellent appara-
tuses have recently been introduced, enable us to add to the list of the
atmospheric agents almost any of the non-volatile substances, provided
they be soluble. Common salt, bicarbonate of sodium, chloride of
ammonium, alum, tannin, and various astringents may be thus used as
required. A proportion of the spray probably passes the glottis, though
doubtless the greater part is condensed on the pharyngeal walls. To
this minimum introduced into the lung we cannot fail to attribute a share
in the marked benefit obtained; and we recognise in it a first step to-
wards the more vigorous topical treatment by intralaryngeal injections,
from which excellent results may be expected in a large number of cases.
The laryngeal insufftation of fine powders is less commonly used, aud,
owing to the ciliary function, it is doubtful whether their action would
extend much below the trachea itself.
BRONCHITIS 45
Counter-irritation is of undoubted value in most forms of chronic
bronchial catarrh, for the treatment of the exacerbations. Its usual
modes of application are the irritating liniments and applications, such as
croton oil, blistering, and the actual cautery. The latter is extensively-
used in France under the name of " pointes-de-feu," for the relief of cough,
of local pain, and of profuse expectoration. For the same objects blister-
ing is invariably useful. Inputrid bronchitis blisters may prove of decided
service in checking both the f cetor and the amount of the expectoration ;
and in those cases where, owing to iibrosis of the lung, Chaplin's treat-
ment by creasote inhalation is not successful, this mode of relief should
be tried.
(iii.) Internal treatment has regard not only to the immediate relief
of the bronchial trouble, but also to constitutional requirements. The list
of those drugs which are beneficial to the membrane need not be given
in full ; their active constituents are usually such as can be exhaled into
the lung, so as to take effect on the bronchial membrane. All the
derivatives of tar, and tar itself, the turpentines, and the balsams are
valuable in the treatment of chronic bronchitis. The more direct ex-
pectorants are also sometimes needed, especially when tonics, which are
otherwise to be preferred, act as a source of irritation. The prepara-
tions of conium, squills, ipecacuanha, senega, in combination with mild
salines, will prove of value in these irritable forms ; and if there should
be much spasm, morphine, belladonna, hydrocyanic acid, lobelia, and like
agents may be required. Of the internal remedies taking special
effect on the secreting function of the membrane four groups may be
especially mentioned : (a) Certain balsams, such as balsam of Peru, of
tolu, and the compound tincture of benzoin ; among the oleo-resins
copaiba, and among the tar derivatives creasote and guaicol (to be
taken in capsules). These remedies stimulate the membrane and tend to
diminish the catarrh. (&) Iodine in all its combinations, and particularly
as iodide of potassium, has the opposite tendency, and is especially useful
when the mucous membrane is dry and the expectoration scanty and
difficult, as in the so-called dry catarrhs, (c) Sulphur and the sulphides
have long enjoyed a reputation for the relief of suppurative conditions,
and their checking influence on the profuse muco-purulent discharge of
bronchorrhcea and the worst forms of catarrhs is striking. When this
can be combined with the tonic effect of a bracing air and with thermal
treatment, results may be obtained such as have established the reputa^
tion of Harrogate in this country; and of Eaux Bonnes, Cauterets,
Luchon, Aix-les-Bains, and other stations abroad.
At all thermal stations patients are subjected to a limited course of
treatment by baths, mineral-water drinking, and exercise in the open air.
When sulphur is administered to a patient treated at home the same
attention should be given to a limitation of the period of administration,
lest irritability of the mucous membrane or irritability of the skin should
be induced. Lastly, (d) cod-liver oil, when tolerated, is an invaluable
remedy.
46 SYSTEM OF MEDICINE
(iv.) Constitutional treatment. — As a rule, a slightly purgative plan is
of great value ; indeed this is one of the favourable aspects of the treat-
ment by sidphur. Various mineral waters may be used, and, with the
same object, patients are sent to various medicinal springs.
The cardiac indication is usually obvious. The right heart needs not
only to be cured of its dilatation, but if possible toned up. Strychnine,
digitalis, strophanthus are thus direct agents in relieving chronic
bronchitis by reducing the pulmonary congestion. We should not for-
get that an excellent way to strengthen the right heart is to strengthen
the left. In chronic bronchitis shortness of breath leads to muscular
inertia and atrophy ; for this there is a remedy in oxygen inhalations, or
in their equivalent, systematic purposive hyperpnoea. Patients would
gain much by training themselves to breathe to the utmost mechanical
advantage, and by cultivating general muscular exercise, at first purely
passive, but ultimately active. A general recovery of neuro-muscular
energy, other circumstances being favourable, will act most beneficially
on the chest through the great improvement in cardiac strength. For
artificial methods of lung gymnastics the reader is referred to the chapter
on Aerotherapeutics in the first volume.
Lastly, haematinic remedies are wanted in a large number of cases ;
this is a special indication in the groups of protracted muco-purulent
and of all severe purulent catarrhs ; and these are also the cases which
most benefit under cod-liver oil. The administration of iron is not to
be limited to those patients whose ansemia and wasting are obvious ;
iron and quassia, or some other bitter, and particularly cinchona, are not
only well tolerated, but of direct value as stimulants to the relaxed and
congested bronchial membrane in cases where venous embarrassment
gives rise to a deceptive appearance of plethora.
In all cases of inveterate catarrh, but particularly in those which
from their severity deserve the name of bronchorrhcea, a warm and
equable climate during the winter is indispensable. Various sheltered
stations have been recommended in this country, such as the Undercliff,
Torquay, Falmouth, Ilfracombe, Minehead, the Scilly Isles, and others.
Some patients will derive great benefit from a winter's residence in the
bracing atmosphere of Thanet. Nevertheless, whenever this is possi-
ble, the Mediterranean seaside resorts are to be preferred ; and among
them the more sheltered, such as Mentone, San,Remo, Alassio, Rapallo,
the Eiviera di Levante,, Capri, Malaga, Corfu, Egypt, and suitable re-
sorts on the North African coast. This large subject is fully treated
in the article on " Climate in the Treatment of Disease " in the first
volume.
Unless the membrane be protected from irritation for prolonged
periods no lasting improvement in the condition can be looked for.
Permanent residence for some years in a favourable district is the only
really curative treatment ; but this may with benefit be combined with a
summer visit to one of the hot sulphur springs ; or to Ems, Soden, or any
of the saline muriated and carbonated springs, suitable for the individual
BRONCHn^IS 47
case. The opportunities for permanent residence in eligible climates
are widening year by year.
Prophylaxis. — (i.) Prophylactic measures between the attacks. — 'No
risks should be incurred by the chronic bronchitic patient. Sudden
changes of temperature, as at sunset, or from walking out of heated rooms
into the cool of the night, or into cold and damp buildings after exposure
to the sun, cold winds, dampness of air and of soil, dusty localities and
occupations, great variations in the amount and thickness of clothing,
chill from damp underclothing after perspiration, and, almost above
all, inactivity of the liver should be sedulously guarded agaiast. The
merely passive avoidance of obvious dangers is, however, a lame policy ;
we should be prepared for those which are apt to fall upon us unawares.
Bracing resorts help us in this by toning up the nerves and tightening
the membrane. A great deal can be done by the patients themselves in
utilising the opportunities afforded by protective climates for the com-
bined development of muscular energy and of respiratory activity. It is
to be observed that vesicular emphysema is almost entirely a passive
change, not brought about directly by voluntary expansion of the chest.
In my opinion, systematic and graduated respiratory exercises, though
they may stretch, tend to strengthen rather than to weaken the elastic
fibre ; and since they are based upon the performance of effective expira-
tions, they would appreciably relieve the passive emphysematous dis-
tension. Much of the hepatic and of the local bronchial congestion
will also be corrected by the greater activity of circulation thus initiated ;
and increased oxygenation will promote the growth of a less irritable
and delicate epithelium.
The same tonic system can profitably be applied to the skin by means
of a well-planned course of rubbing, bathing, and douching. All these
measures need long perseverance before their beneficial effects can be
fully secured ; but their sedulous employment will bring with it an
almost assured reward.
(ii.) Prophylaxis in early bronchial delicacy. — Yet more important is
the subject of prophylaxis in infancy and childhood. The bronchial tubes
are apt to suffer early in life ; worst of all is the mischief arising from a
severe attack of whooping-cough. Inherited family tendencies may in
some children point also to a future liability to bronchitis. Moreover, in
the case of all children, and especially of town-bred children, we have to
deal with the liability induced by climate. All infants in this country,
but in special and varying degrees the offspring of delicate, asthmatic,
bronchitic, and gouty parents, stand in need of the help of preventive
measures. If this were thoroughly understood and our practice regulated
accordingly, a vast saving of life and health would be secured. The pro-
phylactic plan suggested can be summed up in one word. It is a
" hardening" plan carried out with vigilance and discretion ; its essentials
lie in the management of respiration and atmosphere, of temperature, of
clothing, and of the skin.
Eespiration and the atmosphere. — It is not sufficiently recognised
48 SYSTEM OF MEDICINE
that the bronchial tubes and lungs are constructed for the air we live in,
and conversely. Specially strong is the prej udice against night air, which
in itself is exceedingly beneficial. The innocuousness, for the bronchial
membrane, of the higher temperatures of atmospheric air needs no
demonstration ; the innocuousness of extremely cold air, though it is not
usually brought home to us, is evidenced by the ease and comfort with
which respiration is carried on in arctic temperatures. Much of the
objection to night air is generally directed against the dampness of it; but
moisture need not in itself be detrimental ; indeed, as we have seen, it is
often used as a remedy. Nevertheless any of the normal atmospheric
peculiarities may cease to be beneficial and may be turned into a source
of irritation by a systematic substitution of artificial atmospheres for
that provided by nature.
The great prophylactic method is to see that infants and children
live and sleep in the open air as much as possible during the day, and
enjoy as much free ventilation from the outer air at night as may be com-
patible with prudence. The full measure of this fresh-air treatment may
be attained by degrees only ; but it should be persistently aimed at. In
towns this rule is of much greater importance than in the country. The
extraordinary ainount of health enjoyed in London by the children of
the poor, in spite of so much that is depressing, is in great measure to
be explained by the out-door life they are obliged to lead in their dark
streets and alleys.
The skin and temperature. — More serious still than the neglected
training of the aerial mucous membrane is the neglected education of the
heat-generating function in relation to the skin. An excessive amount
of clothing by day and by night, with wraps round the neck and wool
next the skin, excludes too completely the oscillations of the outer
temperature which should act as stimuli to the cutaneous surface. More-
over, the constant moist heat which is thus maintained tends to make
the skin delicate and to depress its power of reaction. Flannel under-
wear is the best and safest for subjects too feeble to keep up their body
heat ; and it is an invaluable provision against unusual variations in the
atmospheric temperature or in cutaneous action, as in athletics, cam-
paigning, rapid journeys through extremes of climate ; but its constant
use is not part of the systematic training of the skin. In healthy children
and adults it is as a rule superfluous at night, although indispensable for
children suffering from rickets, restlessness in sleep, or enuresis. When it
is worn during the day the outer garments should be made proportionately
lighter. To pile up heavy outer clothing over thick flannel under-
garments is bad hygiene, and cannot fail to weaken growing children.
Hygienic treatment of the skin. — Active means of promoting a
vigorous habit of the skin should not be neglected. Massage is almost
superfluous in children, whose life is perpetual movement. The chief
indication is the sponge bath or the douche and rubbing. Pew children
will fail to take kindly to the cold bath if trained with suificient tact to
its use. As a rule, there will be no difficulty in obtaining the glow of
BRONCHITIS 49
cutaneous reaction after the bath, by friction with a coarse towel. In
some constitutions the cutaneous circulation is slow to recover itself, and
some special modification of the bath is called for. An essential pre-
caution is the application of plenty of warmth immediately before and
immediately after the cold sponging. The child may be placed for a
minute or two into a warm bath, transferred to another bath for cold or
tepid sponging, and again put into the warm bath for an equally short
time, before towelling. An alternative, and in some ways a better method
is to sponge the surface rapidly with warm water whilst the child is
standing in a warm- foot-bath. After the cold sponging he is to stand
again in hot water whilst the body is being rubbed dry. The latter
method is extremely simple and very effectual. Adults also who other-
wise might be debarred from the boon of the cold bath are in this way
enabled to resort to it with perfect safety and with enjoyment; In
nurseries a bright fire should be burning before the cold morning baths
are given. The daily cold aifusion is of the greatest value as a direct
protective against " catching cold " ; and its systematic use must be
- reckoned among the most powerful helps in training a habit of resistance,
and of ultimate indifference to all ordinary bronchial or cutaneous
impressions, in those whom inherent debility or inherited predisposition
would otherwise have exposed to ever-recurring risks of bronchitis.
Wm. Ewakt.
eefekences
Bronchitis
Consult also Biermer (1867, u. infra) and Eiegel (in Von Ziemssen's CyalopsBdia,
vol. iv.) .
1810. — Badham. Inflammatory Affections of the Mucous Membrane of the Bronchise.
London.
1820. — Hastings. A Treatise on the Inflam. of the Muc. Menib. of the Lungs.
.1835. — Bamadgb. Asthma, its Species and Oomplications. London.
1837.— Stokes. A Treatise on Bis. of the Chest.
1844.— Fauvel. " Sur la bronchite capillaire suffocante," Mdmoires de la soei£t6 midi-
cale d'observation de Paris, t. ii.
1844. — Legendbe and Baillt. "Rech. nouv. sur quelques maladies des poumons chez
les enfauts," Arch. g€n. de mddecine.
1846. — Beheend. " Toux periodique nocturne des enfants," Gaz. mM. p. 133.
1846. — Beaniss. "Toux periodique nocturne des enfants," Gaz. m^d. p. 353. '
1849. — Fdchs. Die Bronchitis der Kinder.
1850.— Gairdnee. On the Pathological Anatomy of Bronchitis, etc. Edinburgh.
1854. — Lasegue. " Hysterical Cough," Arch. gen. de m4decine, pp. 513-531.
1855. — BiEBMER, A. Die Lehre vom Auswurf.
1860. — FoTHERGiLL. DubUn Quarterly Journal.
I860.— Hyde Salter. On Asthma : its Path, and Treatment, 2nd edit. 1868.
1862.— Fuller, H. W. Diseases of the Chest.
1864. — Waldenburg, L. "Die loc. Behandl." etc., Lehrbuch der resp. Therapie, 2nd
ed. 1872.
1865-67. — BiERMEB. " Krank. der Bronchien- und Lungen-parenchyms," Virchow's
Sand, der spec. Path, und Therap. t. Abth. 1.
1869. — Hayem. "T)ea3ioTichites," These d'agr4gatio7i.
1869. — Barth and Blachez. " Maladies des bronches," Diet, encycl. des so. mtfd. Ifere
serie, t. x. et xi.
VOL. V E
50 SYSTEM OF MEDICINE
1871.— KoBBBTS, Fkedebick. " Bronchitis," Russell Reynolds' System of Medicine,
vol. iii.
1873-74. — Leeert. Klinik der Brustkrankheiten.
1878. — Greenhow. On Bronchitis.
1879. — Paul, Consxantin. "Traitement de la bronchite arthrjtique," Ann. de lasoc.
d'hydrol. t. xxiv.
1881.— March. " Belladonna in Bronchitis," Med. Times and Gazette, 1881, p. 320.
1882. — FoTHERGii-L. Chronic Bronchitis.
1883. — Hare, Chas. J. Good Remedies out of Fashion.
1883. — CuRSCHMANN. " Usber Bronchiolitis Exudativa nnd ihr Verhaltniss znm
Asthma," Deutsches ArchivfUr klinische Medizin, Bd. xxxii.
1884. — Lasegue. tltudes medicates, t. ii.
1884. — Marfan. " Obs. pour servir au pronostic de la bronchite chez les bossus," Areh.
g6n. de midecine, Sept.
1884. — Lee, Kobekt J. Antiseptic Inhalation and the best Method of conducting it.
1885. — Cantani. " La broncost^nosi catarrale diffusa," Klin. Centralblatt, p. 608.
1885-6. — See, G. Bronchites aigues ; Bronchites chroniques.
1886. — Troup, F. Sputum, its Microscopy, etc. Edinburgh.
1886.— Mackenzie, Hunter. A Practical Treatise on the Sputum.
1886.— Davies. Brit. Med. Journ. 20th March, p. 542.
1887. — CuRSCHMANN. " Some Remarks on the Spirals occurring in Bronchial Secretion,"
Oeutsches ArchivfUr klinische Medizin, Bd. xxxvi.
1887. — Fraser. " Dyspnoea — especially on the Dyspnoea of Bronchitis and the Effects
of the Nitrites upon it," The Lancet, 1887.
1887-8.— BuAULT. " Toux amygdalienne," Arch, de laryngologie et de rhinologie, i.
pp. 154-177.
1888. — Ferrand. Legons din. sur les formes et le traitement des bronchites. Paris.
1889. — MuRRKLL, Wm. Chronic Bronchitis and its Treatment.
1889. — EwART, Wm. The Bronchi and Pulmonary Blood-vessels, their Anatomy and
Nomenclature. London,
1890. — Regnault and Sarlet. "Bronchite mfliniteuse," jlram. d'hygiene publ. ; also
Marseille midical, 1891.
1890. — Pansini. Arch.f. path. An. und Phys. Bd. cxxii. Hft. 3.
1891.— Clark, Sir Andrew. "The Barking Cough of Puberty," Med. Soc. Trans, vol.
xiv. p. 142.
1891. — Fagge and Pye-Smith. Text-Book of the Principles and Practice of Medicine.
1891. — Fox, Wilson. Diseases of the Lungs and Pleura. Loudon.
1891. — Leyden. " On Eosinophile Cells in the Sputum of Bronchial Asthma," Deutsch.
med. Woch. 17th Sept.
1893. — Marfan. " Maladies des Bronches " (in Traitg de mid. par Charcot, Bonchard,
et Brissaud) . Paris.
1894. — Gerlach. "The Mode of Production of Cursehmann's Spirals and of the Con-
voluted Urinary Casts," Deiitsches ArchivfUr klinische Med. Bd. liii.
1894. — Hamilton, D. J. Text-Book of Pathology, vol. ii. p. 72.
1895.— Lancereaux. " Les bronchites," Gaz. des hop. p. 108, iii.
1895.— Beaumetz, Dujabdin. " Trait, des bronchites aigues," Bull, de Thirap. briv.
Ter. 15.
1895. — Stoker, G. Transactions of the Annual Meeting of the British Medical Associa-
.tion, London, 1895; and Clinical Society's Transactions.
1896.— Hoffmann. " Die Kkten. der Bronchien," in Nothnagel's Spec. Path, und Ther.
vol. xiii. 3 Theil, 1 Abth.
1896.— Ringer, Sydney. "Belladonna in Bronchitis," Brit. Med. Journ. vol. ii.
p. 1543.
1896. — MuRRELL. " Belladonna in Bronchitis," Brit. Med. Journ. vol. ii. p. 1611.
Plastic Bronchitis
Consult also Riegel'a Bibliography (v. Ziemssen's Cyclopedia) , that by Dr. Samuel
West {Practitioner, vol. xliii.), and that by Professor F. A. Hoffmann (Nothnaeel,
xiii. 3,1). ^ *
1697.— Clarke, Robert, and Lister, Martin. Phil. Trans, xix. p. 779.
BRONCHITIS 51
1783-1784.— Dixon, Joseph. "History of a Case of Angina Polyposa," Med,. Com-
■mentaries,
1836.— Cazeaux. " Bronchite couenneuse aigue," Bull. soc. anat. p. 337.
1847. — Van Meeebbck, " Concretions broncMques ramifie'es," Gaz. hebd. de m4d. et de
chir. p. 263.
1850.— DiTTKiCH. Ueber Lungen^Brand, etc. Erlaugen.
1852. — Babth. Bull. soc. anat. p. 103.
1854. — Peacock. Path. Soc. Trans, vol. v.
1854. — ^Thiekfeldek, Th. " Bronchitis crouposa," Arch. fiir. physiol. Heilk.
I860.— Ogle, J. W. Path. Soc. Trans, vol. xi.
1865. — Haldane. " Fibrinous Casts of the Bronchi," Edin. Med. Jour. p. 657.
1869. — Waldenburg. Berlin, klin. Woch. p. 657.
1870. — TuCKWEiiii. " Casts of the Bronchi," Path. Soc. Trans, xxi.
1873. — Peacock. " Moulded Coagula after Haemoptysis," Path. Soc. Trans, xxiv. p. 20.
1876. — Lucas-Championniere. "De la Bronchite pseudo-membraneuse chronique,"
Thise de Paris, No. 53.
1877. — Bebnouilli. " Bronchitis crouposa," Deutsches Archiv f. klin. Med. xx.
3 u. 4, p. 363.
1878. — FbjLnkel. Charite Annal. Bd. v.
1878. — Degener. Schmidt's Jahrb. Bd. clxxix. S. 168.
1880.— West, Samuel. " Blood Casts in the Bronchi," Brit. Med. Jour. i. p. 282.
1880.— Streets, Thos. H. Amer. Jour. Med. Soc. Ixxix. p. 148.
1881.— RossBACH, M. J. " Papayotin, ein gutes Losungsmittel fiir diphth. nnd croup.
Membranen," Berliner klin. Wochenschrift, 1881, No. 10.
1881. — Prambergeb. " Fibrinose Bronchitis." Graz.
1882. — Jager. Klin. Centralblatt.
1882.— Mader. Wiener med. Woch. No. 11 ff.
1882. — RossEACH. " Ueber die Schleimbildung," etc.. Festschrift zur dritten Saecular
Feier der Alma Julia Maximiliana. Wiirzburg.
1883. — Wolf. Dissertation. Wiirzburg.
1883. — EscHERiCH. Deut. med. Woch. No. 8.
1883. — ViEBORDT. Berlin, med. Woch. No. 29.
1883.— Adseeson. Yirch. Jahresbericht, xi. S. 643.
1884. — MoLLKB. Schmidt's Jahrb. cciv. S. 162.
1885.— Stumpf, Ludwig. "Klin. Beob. iiber Diphth.," Deutsch.Arch. fiir klin. Med.
Bd. xxxvi. S. 73.
1885. — Rossbach:, M. J. " Ueber die Wirkung des Papayotin, etc., eine Entgegnung,"
Ibid. S. 339.
1885. — Sttjmpf, Ludwig. " Entgegnung auf die Bemerkungen Prof. Kossbach's iiber
die Wirkung des Papayotin bei Diphth.," Ibid. S. 586.
1885.— Mazzotti. Klin. Centralblatt, S. 264.
1886.— Sax. Klin. Centralblatt, S. 614.
1886.— Staek. " Zur Casuistik der Bronchitis Fibrinosaf ' Berlin, klin. Woch. S. 221.
1886. — Jaccoud. " Broucho-alveolite flbrineuse hemorrhagique," Clin, de la Piti€, ii.
1886. — West, S. " Plastic Bronchitis " (with bibliography), Prajititioner, vol. xliii.
1887. — Regard. These de Berne.
1887. — Letellibb. " Broncho-alveolite flbrineuse hemorrhagique," These de Bordeaux,
1887.
1889.— Caussade, G. Bull. Soc. Anat. p. 371.
1889.— PicCHiNi, L. Archiv Ital. di din. med. Ap. 1889i
1889.— KisOH. Wiener med. Presse, No. 33.
1890. — Model. " Bronchitis fibrinosa," Dissertation, Freiburg.
1890.— ROQUES. "Un cas de bronchite pseudo-membraneuse," Provence midicale,
Sept.
1892.— Koch, R. Peiersb. med. Woch. S. 83.
1892.— Hampeln. Ibid. S. 336.
1892.— Feitzsche. "Ueber bronchitis fibrinosa," Ref. Schmidt's Jahrb. B. ccxxxvii.
p. 219.
1892. — Bebgengeun. Petersb. med. Woch. xvii. p. 145.
1892.— Deuenee. Ibid. " Tracheal false membrane after use of lactic acid."
1893. — Marfan. " Les bronchites pseudo-membraneuses," Traits de m4d. p. 337.
1893. — Beschobnee. "Ueber chron. essent. fibrinose Bronchitis," Volkmann's
Sammlung, No. 73.
52 SYSTEM OF MEDICINE
1893.— Edgreen. Klin. Centralblait, S. 662.
1893.— DuTEUiL. Ibid.
1893. — SiTTMANN. "Papain bei Erkrk. des Magens," Miinch. med. Woch. No. 29,
p. 548.
1894.— OsswALD. " Untersuch. iiber das Papain (Beuss)," Ibid. 1894, No. 34.
1894. — Fedoroff. Ref. in Gazette des hop.
1895. — KocK, Paul. " Ueber Bronchitis fibrinosa chronica,'' Wien. med. Woch. xlvii
1895. — Magniaux. Recherches sur la Bronchite membraneuse primitive. Paris.
1896. — Hoffmann, F. A. "Die Krankh. der Bronchien," Nothnagel's Spec. Path, und
Therapie, Bd. xiii. 3 Theil, 1 Abth.
Putrid Bronchitis
Consult also the Bibliography of Bronchiectasis, and Lebert's work (v. infra).
1837. — Laycock. "Two Cases of Pulm. Dis. with Remarks," London Med. Gaz. Dec.
1861. — Bamberger. Wiirzb. med. Zeitsch. ii. S. 333.
1863. — Empis. "Du cat. bronch. pseudo-gangreneux," Gaz. des hop. xxxvi. p. 253.
1865. — Gamgee, a. Edin. Med. Joum. March, i. pp. 807, 1124.
1865. — ^Laycock. " On fetid bronchitis," Edin. Med. Journ. p. 901.
1867. — RosENSTEiN. Berl. klin. Woch.
1867. — Leyden and Jaffe. Deutsch. Arch.f. klin. Med. Bd. ii. S. 488.
1869. — Loos, E. Ueber putride Bronchitis. Berlin.
1871-8. — Traube. Gesamm. Beitrage, ii. S. 558 et seq.
1873. — Lancekeaux. Arch, de mid.
1874. — Lebert. Klinik der Brustkrankheiten, i. S. 102.
1875. — TiEDEMANN. Dcutsch. Archivfiir klin. Med. Bd. xv.
1878. — Kannenberg. Chariti-Ann.
1878. — Leyden. Virchow's Arch. Ixxiv. S. 414.
1881. — See. Gaz. mid.
1883.— Leviez. " De la bronchite fetide," These de Paris.
1887. — Lachee. Munch, med. Woch. No. 33.
1889.— Lumniczer, J. Ref. Klin. Centralblatt, S. 51.
1890. — Lancerbaux. Otin. mid. de la Pitii, 3e serie.
1890.— Rendu. Clinique midicale.
1890.— LoEEiscH and Rokitansky. Cent. f. klin. Med. No. 1.
1891.— Thirolodc. " Dilatation des bronches," etc., Soc. Anat. 13 mars.
1891.— KoHLER and Bardeleben. Berlin, klin. Woch. Feb. 9.
1891.— TissiER, P. "Revue criticine sur la bronchite fe'tide," Ann. de mid. sclent, et
prat. Sept. 16, Oct. 7, Nov. 18.
1893.— Marfan. "Gangrfene (j^s bronches," Traiti de mid. par Charcot, Bouchard, et
Brissaud, t. iv. p. 359.
1894.— Bernabei. "Ueber eine durch specifischen Bacillus erzeugte fotide primare
Bronchitis," Boll, delta soc. Lancisiana xiii.; Virchow's Jahresbericht. ii. d.
148. ^
1895.— HiTziG. "Beitrage zur Aetiol. der putriden Bronchitis," Virchow's Archiv,
cxli. p. 28.
Malarial and Parasitic Bronchitis
Consult also Renon (v. infra) on Aspergillosis, and recent periodicals on Actinomycosis.
1857.— Bodgard. " Malarial Bronchitis," Journ. mid. de Bruxelles.
1863-86.— Leuckart. Parasiten des Menschen.
1869.— Cobbold, T. Spencer. Entozoa, etc.
1878.— Bollinger, O. Ueber eine neue Wild- und Rinderseuche. Miinchen.
1878.— KERBF.RT Zoolog. Anzeiger, S. 271-273; also (1881) Arch, fur mikr. Anat. xix
S. 529-578.
1880-81.— Manson, Patrick. Chin. Oust. Gaz. Med. Rep. No. 20; also No. 22 (1881).
1880.— Baelz. Centralblatt f. d. ges. med. Wi.ts.
1882.— PoNFicK, E. Die Actinomykose des Menschen.
1883.— Manson, Patrick. Lancet, vol. i. p. 532.
BRONCHIECTASIS 53
1883.— GiNTRAC. Diet, de mid. et chir. prat. v. p. 669 (mentions Malarial Bronchitis) .
1887.— Israel. "Eiu Beitrag zur Patliogenese der Lungen Actinomykose," Arch. f.
klin. Chir. Bd. jcxxiv.
1888. — Yakimotitch, N. N. Actinomycosis of Lung and Pleura, Vratch.
1890.— Graesek. "Deber einen Fall von Malaria Bronchitis," Berl. klin. Woch.
Oct. 6.
1890.— Schmidt. Ziegler's Beitrage zur path. Anat. und allgem. Path. viii. S. 173
(thrush found in bronchi of five children after death).
1892. — Illich. Beitrag zur Klinik der Actinomykose. Wien.
1892. — Yamagiwa, K. " Ueber die Lungen Distomen Kkht. in Japan," Virchow's
Arch, cxxvii. S. 446-456.
1893.— Manson, Patrick. " Distomum Eingeri vel Pulmonale," in Davidson's Hygiene
and Bis. 0/ Warm Climates. Edinb.
1895.— Ward, Hy. B. "The Asiatic Lung-distome in the United States," Med. News,
March 2.
1897. — Renon. &tude sur V Aspergillose chez les animaux et chez I'homme.
W. E.
BEONCHIECTASIS
Bkonchial dilatation, when slight or limited to one tube, may escape
clinical observation; usually it involves several of the cartilaginous
bronchi, and then gives rise to unmistakable symptoms, constituting a
clinical disease to which the name " bronchiectasis " is appropriated.
The name " bronchiectasis " is also in common use in. descriptive
pathology ; but the affection is far from presenting in its anatomy that
uniformity which we recognise in its clinical symptoms and signs.
Walshe says : " The conditions of disease to which dilated bronchi may
form an adjunct are : bronchitis, acute and chronic ; emphysema ; con-
striction of the tubes themselves ; acute and chronic pneumonia; cirrhosis
of the lung ; phthisis, cancer, and chronic pleurisy with contracted side."
So great are the differences between the various pulmonary lesions thus
apt to be associated with it, that we regard bronchiectasis as a structural
change which may result from a variety of morbid processes, rather
than as a definite and independent pathological product.
Clinically speaking, bronchiectasis is a chronic affection implicating
bronchi of good size ; to this it is that the literature of the subject almost
exclusively refers, and that the present article is chiefly devoted. In
its anatomical sense the name is more comprehensive : it applies to the
secondary and slighter dilatations as well as to those which are some-
times described as primary ; and it belongs with equal right to air-tubes
of all sizes. In a complete clinical nomenclature the affection as it
occurs in the bronchioles should not be left out, and we should recognise
a bronchiolar dilatation or bronchiolectasis, as well as a bronchiectasis ;
both varieties occur independently,- and are clinically important. With
a view to mark the distinction between them, which has not been much
dwelt upon, they will be described under separate headings.
In another group, that of the secondary bronchiectases, tubes of inter-
54 SYSTEM OF MEDICINE
mediate size are commonly involved. This variety does not possess the
same clinical interest, and our references to it will be incidental only.
I. Capillaky bbonchiectasis, ok bkonohiolectasis (including the
so-called " Acute bronchiectasis"). — This type of bronchial dilatation
stands out in clinical contrast with the ordinary variety, while its distinct
pathological features throw light upon the pathology of bronchiectasis
in general. In its most striking form it occurs in children as an acute
process ; and as such it was described by Andral, Rilliet and Barthez,
and others as " acute bronchiectasis." The post-mortem recognition of a
dilatation of the small tubes in connection with certain clinical symptoms
noted during life led observers to infer that in other cases also, which
presented the same symptoms but ultimately ended in recovery, the same
lesions had existed without proving fatal ; and it is upon this assumption,
which is probable enough but not capable of demonstration, that rests
the current belief that children may completely recover from acute bronchi-
ectasis. Granting that recovery may be possible, it may in a proportion
of the cases be but partial ; and in these the dilatations persisting in some
portions of the lung may lapse in the course of years into the common
bronchiectasis of the larger tubes.
In the adult localised dilatations of bronchioles are frequent in chronic
bronchial catarrh, and may follow an acute purulent bronchitis ; but, so
far as I have observed, they do not extend to the whole lung ; and their
accompaniment is not atelectasis, but chiefly emphysema. Their value
is rather that of a complication than of a disease. Since, however, their
symptoms do not difEer from those of a catarrhal bronchitis, and do
not add largely to the fatality of the latter, it would be hard to say
that acute dilatation of the smaller tubes may not occur more often in
the adult, and more often be the origin of true bronchiectasis than is
commonly thought.
In its chronic form bronchiolar dilatation is relatively of small imports
ance. It is a local lesion secondary to the respiratory inactivity of a
pulmonary district disabled by bronchial obstruction, or hampered by
adhesions ; in short, to imperfect expansion of the lung with resulting
accumulation of mucus. Its most common seat is the apex of the lung in
phthisis, where, although an old vomica may have undergone considerable
contraction, the collapsed alveolar substance in its vicinity had failed,
owing to surrounding fibrous changes, to expand again completely. Small
thin-walled bronchi, distended with clear or purulent mucus, may often be
seen in these partially aerated and inactive remains of healthy lung tissue.
The same change may, however, be met with in an opposite associa-
tion, in emphysema due to chronic bronchial catarrh. Where the
emphysema tends to become bullous the dilated bronchioles may take a
share in the formation of the bullae, and occasionally perhaps in the
production of pneumothorax.
The acute form is of much greater clinical interest. In the majority
of cases its mode of origin is tolerably obvious from the clinical
BRONCHIECTASIS 55
history. It is illustrated in the cases collected in Dr. Walter Carr's paper
on " Bronchiectasis in Young Children " ; and it is well displayed in the
drawings reproduced, by kind permission of the editors of the St. Thoma^s
Hospital Reports, from Dr. Sharkey's paper on " Acute Bronchiectasis."
In children the lesion is essentially the result of an acute catarrhal
bronchitis and peribronchitis, with multiple and widely-diffused second-
ary collapse. As immediate factors, the bronchitis of measles and of
whooping-cough probably contributes more cases than any other kind.
The course of the disease and its clinioal features are not very distinctive,
as may be gathered from the brief account given by Dr. Sharkey of his
two cases. The cases were not diagnosed as bronchiectasis during life.
In the first patient, set. 2 (Fig. 2), there was no previous record of illness
e'xcept measles. The lungs after death were pale and curiously dotted
with black pigment spots, hard to the touch. The centre of each of
these was occupied by a small bronchus. The bronchioles were every-
where dilated, and scattered here and there were what appeared to be
small miliary tubercles ; but the other organs were free from tubercle.
Microscopically acute peribronchitis was found, accompanied with ex-
treme bronchiectasis, and a little, but very little, "emphysema. No
genuine tubercles were seen.
The other patient, a child aged 4, was under observation from May 7th
to June 10th, 1893. He had always been healthy till cough began, two
months prior to admission. Since then he had spat up thick phlegm, and
had vomited three or four times a day ; but he was able to attend school
until admission. At that time he presented a dusky flush, rapid breath-
ing, no marked dulness on percussion, no tubular breathing, but crepitar
tions over the whole of both lungs. The pulse-rate was 136 ; the tem-
perature 102-6°; the respirations 44 per minute. The temperature
gradually fell, but on June 3rd subcutaneous emphysema occurred;
otherwise no material change took place till death. The lungs were
found bulky, their surfaces thickly strewn with soft, round, transparent,
bladder-like elevations, the cavities of which were perfectly smooth, and
either empty or full of frothy mucus. Scattered through the lungs these
small cavities, the largest of which was about the size of a pea, gave
a worm-eaten appearance. The larger tubes were not perceptibly
dilated or diseased, but there were numerous patches of broncho-
pneumonia of small size, and here and there some collapse; but no
tubercle. The microscope detected widespread acute bronchitis, peri-
bronchitis, broncho-pneumonia and pulmonary collapse. The bronchioles
were extremely dilated, and there was also considerable emphysema.
A diagnosis of dilatation of the bronchioles cannot be made with any
certainty, even in children; or even when,- as in these cases, the change
is general and extreme. At most its presence can be guessed at.
Neither percussion nor auscultation can fasten upon any trustworthy
sign, and the character of the expectoration does not differentiate the
affection from severe catarrh. In its localised occurrence in the adult
dilatation of the small tubes is still less capable of recognition.
56
SYSTEM OF MEDICINE
Prognosis. — The acute puerile form, as shown by the cases narrated,
is sometimes the result of a catarrh so severe as to be in itself fatal. In
I
Pig. 2.— Acute bronchiectasis. Eeproduced from Dr. Sharkey's Plate I. The figure represents the
external surface of the lung, iv;i:c'.i is seen to be dotted with vesicles. In the fresh state they
projected boldly on the pleural surface.
other cases, perhaps, the bronchiolar affection may be limited to a portion
of the lung; and the catarrh getting well, the small tubes may lose
BRONCHIECTASIS
SI
their dilatation. That this does occur is the view generally held ; but,
so long as a diagnosis of capillary bronchiectasis by physical signs is
^"■"''yj 1^^-^
Fig. 3.— Acute bronchiectasis. Reproduced from Dr. Sharkey's Plate II. A vertical section of the
same lung as in Fig. 2, showing dilated bronchioles distributed over the "whole surface.
impossible, this must remain an unproved though a plausible opinion.
Considerable likelihood has recently been added to it by the successful
results obtained in cases of bronchiectasis in the adult.
The treatment of an affection incapable of diagnosis cannot be
58 SYSTEM OF MEDICINE
laid down •with any definiteness. In the chronic form none may be
needed, the general symptoms being themselves chronic and sometimes
unimportant. In the acute affection the presence of the bronchitis and
of the catarrh supplies all the important indications ; and these are
suflciently dealt with elsewhere. The great object in bronchitis being to
prevent stagnation in the bronchioles, of which this form of dilatation is
one of the results ; the treatment of both diseases is practically identical.
II. Beonchiectasis. — Morbid anatomy. — Since the time of Laennec,
to whom we owe the first anatomical and clinical account of the disease,
three main varieties of dilatation have usually been described : (i.) the
regular or cylindrical, (ii.) the fusiform, and (iii.) the globular or sacculated.
A modification of the globular is the bead-like variety, in which a tube may
present at intervals a normal calibre between successive distensions.
/Saccular dilatations, with that exception, are terminal. The cylindrical ex-
pansions, on the contrary, affect the tubes as they pass towards the peri-
phery. If a further dilatation should occur at their peripheral end, and
cause the latter to become bulbous, the fusiform variety is brought about.
The largest and most extensive bronchiectases are found in more or
less fibrotic lungs. Dilatations occurring in emphysematous surround-
ings are usually either fusiform or bulbar dilatations of single tubes, or
cylindrical expansions of sets of smaller bronchial tubes which may be
filled with catarrhal secretion.
Oongenital bronchiectasis, the varieties of which constitute a distinct
group, may be regarded as a malformation, or as resulting from some
intra^uterine disease, perhaps syphilis. Usually one lung only is af-
fected, and may present a large cyst with a central space branching
into a peripheral set of intercommunicating secondary and tertiary
cysts, with serous contents. Instances of this kind have been described
by Grawitz, by Kessler, by Meyer, and by Frankel. In another variety
described by Grawitz, numerous separate cysts are formed on the bronchi
of the third and fourth order ; some of them communicating with the
bronchial lumen, others being entirely closed. Goitre was found asso-
ciated with this malformation.
In the atelectatic bronchiectasis described by Heller there is an
abnormal growth of the bronchial cartilages, together with remnants of
unexpanded, non-pigmented foetal lung tissue ; and the epithelial lining
is not of the columnar ciliated, but of the pavement type. Cases have
also been described by Gairdner, by Francke, by Herxheimer, and others.
Lastly, congenital bronchiectasis may be due to a dermoid growth
within a bronchus. An almost unique specimen, now in the Museum of
St. George's Hospital, was exhibited by Dr. Cyril Ogle before the
Pathological Society on March 2nd, 1897. The patient, a male aged
twenty-eight, had suffered intermittently for five years with cough and
haemoptysis, and ultimately died from profuse haemorrhage, after a period
of hectic temperature, fetid expectoration, and physical signs suggesting
empyema or bronchiectasis ; both of which were found after death. The
BRONCHIECTASIS 59
dermoid mass, consisting of cheesy sebaceous material -which contained
loose hair and a tooth, was attached to the internal surface of a primary-
division of the right bronchus ; this division -was much dilated, and con-
■tinuous -with a large cavity in the substance of the lower lobe.^
Situation ofthedilatation. — Bronchiectasis may be limited to one lung.
Lebert found in fifty-four autopsies an affection of a single lung in 62 per
cent ; and of both lungs in 48 per cent. Even when restricted to one
lung the dilatations are usually multiple, and they may occur in any
situation. Lebert's figures are interesting in this respect. In his twenty-
eight cases of unilateral bronchiectasis, six (21 per cent) presented an
affection of the upper lobe ; one (3 per cent) of the middle lobe alone ;
nine (32 per cent) of the middle and lower lobes ; and twelve (42 per
cent) of the whole lung. The view held by Laennee, Stokes, and others,
that the apex is the commonest site of bronchiectasis, may have arisen from
an imperfect distinction between tuberculous and bronchiectatie lesions.
In a further series of fifty-five cases, observed only during life, fifteen (29
per cent) presented bilateral signs. In the remaining group of unilateral
cases the upper lobe suffered in six (55 per cent) ; the lower lobe in
fifteen (37 per cent) ; and the entire lung in fifteen (37 per cent). It
would thus appear that in practically half the cases the affection is
unilateral.
ITie distinction between tuberculous cavities and simple dilatation occur-
ring at the apex never presents any difS^culty, except in chronic cases of
phthisis where a vomica has emptied itself of all caseous matter, and
presents a smooth and relatively dry surface. This latter condition was
described by the -writer in the Goulstonian Lectures for 1882. Close
inspection -will show : (i.) that the bronchus opens into the cavity too
abruptly for bronchiectasis ; (ii.) that the bronchial membrane can only be
followed over a small surface immediately adjoining the orifice of the
bronchus ; and (iii.) that the wall of the cavity presents none of that
sculptural detail which identifies the original structure of a bronchus
■even in extreme dilatation.
In a section through a much-contracted fibrotic apex bronchi of normal
size may appear to be enlarged, owing to the disproportion between the
atrophied lobe and its larger air-tubes, which are shortened and slightly
widened by its retraction. Moreover, it should be borne in mind that
destructive tuberculous lesions of any part of the lung render a progressive
dilatation of tubes belonging to the same bronchial set improbable, if
not mechanically impossible ; the damaged portion of the bronchial tree
havir^ become leaky, as it were, and unlikely to sustain much pressure.
In the softening of phthisis the tendency is to an early ulceration and
destruction of the tubes ; and, as stated in the Goulstonian Lectures on
Pulmonary Cavities, although during the progress of excavation the blood-
1 A similar hairy mass, growing in the upper lohe of the left lung, in communication
with the bronchus, is depicted in Albers' Atlas. It was removed from the body of a woman
set. twenty-eight, who had been subject to pulmonary catarrh from childhood, and had for
at least twelve years observed the presence of hairs in her expectoration. She died of
exhaustion after hectic fever, dropsy, colliquative diarrhoea, and pulmonary congestion.
6o SYSTEM OF MEDICINE
vessels may persist for a long time in the trabeculae, the bronchi — even
those of large size — which traverse the diseased region are laid open and
removed by ulceration at an early stage.
In the emphysematous tissue surrounding very chronic and practically
healed lesions of the apex it is not uncommon to find unimportant dilata-
tions of the peripheral air-tubes due to a rarefaction of the lung substance;
these, however, are hardly to be dignified with the name bronchiectasis.
The changes in the mucous membrane and in the outer bronchial coats. — So
long as the mucous membrane escapes destruction — and it is remarkable
how long it will remain intact — it presents the signs of catarrh. In its
later stages, however, it loses the velvety look, and assumes rather a
smooth and shiny appearance consistent with atrophy of the epithelial
layer. Most probably in all cases the atrophic changes prevail ; although
in some they may be limited to the internal coat, the adventitia taking on
an inflammatory action which explains the thickening described as the
alternative change. In Walshe's words, "The walls of such dilated
portions of tube, commonly thick, and exhibiting the several characters
assigned to tubes affected with chronic bronchitis, are, on the contrary,
in rare instances thin and almost transparent." In general the instances
of thickened bronchial membrane are those in which the inflammatory
process extends around the dilated tubes into the pulmonary and
interstitial tissue ; whilst the bronchiectases with thin walls belong to
the emphysematous group.
The condition of the mucous membrane differs much in the several
varieties and stages of the disease ; it is swollen and congested in, the
acute form (as in the acute cases of childhood), and in those chronic cases
which remain free from much accumulation ; congested and atrophic in
cases of an opposite process ; and, lastly,, sometimes ulcerated or even
gangrenous' in the later stages of extensive retention, when septic
inflammation has supervened.
Hanot and Gilbert have connected the occurrence of haemoptysis
in bronchiectasis with the marked alterations described by them in the
blood-vessels, which may form in the submucous tissue an extensive
cavernous network, interspersed with numerous minute aneurysms.
According to Professor Hamilton the basement membrane of the
original bronchus seldom gives way, but becomes stretched and attenuated.
" On the basement membrane stratified columnar epithelium in a wonder-
ful state of preservation may sometimes be found."
The changes in the surrounding pulmonary tissue. — As stated by Walshe,
"The surrounding tissue is either slightly condensed by pressure, hardened
by chronic pneumonia, rarefied by emphysema, or perfectly natural."
Ulceration occurring in a sacculation is prone to set up fatal pulmonary
gangrene. This was observed in twelve cases out of twenty-four by Eapp ;
in three out of forty by Barth; and in five out of fifty-four by Biermer.
The gangrene, as in an isolated case mentioned by Lebert, may perforate
1 Marfan devotes a special chapter to " gangrene of the hronchi," which he regards
as distinct from pulmonary gangrene and from putrid bronchitis.
BRONCHIECTASIS 61
a branch of the pulmonary artery. Perforation of the pleura would
probably be less rare than it is but for the adhesions which so commonly
exist and check the production of pneumothorax and of subcutaneous
emphysema. Both these conditions have, however, been observed.
Sir T. Grainger Stewart has described the process of absorption by
which bands are left stretching across bronchiectatic cavities ; or the
latter may become multilocular, as often seen at the pulmonary base.
Inflammatory changes in the pulmonary tissue in the vicinity of
the lesions are common. Acute pneumonia was recorded in twelve
cases by Biermer, and in five by Lebert. Some inflammation also
extends to the air-tubes in general. Hypertrophy of the bronchial
cartilages, and a calcification of the walls of the dilated tubes — which
in the bovine species is stated by Biermer not to be uncommon — have
been described in isolated cases.
A cystic form of bronchial dilatation has sometimes been described
(Biermer, Briquet) ; the cysts, which average the size of a walnut, being
associated with a bronchial stenosis situated higher up. The contents
may be serous, mucous, caseous, or even calcareous.
TJie secretion found in the dilated bronchi at different stages varies
in its foetor, and in the proportion of its fluid and of its solid constituents.
Among the latter may be found : (a) recent mucus ; (6) small casts,
described by Dittrich and by Grainger Stewart, sometimes presenting
epithelial flakes ; (c) stale, opaque mucus undergoing granular and fatty
degeneration ; (d) micro-organisms of putrefaction (including sometimes
sarcinae and leptothrix pulmonalis, to which is due the purplish colour
reaction of the bronchial casts on the addition of iodine, etc.), but no
bacilli of tubercle. Occasionally the contents are blood-stained. Very
frequently, though not always, crystals of the fatty acids and of chole-
sterine are found, especially in the fetid stage. Calculous concretions
(Stokes, Dittrich) have also been observed.
PatJiological changes in distant organs. — ^Variou^ accidental complica-
tions have been described, such, for instance, as cancer, which Barth recog-
nised in 8 out of 43 cases. The associated changes special to the disease
are chiefly those connected with the obstructed circulation through the
lungs : secondary dilatation of the right side of the heart, and venous con-
gestions in the portal and in the systemic circuit. Valvular lesions may
coexist, but do not appear to be traceable to the disease; pericardial adhe-
sions sometimes occur as an extension of the pleuro-pulmonary fibrosis.
The liver is almost always congested ; it may present fatty change, and is
sometimes lardaceous. Lardaceous degeneration also occurs in the kidney ;
and catarrhal nephritis has been recorded. Septic abscesses may be set
up in various situations ; one of their most common sites is the brain.
An articular affection, analogous to gonorrhceal synovitis, or to that
sometimes following dysentery, has been described by Gerhardt in two
cases of bronchiectasis, and is regarded by him as secondary to the
bronchial trouble.
We should also mention the skeletal changes, not limited to this
62 SYSTEM OF MEDICINE
disease, described by P. Marie and by SouzarLeite under the name of
Hypertrophic Pulmonary Osteo-arthropathy, and previously noted by
Bamberger. In extreme cases there may occur, in addition to the usual
clubbing of the finger-ends, an enlargement of the joint ends of the
phalanges and metacarpals, of the long bones of the arm, and even of
the vertebrae. Similar changes are also traced in the bones of the
lower limb {vide vol. iii. p. 153].
Bamberger believes that the changes in bronchiectasis constitute a
separate variety distinguished by the painful swelling of the epiphysis,
and by the condensation occurring in its spongy substance as well as in
its shell of hard bone.
General and clinical causation. — The insidious beginnings and the
chronic course of bronchiectasis are not favourable to a study of its causes.
Statistics of the disease at ■vanoMS ages can only deal with approximations.
Lebert, in a series of 83 cases, found 47 per cent occurring before, and
53 per cent occurring after, the age of 40 :
7 per cent occurred under the age of 10
8
) 1)
)»
20
20
, from the
age
of 20 to 30
12
1 If
n
31 „ 40
18
7 1>
n
41 „ 50
11
» J)
?)
51 „ 60
24
1 J)
j>
61 „ 85
The congenital dilatations are exceedingly rare.
The male sex is more often affected than the female, according to
Trojanowski and Bamberger ; but other authors (Biermer and Willigk)
have traced no difference. Occupation does not influence the production
of the disease in any direct way, though it may act indirectly by setting
up pulmonary and bronchial changes favouring a dilatation. Depressing
circumstances of all kinds might also have an indirect effect.
Clinical antecedents. — We have no proof that the change ever arises
spontaneously dui-ing extra-uterine life. In children we are able to trace
its acute form to bronchitis. Fatal cases of this kind furnish us with the
only direct evidence in favour of a definite causation from acute inflam-
matory disease ; but clinical observations, although less conclusive, lend
their support to the same view. When not traceable to an acute attack,
dilatation is probably secondary to some chronic bronchial or pulmonary
affection, and the precise time of its onset becomes difficult to determine.
As regards the immediate etiological factors Lebert's results are prob-
ably trustworthy. In a quarter of his series there had been previous
emphysema; in another quarter an acute pleiirisy or an acute pneumonia
had preceded the disease ; and in a large number the history was one
of long-continued bronchitis with intercurrent acute attacks (Wilson Fox).
Thus, bronchitis in all its forms, but especially when complicated with
spasmodic cough, as in whooping-cough (Laennec) and in asthma (Hyde
Salter), contributes a well-marked etiological group ; pulmonary diseases,
BRONCHIECTASIS 63
whether acute or chronic, rarefying or condensing, forming a second
group ; and pleuritic affections a third. A fourth group is that in which
a temporary or permanent narrowing of a large bronchus, as by an aneu-
rysm,has led to increased strain or to accumulations withinits subdivisions.
The relation which the bronchial affection may bear to tuberculous
disease has been much discussed. Some, including Eokitansky, have
regarded the two diseases as almost incompatible, and as mutually
protective. Nevertheless, true bronchiectasis may occur in the subjects
of chronic tuberculous disease ; for instance, at the base of a lung with
an indurated apex. And, conversely, sufferers from chronic bronchiec-
tasis may end in tuberculosis, though this is rare.
Wilson Fox suspected that the fibrotic induration around the tubes
was probably tuberculous in its origin ; the other tuberculous deposits in
the same lungs having been slight and obsolescent : but this opinion
does not appear to have had the support of any direct evidence.
Biermer, who quotes Trojanowski as reporting tuberculosis in 21 out
of a series of 68 cases, could find only 3 in his own collection of cases.
As pointed out by Wilson Eox, discrepancies of this magnitude can only
be explained on the score of some confusion between tuberculous lesions
and those due to bronchiectasis.
Pathological etiology. — The history of the subject is a record of hypo-
theses as varied as the associated intrathoracic conditions ; but they may be
briefly classified as attempting to identify the causation (1) with changes
limited to the tubes themselves, (2) with changes in the pulmonary tissue,
(3) with changes in the pleura, or lastly (4) with a combination of the
bronchial, pulmonary, and pleural changes.
Some cases carry their own explanation : cicatricial stricture, lateral
pressure from aneurysms or morbid growths, internal obstruction due to
tumours, and particularly the impaction of foreign bodies are occasional
causes of bronchiectasis; but those needing elucidation form a much
larger group.
Laennec regarded the dilatation as due to an accumulation of mucus.
Andral accepted this view only for the bead-like form, and attributed the
other dilatations to a process of hypertrophy analogous to that of other
hollow organs ; this was also in part the view of Louis. Eokitansky,
and subsequently Hasse, assumed a stenosis of the larger and an oblitera-
tion of the smaller bronchi, with compensatory dilatations elsewhere.
Stokes and Williams traced the production of dilatation, under stress of
cough or of accumulating secretion, to impairment of elasticity and of
muscular contractility by inflammation. Atrophy of the bronchial mus-
cles has been described by Bamberger, by Trojanowski, by Lebert, and as
a primary and probably constitutional defect, by Sir T. Grainger Stewart.
Lebert also suggested that dilatation might be due to atony dependent
upon defective innervation. Various other pathologists (Beau, Maissiat,
and Mendelssohn) have insisted on the share taken by cough in the pro-
duction of dilatation.
Wilson Pox considered all forms, except those secondary to a con-
64 SYSTEM OF MEDICINE
striction, as essentially inflammatory in origin ; the loss of elasticity and
muscular contractility of the tubes themselves being the only essential
changes, and sometimes the only changes found ; whilst on the other
hand the dilatation -would be favoured by the coexistence of a pneumonia,
or of a broncho-pneumonia, or by pulmonary collapse or tuberculous indu-
rations in the surrounding tissue. The acute bronchiectasis of infantile
bronchitis he regarded as due to cough pressure rather than to any
inspiratory mechanism, or to any indirect effect of collateral collapse ; but
the proofs upon which he based this view were not fully stated by him.
As an explanation of the infrequency of bronchiectasis, in spite of the
great frequency of bronchitis, Wilson Fox alleged that the dilatation is
readily recovered from in children ; and that in adults chronic bronchitis
tends to hypertrophy rather than to weakness of the muscular fibres, in
contrast with its action upon the pulmonary parenchyma.
It is noteworthy that Biermer traces as many as a quarter of the
aggregate cases to acute pneumonia. The strict priority of the pneu-
monia is in many cases difficult to establish, and therefore open to some
doubt.
Biermer is also a believer in the influence of pleural adhesions, which,
according to Wilson Fox, are more easily explained as a secondary pro-
cess. A compression of the lung by fluid was regarded by Buhl as most
likely to lead eventually to bronchial dilatation. In this connection it
may be pointed out that in simple pulmonary collapse no dilatation can
occur in previously healthy tubes, so long as they receive evenly from all
sides the strong support of carnified tissues ; and that on the other hand
the appearances of dilatation are very apt to be simulated by the shorten-
ing and retraction of tubes within a collapsed portion of the lung.
The explanation given by Sir Dominic Corrigan of the mechanism of
the dilatation in cirrhosis of the lung has become classical. Owing to the
rigid connection of the surface of the fibrosed lung with the chest wall,
not only will the spontaneous shrinking of the fibrous tissue lessen the
distance between the chest wall and the bronchial wall, but every in-
spiratory effort of the former will take effect in dilating the cavity of the
bronchus. Corrigan's theory was subsequently adopted almost unaltered
by Eokitansky and by Lebert. The latter based the etiology, at least in
fibrotic cases, on some antecedent pZeMriJis_p?-q/Mnda setting up a prolifera-
tive irritation in the pleuro-pulmonary connective tissue.
Dr. David Drummond has favoured me with the following statement
of his views on the production of bronchiectasis fvom. pleuro-broncMtis : —
" The common form begins as an acute bronchitis and pleurisy, to
which the name pleuro-bronchitis is fairly applicable. The process leads
early to blocking of some of the larger tubes by hypertrophic thickening
of the mucous membrane, and in consequence to collapse of lung and
diffuse broncho-pneumonia. This form of pleurisy is essentially progres-
sive. The fluid becoming absorbed, fibrous thickening of the pleura sets in.
Tube after tube becomes blocked and subsequently dilated from pent-up
discharge, which in time bursts away. After death the tubes first attacked
BRONCHIECTASIS 65
are found surrounded by fibrous tissue; but those affected later are
devoid of fibrous tissue, and only nuclei and collapsed lung can be found
in tbeir vicinity, showing that the fibrous tissue is developed after the
dilatation of the tubes."
Most of these hypotheses are summed up and criticised by Sir T.
Grainger Stewart and Dr. Gibson under the headings of: — (1) Direct
pressure of stagnating secretion — a mechanism in which they do not
believe ; (2) Concentrated air pressure, as in cough (Reynaud, Williams)
— an explanation which they regard as inadequate apart from another
factor, that of an essential debility of the bronchial wall; (3) Extra-
bronchial traction — which they recognise only in cases of pulmonary
•cirrhosis, and not in all of these, since in as many as 20 per cent Bastian
found no dilatation ; (4) Inflammation of the bronchial wall causing loss
of elasticity, of contractility, and of ciliary movement (Stokes) — a view
. which, according to them, leaves unexplained the infrequency of bronchi-
ectasis in spite of the great prevalence of bronchitis ; (5) Dilatation as
a result of defective innervation and loss of tone, as alleged by Lebert, an
origin which they regard as unproved ; (6) Lastly, Sir T. Grainger Stewart's
own hypothesis, first published in 1867; which refers the origin of a
large proportion of the cases to a constitutional, or possibly, as held by
Leroy, to an hereditary weakness, a " primary atrophy " of the bronchial
wall, unfitting the bronchi for stress even within the physiological limits
of powerful inspiratory efforts, of cough, and of violent exercise. Once
originated in an insidious manner, this primary bronchiectasis progresses to
the fully developed forms with the well-known symptoms.
In another large group — that of the secondary bronchiectases, including
a general and a local variety of dilatation — the same authors recognise
among the determining causes the influence of pertussis, of capillary
bronchitis, of bronchial stenosis or impaction, of pulmonary cirrhosis.
Most of the explanations hitherto attempted have, according to them,
been limited to these secondary varieties. Here again individual delicacy
or inflammatory impairment of the contractility or of the elasticity of
the bronchi may be frequent factors in the result.
The writer's view's. — The first essential for a comprehensive theory of
bronchiecta,sis is a sufficiently broad basis. There is one feature which is
common to all ; namely, the faulty distribution of space between the
air-tubes and the pulmonary tissue. In health the intrathoracic space is
suitably distributed between its several contents ; the functions of which
are regulated for the avoidance of undue stress on any one of them. Any
excessive stress ultimately finds out the least resistant tissue, and this is
most often the pulmonary tissue. Why, in exceptional instances of
sustained intrapulmonary pressure, the bronchi should suffer rather than
the pulmonary tissue, has never been explained. The possibility that
disorderly nutritive changes may occur at an early period of development
must be borne in mind ; and hereafter vascular disease may be found to
take as leading a part in the production of btonchiectasis as it does in
that of emphysema. On the whole, however, there is little support for
VOL. V t
i66 SYSTEM OF MEDICINE
the view that bronchiectasis is a progressive deterioration due to an innate
local delicacy, independently of disease.
In disease, mechanical factors arise ■whicli are entirely foreign to the
natural play of the organ, and which do not necessarily seek out the
weakest part. To these belong, within the tubes themselves, an accumu-
lation of mucus and the antecedent or the resulting degenerative changes
in the bronchial wall.
A second influence is that of changes induced in the lung tissue.
In a rather large proportion of cases bronchiectasis is accompanied by
more or less emphysema. Much of this is clearly a result rather than a
cause, since the ordinary vesicular emphysema does not carry with it
any accessory bronchiectasis.
Another frequent accompaniment of bronchiectasis is pulmonary
collapse. When occurring unevenly, at one side of a bronchial tube,
this may act as one of the agents of dilatation. Not only in advanced .
bronchiectasis do we often observe a proportionate amount of con-
densing fibrosis of the lung, but in any recent dilatation, such as
that witnessed in the infant after bronchitis or whooping-cough, the
incipient bronchial bulgings occur side by side with considerable lobular
collapse.
A further set of structural changes contributing, in a large proportion
of the cases, to faulty allotment in space, are those of the pulmonary
stroma, which includes the subpleural, the perilobular, and the inter-
lobular systems.
As to the general mechatiism of the dilatation we must again look for
some elementary factor common to all varieties ; and this we find in
" obstruction," Understood in the broadest sense of the word.
In the alimentary tract and in most animal tubes the obstruction is
invariably situated forward, beyond the dilating segmetit In the
bronchial tract no such local restriction obtains. Neither is. the nature
of the obstruction necessarily limited to stenosis or to impaction. Owing
to the alternating direction of the respiratory air-currents, an obstruction
may lead to dilatation either on its proximal or on its distal side. Again,
the 'dilating force is not usually, as in other tubes, the pressure of an
accumulation within the dilating bronchus. This mechanism may occur
in the bronchial system : an instance in point is the thin-walled saccula-
tion, completely filed with stiff gelatinous mucus, sometimes found
beyond a bronchial stenosis. But much more often the obstruction has
its seat on the distal side of the dilatation amd is not a bronchial stenosis,
but a terminal occlusion of a respiratory district of the lung ; and the
dilating force, far from being exclusively due to the pressure of an
internal accumulation, is then applied to the outside of the tube ; it is an
aspirating, not a foncing pressure.
If we bear -these eleipentary data in mind we shall find that the
details oi the problem work out. Thus, whereas in the normal state
each pulmonary constituent preserves its relative position and its allotted
space, the local failure of any individual constituent to perform its
BRONCHIECTASIS 67
respiratory function would interfere with the perfect adjustment of other
parts during the phases of respiration. How readily bronchiectasis
might result from this disturbance will be seen from a consideration of
the forces which normally protect the weaker non-cartilaginous tubes
against the dilating influences of atmospheric pressure. The elasticity
proper to the inflated pulmonary tissue through which they pass tends to
widen them ; but this tendency is counteracted by the inspiratory
elongation of the lung, and probably never goes farther in health than to
ensure their patency, thus acting in the depth of the lung in lieu of a
cartilaginous armature. On the other hand, both during inspiration and
during expiration, the small tubes receive lateral support from their closely
fitting environments. Let this support be withdrawn at any one spot by
the persistent inspiratory inactivity of one of the adjacent lobules, even
though this were merely a delay in the fulfilment of inspiratory inflation,
then the imperfectly resisted intrabronchial pressure would gradually
bulge out the yielding wall into the space rendered available, and thus
establish the first stage of a progressive dilatation. Or, to put the matter
more clearly, the inspiratory traction made by the chest wall, if it should
fail to expand an obstructed lobule, might be transmitted to the delicate
air-tube adjoining the latter, and might dilate it.
Owing to the solidarity existing between all parts of the lung, this
encroachment of 'bronchial space into the vacaied pulmonary space may occur at
a distance from the original collapse. The same mechanism might there-
fore be concerned in some measure in the production of almost every
variety of bronchiectasis. Its more strictly local operation is probably
alone concerned in the early stages of the afi'ection when the pulmonary
tissue is still free from induration. In some instances bronchiectasis
remains permanently uncomplicated with any pulmonary fibrosis, or with
any peribronchial thickening. It is in these cases that the bronchial
membrane preserves its delicate and transparent thinness. The plug of
semi-gelatinous mucus which sometimes fills simple dilatations of this kind
in the midst of soft spongy lung tissue suggests the idea that the mucus
itself was originally the obstacle to the free inflation of the collateral
lobules, whilst its accumulation eventually assisted in producing the dis-
tension.
The progresswe increase in the dilatation may conceivably be brought
about by the various mechanisms assumed by the so-called inspiratory
and expiratory hypotheses ; although much that has been advanced in
connection with them is lacking in strict proof. Thus : —
(i.) The inspiratory hypothesis of Laennec asserts that the abnormal
inspiratory effort preceding cough throws damaging stress upon the
weakened parietes of the bronchial tube. In the diagram (Fig. 4)
which illustrates this supposed agency, if we imagine the shaded zone
to remain rmexpanded, the arrows would represent the inspiratory
traction thus transferred from the alveolar to the bronchial walls.
The same explanation has been applied to the condition which may
result from a proximally situated stenosis, when the impeded removal of
68
SYSTEM OF MEDICINE
the products of catarrh from the terminal districts has led to an irregular
lobular collapse with consequent disturbance of the balance of pressures.
(ii.) The expiratory hypothesis has also been pressed into the service of
bronchiectasis as well as of emphysema. Were it not that one of the
chief functions of man in earning his bread by manual labour is the per-
formance of muscular strain mth closed glottis, and that his organs are
specially constructed for that purpose, the wonder would be that the
prevalence of bronchiectasis and emphysema is not universal.
As a fact, nothing gives way within our visceral cavities under the
Fig. 4.— niustrating the alleged meclianisni of dilatation, according to the inspiratory theory.
high pressures due to muscular strain so long as every part is sound and
works true. The extent to which we are dependent for this immunity
upon a perfect distribution of pressiu-es is illustrated by some of the
delicate valvular membranes of the heart which could not perennially
resist the stress to which they are exposed, were not the pressure exerted
upon one of the two surfaces neutralised by equivalent pressure or
support on the other. So must it be also with the delicate bronchial
membranes. The range of pressures to which they are exposed is not
so great, but their risk is multiplied by the number of their subordinate
districts. A loss of the even balance between the intra- and the extra-
bronchial pressure occasioned by imperfect 'inflation of any of the latter
might in delicate and predisposed subjects cause the bronchial wall to
yield, and to suffer progressive dilatation.
BRONCHIECTASIS
69
Cough is a special instance of muscular stress ; it is often complicated
by the mechanical influence of the secretion which excites it. The
diagram (Fig. 5) illustrating the mechanical theory of expiratory pres-
sure will also serve to explain this point.
The cough which may be powerless to dislodge and evacuate the
contents may yet propel some of them far enough to cut off the dilated
chamber from the main bronchial channel. The moment represented is
that of the explosive expiration, when the air accumulated under high
Fig. 6.— Eluatiating some of the effects of cough in bronchiectasis. (From Clin. Jamiwl, Feb. 1894.)
pressure leaves the chest without any further hindrance. Alone in the
dilated tube the pressure, indicated by the curved arrows, will remain at
that moment nearly as high as during the period of closure of the glottis ;
and its dilating effect is but feebly counteracted by the released elasticity
of the immediately surrounding lung tissue. Slowly, with the ensuing
inspiration, the plug may be sucked in again ;■ and this suction is the
most likely explanation of the long-drawn, semi-musical, or croaking
rhonchi and rSles of bronchiectasis.
The practical results of a recurring valvular obstruction of this kind
would be not only a continued fulness of the dilatation, whilst the
surrounding tissues are being relieved of much of their air, but a main-
tenance within it of the highest air-pressure at the time when the air-
pressure in its vicinity is at its minimum. Neither should we lose sight
70 SYSTEM OF MEDICINE
of the possible injection into the tributary bronchioles and lymphatics of
some of the bronchiectatic contents.
Most cases may begin and progress after the mode suggested ; but,
except in fatal cases of bronchitis and whooping-cough in children where
these etiological relations are well displayed, an opportunity of examining
the lung at this stage is not often afforded ; and ulterior changes of a
very different kind usually obscure, more or less completely, the original
mechanisms.
The influence of catarrh seems entitled to be regarded, as it has been
by most writers since Laennec, as the chief and earliest etiological factor
of bronchiectasis. The inflammatory softening and weakening of the
bronchial wall, the changes in its muscular and fibrous coats, whether in
the direction of atrophy or of overgrowth, are all possible accessory
agents ; but the special action of catarrh consists in the mechanical plug-
ging of bronchioles. AVhen a bronchiole becomes occluded the amount
and the pressure of the air within its district are rapidly altered, and the
balance of pressures will be disturbed to the special detriment of the
tube from which the bronchiole sprang. If the pressure can be speedily
readjusted by collateral expansion in the vicinity any strain or dilatation
thus induced wiU be corrected. Failing this adjustment, however, the
existing catarrh will aggravate the dilatation by a tendency to accumula-
tion and by the impairment of the respiratory mechanisms of relief.
The successive obliteration by catarrh of many tributary bronchioles
is probably the mode of extension of bronchiectasis. The greater the
stretching of the dilated bronchial membrane and the accumulation
within it, so much the greater will be the number of collateral bronchioles
obliterated by stretching or by plugging, and so much the greater the
extent of the resulting atelectasis.
A direct influence aiding the dilatation is that of any impairment of
the muscular coat, whether in its structure, as in the atrophic fibrosis
described by Lebert, or the simple atrophy of Grainger Stewart; or in its
function, as in atony from defective innervation, or from insensitiveness
of the mucous membrane.
Indirectly, the process of dilatation might be favoured, as in pertussis
and in acute bronchitis, by the opposite condition of bronchial spasm,
since this would lead to a narrowing and to a more ready plugging of
the smaller tubes.
The influence of interstitial pneumonia and fibrosis. — In whatever way it
may have arisen, a sacculation of a small bronchus is fatally exposed to
an accumulation of secretion during periods of catarrh, and to irritation
not only within its own terminal divisions, but probably, by overflow and
by inhalation, in collateral lobules also. This is the beginning of an
interstitial pneumonia, the ultimate result of which may be a conversion
of the pulmonary substance into structureless fibrous tissue. The loss of
expulsive power is progressive, and the shrinking of the chronically
inflamed parenchyma favours the encroachment of the sacculation; whilst
the implication of the lymphatics of the lobule causes an extension of the
BRONCHIECTASIS 71
changes along the perilobular system. In this way the pulmonary
■degeneration is promoted along two lines, by intralobular and by peri-
lobular agencies. How far it may extend will depend upon the vary-
ing ability of the remaining pulmonary tissue by its increased expansion
to replace some of that which has atrophied. Dense adhesions would
largely interfere with this compensatory process.
The, infiiience of pUwo-jpneumonic fibrosis. — The close relationship
existing between the pleura and subjacent stroma and the lymphatic
system of the lung explains the influence which agglutination of the
pleural surface exercises on the course of the interstitial pneumonia,
and on the etiology of bronchiectasis. Extensive pleuritic thickening
at the base, with obliteration of the groove and agglutination of the
surface of the diaphragm, cripples the lung. The respiratory function of
the base is almost entirely lost, or can be carried on only by consider-
able mechanical effort on the part of the diaphragm, and of the inspira-
tory muscles ; an effort which must tell on the pulmonary tissue as a
constantly recurring and irritating traction. The lymphatic circulation
may also be impeded. The result is usually a considerable shrinking
of the side affected, and a compensatory hypertrophy of the sound lung,
with great distension of that side of the thorax.
The process which has just been sketched is essentially that originally
described by Corrigan under the name of " cirrhosis of the lung."
The influence of stenosis. — Dilatations are by no means the invariable
result of bronchial stenosis. When a bronchiectasis occurs beyond the
stenosis its mechanism is generally held to be analogous to that of em-
physema from a partial obstruction of tubes, which allows a slow entrance,
but unduly delays the escape of air. Syphilis, being a well-known
cause of bronchial stricture, should be allotted a place among the
recognised factors of bronchiectasis. It is not. improbable that in some
cases the occurrence of a late ulceration of the dilated tubes may be
due to the same influence.
Hoffmann believes that sufficient attention has hardly been paid to
the probably frequent origin of bronchiectasis from inhalation of solid
^articles, and he refers to the experiments of Cohn which show that
dilatation occurs not beyond but at the seat of impaction, around the.
impacted foreign body.
Lichtheim's experiments go to prove that total closure of a bronchial
tube leads within twenty-four hours to a complete atelectasis of the
pulmonary district, with purulent accumulation within the tubes. After
several weeks the latter become more or less .dilated, the surroimding
tissue being completely compressed by the distended bronchi, or expanded
by collateral emphysema.
Beyond any valvular obstruction micro-organisms, which easily pene-
trate through the stenosis, may set up fermentation, and the secondary
results of putrid decomposition will follow.
Symptoms. — The severity of the disease varies greatly in different
individuals and at different stages in each. Its- course and its symptoms
72 SYSTEM OF MEDICINE
are largely determined — (a) by the mechanical factors, such as induration
or persisting elasticity of the surrounding tissue, position of the dilatation,
its single or multiple character ; (6) by constitutional factors special to
the individual or to phases of his' general health ; and (c) by climatic
and atmospheric factors, including not only temperature and humidity,
but also purity of air, in the sense of relative freedom from septic germs.
It has already been stated that in exceptional instances bronchiectasis
may be latent for some time after its commencement : in a few cases also
there may be periods of quiescence during vrhich it might pass unobserved.
These are the' milder forms, of a catarrhal and emphysematous type —
non-indurative, non-septic, non-ulcerative, progressing but slowly, and
compatible with relative longevity. All cases are liable to exacerbations
in the symptoms, to occasional or periodical increase in the expectoration,
to recurring intervals of f etidity of the sputum, and to intercurrent attacks
of general bronchitis or catarrh.
Constitutional symptoms. — For long periods the flow of expectoration,
sometimes even when fetid, may proceed without making any obvious
impression upon the general nutrition or functions; but these are
gradually involved as the diminution of respiratory surface and con-
sequent loss of energy advance ; and ultimately the system is contamin-
ated by the septic matters inhaled, absorbed, and swallowed. The
constitutional symptoms set in at different stages, and at first may not
be permanent, but coincide with transient periods of fcetor of the sputum.
In the worst forms these deteriorations are lasting. Sooner or later the
pulse and respiration become permanently accelerated, and the tempera-
ture moderately hectic, or at the least remittent, with an evening rise
to 101° or 102°, and in a few cases with associated night-sweats.
Diarrhoea may be among the septic symptoms, and sometimes vomiting
alsQ. Vomiting as a mechanical result of cough is not so common in
bronchial dilatation as in phthisis.
Failure of cardiac energy lies at the root of the final cachexia. In
addition to the previous lividity and cyanosis oedema supervenes, and
the patient becomes a bed-ridden invalid. At this stage, or prior to
it, intercurrent albuminuria may be observed ; or in association with
. lardaceous disease it may become permanent. Various complications
may cut short the gradual process of exhaustion ; low pneumonia, putrid
bronchitis and gangrene, septicaemia or pysemia, cardiac or renal disease,
and cerebral abscess are among the most common. In the more favour-
able cases, especially when helped by the advantage of climate and treat-
ment, the sufferers may live with their trouble for years, and die from
other causes. Those who reach a relatively mature age are more and
more exposed to catarrh and emphysema with their attendant symptoms,
and the disease, whether directly or through its complications, is
usually responsible for death.
Pulmonary symptoms. — Under this heading we must briefly review
the changes in the respiratory function — the cough, the expectoration,
and haemoptysis.
BRONCHIECTASIS 73
Dyspncea. — There is often a cardiac element in the dyspnoea observed
in bronchiectasis. Much cardiac and nervous depression is induced at
times by septic absorption from the bronchial tubes and through the
breath, especially in ulcerative cases. As a rule, during the major part
of the clinical history the dyspncsa is not excessive ; but it varies much
with the degree of emphysema or of fibrosis, and with the amount of
intercurrent catarrh. In the ultimate stages dyspnoea becomes a pro-
minent feature.
Cough. — A leading peculiarity of the cough of uncomplicated bronchi-
ectasis is its intermittence. It would seem as though the sacculated
membranes lost their sensitiveness, and that cough were excited only
when the tide of accumulation reaches the level of some healthier part of
the bronchial tubes. It is often observed that for long periods, during
which a patient preserves the posture which acts as a protection, no cough
is set up ; but change of position will bring on severe spasmodic cough
and profuse expectoration. The severity of the cough and its paroxysmal
character are explained by the irritating quality of the secretion which
has to be forwarded through the sensitive upper passages ; and also by
the difBculty, or impossibility in some cases, of complete relief on account
of the position of the sacculations. "Whereas a partial emptying of the
surplus of the bronchial contents is comparatively easy, nothing short of
an inversion of the patient could empty some of the ultimate dilatations,
especially when surrounded by fibrous tissue. The creasote inhalation
method introduced by Dr. Chaplin has demonstrated that the foBtor
of this residual material is much in excess of that of the tidal output,
a point which should be borne in mind as of the utmost importance
in treatment.
Expectoration. — The sputum in bronchiectasis varies considerably in
amount and in character. Sometimes it remains sweet and almost purely
mucous for long periods ; more usually it is muco-purulent throughout.
In most cases it becomes fetid at times ; or this may be the habitual
condition. Very often, when ulceration has taken place or after severe
paroxysmal cough, it is slightly blood-stained.
A third of a pint or half a pint is not an unusual daily quantity; but
this amount is often much exceeded. The way in which the expectora-
tion pours out of the mouth in some cases is almost distinctive, though
the same peculiarity may be observed in phthisis. At intervals the
expectoration may be much lessened or completely absent. Complications,
especially bronchitis or pneumonia, commonly reduce the amount.
The sediment deposited by the expectoration, which may separate
into an upper frothy mucus, and a lower puriform layer with an inter-
vening watery layer, presents, besides bronchial epithelia, numerous pus-
cells, granular debris, bacteria and vibriones, fatty acid crystals ; and
occasionally sarcinse, leptothrix, Dittrich's plugs, and Charcot -Leyden
crystals. The presence of elastic fibre would be a proof of ulceration.
The foetor is apt to be great, but it is occasionally more marked in the
breath than in the sputum.
74 SYSTEM OF MEDICINE
Hsemoptysis was among the symptoms deseribed by Laennec. Walshe
failed to observe hsemoptysis except in the presence of mitral disease
or of tubercle. Lebert observed hsemoptysis, of varying degrees but
decidedly more marked than that which belongs to ordinary pneumonia,
in oiie-sixth of Ms cases. Biermer reports one case of fatal haemorrhage
in non-tuberculous ulcerative bronchiectasis. Wilson Fox, who quotes
these authors, refers to it as not beiQg rare. It may occur early and
independently of any ulceration. On the whole, it is to be regarded
rather as a frequent complication than as an invariable symptom.
The respiratory symptoms vary with the degree of the pulmonary
atrophy. Among them are to be noted frequency of breathing and
dyspnoea on exertion, and, in unilateral eases, iaability to lie on the
sound side.
Physical examination of the chest. — Inspedknu. — There is no dis-
tinctive chest shape peculiar to bronchiectasis ; and the thorax does not
present the characteristics of phthisis, even though one side may be much
retracted. Whatever amount of flattening may be present locally, this
is compensated elsewhere by active thoracic expansion. The immunity
of the apex in the majority of cases and its compensatory expansion,
coupled with the fulness of the neck, establish at first sight a distinction
from the ordinary case of phthisis. Often, on the other hand, the
deformity peculiar to emphysema may be more or less fully established.
The unilateral character of the group of cases described by Corrigan as
cirrhosis of the lung is usually made obvious by the cardiac displacement,
and by the extreme disproportion between the size and the respiratory
m.ovements of the two sides of the chest. But in some unusual eases,
owing to considerable encroachment of the sound lung across the middle
line, the thorax on the side afiected is much less collapsed than the lung
which it contains. Cases of this kind are deceptive, and need, for an
accurate determination of the size of the lung, a very careful percussion of
the boundaries of the cardiac dulness. I have described a case of this
sort. This cirrhosis of the lung without thoracic deformity is much
less readily distinguished from phthisis or from chronic bronchitis than
the usual form.
Among the bilateral cases the emphysematous variety is to be diagnosed
from phthisis, on mere inspection, by the dusky and congested complexion,
the prominent veins and deeply coloured lips, the high, deep, and broad
ohest, and the relatively good nutrition.
In the remaining groups the diagnosis may be assisted by a knowledge
of the following points : — (a) A solitary bronchiectatic lesion is seldom
localised at the apex ; this is the customary site for the tuberculous lesion.
(6) The supraclavicular area is usually not implicated in any dulness due
to bronchiectasis ; it is invariably implicated in the apex dulness of
phthisis. (c) In phthisis, as pointed out by Stokes, consolidation pre-
cedes, excavation follows ; in bronchiectasis this is otherwise. And
again, extension of the excavation is peculiar to phthisis (Stokes), whilst
a stationary size belongs to bronchial dilatation (Walshe). {d) The
BRONCHIECTASIS 75
almost daily alternations between the signs of fulness and those of
vacuity greatly help the diagnosis of sacculation. This peculiarity is
usually absent or inconstant in excavating phthisis, (e) The normal site for
tuberculous disease is the apex ; it hardly ever involves the base. The
site of predilection for bronchial dilatation is the base ; but bronchiectasis
also favours the middle and lower third of the back and may affect
various other situations vidthout any hitherto ascertained regularity of
order ; it is specially uncommon in the district of the vertical bronchi
ascending to the apex. (/) It is unusual in phthisis for multiple excava-
tions to form in the same lung with the intervention of sound pulmonary
substance, except in the situations described in the Goulstonian Lectures
for 1882, and by Dr. J. Kingston Fowler in his Dictionary of Medicine.
Even these secondary deposits are commonly almost continuous with
the upper zone of disease. In multiple bronchiectasis a truly sporadic
arrangement is the rule, (g) Unilateral indurative tuberculous phthisis
invariably excavates and condenses the apex first, even if later it should
extend downwards. The fibroid change associated with bronchiectasis
originates as a rule at the base and spreads upwards, (h) The dis-
placement of the heart towards the diseased side of the chest in the usual
cases of unilateral phthisis follows an oblique direction upwards ; a hori-
zontal displacement is exceptional and suggests some complicating basic
pleural factor. In unilateral bronchiectasis the displacement is, practically
speaking, always horizontal ; not only by reason of the basic origin of
the disease, but largely also owing to the lowering of the diaphragm
on the sound side, with extension of the cardiac beat into the epigastric
notch.
Attention to these general guides may often prove of greater value
than a close search for points of difference in the auscultatory and
percussive sounds.
Percussion in advanced cases may yield different results in the same
chest at brief intervals of time, according to the amount of retained
secretion; and this variability is perhaps the most distinctive feature
obtainable by the method. If in a chest otherwise resonant patches
of dulness be found scattered in the middle and lower third, and particu-
larly over the back, and if some of them yield a cracked-pot sound, a
strong suspicion of bronchiectasis will arise. The high-pitched, the tym-
panitic, the amphoric, the splashing, and other varieties of percussion
note which have been described cannot be expected in every instance.
Much emphysema may almost preclude a diagnosis by percussion
alone ; although with a previous knowledge of the existence of
sacculations their site could in most cases be made out by an expert
percussor. The strong element of dulness in the fibroid variety of the
disease, coupled with the boxy note obtained over the cavities when
empty, is a much more definite guide ; although the diagnosis from a basic
cavity of tuberculous origin would still have to be made.
Auscultation, although not always capable of establishing a diagnosis
between slight bronchiectasis and bronchial catarrh, seldom fails to
76 SYSTEM OF MEDICINE
identify advanced dilatation, from a joint observation of the respiratory
sounds and of the rales.
As regards the respiratory sounds, the peculiarity of the emphy-
sematous variety of bronchiectasis is the intimate blending of the
tubular with the vesicular breath-sounds ; the iibrotic variety is dis-
tinguished by the local absence of the latter.
The riles occurring in small dilatations, and in those which are mainly
cylindrical, do not differ from ordinary catarrhal rS,les of medium and of
large size. A distinctive character belongs to those produced in the
sacculations. The sound, which is best described as "croaking," is
partly due to the valvular action of the viscid and confluent secretion,
and partly to the free communication and continuity subsisting between
the sacculations and the corresponding bronchus. The undiminished
length of the latter, and the branches which open into it above the
terminal sac, are probably additional factors. An explanation of the
mode of production of this sound is suggested above in connection with
Fig. 5. The croaking sound is most distinctly produced in sacculations
surrounded with more or less spongy tissue. In the iibrotic variety the
solid medium through which it is conducted to the ear imparts to it a
more metallic character.
It is unnecessary to dwell upon the common catarrhal sounds, the
sibili and the rhonchi, which may spread over the lung as a result of
general bronchitis. They may complicate the diagnosis by veiling to a
certain extent the diagnostic sounds which have been described, although
they seldom mask them entirely.
The voice sounds sometimes supply definite data. Bronchophony and
sego-bronchophony are yielded by the extensive and multiple sacculations
of a partly cirrhosed lung, and sometimes by those not surrounded with
fibrous tissue, if sufficiently large and superficial. Hollowness of the
voice sound would, however, disappear if the cavity were to fiU completely.
The vocal fremitus varies considerably in different cases, the pleura being
unaltered in some, in others greatly thickened.
Diagnosis. — The diseases most likely to be mistaken for bronchiectasis
are the various forms of bronchitis and phthisis. Less commonly the
difficulty may be to distinguish it from emphysema, pulmonary gangrene,
and cancer.
When originating in a general hronchitis, dilatation, in its earlier stages,
can only be inferred. Subsequently foetor of the sputum necessitates a
diagnosis from fetid bronchitis or bronchorrhoea ; and, apart from any
previous knowledge of the case, the distinction may be extremely difficult
if a general catarrh should coexist. In the absence of the latter, dilatation
would be known by the localisation of the large rS,les in the situations
which present some alteration of the percussion note ; and the same
observation would also be a help in the more complicated condition.
Again, the mode of the expectoration, even more than the nature of it,
might throw light on the case; although in fetid bronchorrhoea the
expulsion of the bronchial contents is often sudden and paroxysmal.
BRONCHIECTASIS 77
Pulmonary gangrene, occurring in aged or broken-down subjects and
preceded by a history of chronic bronchial catarrh, would suggest
bronchiectasis culminating in ulceration. Most commonly the onset of
pulmonary gangrene is sudden and marked by extreme prostration;
that of gangrenous ulceration of a bronchiectasis is gradual. As pulmon-
ary tissue is expectorated in both cases, our guides must be the clinical
data and the clinical history. But commonly in bronchiectasis a
gangrenous odour occurs apart from any tissue necrosis; and a fruit-
less search for elastic fibre would strengthen any direct evidence of
bronchiectasis otherwise obtained, and any negative evidence as to
the existence of broncho-pneumonic or tuberculous processes such as lead
to gangrene.
The intra-bronchial ulceration of an empyema may closely simulate
bronchiectasis. Its presence will be sufficiently indicated by the history
of an absence or insignificant amount of expectoration prior to the
bursting; and of the considerable relief given by the latter to the
cough, dyspnoea, pain, and thoracic deformity. The expectoration of
an empyema is usually distinguishable at first sight, by its freedom
from mucus, from that of bronchial dilatation. According to Biermer,
it contains crystals of cholesterin and of hsematoidin. In any special
case a physical examination of the chest would probably remove any
lingering doubt.
Prior to the discovery of Koch's bacillus the diagnosis from phthisis
had to be made almost exclusively from physical signs, and was often
very difficult for persons unfamiliar with the physiognomy of bronchi-
ectasis. A microscopical examination of the sputum now decides the ques-
tion. Nevertheless, the other elements of diagnosis — (a) the clinical
history, (J) the general clinical state and aspect, and (c) the physical
signs — ^are too important to be neglected.
(a) In most cases phthisis can be traced back to characteristic
beginnings, the constitutional efiects of the invasion being out of propor-
tion to the pulmonary symptoms existing at that time. This is not the
history of bronchiectasis, which begins with a definite bronchial affection,
or with a pneumonia or a pleurisy ; the worse constitutional symptoms
being relegated to the late stages. Again, when the patient's affection
begins with a profuse haemoptysis the probability of its tuberculous nature
is great.
Moreover, the duration and the progress of the two diseases are
strikingly different. Cough and expectoration of many years' standing,
in a subject not markedly marasmic, would not be features of the common
phthisis ; though we should not forget that unilateral phthisis may, and
often does, run an exceedingly protracted and mild course. In such a
case the signs would be unmistakable and strictly apical, and therefore
tmlike those of bronchiectasis which, when single, hardly ever implicates
the pulmonary summit.
(b) Between ordinary pulmonary tuberculosis and ordinary bronchi-
ectasis a very marked contrast in the general clinical appearances is at once
78 SYSTEM OF MEDICINE
perceptible. In the ultimate stage of pulmonary consumption there is no
difficulty in the diagnosis ; the patient carries it written large in every
feature. At a rather earlier period in the complaiat, when doubt might
be possible, the same peculiarities are apparent, although not yet so
manifest as to strike the superficial observer. They are briefly these —
wasting of the subcutaneous fat in general, and in particular of the fat of
the orbit and of the cheek; wasting of the muscles; visible loss of
energy ; pronounced ansemia, in the strict sense of the word, namely,
reduction in the total amount of the blood, the patient being bloodless
and withered. These are not features of bronchial dilatation, uncompli-
cated with tubercle, at a like interval after the beginning of the
affection : emaciation usually exists, but it is not extreme ; there
may be slight anaemia also, but it does not confer the characteristic
wan look of phthisis. The hollow orbit, with undue exposure of the
sclerotic, the sunken cheek with projecting malar eminence, and the thin,
drawn lip are all conspicuously absent. Instead of these bronchiectasis
often presents outward peculiarities of its own ; a certain fulness of
the eye, of the lip, and of the features, and a slight duskiness of the
complexion suggestive of congestion rather than of anaemia : and the
veins, the jugulars in particular, are commonly conspicuous, if not
turgid. On analysis these peculiarities will be found correlated with the
state of fulness of the right side of the heart, which in advanced phthisis
is never surcharged, in spite of the great obstacle to the pulmonary circu-
lation. In short, the bulk of the blood is not reduced in proportion to
the pulmonary destruction, as is the case in phthisis. For the same reason
also the depressed and devitalised aspect peculiar to phthisis is not noticed
in this disease.
Another striking peculiarity is the unusually bulbous expansion of
the finger-tips, associated with a very marked incurvation of the nails.
In phthisis the nails are aduncate, but the finger-ends are seldom much
clubbed ; nay, the pulp of the finger is often wasted.
Prognosis. — The spontaneous cure of acute bronchiectasis, such as it
occurs in the growing lung of infants, cannot be expected at a later age ;
and a restoration of the damaged lung is impossible. In rare instances,
where the dilatation is single, and where it is no longer the seat of
catarrh, as in the exceptional case of the cicatricial closure of its bronchus
higher up, the disease may become obsolete. Lebert quotes a case of
Bamberger's, in which the formation of an external fistula eventuated in
a cure ; and a similar result might be hoped for from the surgical treat-
ment of a solitary dilatation. In the great majority of chronic cases, so
long as the original conditions persist, the disease, if left to itself, is in-
evitably progressive ; and therefore less likely as time goes on to be per-
manently relieved. The most favourable achievement to be gained by
treatment is often no more than a relative quiescence of the trouble ; or a
reduction in the rate of a progressive destruction of the lung.
As regaa-ds duration of life, the great diversity in the kind, degree,
and multiplicity of the lesions, and of their bronchial, pulmonary, and
BRONCHIECTASIS 79
pleural complications, must establish a "wide difference l)etween the chances.
Of this some idea is given by the figures obtained by Lebert in a series
of fifty-two cases.
The period of survival was : —
Of one year .... in 21-1 per cent
Of one to two years . . . „ 7'7 „
Of three to five years . . , „ 30-7 „
Of six to ten years . . . „ 15"5 „
Of upwards of ten years . . „ 25-0 „
Apart from all other difficulties, an exact determination of the extent
and number of the lesions is so tmlikely to be attained by physical
examination, that the physician's forecast in the individual case must be
based on very broad considerations : such as the age, temperament, ante-
cedents, energy, nutrition, and general circumstances of the patient ; the
unilateral or bilateral character, and the cirrhotic, emphysematous, or
stenotic type of the affection ; the presence or absence of heart, kidney,
or liver disease ; the present and the previous state of the expectoration,
and the effects of treatment on the catarrh.
Often enough, when all has been taken into account, great uncertainty
must still surround the prognosis, and it will be wise not to venture upon
too precise a statement of the probabilities. In the future much more
may be expected from an improved diagnosis, and from the earlier
adoption of improved preventive, palliative, and curative measures, than
from surgical interference, which is not likely to prove more successful
than in the past.
The worst prognosis will probably always belong to the bilateral cases
and to the unilateral cirrhotic variety, especially when associated with
some defect of the other lung or pleura. Haemorrhage is occasionally a
fatal complication ; it is apt to be profuse in cases of valvular disease or
of secondary cardiac dilatation. The occurrence of perforation and
pyopneumothorax, or of ulceration with the attendant dangers of gan-
grene, of putrid bronchitis, of pysemia, and of septicsemia, would justify a
grave prognosis. Mere foetor of the expectoration is not in itself an
alarming sign.
In those most favoured cases which remain free from all serious
complications life may not be greatly shortened.
Treatment. — The acute bronchial dilatation of early childhood,
depending upon temporary impairment of the expansion of lobules, and
of the pulmonary and bronchial elasticity, is capable of spontaneous
recovery. The general principles on which such cases should be con-
ducted are too well known to need comment.
Inveterate bronchiectasis, though not, strictly speaking, curable, is
often susceptible of considerable amelioration. The extent to which
positive results may be hoped for must largely depend upon the extent
of the bronchial lesions, and especially upon the condition of the sur-
8o SYSTEM OF MEDICINE
rounding tissue; the most unpromising cases being those in which
ulceration or considerable fibrosis has already taken place. ■
In addition to the therapeutic measures specially intended for the
pulmonary condition, we shall consider those meant for the relief of com-
plications and for the improvement of the constitutional state.
The constitutional treatment, an essential adjunct of the pulmonary
treatment, need not detain us long, since its climatic and hygienic aspects
are included in the account to be given of the latter. It cannot be
regarded as curative, nor even as being aimed at the cause of the
affection; but it undoubtedly promotes the patient's chances and the
results to be obtained from symptomatic treatment. The only instances
in which it might claim to be in any sense specific are those in which the
disease has been traced to syphilis, and in which mercury, a drug possess-
ing also general advantages as an antiseptic, should have a trial.
Iron, quinine, and cod-liver oil perseveringly administered, with intervals
of rest and interludes of hepatic treatment, are still, so far as we know,
the best means to the end of strengthening both fibre and function.
Syrup of the iodide of iron in liberal doses, or the hypophosphites of
calcium, of sodium, and of iron also freely administered, are remedies
specially adapted to counteract the exhausting effect of catarrh on the
serous and glandular elements. A liberal, varied and nutritious diet,
and a moderate allowance of burgundy or of port wine are indicated.
Much general tonic effect may also be obtained by systematic treatment
of the skin and by salt-water baths — subjects to be discussed presently.
Neither should we lose sight, in cases showing a tendency to venous
stasis and to cardiac dilatation, of the great value of derivative,
alterative, and mildly hepatic treatment. Much might be effected in
early stages by hygienic and medicinal measures of this kind ; but too
often the opportunity of recommending them is not afforded until it is
almost too late for their successful employment.
The treatment of complications. — ^As in other chronic affections, medical
advice may at first be called in for the treatment of aggravated symptoms,
of complications, and of emergencies. Among the latter, haemorrhage — for-
tunately rare in its worst form, that of ulcerative perforation of an arterial
branch — calls for immediate action, and must be treated on the usual
principle of reduction of blood -pressure, by subcutaneous injections of
morphia, by calomel by the mouth, and by an enema of glycerine (not of
a large bulk of fluid) ; all of which should be administered as soon as
possible.
The febrile exacerbations of the bronchial catarrh, the complications
of pneumonia and of pleurisy, the severe symptoms attendant upon
absorption of septic material, and the occurrence of ulceration, with
threatenings of gangrene, will need measures adapted to each event. In
all of them a supporting plan of treatment will be necessary, and, in those
last mentioned, stimulants, both medicinal and alcoholic, must be freely
administered.
The special treatment of the respiratory organs should be guided by
BRONCHIECTASIS 8l
the following indications : (i.) the emptying of the cavities ; (ii.) the relief
of the foetor ; (iii.) the reduction of the catarrh ; (iv.) the protection of the
membrane from further irritation ; (v.) the diminution of the size of the
dilatations, and (vi.) the improvement of the respiratory function in
general. Until recently these indications have been very imperfectly
fulfilled. The methods employed have acted as palliatives, but their
inability to check the progress of the worst cases has been one of the
reproaches of medicine, and has led within recent years to a desperate
resort to surgical measures, the hopelessness of which has now been made
apparent ; and indeed was almost foretold in the anatomical peculiarities
of the affection.
As regards the emptying of the dilated tubes, sufferers often dis-
cover at an early stage the value of posture as a mechanical aid to the
bronchial outflow. With the majority, lying down or turning to one side
or to the other will bring on more or less cough and expectoration ; but
in others, when the dilatations are situated at the back, it is the change
to the sitting posture which induces the paroxysm of cough. In this
disease, even more than in phthisis, lowering the head, either over the
edge of the bed or whilst standing, will allow the accumulated secretion
to gravitate out of the sacculations and into the receiver. Some patients
are in the habit of practising this method of relief. Its regular em-
ployment should be suggested whenever no contra-indications exist. In
the case of multiple bronchiectasis systematic treatment should also
include, unless there be good reason to the contrary, the yet more
effectual resort to an emetic ; and it is well to administer, for two days
prior to this, repeated doses of an expectorant mixture containing
ipecacuanha, small doses of vinum antimoniale, and iodide of potassium, —
a mixture to be subsequently continued until a second emetic shall have
been taken at an interval of a few days. The object is to wash out the
stale secretion by a more abundant flow of watery mucus. Much will
have been gained if this result can be secured.
For the relief of the foetor two methods have hitherto been adopted
alternately or combined : (a) the inhalation, and (6) the internal adminis-
tration of deodorising and antiseptic agents.
(a) Inhalations as a rule fail to influence the bulk of the accumula-
tions, though they may reach the uppermost layers. A noteworthy
exception must be made in favour of those inhalations which set up
cough and copious expectoration.
Theoretically, oxygen was expected to fulfil a double purpose, as an
aid to respiration and as a disinfectant ; but it has really proved of little
service, partly perhaps because of its tendency to diminish rather than
to increase the activity of the respiratory movements.
Some relief may be obtained from the inhalation, from a jug,
of vapour impregnated with thymol, eucalyptol, wool fir oil, or other
antiseptic.
Inhalation may also be practised with the dry inhaler, through which
air is drawn over a sponge or a quantity of cotton wool steeped in the
VOL. V G
82 SYSTEM OF MEDICINE
solution to be used. Since only those constituents are inhaled which are
volatile at the ordinary temperatures, substances such as carbolic acid,
creasote, tar, terebene, and others can be used fairly concentrated.
Iodine can also be used with proper precautions.
Lastly, inhalation may be conducted on the principle of the spray.
Steam sprays, at one time much in use, have their drawbacks, but in
some respects are convenient : they may be made the vehicle of a great
variety of medication. The complication of steam is avoided in the
mechanical spray-producers which " atomise " the solutions to be inhaled,
by forcing them through the minute orifice of the outlet with a jet of
compressed air worked by an india-rubber hand-ball. In this case the
solutions are not diluted by steam, and must be prescribed of an ap-
propriate strength. The dripping and dampness inseparable from the
steam are avoided ; and the nozzle of the instrument can be introduced
into the nose or mouth, thus almost ensuring actual inhalation of a
large proportion of the remedies. The finest subdivision is obtained —
as in Oppenheimer's "nebuliser" — by combining strong pressure with
smallness of orifice. The latter condition unfortunately limits the supply
of the medicated atmosphere.
(J) The internal administration of creasote, tar, terebene, the essential
oils, the oleo-resins, and the balsams has long been in use. Only of late
years, however, have the improvements in pharmaceutical detail enabled
ef&cient doses of the more powerful of these agents to be taken with com-
fort. Copaiba, tar, and especially thymol, eucalyptol, guaiacol, and
creasote, can be administered in the shape of capsules at frequent intervals
throughout the day ; and, by the persistent action kept up on the
respiratory mucous membrane, may be of great benefit. Fifteen centi-
gramme capsules of myrtol, taken every two hours throughout the day,
are well spoken of in Germany ; and are worthy of trial in cases in which
none of the measures about to be described can be carried out.
The fault of most of these methods is their inadequacy ; they do not
deal with the evil at its chief seat in the depths of the lung. A new era
in the prognosis of bronchiectasis has happily been opened up by the more
thorough methods associated with the names of Dr. Vivian Poore, Sir T.
Grainger Stewart, and Dr. Arnold Chaplin ; these methods consist re-
spectively in the internal administration of garlic, in the intralaryngeal
injection of disinfecting solutions, and in the systematic inhalation of
the vapour of coal-tar creasote.
(1) Dr. Poore's method is based upon the penetrating properties of
some of the volatile constituents of garlic, and upon their stimulating
and antiseptic as well as odoriferous virtues. Garlic probably acts as a
general tonic as well as a local stimulant. Its local effect is produced at
the surface of the mucous membrane by exhalation ; but the fact that the
smell of garlic is also given off by the skin suggests that the constitutional
influence of the drug may be widespread and important.
The favourable results reported by Dr. Poore in his work on Nervous
Affections of the Hand and other Studies were obtained from the continued
BRONCHIECTASIS 83
administration of sufficient garlic to render tlie odour permanent in the
breath. In the cases to which he refers the original foetor of the ex-
pectoration was replaced by a pungent smell reminding one of that of
syringa. The discharge was greatly diminished; and a remarkable improve-
ment took place in the health, in the strength, and in the weight of the
patients. The treatment is generally well borne, and, if the remedy be
taken with meals, patients submit to it without much inconvenience. A
clove of garlic is chopped up and mixed with the beef-tea, or preferably
enclosed in gelatine capsules. I have administered as much as eight
capsules daily, each containing thirty grains of chopped garlic. An
extract might also be used. Dr. Poore suggests that sulphide of allyl,
which is contained in the essential oil of garlic, is probably the remedial
agent. The oil of allyl has an exceedingly penetrating smell. It
should be taken immediately after meals. I have prescribed it in three-
minim capsules three times a day ; but this dose is too large, and soon
disagrees. Capsules containing half a minim of the oil will be found
more convenient. The remarkable results obtained by this method are
not limited to cases of bronchiectasis, but have also been obtained in
phthisis. The chief theoretical objection to the treatment by garlic
is that, whilst it provides for the disinfection, it does not ensure the
complete clearance of the dilated bronchi, nor directly assist their con-
traction.
(2) Intratracheal injection, suggested years ago, and experimentally
tried in animals, was first performed with the hypodermic syringe, — a
valuable method in some cases, and was described by Dr. Sehrwald.
The idea was applied in a practical form to the treatment of pul-
monary affections by Rosenberg, Colin Campbell, Jamieson, Downie,
Byrom Bramwell, and by Sir T. Grainger Stewart, who treated with
great success by the intralaryngeal method an inveterate case of fetid
bronchiectasis in which all other measures had failed. The treatment
consisted in injecting twice daily into the trachea (through the glottis)
one drachm of a solution of 10 parts menthol and 2 parts guaiacol in
88 parts of olive oil. The injections were continued for a considerable
time with benefit.
This method, which has now been fairly tried and seems likely
to lead to important results, is the only one which aims at disinfecting
the secretions in the lung by fluid admixture with the disinfectant, and
at treating the mucous membrane locally by soluble applications. What
proportion of the injection may reach the dilatations will depend upon
circumstances not easily controlled, but chiefly upon the posture adopted
by the patient at the time of the operation and afterwards. At any rate,
the efifect on the bronchial mucous membrane must be widespread and
decided, and, with a systematic use of the treatment, would finally extend
to that of the diseased mucous membrane also. The possibilities opened
up by this therapeutic innovation are obviously great, and its applica-
bility is not restricted to the disease under discussion, nor to the stated
formula. Chronic bronchial catarrh, fetid or putrid bronchitis, and
SYSTEM OF MEDICINE
bronchorrhoea, especially of the purulent variety, are suited for its
adoption.
Although in common with those who have tried this method I have
wondered at the facility with which the pulmonary lymphatics dispose of
the injected solution, we are left too much in the dark as to the destina-
tion of the latter. It is much if, by carefully directing the nozzle of the
syringe and adjusting the patient's posture, we can ensure the treatment
of one lung rather than of the other ; but we are unable to control the
injected fluid in its course down the tubes. In the majority of cases
nothing but good happens. In tuberculous cases, however, there may be
some misgiving as to the possible dissemination of the infection from the
upper into the lower lobes. From personal observation I regard the
use of the method in cases of phthisis with grave suspicion ; and it
has been my regret to witness, after its repeated use, the appearance
of persistent rS,les, of bronchial engorgement, and of catarrhal pneumonia
at both bases in a case which ended fatally.
(3) No objections of this sort can be urged against Dr. Arnold
Chaplin's creasote method, which both theoretically and in its results is
the only one hitherto claiming to be strictly rational and thoroughly
adequate. Its principle is to obtain an amount of coughing sufficient to
squeeze out every remnant of the noxious secretion, and to keep up local
disinfection by inhalation for a sufficient time, and in sufficient strength,
to enable the mucous membrane and the lung itself to be completely
purified. These indications once fulfilled, nature will do the rest.
Living in an atmosphere of the disinfectant would carry out an important
part of the treatment ; and Dr. Chaplin originally noted the tradition,
which exists among workmen constantly employed in an atmosphere
of creasote, that the fumes " clear the chest of phlegm," and confer an
immunity from " asthma " and consumption. But in bronchiectasis the
object is to bring about a complete expectoration of the bronchial
contents; and with this view the creasote atmosphere has to be made
almost intolerably strong, so that it can be inhaled for short periods only.
This concentration of the vapour is the irksome side of the treatment ;
but any objections connected with the hardships of the method will, after
a brief trial, be laid aside when the patients have experienced the
remarkable relief afibrded by its use. In addition to the intense cough,
which has the advantage of leading to inhalations of the disinfecting agent
proportionately deep, the discomforts are chiefly the irritating action
upon the other mucous surfaces and the eyes, the strong smell which
clings to the hair and clothing, and the diffusion of the smell into the
surrounding space. So pervading is the odour that it may be complained
of even within neighbouring houses, and it is desirable to provide an
entirely separate inhalation chamber at some distance from the doors and
windows of other buildings. The remaining difficulties are met by loosely
plugging the nostrils with cotton wool, by wearing over the eyes watch-
glasses framed in bandage or sticking-plaster, and by covering the
garments and the head with oiled silk or mackintosh.
BRONCHIECTASIS 85
The inhalation chamber should be of small size, 6 or 7 feet wide by
8 feet high, and should be made as air-tight as possible, with cotton wool
or tow, in order to obtain a dense creasote atmosphere. In vaporising the
creasote proper care must be taken to prevent a conflagration. A fair-
sized metallic evaporating dish is the best, and into this it is convenient
to place some dry sand. Some more stable support than the common
tripod should be used, and gas flames must be avoided.
At the first sittings the patient may with advantage enter the room
before the spirit lamp is lighted under the dish containing the sand and
creasote ; but subsequently time may be saved by vaporising before-
hand some of the creasote. The duration of the exposure is gradually
increased from a quarter of an hour to an hour or more. The residual
phlegm dislodged by the searching cough is exceedingly oifensive ; but
the foBtor is partly covered by the strong creasote odour. The treatment,
unless contra-indicated, is to be continued daily until little is coughed
up in the chamber, and until no expectoration is brought up spontaneously
the next morning. In an average case this will imply a treatment of
from four to six weeks.
In itself the adventure is a valuable respiratory exercise. Whilst the
cavities are being cleared and disinfected collateral expansion of the lung
is induced by the cough, and the gradual contraction of the sacculations
is promoted. A remarkable improvement takes place in the general
health and strength, as well as in the respiratory capacity. In the seven
cases originally reported by Dr. Chaplin excellent results were obtained.
Notes of equally successful cases have been kindly communicated to me
by Dr. Devereux of Tewkesbury. A full account of one of his cases has
been published by Dr. Brian Dobell. Through the kindness of Dr.
Dobell and of the Editor of the British Medical Jcumal the temperature
chart of this case is reproduced on the following page as a striking illustra-
tion of the reduction of temperature which is obtained in pyrexial cases.
A case of inveterate bronchiectasis under my own care is for the
present cured. In another the relief seemed to be complete, but was
followed by a relapse which did not yield thoroughly to a second course.
Eeduction of temperature and of the expectoration and general improve-
ment were also observed in a third patient with fibroid disease of the
lung and profuse oifensive expectoration ; but the treatment has been
temporarily interrupted, whilst these pages are being written, because
of an intercurrent aggravation of the catarrh, due perhaps to irritation by
the fumes.
The freedom from risk and the brilliant results hitherto secured in
most of the cases reported leave us no choice : so long as we have
no better method, every sufi'erer should have the benefit of a trial of
the inhalation method. A combination with it of the administration of
garlic, whilst adding a fresh therapeutic infliction to a trying treatment,
would probably curtail the duration of the latter. Lastly, for cases not
jrielding sufficiently good results the intralaryngeal injection method
would still be available.
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BRONCHIECTASIS 87
The prospect of a permanent cure will be greater the earlier the
creasote treatment can be applied. Some of the inveterate cases which
have long resisted all other remedies may fail to end in a complete
recovery, and may need repetitions of the course. But their number
will decrease as the method comes into more general use. Indeed, it is
not improbable that in the future, when cases are treated sufficiently
early, bronchiectasis may cease to be regarded as an incurable disease.
Surgical treatment. — An attempt was made some years ago to treat the
lesions by injecting weak solutions of carbolic acid, of iodine and of
other antiseptics through the chest wall into the surrounding pulmonary
tissue. No good results were obtained by this method, which has since
then been almost forgotten.
Treatment by incision and drainage was proposed and attempted as a
last resort a few years prior to the recent advances. Although this may
now be regarded as a closed chapter in the history of pulmonary thera-
peutics, it calls for a few retrospective remarks. The few cases of
operative interference which have been reported in this country and else-
where are not encouraging. Hofmockel, who gives a review of eighty
cases of operation for abscess, for gangrene, or for bronchiectasis, finds
that the worst results were obtained in the cases of bronchiectasis.
A disastrous experience has shown that success can be looked for only
where a single dilatation exists. These are, however, the cases in which the
symptoms are least urgent as well as least refractory to the ordinaiy
measures. Where help is most needed — ^in the instances of multiple
sacculations^ — surgery is doomed to failure. To attempt multiple in-
cisions is to multiply the risks of septic infection of the pleura ; and to
open only one of the sacculations is not only to leave a great part of
the disease unrelieved, but to place its remaining foci in a worse position
than before, by weakening the expiratory mechanism of cough owing to
the direct leakage of air, and to the unavoidable interference with the
freedom of the thoracic movements.
The mechanical hygiene of respiration and the climatic treatment may be
considered under one heading. They are both necessary adjuncts to any
method of treatment, although in the future their relative importance will
probably be less than it has been heretofore.
For the control of the catarrh and for the protection of the mucous
membrane from further irritation we had until recently looked with
greater confidence to the effect of climate than to medicine. The great
indication was to strengthen the clogged and sodden mucous membrane
by constant contact with the purest air, whilst invigorating the system
by prolonged residence in a warm and equable climate, where patients
might live in the open. The dry and stimulating climates to be found
on the table-lands of South Africa, in South California, on some of the
slopes of the Andes, or at high elevations in islands, as in the West
Indies, or even in the Mediterranean, as at Ischia or Capri, are
specially indicated ; and along the shores of the Mediterranean there is
a large selection of suitable sites. For a fuller discussion of this part of
88 SYSTEM OF MEDICINE
tte subject the reader is referred to the chapter on " Climate and Disease "
in the first volume of this work.
Patients who at a sufficiently early date adopt and adhere to this
thorough treatment by climate might hope for a permanent arrest of
their catarrh, and, thanks to the increasing pulmonary expansion due to
open-air life, might ultimately secure a degree of improvement almost
equivalent to a cure. For this happy result a life-long treatment is now
less indispensable, nor need we expatriate our patients. The climatic
treatment is henceforth, as in the case of other diseases, an after-cure.
A suitable climate for the winter retains its importance ; but its selection
is no longer limited as formerly when the consequences of any incidental
catarrh were much less within our control. We might, for instance,
without serious risk, in the case of some convalescents not advanced
in years, recommend the dry, cold atmosphere of the Alpine winter and
the outdoor life and physical exercise, which are not the least of the advan-
tages of the Alpine cure ; whilst for those unable to travel our home
resorts and seaside places afford eligible climates, among which Thanet,
Folkestone, Eastbourne, and Brighton deserve special mention.
Warm seor-water laths may be of considerable value. For some patients
a stronger effect might be sought from the artificial Nauheim salt-water
baths. In any case the temperature and the duration of the bath
must be adapted to the individual. An important part of the balnear
treatment is the tepid, and ultimately the cool or cold affusion terminating
the bath, followed by strong friction of the surface.
Among the medicinal springs the sulphurous thermal waters enjoy a
deserved reputation in the treatment of this affection. Harrogate, Moffat,
Challes, Aix-les-Bains, Eaux Bonnes, Eaux Chaudes, Cauterets, Bagnferes-
de-Luchon, and a variety of other spas might be visited with' profit ; but
for patients unable to leave home a substitute may be found in tonic
baths combined with the internal administration, for recurring periods,
of some preparation of sulphur.
At most of the foreign health stations and at some of our own various
hygienic measures are recommended in addition to the use of baths or
waters.
Among them special value attaches to the following : —
(a) The inhalation of an oxygenated and terebinthinated atmosphere ;
(6) systematic exercise, at first passive only, of the thoracic muscles and
of the abdominal muscles, including the use of dumb-bells or clubs, and
a variety of postural exercises ; (c) systematic respiratory gymnastics,
such as deep inspirations followed by deep expirations in various attitudes,
reading aloud or singing; {d) general massage and passive resistance
movements followed by brisk rubbing. An improved circulation through
the skin and a general bracing of its nerves are special objects of this'
form of treatment ; another is the tonic effect on the right heart and
pulmonary circulation, and the help which the mucous membrane may
derive by sympathy from a healthier cutaneous surface, and from its
improved reaction to atmospheric influences.
BRONCHIECTASIS 89
The importance of these systematic methods lies in the regularity
with -which they can be enforced ; but the benefit they can confer might
equally well be secured by a perpetual out-door life in a really suitable
climate, and by progressive exercise gradually pushed to the extent of
slight breathlessness.
The contraction of the sacculations and the general improvement of
the respiratory function, which are the final aims of our treatment, are
directly promoted by all the measures which have been detailed ; and in
none of the ordinary cases, nor even in fibrotic cases if one lung be perfectly
sound, need we despair of their partial attainment.
Wm. Ewart.
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60 SYSTEM OF MEDICINE
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W. K
PNEUMONIA
Definition — Nomenclature — Historical sketeli — Clinical course —
Symptoms and physical signs — Diagnosis — Complications and
sequels — Secondary Pneumonia and other Clinical Varieties —
Morbid Anatomy — Histology — Bacteriology — Pathology — Eti-
ology— Prognosis — Treatment — Statistics of four hundred and
thirty-flve cases — References — Catarrhal Pneumonia — Chronic
Pneumonia.
Synonyms. — Peripnewnony, irepnrvevfji.ovla, Hippocrates and later
Greek writers.^ Pnewnonia, Tvevfiovia (Attic form irkm^i.ovl.a., used by
Plutarch). Peripneumonia vera (Sydenham), as distinguished from
Peripneumonia notha, " obstruction of the lungs by a heavy, viscid
pituitous matter," that is, in modern nomenclature, bronchitis. Pneumonic
fever ( Huxham). Pleuro-pneumonia ; Acute or Sthenic pneumonia ; Lobwr
pneumonia/ Croupous or Fibrinous pneum^onia ; Pulmonary fever.
^ "Vehemens et acutus morbus quem irepnrvEVii.ovi.Kbv Grseci vocant." — Celsus, lib. iv.
cap. vii.
92 SYSTEM OF MEDICINE
Definition. — A febrile disease, running a short course, with a special
form of acute inflammation of one or both lungs.
The disease which is now understood by the name Pneumonia, when
stated without qualification, has been a common acute disorder in all
historical times, in all climates, and at all periods of life. It is one of
the most striking and characteristic of maladies in its symptoms and
physical signs, and not less so in its morbid anatomy. Other forms
of acute inflammation of the lung bear the same name ; but they
bear it with a diiference : they are, or should be, always distinguished as
broncho - pneumonia, lobular, or catarrhal, hypostatic, tuberculous, or
pyeemic pneumonia. These all difi'er pathologically and clinically from
the disease now under consideration ; and no less different is a chronic
interstitial inflammation of the lungs — also known as iron-gray or slaty
induration — which is sometimes called chronic pneumonia. It would be
well if the historical name pneumonia could be restricted to the acute
disease with lobar hepatisation ; and the other inflammatory affections
of the lung be named pulmonary catarrh, pulmonary abscesses, and
cirrhosis of the lung.
History. — Before morbid anatomy was studied, or physical diagnosis
invented, acute inflammations of the chest, whether affecting the parietal
pleura alone or the lung with its pleural covering, were described under
the name peri-pneumonia ; that of " pleurisy " being applied to the sharp
characteristic pain in the side which accompanies both diseases. Charle-
magne is said to have died of a " fever, with a pain in the side which
the Greeks call pleurisy." We now recognise the pain as due to in-
flammation of the pleural membrane, and the name of the symptom is
applied to the anatomical change which it accompanies ; pleurisy always
accompanies acute lobar pneumonia, although it is often present independ-
ently ; and the name pleuro-pneumonia is therefore superfluous.
The characteristic clinical features of pneumonia were identified with
solidification of the lungs by Morgagni. Baillie described them as some-
times converted into a solid mass very much resembling liver (hepatisa-
tion). But Laennec, Cruveilhier, and Eokitansky completely described
the anatomy of the disease. The diagnosis of pneumonia by auscultation
was one of the most important results of Laennec's great discovery.
The chief steps since made in advance have been the proof by Addison
that the exudation of pneumonia is not into the " interstices " of the lung,
but into the air-vesicles themselves ; the distinction between fibrinous or
lobar and catarrhal or lobular pneumonia, which is due to Eokitansky ;
and the discovery of a specific pathogenetic microbe, which has been
the work of numerous observers.
Clinical features of the disease. — Onset and early symptoms. — The
symptom which commonly marks the onset of pneumonia is a feeling of
chilliness, a fit of shivering. When this initial rigor has passed off,
the patient often feels prostrate, with headache but without the severe
lumbar pains which mark the onset of some acute diseases. He becomes
thirsty, the skin is hot and dry, and the pulse is quickened ; the tern-
PNEUMONIA 9 J
perature rises rapidly from the beginning, and by the evening of the
first day often reaches 103°, or in children 104°.
When twelve or more hours have passed from the onset of the
disease the patient's aspect is characteristic ; the face is flushed, the
eyes bright and watchful, the expression that of constraint and
apprehension. He usually lies on his back without marked orthopncea.
Breath is short, frequent, and shallow, deep and efficient respiration
being hampered by a sharp pain in the side ; the pulse is quickened,
full, and of increased tension, but varies less from the normal than the
temperature, and still less than the ■ breathing. The skin is dry and
pungent. Except scarlatina, and ague in its second stage, there is
scarcely any disease which gives such a sensation of burning heat to
the hand of the observer, a character probably due to the absence of
perspiration.
Not infrequently an eruption is seen upon the face, which consists
of a group of small, clear vesicles on a reddened patch. This herpes
labialis is most commonly seen on the upper lip in the neighbourhood
of one or the other nostril; but it may be seen on the lower lip at
the angle of the mouth, or upon any part of the cheek, chin, or jaw;
hence it is sometimes called herpes facialis. Although frequent enough
to form a characteristic feature of pneumonia, it is probably not present
in more than two-thirds of the acute idiopathic cases we are now describ-
ing; and it is the exception instead of the rule when pneumonia is
secondary to another disease. Moreover, exactly the same eruption may
occur with slight pulmonary catarrh, or bronchitis without broncho-
pneumonia, or with a mere cold in the head. Indeed some persons have
an attack of herpes labialis with almost every accidental catarrh. It is
occasionally seen in other febrile attacks also ; or it may even follow a
rigor without subsequent fever. The little vesicles cause no irritation
or pain ; they become purulent and dry up, leaving their dark crusts,
which drop oflF and leave no trace. The eruption lasts from ten days to
a fortnight.
As in other febrile disorders, there is complete loss of appetite, with
constipation. By the second or third day the tongue is thickly plastered
with white fur, particularly if the patient is kept on a diet of milk.
It closely resembles the appearance of the tongue at the beginning of
acute rheumatism and of scarlatina.
Physical examination of the chest diu-ing the first few hours will
often determine the nature of the case by the presence of a pleuritic
rub, or a small crepitant ra,le ; and towards the end of the first twenty-four
hours, or on the second day, consolidation of a part of the lungs will be
recognised by its physical signs. These will be conveniently considered
together after the account of the external symptoms has been completed ;
but it must be stated here that the evidence of physical changes in the
lungs, derived from auscultation, is occasionally absent on the first, the
second, and even the third day. In these cases there is no reason to
suppose that the local change is present without its appropriate signs ;
94 SYSTEM OF MEDICINE
nor are we aware of any such case in whicli the opportunity occurred of
ascertaining the state of the lung ; in the absence of such direct observa-
tion, we are justified in believing that the pneumonic fever with all its
characteristic symptoms may precede the pneumonic hepatisation not only
by hours but by days.
Clinical course. — The temperature, after an abrupt and rapid rise on
the first day of the disease, continues at the degree then reached, or
rises somewhat higher; the mean range being from 103° to 104°. In
severe cases it may reach 105° and upwards; while in slight cases,
particularly in children, it is often a degree lower. The same is true,
even of severe cases, in elderly people. The moderation of the pyrexia,
not uncommon in children, depends on the rule that the mildest cases
of pneumonia, as of enteric fever, occur in children; the lower tem-
perature in elderly pa,tients on the still more general rule that the
same degree of febrile disturbance, as measured by other symptoms and
by local changes, will produce a higher temperature in a child or young
adult than in an aged patient. The morning remission and evening
rise, which are rarely quite lost in any case of pyrexia, are present in
pneumonia' ; but they are less marked than in enteric fever, and still less
than in suppurative fever. Hyperpyrexia is not an uncommon event;
some cases indeed, and these not always the most severe in their sub-
sequent course, manifest a, very high temperature on the first or second
day. The pulse usually lags behind the rising temperature, and the
respiration follows rather the extent of the local changes in the lungs
than the course of the fever. (Appendix, p. 134.)
Sometimes at the very beginning of the attack, sometimes later on
the first day or in the course of the second, the patient feels a sharp
pain like a magnified stitch in the side. This pain, independently of
auscultation, tells us which lung is affected; for although the pain is
pleuritic, the pleurisy is part of the pneumonia. It is usually referred to
the front of the axilla an inch or so outside the nipple ; sometimes to
the post-axillary line a little outside the angle of the scapula ; occasionally
it is felt in the mid-axilla, and still more rarely towards the base of the
lung. A friction sound can usually be heard at the seat of pain ; but
inspection of a pneumonic lung after death shows that the pleural inflam-
nrntion is more extensive than the point on the chest-wall to which the
pain is referred. It is certainly rare to hear a rub under the clavicle,
or above the scapula in cases of apical pneumonia; and the same
remark applies to the pleurisy which so frequently accompanies tuber-
culous disease of the apex.
The pain felt on taking a deep breath makes the breathing shallow
and hurried, without dyspnoea; and the cough is short, dry, and
restrained by the patient.
The urine, from the first day onward, shows the characters of pyrexia
in a marked degree. It is like that of rheumatic fever, of quinsy,
scarlatina, or typhus ; scanty, high-coloured and very acid. The lithates
of soda and potash are deposited as it cools, partly from want of water to
PNEUMONIA 95
dissolve them, partly from a strongly acid reaction, and partly also from
an increase in tie output of uric acid. The daily excretion of urea is
also larger than in health.
The inorganic salts excreted in the urine — the phosphates, sulphates,
and chlorides, and particularly the chloride of sodium — are diminished
as in other febrile disorders; but in a much greater degree. When
nitrate of silver with excess of nitric acid is added to the urine of
pneumonia, it is not uncommon to see an opalescence only in place of a
thick opaque precipitate. This diminution of the saline constituents of
the urine does not depend merely on the patient's diet, as experiment
has proved, but is probably due to the abundant exudation of salts
into the lungs. Hepatised lung is found to contain considerably more
saline constituents than healthy limg, and during convalescence there is
excess of salt in the urine.
Another feature of febrile urine in general is particularly frequent in
pneumonia, namely, the presence of albumin. This has been observed by
different authors in one-third, one-half, or two-thirds of the cases. It is
probable that even the last estimate is below the truth, and that some
amount of albumin is present in almost every case of primary acute
pneumonia.
The sputwn which the patient coughs up is characteristic. It is not
abundant, not very frothy, and is unmixed with sahva or with pus. It
consists of clear, tenacious mucus with a few air-bubbles, and is more or
less deeply stained with blood. It hangs on the patient's lips and clings
to the vessel in which it is received. The colour, when most char-
acteristic, deserves its traditional name of "rusty"; it is a bright orange-
brown, resembling the burnt sienna of the colour-box. When the sputum
is abundant and thin it loses its bright chestnut colour, and has been
aptly compared to the juice of dried prunes when stewed. Under other
conditions the reddish tint is lost and is replaced by a greenish yellow ;
the sputum is then compared in colour to greengages. When the
amount of blood is scanty, a bright lemon colour is no less characteristic
than the more usual rusty sputum ; when, on the other hand, it is excessive,
the yellowish brown is replaced by a more decided red, and in some cases
pure blood is spat up. This haemoptysis is sometimes very free, and
denotes, we may presume, unusually intense congestion or unusual
fragility of the pulmonary vessels. Whatever its immediate cause, it
does not appear to have any unfavoiurable import, and certainly it does
not point to subsequent tuberculous disease. But the " prune- juice " and
the " greengage " varieties of pneumonic sputum are justly held to be of
graver significance.
On microscopic examination, beside transparent structureless mucus
with a few small air-bubbles, the sputum of pneumonia is found to con-
tain abundant blood-discs, a few leucocytes, and frequently minute casts
of the smallest bronchioles. When treated by appropriate staining, the
pneumococcus or diplococcus described by Fraenkel — an oval or rounded
organism with a thick transparent capsule — is revealed ; some of them are
96 SYSTEM OF MEDICINE
separate, some in groups of three or four ; but almost every slide will
show several pairs united two and two in characteristic fashion.
The rusty sputum has of all the symptoms of the disease the best
right to be called distinctively pneumonic. Its peculiarity is due to the
hsemorrhagic quality of the inflammatory exudation itself, which may be
compared in this particular to that of acute glomerular nephritis. As in
the smoky urine of this disease so in the rusty sputum the blood-discs have
been poured out uniformly and continuously from the first, and are there-
fore more equally distributed than when hsemorrhage is added to inflam-
mation as a subsequent event. Accordingly we do not find the charac-
teristics of " rusty " sputum in the haemoptysis of phthisis, of aneurysm,
of purpura, or of laryngeal or tracheal ulceration. Nor is it, as a rule, to
be seen in cases of cardiac disease with consecutive pulmonary hsemor-
rhage. In these cases the blood is more separate from the sputum.
When, as sometimes happens, characteristic rusty sputa are observed in
the course of heart disease, it is probable that the haemorrhage is compli-
cated by local consecutive hepatisation. This is often recognised during
life, but still more often it is ascertained after the patient's death.
It is well known that children do not expectorate ; hence we lose in
these cases the important help derived from inspection of the sputum.
Even as late as the age of eleven and twelve years the patient may be
unable or unwilling to bring up the phlegm. When a child vomits after
coughing we may sometimes observe characteristic rusty sputa in the
basin. Old persons, as a rule, are like children in this respect ; they seem
unable to expectorate the sputa.
The nervous system is less frequently and severely affected in patients
suffering from pneumonia than in most cases of typhus or enteric fever ;
but more frequently than in rheumatism without hyperpyrexia. From
the beginning the patient's rest is disturbed ; and if the case be protracted,
insomnia may become a grave and distressing incident. Some degree of
nocturnal delirium probably accompanies almost every state of pyrexia,
even that which attends a feverish cold ; and it is sometimes severe in
attacks of influenza othervrise mild. In this slight degree, shown by the
persistence of the impression of dreams, and by confusion of time and
place, delirium is probably present in every case of pneumonia. It seems
never to take the terrible form occasionally seen in rheumatic fever, and
associated with hyperpyrexia and pericarditis ; but it is sometimes import-
ant from its preventing sleep and prompting attempts to get out of bed.
When an intemperate person is seized with pneumonia, the febrile de-
lirium, as in other cases of this nature, assumes the characters of delirium
tremens ; and the gravity of the case is at once apparent. But even in
pneumonia of the most temperate persons diurnal delirium is a serious
symptom.
Termination. — In a slight case of pneumonia, particularly when affect-
ing a child, after a sharp onset and a day or two of ' fever the tempera-
ture falls rapidly, the skin begins to act, refreshing sleep is obtained, and
the patient awakes on the third day to find convalescence begun. These
PNEUMONIA 97
cases are, however, the exception. The symptoms much more often,
even in favourable cases, last till the fifth, the sixth, or the seventh day ;
and in many persons who make a good recovery the illness is prolonged
into the second week, so as to give a duration of eight, nine, or ten days.
Beyond this the duration of the disease, unless due to some local cause,
is certainly rare. The most frequent extension of the inflammation is to
the other lung ; but pleuritic effusion, and particularly effusion of pus,
pericarditis, or severe and persistent bronchial catarrh may protract the
disease beyond its natural limit. (Appendix, p. 135.)
In unfavourable cases it is very rare for death to take place on the
first or second day, as in malignant variola or scarlatina. Even with
double pneumonia the patient seldom succumbs before the fourth day ;
the time of greatest anxiety is that of the latter days of the first and the
early days of the second week. In such cases, while the temperature
still ranges high, the insomnia and delirium become more severe ; the
tongue is dry and brown as in typhus, and the pulse more frequent,
weaker, and perhaps irregular. The rapidity of breathing, the dyspnoea and
the cyanosis depend upon the extent of lung involved. When the whole
of one lung is hepatised, the other rarely escapes ; and in such cases addi-
tional difiiculties in aerating the blood are often caused by profuse bron-
chial secretion which chokes the air-passages, passes up and down with
each weak breath, and is not expelled by a vigorous cough. In the other
cases, even with moderate secretion and without signs of cyanosis, the
heart begins to flag, the pulse grows small and weak, and the condition
becomes like that of a typhoid patient at the end of the third week.
The favourable close of an attack of pneumonia, whether earlier or
later, will almost always be marked by a critical fall of tempera,ture ; and
even in cases which prove fatal by some intercurrent complication, this
crisis may often be observed. Indeed a gradual fall of temperature, or a
temperature which continues high after ten or twelve days, should lead to
a revision of the diagnosis, and to a careful search for some disturbing
condition apart from the primary disease.
Phjsical signs. — The auscultatory evidence of pneumonia, which was
discovered by Auenbruger and Laennec, and has since been confirmed,
corrected, and elaborated by a succession of physicians, is in the
majority of cases striking and unequivocal. It suffices for the re-
cognition of the presence, extent, and course of pneumonia without the
aid of other symptoms ; just as a sure diagnosis of the disease can be
made from the aspect of the patient, the pain, the sputum, the urine and
the fever, without the aid of percussion or auscultation. Together
they make the recognition of primary pneumonia one of the easiest
of the physician's tasks.
It is seldom that we have the opportunity of examining the chest at
the beginning of the disease. "Within a few hours of the initial rigor
and rise of temperature we often find the percussion note at the base of
one lung less clear and flatter than at the other ; the respiratory murmur
has lost its normal character, and has assumed more or less of the bronchial,
VOL. V H
98 SYSTEM OF MEDICINE
tracheal, or tubular quality. Sometimes, however, mingled with this
diminished dulness and with the "vesiculo- bronchial" breathing, or
even preceding it by a few hours, may be heard an adventitious murmur
which is very characteristic, and was thought by the earlier auscul-
tators to be even more frequent and more decisive than later ex-
perience has confirmed. This is the rdle crdpitant of Laennec, who briefly
described it in the following words : — " Dans le premier degr^ de la
p^ripneumonie, la respiration s'entend encore dans le point affect^, soit
que la percussion donne en cat endroit un son mat, soit qu'elle n'indique
aucune difference sensible, ce qui varie. Mais la respiration, quoique
sensible dans le lieu affects, est cependant beaucoup moins grande et
moins sonore que dans les autres parties de la poitrine ; elle est, en
outre, accompagnde, dans Tinspiration surtout, d'une espfece de crepitation
ou de r41e l^ger, dont le bruit peut Stre compart k celui du sel que Ton
fait decr^piter en le chauffant dans une bassine; ce rale, que j'appelle
r^le crepitant, est le signe pathognomonique du premier degr^ de la p^ri-
pneumonie. II serait difficile de le mieux d^crire ; mais il suffit de I'avoir
entendu une seule fois pour ne plus le m^connaitre" (17, § 209).
In other places the illustrious French physician admits that the same
" rile crepitant " may be heard in cases of oedema of the lung. He says :
"Le cylindre, dans ce cas, offre deux moyens de reconnaltre I'alt^ration
du poumon. La respiration s'entend beaucoup moins qu'on ne devrait
s'y attendre, k raison des efforts avec lesquels elle se fait et de la grande
dilatation du thorax dont elle est accompagn^e. L'on entend en m^me
temps, comme dans la p^ripneumonie au premier degr^, une 16g6re crepita-
tion plus analogue au rale qii'au bruit naturel de la respiration. Ce rile
crepitant .est mois fort que dans la p^ripneumonie au premier degr^ :
cependant on doit avouer qu'il est fort diflBcile de distinguer ces deux
affections I'une de I'autre k I'aide des seuls signes donnas par le cylindre,
et qu'il est n6cessaire d'y joindre la comparaison des sympt6mes g^n^-
raux" (17, § 500).
This remarkable sound is, as Laennec says, inspiratory ; occasionally
it may be heard with expiration also, but this is exceptional. It is a
" moist " sound, or, to speak more strictly, it is an interrupted sound ;
the parts of which it is made up are very short, very numerous, and uni-
form in duration and quality. Though perfectly audible and distinct, it
is not loud ; lastly, its quality is thin, rather high pitched, and what is
called "musical," "bright," or "clear"; that is to say, it has more tone
and is farther removed from a mere noise than the respiratory murmur,
a sonorous rhonchus, or than the bubbling ri,les in the trachea which form
the death-rattle. On the other hand, it is more of a noise, and has less
tone or musical quality than the metallic tinkling heard in a large cavity,
or the clear percussion note of pneumothorax or of gastric distension.
Unlike other rMes, it is not influenced by coughing. It sometimes
persists for a few hours only; sometimes it lasts until dulness and
tubular breathing show that the lung is completely solid ; sometimes it
leaves the place where it was first heard, and ascends with the advancing
PNEUMONIA 99
line of hepatisation ; or it appears on the opposite side as the first sign of
extension to the other lung. Lastly, under the title " crepitus redux,"
it may reappear, somewhat larger, louder and less musical, when the
solidified lung is recovering and again admitting the air.
This pneumonic crepitation is so peculiar and remarkable a sound
that after it has been heard two or three times it is easily recognised ;
but, beside the account of its acoustic properties attempted above, it
may be compared to some other sounds. Laennec's own illustration,
quoted above, is that of the crackling sound produced by heating salt
over the fire ; this resembles the rMe in being an interrupted sound, and
in the clear sharpness of its quality ; but the crackles are fewer, larger,
and louder. The late Dr. C. J. B. Williams compared pneumonic crepita-
tion to the sound heard when a lock of hair is gently rubbed between the
fingers close to the ear. My own illustration for students was by squeez-
ing a piece of the porous indiarubber, formerly much used instead of a
toilet sponge, after it had been soaked in water. The late Dr. Sturgea
reproduced the sound by pressing dry tissue-paper into a ball, or by
squeezing and relaxing a piece of sponge dipped in gum-water.
The " redux " crepitation is sometimes indistinguishable from that of
pulmonary haemorrhage, or of broncho-pneumonia, or from that which
is commonly regarded, since Laennec's time, as a sign of oedema of the
lung.
The true pneumonic crepitation undoubtedly diifers from these in
being finer or smaller, that is to say, the crackles are shorter and more
numerous ; they have more tone and are less loud ; they are more often
confined to inspiration, and are uninfluenced by deep breathing or by
cough.
Nevertheless the ear of most auscultators tells them that these sounds
are all similar j thus from the more definite pneumonic crepitation we
pass by small gradations through " redux " crepitation to that of broncho-
pneumonia, and so on to the smaller consonating riles of phthisis.
On the other hand, pneumonic crepitation is quite unlike any respiratory
murmur, modified or unmodified ; unlike sibilus or any other continuous
sound, and unlike nou- consonating rSles of every degree. The only
sound heard in the chest which may simulate it is a very soft pleuritic
rub, not loud, but clear and audible at the end of inspiration.
The physical explanations of this remarkable auscultatory sign are of
doubtful validity. Probably the most generally received opinion is that
it is caused by the opening out of the small extra-lobular bronchioles, by
the inspired air, while their walls are covered with viscous exudation.
This explanation, however, appears improbable, as it can scarcely be
applied to the explanation of expiratory crepitation ; and we have no
evidence that collapse of the channels of the air-passages occurs as a
matter of fact. Moreover, true pneumonic crepitation is thus too widely
separated from the allied sounds above enumerated. From these indeed
it may be distinguished by the practised auscultator, who rightly teaches
students to make the same distinction ; nevertheless we must admit
SYSTEM OF MEDICINE
with Laennec that the distinction is sometimes difficult. The air-vesicles
cannot be the seat of this crepitation any more than they can be the
seat of the normal respiratory murmur, or indeed of any auscultatory
events ; for the air in the vesicles is not changed save by diffusion : the
strongest efforts of respiration produce a current in the air-passages only,
which does not reach the lobules. Pneumonic crepitation is an inter-
rupted and probably a "moist" sound, that is, a sound made by
bubbles bursting, and is a consonating rale, that is, a sound trans-
mitted through a solid lung. Regarding it, then, as the finest or smallest
of this group, we may ascribe its production to the same cause, namely,
to air passing through fluid and making a series of crackles which are
transmitted to the ear through a hepatised lung.
There is little reason to acquiesce in the three stages of pneumonia
described by Laennec, either on anatomical or clinical grounds. The
first stage, that of engorgement or active congestion, is in all probability
the beginning of hepatisation, and with the afHux of blood comes the
exudation ; congestion and hepatisation begin and go on together, and
the consonating rfile just discussed is the earliest sign, not of preliminary
hypersemia, but of actually existing inflammation. Hence we find it
mingled with the signs next to be described, signs which are admitted
to denote complete solidification of the lung.
These are bronchial breathing, bronchophony, and increased vocal
fremitus.
This is not the place to discuss the difiicult questions involved in the
physical theory of the respiratory murmur and its modifications in dis-
ease. It must suffice to assume, as most in accordance with physical
facts and least contradicted by clinical experience, the hypothesis
which refers the normal respiratory murmur to vibrations of air due to
a fluid vein, which is produced in inspiration and expiration by the
passage of the air through the narrow chink of the glottis into the wide
channel of the trachea in the one case, and of the upper larynx in the
other. The sounds thus produced are heard by a stethoscope placed
upon the larynx or trachea ; where they have the loud, somewhat harsh,
continuous, blowing character, which is recognised as tracheal, or an
extreme degree of bronchial or tubular breathing. On listening to the
patient's voice with a stethoscope on the trachea we hear the loud vocal
resonance which is known as bronchophony. The same inspiratory and
expiratory murmur and vocal resonance are heard in most persons over
the manubrium ; and in some on applying the stethoscope between the
shoulder-blades, or over the inner part of the first right intercostal space :
but the sounds thus transmitted (not by the column of air, but by the
walls of the trachea and right bronchus), while still harsh and blowing,
are less loud than the tracheal murmur just described. This bronchial
breathing is certainly no new sound ; it is the tracheal murmur diminished
in intensity, because less directly conveyed. As soon as we leave the
neighbourhood of the trachea (that is to say, over nearly, if not quite, the
whole of the chest) we find the resonance of the voice much diminished,
PNEUMONIA
even when it is that of a strong man with thin covering of the thorax ;
while if the thorax be thickly covered by clothing, subcutaneous fat,
or even thick muscles, or if the voice, as in women and children, be
shrill and comparatively feeble, the vocal resonance is weak and not
infrequently absent.
Since the vibrations of speech in the larynx are conducted by the walls
of the air-passages, and when they reach the surface of a healthy lung
are still the same sounds, though diminished in loudness or modified in
character ; and since again the sound of the voice is greatly altered when
transmitted through a solid lung, or through pleui'al effusion, or through
emphysematous lung, or through pneumothorax, yet, however altered or
modified, is still the sound produced by the vibration of the vocal cords
— so, according to the hypothesis now advocated, the breath-sounds
heard over the chest are not produced in the pulmonary vesicles, the
lobules or the bronchial tubes, but in the larynx.
The pulmonary murmur is heard indeed over the lungs, but does
not arise there. It is the same sound which over the trachea we call
tubular, with its loudness diminished and its quality altered by trans-
mission through the spongy lung.
On this view we do not start with a so-called vesicular murmur in
the lung, which becomes bronchial in the bronchi and tracheal in the
larynx ; but in breathing and in voice we regard the audible vibrations as
formed at the glottis and altered, whether in health or disease, by trans-
mission through various media.
Now when, as in pneumonic hepatisation, the laryngeal breath-sounds
are transmitted through a solid lung, they retain much of their loudness
and quality. The expiratory murmur is not shortened and weakened, or
even rendered inaudible, as in health. Inspiration and expiration are
accompanied by a murmur nearly equal in length, loudness, pitch and
quality.
The simplest way of describing the breath-sounds heard in pneumonia
is to call them tubular, bronchial, or tracheal ; and to define them by
reference to the respiratory murmur as heard over the trachea or the
manubrium in health. But, simple as it is, this comparison is not com-
pletely accurate ; it may help the student in the rudiments of auscultation,
but it will probably hinder him when he hears well-marked pneumonic
breathing. It seems that in phthisis, lobular pneumonia of children, and
other conditions of partial solidification, and again in some cases of
narrowing of a large bronchial tube whether by stricture or compression
from without, breath -sounds may be heard which are very different
from the pulmonary murmur, and which closely approach that heard
over the larynx. These may be fairly called bronchial or vesiculo-
bronchial sounds. They differ from the tracheal murmur chiefly in loud-
ness, so that expiration loses its later part and becomes shorter than
when heard over the larynx, though longer than over a healthy lung.
The word " tubular " is often applied indiscriminately as a synonym
of tracheal or bronchial breathing; but by many writers, and I think
SYSTEM OF MEDICINE
■with advantage, it is reserved for the special modification heard most
perfectly in eases of pneumonic hepatisation.
This modification essentially resembles laryngeal, tracheal, and bron-
chial breathing, and differs essentially from the healthy pulmonary
murmur. It has a blowing rather than a breezy quality ; and expiration
is often as loud and usually as long as inspiration ; but it differs from
the normal laryngeal murmur in the following points : it is not so loud,
nay, it may be softer than the bronchial breathing above described ; but,
however subdued, it is remarkably distinct — audible, that is, by reason of
its peculiar quahty, when a much louder breath-sound might pass un-
noticed. Again, it is higher pitched than the pulmonary murmur and
than laryngeal or tracheal breath-sounds ; thirdly, it has the quality of
tone, that is to say, it is farther removed from a mere noise, and ap-
proaches though it never reaches the quality of a musical note. To
these characteristics we may add that expiration does not follow inspiror
tion so immediately as in health — possibly because the solidified lung
does not contribute its resilient energy to that of the rest of the lungs,
or it may be because of some disturbance of the nervous mechanism
of respiration. In short, the laryngeal vibrations in breathing are trans-
mitted to the ear better than in health, less changed and changed in
another direction.
Along with the tubular breathing marked bronchophony is present, that
is, when the patient either speaks or coughs, the laryngeal voice is heard
more loudly and distinctly than with a healthy lung. The tactile
fremitus is also more perceptible, that is, the laryngeal vibrations are more
perfectly transmitted to the touch as well as to the ear.
A remarkable variety of vocal resonance usually heard over a pneu-
monic lung is that called by Laennec "pectoriloquy"; in which case not
only the laryngeal voice but also the articulated sounds in the mouth are
transmitted, so that words as well as vocal sounds are heard. If the
patient speak in a whisper, the latter of course are absent, and we hear the
former alone, just as if a loud whisper were directed into the stethoscope.
Thus pectoriloquy is best distinguished as whispered pectoriloquy, but vocal
pectoriloquy is just as real a phenomenon, and was what Laennec first
described.
There are some curious exceptions to the regularity of these physical
signs. Occasionally the percussion note loses its resonance, but at the
same time rises in pitch ; this condition, sometimes found over a very
tense coil of intestine, is known as tympanitic dulness. Still more rarely
a solid and hepatised lung has been found by good observers to yield a
resonant note, even in the presence of bronchial breathing and broncho-
phony. Occasionally, instead of the ordinary dull or flat toneless
percussion note, a " cracked-pot " sound may be heard, particularly in
children.
In some cases, where presumably there is a plug of fibrinous exuda-
tion, bronchial breathing and the associated signs are absent : such a
case resembles a pleural effusion save that the heart is not displaced.
PNEUMONIA 103
Since pneumonia is always accompanied by pleurisy, a pleuritic rub
■will almost always be heard early in the attack ; most often to the
outer side of the nipple or near the angle of the scapula.
The physical signs just described undergo little alteration as during
the progress of the disease hepatisation spreads upward, or attacks the
other lung : pneumonic crepitation may be heard at the advancing border,
and the area of dulness and tubular breathing extends. When the crisis
arrives, the solidified lung clears up, but more slowly than the symptoms.
The dulness gradually gives place to resonance ; the " redux crepitation "
is often heard, and instead of tubular breathing we hear riles, at first
consonating and then losing this quality as they become larger and looser.
Sometimes the signs of consolidation continue for a week after the
temperature has become normal, , or even longer than this. Sometimes
they are succeeded by the signs of pleural effusion.
Diagnosis. — It is customary, after describing the symptoms and
signs by which a disease is recognised, to add special directions for
distinguishing it from other diseases. But it is often impossible to
predict what maladies may be confused in a given case ; and when we
draw up tables of distinguishing signs, although the exercise is useful for
a student, we find, on the one hand, that each has to be so guarded and
qualified that it ceases to bear the weight put upon it, or on the other
that we are making our statements more absolute than facts will bear out :
thus we may mislead rather than help the reader. There are no patho-
gnomonic symptoms of any disease, nor is there any royal road to diagnosis.
In some cases, as in the discrimination of external tumours, in the
distinction between measles and rubeola, rheumatism and gonorrhceal syno-
vitis, psoriasis and scaly syphilis, tuberculosis and enterica, it is practically
useful to keep the contrasted features in our minds ; though in each of these
cases we may rely too much upon them, and may fail to observe other
points of greater importance. But pneumonia is so well marked a malady
in its symptoms and course, and auscultation gives us such clear and precise
evidence of its presence, that, once suspected, it can always be discovered ;
and the disease is too common and striking not to be thought of whenever
an acute febrile attack is before us.
In children, confluent pulmonary catarrh may simulate lobar pneu-
monia in its physical signs ; but its onset and course are very different,
so that we have only to bear in mind that true pneumonia may affect
young children and even infants at the breast.
Apical pneumonia has been mistaken for phthisis ; but if the sputa
and the curve of temperature do hot distinguish them, the onset and the
crisis are decisive.
When pneumonia comes on in its secondary form as a complication of
some chronic disease, it may be easily overlooked ; but, if sought for, the
characteristic physical signs prevent all doubt of its presence. A rise of
temperature, with rapid breathing or quickly ingravescent muscular weak-
ness, are the symptoms that should at once lead to auscultation of the
lungs. When pneumonia complicates fevers we are already on the watch,
!04 SYSTEM OF MEDICINE
and an increased ratio of respiration to pulse and temperature at once
excites suspicion and indicates the danger. In the course of dehrium
tremens we must always be on the look-out for the supervention of pneu-
monia ; for the entire lower lobe of a lung may be hepatised before the
appearance of characteristic symptoms.
In children, fever, dyspnoea, and cough may coincide with dulness on
percussion and characteristic tubular breathing at the base of one' lung,
and the cause may be not hepatisation, but pleural effusion, most often
purulent. No sputum is obtainable, and the voice fails to give help. In
such cases, and in such only, we are driven to leave the art of
diagnosis by physical signs, and to solve the problem by puncture with a
hypodermic syringe.
Other difficulties of diagnosis turn. rather upon disputed pathological
points than on technical skill in interpreting symptoms and signs.
The first depends upon the distinction of true pneumonia from what has
been often described as " acute pulmonary congestion." This affection,
described by practitioners in England, and admitted by some pathologists
in France, may be defined as an acute disease with the symptoms but
without the pliysical signs of pneumonia, running a short and for the most
part a benign course, usually calling for and sometimes obtaining anti-
phlogistic treatment. That an attack of pneumonia occasionally aborts,
that the physical signs of pneumonia are sometimes delayed for two or
three days after the symptoms have appeared, and that they are some-
times strangely obscured or difficult to detect, are facts that probably
explain most of these cases. The remainder may perhaps be regarded as
examples of acute pulmonary oedema, like that which not infrequently
attends the later stages of Bright's disease. In any ease acute arterial
congestion vnthout exudation — hypersemia without inflammation — is
a pathological event the existence of which has never been proved, and
cannot be admitted until supported by the results of post-mortem
examination.
Another question of diagnosis depends upon our view of the
relation of lobar and lobular pneumonia in children. When patches of
catarrhal pneumonia become confluent, the physical signs closely resemble
those of fibrinous hepatisation ; the symptoms are also more acute in
these cases, and may be undistinguishable from those of the latter. Even
anatomically it is so difficult to distinguish them that some good patho-
logists give up the attempt. Moreover, the pneumococcus may be present
in lobular as well as in lobar pneumonia. The distinction rests on the
more gradual onset, the relation to previous bronchitis, measles, and other
primary disease, the more scattered localisation; anatomically, on the
separate lobules being distinguishable, the surface less firm and granular ;
and microscopically, on the greater amount of leucocytes and epithelium,
and the smaller amount of fibrin and blood-discs. Confessedly difficult
as is the diagnosis between true lobar pneumonia and lobular catarrhal
consolidation, there does not appear to be sufficient reason for giving up
the attempt. The two diseases differ essentially in their natural history.
PNEUMONIA los
origin, incidence, course, and histology ; and the difficulty of distinguishing
them in what is after all a small proportion of cases is no more a reason
for confounding them than in the similar occasional difficulty of distin-
guishing between rubeola and morbilli, osteoarthritis and gout, carcinoma
and alveolar sarcoma. If the whole duty of medicine were the practical
one of healing the individual patient, we might be content with the
knowledge that in the doubtful cases, which sometimes occur in children,
the determination of the question is not of practical importance.
The third difficulty in diagnosis is between pneumonia with hepatisation
of the lung and the cases of acute pleurisy and even of acute meningitis,
cerebral or cerebro-spinal, of acute pericarditis, or ulcerative endocarditis,
which, as it is asserted, have the same general symptoms and course, the
same infective microbe, the same origin and pathological nature, and yet
no affection of the lungs — pneumonic fever without pneumonia.
The diagnosis in these cases would rest upon the absence of the
physical signs of a solidified lung and of rusty expectoration and other
strictly pulmonary symptoms. The evidence for the theory in question
will be noticed again in the section on pathology.
Complieations and Sequels. — Pneumonia is more uniform in its
course than most febrile disorders, and offers in this, as in other respects,
a marked contrast to enteric fever. Its complications are few and rare.
Hyperpyrexia is comparatively rare. The temperature runs high, but
seldom exceeds 106°; and deaths from this cause alone are uncommon.
At the same time a temperature above 104° marks a severe attack, at any
rate in an adult.
Pleurisy is, not a complication, but part of the disease. In its usual
fibrinous form it is insignificant except for the pain it causes. Serous
effusion is seldom considerable, and rarely needs attention ; but after the
pneumonia has subsided, it sometimes happens that the dulness persists
longer than usual, and the temperature rises again after the initial fall
— the interval in Dr. White's 26 cases was from one to four days.^ This
almost always points to the presence of fluid in the pleural cavity, and as
a rule this fluid is purulent. In a case lately under my own care, the
pus, when drawn ofi", was found to be a pure cultivation of Frankel's
pneumococcus ; and this is frequently the case. But more often the
organisms found in the effusion are the strepto- or staphylococci of
non-specific suppuration. It is certainly remarkable that the diplococcus,
which usually produces non-suppurative inflammation of the lungs and
pleura, should occasionally cause the purulent infiltration which marks
the last stage of hepatisation, and the empyema which we are considering :
the two conditions, though so far comparable, seldom or never exist
together ; a mixed infection might rather have been anticipated, pyogenetic
^ In a paper in the Qmfs Hospital, Reports for the past year (vol. li.) by Dra. Hale Wlite
and A. C. Pearse, 26 cases of empyema are recorded following 890 oases of lobar pneumonia.
The percentage on the total is three, but in different years it varied widely from none up to
more than five per cent. Of 708 oases of pneumonia recorded in the St. Thomas's Hospital
Reports (vol. xix.), only 6 were followed by empyema.
io6 SYSTEM OF MEDICINE
microbes being added, as in the latter stages of enteric fever, to those
which are specific. On this point further evidence is needed.
From the clinical point of view it seems very doubtful whether time
will justify the belief entertained by some French pathologists, that an
empyema of diplococcous origin is benign, and may be absorbed without
surgical interference, while the contrary is true of one in which strepto-
cocci are found. In the case above mentioned a second paracentesis was
necessary, and ultimate incision and drainage before recovery ensued.
A common and more dangerous complication is pericarditis,
which, when it complicates double pneumonia, is most often fatal. It
occurs during the height of the fever, and is recognised by the usual
friction sound, which must be distinguished from a pleuritic rub produced
by the impulse of the heart. The effusion is usually plastic and serous,
but occasionally it is purulent. There is no added pain, but dyspnoea and
orthopnoea are increased, and the pulse becomes smaller and irregular.
Another complication or sequel is ulcerative endocarditis. Dr. Osier,
who in 1885 drew attention to this connection of the two diseases, met
with it sixteen times in 100 cases. This was probably an accidentally
high number. In the 425 cases tabulated by myself it occurred seven
times. It often accompanies empyema.
A rarer complication is acute meningitis. Of this I have had but
small experience. In the few cases I have seen, the pneumonic diplococci
were found in the lymph at the base of the brain ; and this appears
to be the rule. Meningitis is often associated with acute ulcerative
endocarditis.
Dr. Bristowe and other writers have described a membranous catarrhal
or ulcerative colitis as complicating acute pneumonia. There have been
several cases at Guy's Hospital during the experience of many years, but
I have myself only once found this condition of ulceration of the colon.
It is certainly far more common in cases of Bright's disease.
Severe epistaxis occasionally marks the onset of pneumonia, and may
recur during its course. Except in elderly patients, this is not a serious
symptom.
A curious occasional complication of pneumonia is jaundice ; and this
is more often observed when the right lung is afiected. None of the
attempted explanations of its occurrence is satisfactory. There is no
evidence of catarrh of the bile-duct (if catarrh is ever the cause of icterus),
there is no reason to suppose the blood differently constituted in these
particular cases (if there be such a thing as hsematogenous jaundice),
the hepatic circulation is not more obstructed in these cases than in others
without the symptom in question, and deficient movement of the
diaphragm, if a cause, would be more likely to induce jaundice in cases
of right hydrothorax or phrenic pleurisy. It does not appear to affect
the course of the attack or its prognosis.
Relapse after recovery from pneumonia has been often reported ; and
cautions are given to guard against it. But I have never met with a case,
and believe that a relapse occurs very rarely, if ever. The spread of
PNEUMONIA 107
pneumonia to the other lung when it had subsided in the first, or the
supervention of empyema, may perhaps have been thus misinterpreted.
Recurrence of pneumonia after several months or a year's interval is,
however, often observed. In the 425 cases tabulated, such recurrence is
noted in eighteen. This shows that pneumonia does not protect against
a future attack like small-pox or measles, not perhg-ps that it disposes
to a repetition like erysipelas ; occasionally the same patient may suffer
five or six times from pneumonia in his lifetime.
Secondary pneumonia. — The description of the symptoms and
course of pneumonia above given refers with comparatively small variation
to cases of primary, or, as we say, idiopathic pneumonia ; to cases, that
is, in which the disease, whatever its cause, is not a complication of any
previous malady, but attacks a person in apparent health. There are,
however, numberless cases in which after death we find lobar hepatisation
as the closing event of preceding disease, acute or chronic. The anatomy
to the naked eye is the same ; and neither histological nor bacterial
investigation enables us to distinguish the forms of primary from those of
secondary pneumonia ; or to distinguish one from another those which
occur in the course of typhus, rheumatic fever, diabetes, or Bright's
disease.
It would be an arbitrary proceeding to separate the one group of cases
from the other : for, in the first place, the anatomical changes of disease
are by far the safest guide in their discrimination and recognition ; and,
secondly, although the symptoms of these secondary forms of pneumonia
are less clear and distinct than in the primary cases, yet they are present,
curtailed or obscured it may be, but capable of detection, and accompanied
by the same physical signs which denote the presence of primary pneu-
monia.
Moreover, we find a connecting link between primary and secondary
pneumonia in cases following influenza, which in other respects have the
character of the idiopathic disease rather than that of a complication or
sequel.
When one disease supervenes upon another, the former is not likely
to preserve the distinctive features which mark its invasion of a normal
organism. The contrast between health and disease is more obvious than
between one kind of sickness and another. The antecedent disorder
of the pulse, temperature and respiration, of the appetite, of the blood,
of the tongue, and of the skin, blurs the outline of those striking changes
which in a healthy subject denote the advent of pneumonia. In like manner
after death we may discover the ulceration of enteric fever which has
supervened in a course of protracted rheumatism with relapses ; or cancer
in the body of a patient who has died from alcoholic intemperance ; or
Bright's disease in a case of emphysema and bronchitis ; or phthisis latent
in a diabetic or insane patient.
The diseases in which secondary pneumonia frequently occurs as a
complication are the following : typhus, enteric and relapsing fevers,
small-pox, erysipelas, puerperal septicaemia, and occasionally diphtheria.
io8 SYSTEM OF MEDICINE
Lobar fibrinous pneumonia, of wbich alone we are now speaking,
is rarely seen as a complication of measles, but it is less rare in
scarlatina. It seldom appears in the course of phthisis, or again of
quinsy, bronchitis, pleurisy, or asthma. It may be seen as a complication
of cardiac disease, but is much more frequent in both the acute and
chronic form of Bright's disease. It is an occasional and often fatal com-
plication of rheumatic fever ; and is almost invariably fatal when associated
with pericarditis. Acute lobar pneumonia of the base is often found as
the cause of death in diabetes, and in chronic alcoholic poisoning ; and it
may occur as a fatal complication in the course of many chronic diseases,
such as paraplegia, tabes, or cancer. Pneumonia, probably of septic origin
but neither lobular nor suppurative, is also not an infrequent cause of
death after surgical operations. It was remarked by the great Dr. Arbuth-
not, in the 3rd chapter of his book on Diet, that a peripneumony is the last
phase of every disease ; for nobody dies without a stagnation of the blood
in the lungs. If we include broncho-pneumonia and hypostatic congestion
under the name of pneumonia, as Arbuthnot, no doubt, would have done,
the proposition is not very far from the truth.
In what points do these secondary forms of pneumonia differ from the
primary ? In the first place, they are far more dangerous. Secondly,
although their anatomy and their physical signs are the same, they lack
some of the symptoms of the idiopathic disease : more particularly it
may be observed that the initial rigor is frequently, perhaps usually,
absent ; that the temperature does not rise so abruptly or so high ; that
although pleurisy is present, and a rub may be heard if sought for, yet
pain in the side, instead of being a constant symptom, is often absent ;
that a cough may also be wanting ; that the burning heat of the skiu
and the characteristic conditions of the urine may be absent or sUghtly
marked. Herpes is usually absent. The sputum is rusty, and con-
tains diplococci ; but often in these cases, either from absence of bronchial
irritation or from the weakness of the patient, no sputum is expectorated.
If all these symptoms are wanting, and fever already present, a secondary
pneumonia may be called latent ; and we have then to depend entirely
upon physical examination of the chest for its recognition. Apart from
these signs, probably the most important symptom is increased frequency
of respiration.
Other clinical varieties. — Beside the distinction between primary and
secondary pneumonia, certain other divisions of the disease have been
made, by some writers, into varieties which scarcely deserve separate
nomination.
Abortive or ephemeral cases, which last only a day or two ; wandering
pneumonia {P. migrans), in which form the disease attacks first the right
base, then the left, and then perhaps returns to the right apex ; malarial
pneumonia, in which under the influence of this poison the fever assumes
an intermittent character, are among the varieties which might be multi-
plied without advantage.
In children, pneumonia is comparatively rare, its course usually short.
PNEUMONIA 109
and its prognosis very good. The pneumonia of old people is often
attended by only moderate fever ; bronchitis is common and exhaustion
speedy. The drunkard's pneumonia is complicated with early delirium.
Epidemic pneumonia, apart from that consecutive to influenza, has
been frequently observed in former and recent times. An interesting
historical account of it is given by the late Dr. Wilson Fox (12) (13),
and also in Sturges' and Coupland's valuable monograph. Eecent epi-
demics have been described by Dr. Whitelegge in the first volume of
the present work (p. 655).
Morbid anatomy. — The anatomy of pneumonia is no less striking
and characteristic than its symptoms or its physical signs. The hepatised
lung does not collapse on exposure to atmospheric pressure. It feels
heavy when lifted out of the chest, and readily sinks in water. Its
surface is covered by a more or less extensive layer of fibrin. This
false membrane, or coagulated lymph as it used to be called, is some-
times a thin, adherent gray film, contrasting with the smooth and
shining portions of the membrane which are unaffected. Sometimes
it is in thick and comparatively tough layers, which can be peeled oflf;
sometimes in soft shaggy masses of moist fibrin ; and sometimes, together
with the solid exudation, there is more or less of serum or pus.
On cutting into the lung the section is seen to be dark red, the
colour of liver ; or at a later stage a pale and yellowish gray. The
advancing border is red and oedematous, but not yet solid. The surface
is granular, uniform, and dry compared with most other morbid states
of the lung. As in other acute inflammations, the tissue is so softened
that it readily breaks down under pressure. A scanty, blood-stained liquid,
characteristically free from froth, issues from the squeezed tissue ; and
this becomes more abundant, paler, and thicker in the parts longest hepatised
— that is to sa,y, in the gray as compared with the red hepatisation.
The traditional stages of pneumonic hepatisation are — (1) Engorge-
ment (Bayle), that is, acute congestion with oedema, but without solidity ;
(2) Red hepatisation, that is, solid exudation with hyperaemia ; (3) Gray
hepatisation or solid exudation with ansemia from pressure on the blood-
vessels ; (4) Purulent infiltration, the gray tissue yielding thick purulent
exudation.
Histology. — On scraping the cut surface we obtain a turbid liquid, of
which a drop under the microscope shows abundant red blood-discs, with
a few leucocytes ; or, in the latter stages, abundant leucocytes, and a few
blood-discs, together with minute fibrinous casts of the vesicles. Larger
branching casts, plainly visible to the naked eye, can often be pulled out
of the bronchioles with forceps. Diplococci may be detected after stain-
ing, and sometimes streptococci in addition.
A thin section of the hepatised lung shows the vesicles and intra-
lobular air-passages, as well as the smallest bronchial tubes, to be com-
pletely filled with exudation : blood-discs, threads of fibrin, and leuco-
cytes, the latter at first few in number, but becoming more numerous as
the red turns to the gray stage.
SYSTEM OF MEDICINE
The absence of epithelial cells is important. The walls of the air-
vesicles are usually thickened, but no other change of the texture of the
lung is apparent, no alteration of the elastic fibre, and no increase of the
exceedingly scanty interstitial connective tissue of the healthy lung.
The capillary blood-vessels in the early stages of hepatisation are dilated ;
but the blood is gradually squeezed out of them as consolidation goes on
until red gives place to gray hepatisation, when the lung becomes very
anaemic. The remarkable friability of a pneumonic lung is caused partly
by the swelling and softening of the tissue, but chiefly by its being
solid instead of spongy, so that instead of yielding to pressure, it resists
and breaks down under it. In the later stages the blood-discs are no longer
seen, or only few of them ; the leucocytes, on the other hand, have greatly
increased in number, and have assumed the granular character of pus-cells.
The air-vesicles, being thus stuffed and swollen with inflammatory exuda-
tion, expel the blood from the pulmonary capillaries and cause the
exsanguine pale aspect of gray hepatisation. The gray colour is due to
the accidental pigmentation with granules of carbon due to inspiring
smoky air, and is absent when the hepatisation of the lungs is observed
in children or in cattle.
Anatomical distribution. — The site of hepatisation is important. In
the majority of cases (288 : 92) it begins at the base of the lung and
travels slowly upwards— in the reverse direction to that characteristic of
phthisis. The epithet lobar is to some extent unfortunate ; for the
process is seldom exactly bounded by the fissures of the lung. The lower
lobe may be hepatised only in its posterior-inferior part, or in all but its
apex ; or the back of the upper lobe and the whole of the middle and
lower lobes of the right lung may be solid and the apex alone escape.
Sometimes every part of one lung is found solid after death ; the base gray
and the upper parts red, with hepatisation of the base of the other lung.
Not infrequently, however, pneumonia attacks the apex and travels
downwards. This local variety is more common in children than in
adults ; it is often latent, and is said to be more often associated with
delirium. The prognosis of apical pneumonia, when it occurs in an adult,
does not seem to be better or worse than that of the ordinary basal form.
Apical pneumonia of one lung is often accompanied by basal pneu-
monia of the other. Double apical pneumonia is very rare.
A third site, still more seldom selected by the pneumonic process, is
the deep part of the lung near its root. This " central pneumonia " is
naturally difficult of detection before it has advanced towards the
surface.
Occasionally the anterior tongue-like process of the left lung is alone
affected on that side.
Right pneumonia is rather more frequent than left, whether it affect
base or apex,^ and unilateral is happily more common than double pneu-
monia. (See Appendix, § 4, p. 132.)
^ It happens that in the cases collected by the writer there were rather more of the left
than of the right base (151 : 137), but in larger numbers the proportion is reversed.
PNEUMONIA
Anatomical events. — Jn the majority of the cases pneumonic inflamma-
tion ends by resolution. The exuded blood-discs, and leucocytes, and
fibrin are no longer expectorated as such, but degenerate and are
broken up into granules, chiefly fatty in nature. These are partly
mingled with the bronchial secretion and coughed up, but probably a
larger proportion are absorbed by the lymphatics, conveyed to the veins,
and finally excreted. The abundant salts (chiefly sodium - chloride)
deposited in the inflamed lung are rapidly carried off by the veins, and
discharged in the urine. The air re-enters the minute bronchi and air-
vesicles as they re-expand in inspiration. The lung more or less rapidly
regains its spongy character, and the pleural exudation is gradually
absorbed. Once only have I had the opportunity of seeing a hepatised
lung in process of recovery about ten days after the crisis ; it was a case
in which death occurred from another cause. The tissue contained air,
exuded frothy serum, and floated in water ; it was ansemic rather than
congested, did not break down under pressure, and was very oedematous.
As above stated, we learn from physical examination of the chest that
the hepatised lung sometimes continues solid for several days after the
raised temperature and other febrile symptoms have disappeared.
In fatal cases we may find any stage of hepatisation, as above
described, and any combination of these stages. There is no reason to
conclude that gray consolidation, or even purulent infiltration, is incap-
able of resolution; but the contrary opinion is obviously almost as,
difficult to prove as to disprove.
When the lung has passed into gangrene the surface is obscured by
a cloudy film ; the tissue breaks on the slightest handling, is of a very
dark colour, and emits a characteristic foul and pungent odour. Under
the microscope no air-vesicles or other structural forms are distinguish-
able; the organ and the exudation are alike dead and disintegrated,
and blood-vessels and elastic tissue alone remain. Gangrene is always
limited in extent, but perhaps never by a separating capsule. In many
cases, probably in most, the cause of the gangrene can be ascribed to
the presence of particles of decomposing food which have gained an
entrance to the air-passages in the last day or two of the patient's life.
It has been stated by Addison, and by other pathologists, that
occasionally a pneumonic lung never recovers its permeability to air,
and may gradually pass into an unnaturally firm, pale, solid state,
containing an excess of fibrous tissue, a state which has been included
by some writers under the head of cirrhosis. Addison described it as
"marbled induration." This condition must be a very rare one, and it
does not appear to lead to the contraction of tissue or the dilatation of
bronchi which mark Corrigan's cirrhosis.
Equally supported by credible authorities, both past and present,^
is the statement that pneumonic hepatisation may end in abscess
of the lung. Of this, as of the previously mentioned condition, I
have no experience, and without denying the occurrence of either,
' Among the former may be mentioned Stokes, among the latter Osier.
SYSTEM OF MEDICINE
would regard this also as an extremely rare event. The "abscesses
of the lungs" of the physicians of the 17th and 18th centuries
were tuberculous vomicae. Multiple pyaemic abscesses, now happily
seldom seen, are well-known morbid conditions, but they do not follow
true pneumonia. A small circumscribed empyema following pneumonia
may burst and simulate an abscess during life, and may even be mis-
interpreted after death. And when the stage of purulent infiltration
has been reached, it is not difficult by pressure or accidental laceration
of the rotten tissue to produce a cavity fiUed with purulent fluid not at
all unlike an abscess. These facts are, however, familiar to the able
pathologists who describe abscess as a not infrequent event of (acute,
lobar, fibrinous, or " croupous ") pneumonia, and therefore its occurrence
cannot be denied : but subsequent experience has certainly confiirmed the
observation of Laennec — "II n'y a pas de lesion organique plus rare
qu'une veritable collection de pus dans le tissu pulmonaire " (22, § 192).
Other organs. — -In an autopsy on a case of primary pneumonia we
expect to find the lungs only diseased, and an exception is rare. There
will always be lymph on the visceral pleura, and sometimes pleuritic
effusion, serous or purulent. The bronchial lymph-glands are soft and
swollen. Occasionally the pericardium or endocardium, the meninges,
larynx, or large intestine may show the lesions above described.
The blood in pneumonia when drawn coagulates slowly, and forms
•an abundant and firm clot with the " buffy coat," due to the red discs
having subsided before becoming entangled in the meshes of the fibrin
as it forms. This condition (so-called hyperinosis), like the pneumonic
pulse and fever, is present in many other inflammatory diseases. The
leucocytes of the blood are also considerably increased in number, a
fact first observed by Piorry, confirmed by Virchow, and more recently
by Billings.
Baeteriolog'y. — Klebs, in 1877, was the first to describe a microbe
characteristic of pneumonia ; but it was probably not the same as that
afterwards discovered by Friedlander, and certainly not the same as
Frankel's diplococcus. The former was described by the late- Dr. Fried-
lander in 1882 as an oval body 1 ^ in length, occurring in pairs {diflo-
cocaos) or in chains {streptococcus) ; and, as was soon after ascertained,
enclosed in a thick transparent envelope. On cultivation in gelatine it
forms a colony of a characteristic nail-shape. When inoculated it pro-
duced pleuro-pneumonia in mice, and often in guinea-pigs, but not in
rabbits. Accordingly it was named Pneumococcus (15).
It was soon ascertained, however, that this organism is not a coccus,
but a bacterium or bacillus ; that it is not invariably present in pneu-
monic lungs or sputa ; and that it is often to be found in the mucus
of the nose and bronchi, in the absence of pneumonia.
In 1884 Dr. A. Frankel brought forward another claimant to the
distinction — a microphyte, also oval or lancet-shaped, also occurring in
pairs, also encapsuled, but dififering in the conditions and results of
successful cultivation. It also produced death in rabbits (but not pneu-
PNEUMONIA 113
monia), and pneumonia in mice and guinea-pigs (14). The same microbe,
in all likelihood, had been independently detected in hepatised lung by
Talamon (30) ; and this again was the streptococcus observed by Dr.
Sternberg of the U.S. Army in 1885, named by him "Micrococcus of
Pasteur," and identified by many observers with that of sputum-septi-
caemia, and with a similar organism occurring in healthy human saliva —
"Bacillus sjpwtigenus," "Bacillus saHvarms" (26).
The extended researches of Weichselbaum in Vienna on 129' cases
of pneumonia (in the wide sense of the term) resulted in the discovery
of Frankel's diploeoccus in 94, of Friedlander's " pneumococcus " or
" bacillus -pneumonie " in only 9, streptococcus pyogenes in 21, and
staphylococcus pyogenes aureus in 5 (33). This appears to show that while
one microbe is most frequently present, others are competent to produce
" pneumonia " ; but, unfortunately, it is not clear what precise kind of
pulmonary disease was present in the several instances.
The experiments of Gamaleia in Pasteur's laboratory led him to
believe that the pathogenetic organism is to be found in the diploeoccus
described by Frankel (now often called pneumococcus, in succession to
the title enjoyed for a short period by Friedlander's bacillus), which,
however, he identified with that of Talamon and Sternberg, and calls
"Streptococcus lanceolatus Pasteuri" (16).
Lastly, we must remember the mobile rod-shaped microbe which
was found by Dr. Klein (20) in the epidemic pneumonia of Middles-
borough.
While recognising the interest and importance of these laborious
researches, we must observe that even the diploeoccus of Talamon and
Frankel does not fulfil -Koch's three tests of a pathogenetic organism ; as
they are fulfilled, for example, in anthrax, relapsing fever, and tuber-
culosis. It is not invariably present in the tissue of pneumonic lung ; it
does occur in other situations in health ; when injected as a pure
cultivation it does not always reproduce itself and cause a fresh case of
hepatisation of the lungs. Nevertheless the frequency of its occurrence,
and the fact that it often reproduces the disease by inoculation, make
it probable that it plays an important part in the natural history of
pneumonia.
There are, indeed, two other and preliminary postulates which are
no less important than the three of Koch, but which have not always
been kept in view in these or in similar investigations.
The first is that the microbe of which the action is under investigation
shall be "specific" — that is, it shall be possessed of definite and con-
stant characters; it must be a good botanical species which can be
identified beyond dispute. The mere shape is admitted to be illusory.
The same microphyte varies in different stages of its growth and under
different conditions, and may almost arbitrarily be described as a micro-
coccus, a diploeoccus, or a streptococcus ; as an oval or lancet-shaped
bacterium, or as a bacillus. The presence of a capsule is not a con-
stant distinction ; and even the reaction to staining agents and the
VOT/. V I
114 SYSTEM OF MEDICINE
shapes assumed under various methods of cultivation are not always
decisive.
But if a certainty that different observers are discussing the same
microbe is essential before their results are compared, it is no less essen-
tial that they should be agreed as to the disease which is under inves-
tigation. Septic pneumonia, lobular broncho-pneumonia, and lobar fibrin-
ous (" croupous ") or vesicular pneumonia are different pathological
conditions ; and unless they are carefully discriminated, statistics of
" inflammation of the lungs " are as useless as would be similar facts with
regard to "inflammation of the joints" or "inflammation of the skin."
Pathology. — ^Looking back at the natural history of the disease now
described, to what conclusion concerning the nature and essential characters
of pneumonia and its relation to other disorders are we led ? Are we,
like Laennec and his successors, to regard it as an acute inflammation of
the lung, of which the pyrexia and other symptoms are only the effects ?
Or are we, with most modem writers, to look on the local lesion as hut
one element in a specific infective fever ? Or is any alternative opinion
open to us ?
In the first place, the attempt, which has more than once been made,
to disprove the inflammatory nature of pneumonic hepatisation has
certainly failed. We have the hypersemia and softening of the tissue
which are the characteristic signs of acute inflammation everywhere ; we
have the pyrexia and other febrile symptoms which also attend acute
inflammation ; we have the exudation of liquor-sanguinis, with leucocytes
and fibrin; the last stage of the process is purulent infiltration of the
affected lung, and, lastly, in every case of pneumonic hepatisation we
find the obviously related pleurisy, which no one can deny to be
inflammation.
It is true that pneumonia cannot be produced by injury, or by
ordinary irritants, as is proved by experience in men and experiment
on animals. The few supposed cases of pneumonia of traumatic or
irritative origin are mostly accidental coincidences. It does not arise by
extension from capillary bronchitis, nor by the irritation of dust, nor by
the more specific stimulus of the tuberculous microbe; but this only
shows that the process is a special, peculiar, or, as we say, specific kind
of inflammation. Much the same is true of the tubal nephritis of acute
Bright's disease, which is no doubt inflammation, but inflammation of a
peculiar kind ; not traumatic, or irritative, or septic.
Admitting, however, that pneumonia is truly inflammation of the
lungs, are all its symptoms due to this local inflammation ? This cannot
be maintained, for occasionally we find the symptoms precede the signs
of hepatisation by several days ; the temperature and even the number
of respirations fall when the crisis comes, long before the solidified lung
has cleared up; the violence of the fever is not in proportion to the
extent of the local lesions, although the amount of lung involved does
produce its direct effects on the heart.
On the other hand, the differences between pneumonia and the
PNEUMONIA IIS
group of diseases to wliich typhus, small-pox, and measles belong must
not be overlooked. It resembles them in its sudden onset, in its
pyrexia, its definite course, and its limited duration; but in the vast
majority of cases it is sporadic and idiopathic. It does not in common
experience arise from previous cases, nor produce fresh ones ; it does not
protect from future attacks, but rather disposes to them. Although epi-
demics of pneumonia undoubtedly occur, they are local, and the most
striking cases are those which follow influenza, a true specific fever,
just as nephritis follows scarlatina. Moreover, unlike the local lesions of
enteric fever or of mumps, hepatisation of the lungs is found in the
course of other fevers, and of chronic affections such as Bright's disease.
Against these broad differences the fact of a distinctive microbe being
present is inconclusive ; for, not to insist on the absence of any such
microbe in some of the most definite specific fevers, its presence is not
constant in pneumonia. It is associated with other microbes, strepto- and
staphylococci, and is sometimes replaced by a bacillus which Dr. Klein
found constant in an epidemic of pneumonia at Middlesborough in 1889
(vol. i. p. 658). The diplococcus, which is almost constantly present, is
sometimes found in lobular pneumonia, sometimes in pleurisy without
pneumonia, and sometimes in healthy saliva.
The fact seems to be that in this case, as in so many others, the
phenomena of disease cannot be fitted into current classifications.
Inflammation itself is a much more variable condition than it was
once thought to be. It differs as the cause which produces it, and
as the organ or tissue which reacts to the irritant. Bacterial diseases
differ also among themselves. The constancy of the presence of a
peculiar bacillus in phthisis is most important, but phthisis remains a
very different disease from tuberculous meningitis, or pulpy disease of
the knee; while diphtheria, erysipelas, gonorrhoea, and relapsing fever
differ in almost every particular except in respect of a specific microbe.
At present our knowledge is too imperfect to decide the true nature, origin,
and pathology of pneumonia ; but we can affirm that, on the one hand,
it is not an ordinary inflammation produced by injury, or mechanical
irritants, or cold, with symptoms directly proportionate to the extent of
the tissue inflamed ; and that, on the other hand, it differs from such
specific fevers as measles, enterica, and small-pox in that, though self-
limited and definite in its course, it is not strictly "specific," not contagious,
and often not idiopathic but secondary.
We may admit that the presence of a special microphyte is nearly
constant in the disease; so that its presence in the sputum, like
that of Koch's vibrio in cholera-stools, is a useful means of diagnosis :
nevertheless, the disease is a local inflammation ; not a common inflam-
mation produced by common irritants but an inflammation peculiar to
the lung, and incapable of artificial reproduction. Of many, perhaps
of most organs of the body we may say that they are capable of three
kinds of inflammation at least : that which is acute and suppurative,
marked by abundant exudation of leucocytes, by the presence of some
Il6 SYSTEM OF MEDICINE
forms of staphylococcus or streptococcus, and accompanied by what
used to be called constitutional disturbance ; secondly, a chronic
interstitial inflammation with hardening of the tissue, shrinking and
destruction of its peculiar elements by the new inflammatory growth;
and, thirdly, an acute form of inflammation, not suppurative and peculiar
to each organ. . Pneumonia belongs to the last of these classes, and may
be compared with acute Bright's disease, acute atrophy of the liver, and
acute myelitis.
Of late years attention has been directed by Dr. Washbourn and
others to the possibility of cases of acute pleurisy depending on the
presence of the specific diplococcus of pneumonia, and running a short
febrile course with the clinical features of pneumonia, but without the
physical signs of hepatisation of the lung. If in such cases the lung
really remains unaffected, and is found after death anatomically sound,
while the pleura is the seat of a specific diplococcous inflammation, our
notion of the disease pneumonia will be much modified ; we shall have
to admit it without reserve among the specific fevers, and to regard the
inflammation of the lung as a very frequent but not a constant lesion.
Causation. — Of the causes of pneumonia we are still ignorant.
Unless we disbelieve careful observations, because they do not fit a hypo-
thesis, pneumonia can exist without the pneumococcus ; and the same
microbe may be found, not only in disease without pneumonia, but under
healthy conditions also. Whether under certain circumstances this usually
innocent microphyte acquires virulence, or whether a noxious and a
harmless parasite resemble each other too closely to be distinguished, we
cannot yet say ; nor can we define the exact conditions which favour the
occurrence of the disease. It is certain, however, that pneumonia is con-
nected with cold, with north winds, with high ground, and with sudden
fall of temperature.
Excluding bronchitis and ophthalmia, in which cold air seems to act as
a direct common irritant, we may say that pneumonia affords the best
evidence that there is truth in the common belief that a chill may "strike
inward," and lends probability to the view that other acute inflammations —
as pleurisy, colitis, acute Bright's disease, and even myelitis — may some-
times be due to a similar proximate cause.
We must also recognise as occasions of pneumonia certain previous
morbid states, of which the most striking and important is influenza.
Pneumonia following this disorder forms an important link between
primary idiopathic pneumonia and the secondary pneumonia of fevers
and septicsemia. Of the latter group of diseases, pneumonia appears
to occur most frequently in typhus, less frequently in enteric fever,
and in certain epidemics only of relapsing fever. Jt is not common
in fatal cases of scarlatina or variola, and seldom takes the place of so-
called lobular pneumonia in measles, whooping-cough, or diphtheria. In
rheumatic fever its occurrence is happily infrequent. Among chronic
diseases it is perhaps most frequent towards the termination of Bright's
disease ; but certainly it is not nearly so common as acute cedema of the
PNEUMONIA 111
lung, or pleurisy, or pericarditis. Pneumonia is probably more common,
and is certainly not less fatal in the latter stages of diabetes. Beyond
these there is perhaps no chronic disease in which its occurrence is
sufficiently frequent to be of etiological or practical importance ; but
pneumonia is one of the intercurrent maladies which bring invalids to
their end.
It is important to notice that lobar pneumonia is very rare as the
consequence of phthisis, or of bronchitis, whether acute or chronic.
Natural history and incidence, distribution and local prevalence. —
Pneumonia, as we see it in this country, is a sporadic and endemic disease.
In its primary form it appears to be more common in winter and spring.
It is common all over temperate Europe, in the United States, and in
the inhabited parts of the South Temperate Zone — in Australia and New
Zealand, at Buenos Ayres, and in South Africa. It is less common in
the Tropics ; but on the hill stations of India it is far from infrequent
during cold weather. It is also common in the highlands of Central
Asia. In Cabul and Beloochistan it is ascribed, as in Italy, to the sudden
change from the scorching heat of the day to the severe cold after
sundown.
Pneumonia sometimes occurs in an epidemic form. From the Middle
Ages downwards we have accounts of acute epidemic disorders, which
seem more like pneumonia than anything else ; and from time to time
circumscribed epidemics are still reported in this country and in other parts
of Europe. There is, however, no instance of prevalence of the disease so
widespread as that of plague or cholera. All that happens is that a
disease never uncommon becomes more common at certain times or in
certain locahties. This prevalence can sometimes be referred to a coinci-
dent prevalence of cold, dry winds, and sometimes is confined to a parti-
cular locality ; but on the whole the phenomena do not seem to be of a
different order from those which at certain seasons determine a greater
prevalence of rheumatic fever, or quinsy, or bronchitis, or diarrhcea.
What is more important is that we sometimes find a group of cases of
pneumonia occurring together in the same village or in the same house.
When influenza is epidemic, pneumonia follows it so often as to simulate
an epidemic.
Sex and Age. — Pneumonia affects men more commonly than women —
a preference usually explained by the greater exposure of men to changes
of weather (Appendix, § 1).
No period of life is exempt from lobar pneumonia. It is, however, rare
in infancy ; and it is less common in children than in adults (Appendix, § 2).
It must be remembered that these facts concerning the incidence of
pneumonia refer to the primary disease. Very little is known of the
conditions under which pneumonia supervenes as a fatal complication of
other diseases.
Prognosis. — There are few diseases of which the forecast varies so
much with circumstances as it does in lobar pneumonia. Speaking broadly,
primary pneumonia is much less dangerous than secondary ; and in cases
Ii8 SYSTEM OF MEDICINE
of primary pneumonia the danger increases, first, ■with the extent of the
lung involved ; secondly, ■with the age of the patient.
Age. — The latter point is one in ■which pneumonia agrees -with most
acute specific fevers — ^particularly ■with typhus, enterica, and variola. In
this point of increasing danger ■with increasing age pneumonia is in strik-
ing and instructive contrast, not only ■with scarlet fever, but also with
rheumatism and ■with diabetes.
Lobar pneumonia is rare in infancy and diflScult to distinguish from
extensive lobular catarrh ; not only during life, but sometimes even after
death. When present, ho^wever, as it often is in children bet^ween two
or three and thirteen or foittteen years of age, lobar pneumonia is a most
satisfactory disease to treat. Its symptoms and physical signs are well
marked ; the fever is high, and the condition of the patient threatening,
but, with few exceptions, the temperature ■wiU faU on the fifth or sixth
day, if not earlier, the symptoms -will rapidly subside, and the recovery
of the patient will be as safe and permanent as it is rapid.
With girls and boys between fifteen and twenty the extent of
pneumonia is commonly greater than at a younger age ; and the disease is
more often severe and prolonged ; but the prognosis is nearly or quite as
good. Between twenty and five-and-thirty or forty the pneumonia of
young adults is still of good augury on the whole ; but at this time of
life it is more frequent for both lungs to be affected. Intemperate
habits begin to weigh in the scale; and cases of pneumonia, secondary
to rheumatism, to influenza, to disease of the cardiac valves, to Bright's
disease and to diabetes, begin to bring down the proportion of recoveries;
although it is still high for idiopathic cases. After the age of forty
acute pneumonia is always a serious disease. The prognosis in primary
cases depends upon the temperate habits of the patient, on his being
neither over-fed and obese on the one hand, nor, on the other, under-
fed and enfeebled by want and misery ; on his being early put to bed
under judicious treatment ; on the extent of pulmonary tissue invaded,
the height of the fever, the presence of cyanosis, and the effect of the
pulmonary obstruction upon the heart. Secondary pneumonia at this
age is a more dangerous disease than at the earlier period of adult life ; but
we see recovery from it in cases of enterica, of rheumatism, and even
of Bright's disease and diabetes.
In old age pneumonia is a very fatal malady. As a secondary com-
plication it frequently decides the termination of fevers, of chronic
disease of the kidneys, of internal carcinoma, of lingering cases of hemi-
plegia, and other chronic affections of the brain and spinal cord. Even
primary pneumonia, limited to a single lung, is dangerous in an aged
patient, and we see recovery after the age of 70 with surprise. It does
however occur, and sometimes even at so advanced an age as 80, but
the cases are very rare.
Extent. — With respect to the area of pulmonary tissue affected, it is
well known that double pneumonia is of graver prognosis than single
( Appendix, pp. 133, 136). Pneumonia affecting the whole of one lung, from
PNEUMONIA 119
base to apex, though serious enough, is probably less so than that which
affects a part of both bases. Apical pneumonia is more common in chil-
dren than in adults, and probably for that reason is believed to be less
dangerous. If, after one lung has partly or entirely cleared, pneumonia
attacks the opposite one, the prospect of recovery is better than vi^hen
both are hepatised at the same time.
Frognostic complications. — Of the conditions which affect the prognosis
of pneumonia, probably the most important, apart from the age of the
patient and the local extent of the disease, is intemperance. Such patients
almost invariably become delirious, and the combination of delirium tre-
mens and pneumonia is almost always fatal. Scarcely less serious is the
presence of chronic renal disease ; and next in gravity is that of valvular
cardiac lesions. These two conditions, however, make the disease no
longer primary but secondary.
Of the complications of idiopathic pneumonia, much bronchitis, and
particularly bronchitis with bronchorrhea of the unaffected lung, is
perhaps the most serious. Pleurisy, or even purulent effusion, is much
less important ; but pericarditis is a not infrequent and an extremely
dangerous complication. Double pneumonia with pericarditis is almost
invariably fatal (Appendix, p. 189).
A weak sound of the heart and a very rapid pulse are well-known in-
dications of danger. Cyanosis, with very frequent breathing and action of
the alse nasi, is equally grave ; and the two conditions often go together.
They are partly due to the mechanical obstruction to the lesser circula-
tion, and partly to the direct effort of the high temperature on the cardiac
muscle ; but in many cases both are aggravated by more or less pro-
nounced saprsemia (24). Tympanites is a very unfavourable symptom in
pneumonia, as in most other diseases ; so also are hiccough and subsultus
tendinum. When delirium persists during the day, and above all when
it prevents sleep, the symptom is a grave one, and calls for decided treat-
ment. Very high temperature indicates a severe case, and often goes with
failure of the heart ; but of itself hyperpyrexia is seldom fatal (Appendix,
p. 1 40). Febrile albuminuria, even when abundant, is not of bad omen,
and seldom or never persists after recovery. Free rusty expectoration
or even haemoptysis need give no anxiety. Diarrhoea is neither common
nor dangerous, and if necessary it can be controlled without difficulty.
Sweating during the height of the disease is not common, and when
present is not of bad import. A profuse sweat, an abundant discharge
of urine, or a sharp attack of diarrhoea, sometimes accompanies the critical
fall of temperature.
Treatment. — Historical sketch, — Acute pneumonia is so striking
and so severe a disease that as soon as it was definitely recognised it was
attacked by all the resources of medicine. During the whole of the
present century the treatment of pneumonia has reflected the various
theories of disease and the changing practice of therapeutics.
The conception of pneumonia current at the end of the last century
was that of an acute inflammation, directly produced by cold, and
SYSTEM OF MEDICINE
attacking a healthy subject. The business of the physician was
to combat the enemy by the potent weapons of bleeding, blistering
and starvation, aided by purgative and alterative drugs. The high
fever, the flushed face, the acute pain and the burning skin were evidence
of a " sthenic " inflammation. The physician felt confident that by
antiphlogistic remedies he could subdue the disease ; and his only fear
was lest the patient's strength should fail under the necessary treatment,
that he might die, not of the disease, but of the weakness attending its
cure — mart guiri. The " corroborant " practice of the Brunonian school of
medicine never obtained such vogue in England as on the Continent. It
was as baseless as the iatro-chemical or the iatro-mechanical systems
which prevailed earlier in the 18th century, and had deservedly fallen into
disrepute. During the first half of the present century the antiphlo-
gistic treatment of pneumonia and of other acute inflammations continued
to be the only one followed in civilised countries — in Dublin as well as in
Edinburgh, in Vienna as well as in Madrid; and precisely the same
treatment was adopted by surgeons for compound fractures, inflammations
of the eye, and for what we now call pysemia. To realise the confidence
and energy with which this absurdly called "heroic" treatment was
carried out, one must have seen, as I saw so late as 1863-64, the treat-
ment not only of pneumonia and pericarditis, but of rheumatic and typhoid
fever, by Bouillaud at the Charity ; or one must read the lectures of the
late Dr. Peter Latham (1845), in which with admirable rhetorical skill he
enforces the dogmas of the day.
The only important modification of the antiphlogistic treatment of
pneumonia introduced during the period between 1790 and 1850 was the
introduction of large and repeated doses of antimony by Easori (1808), a
practice much followed for a time both in Italy and France. The
undoubted efiects of this drug, in producing nausea and disinclination to
food, lowering the blood -pressure, and causing diaphoresis, were quite in
harmony with the effects of bleeding, purging and salivation.
It was and still is true, when a patient is suffering from acute pain in
the side with fever and a frequent, strong, and hard pulse, that vene-
section and free purging will relieve the pain, reduce the arterial tension,
and give him grateful relief from his sense of fulness and oppression. It
was no doubt from observation of these effects, which were well known to
Sydenham, Mead, and Boerhaave, that the antiphlogistic practice began;
and when the discoveries of Laennec made it possible to recognise
pneumonia from the first, and to trace its daily progress, it seemed right
to continue and to reinforce the treatment apparently so appropriate.
The mistake lay in having no control-observations. Physicians saw
patients in an illness apparently desperate, and under treatment by bleed-
ing and antimony they saw most of the symptoms relieved ; frequently,
after a battle of several days, the disease was subdued and the patient con-
valescent ; but they did not know, because they never ventured to try,
what would happen if these remedies had been omitted. It is a humili-
ating but instructive fact that the possibility of recovery from acute
PNEUMONIA
disease without active treatment was established by the assumed success
of a demonstrably futile system of therapeutics, the last, we may hope,
of attempts to answer the absurd question, " On what universal principle
should disease be treated ?" When it could not be denied that persons
suffering from pneumonia and other acute disorders did recover when
treated with infinitesimal doses of useless drugs, it could not be long
doubted that some acute diseases might get well of themselves.
The report of some cases of pneumonia which recovered in the Homoeo-
pathic Hospital at Vienna awakened thought on this subject, and an
article by the late Sir John Forbes, which appeared in the British and
Foreign Medical Chirwgical Review (1846), pressed the lesson home. Skoda
had given fair trial to other methods of treatment, and found that his mor-
tality from acute pneumonia was much less than when treated by bleeding,
blisters, and antimony. These facts were made known in England by Dr.
Geo. Balfour, who had followed Skoda's practice in Vienna (6). Dr. Hughes
Bennett of Edinburgh also published a series of cases of pneumonia
treated without bleeding, antimony, or mercury with unusually small
mortality (1848); and he gave an interesting account of the arguments
of Alison, Watson, Christison and Markham (8). Discussion followed,
but it was less prolonged than might have been supposed; as so
often happens, general opinion had been gradually altering, and was
ready to turn at the first summons. Moreover, the advocates of anti-
phlogistic treatment threw away their case by the assertion that they
were right in bleeding before, and right in doing nothing afterwards — not
because their opinions but the nature of the disease had changed ; and a
presumed " sthenic type " of fevers and inflammations, with a successful
heroic treatment corresponding thereto, was dwelt upon with the same
satisfaction that an old man contrasts the. hard frosts and heroic exploits
of his youth with the mild winters and feeble powers of his contem-
poraries. For a long time the antiphlogistic treatment held its ground
in books and lectures ; but those who taught it always found in practice
an excuse for disobeying their own precepts. By 1860, however, the
change in treatment was nearly universal ; and during the latter half of
the 19th century, English physicians, under the guidance of Jenner and
of Grull, have given up the " heroic " treatment of pneumonia.
In too many cases the treatment which supplanted it was of a purely
negative kind, disguised under such platitudes as the prescription of
rest in bed for a patient who could neither sit up nor rest ; of light and
nourishing food, as if the opposite was ever ordered for a fevered man ;
and of avoiding cold for a patient with a temperature of 104°.
At present we may hope that a more rational system is established.
We know that under favourable circumstances pneumonia needs no
treatment beyond the following of the indications of the patient's own
feelings, and awaiting the favourable result which will follow in the course
of a week.
Abortive treatment. — It is clear that no means known at present can
cut short pneumonia. There is nothing absurd, however, in supposing
•
SYSTEM OF MEDICINE
that this may one day be done. We do cut short the manifestations
of syphilis and of ague, of hydrophobia, and of diphtheria.
Since the presence of microbes has been ascertained in pneumonia,
and the pathogenetic significance of the diplococcus of Talamon and
Frankel has been admitted by physicians with more or less confidence,
it is not surprising that attempts have been made to apply the theory
of immunity in treatment. The method adopted has been to render
animals immune from the disease by introduction of the supposed
pathogenetic microbe in doses of increasing strength until this immunity
is attained, and then to inject the serum of such an animal into the veins
or tissues of patients suffering from pneumonia. This practice was intro-
duced by F. and G. Klemperer in 1891, and has been followed by some
apparent success (21).
Whether pneumonia can be cut short or not, it may be successfully
guided. No reasonable observer would deny that, although we are
rarely able to say that a patient's life was saved by such and such a
timely measure, yet in the long run the expectant method of treatment,
which interferes only as occasion requires, is followed by a far lower
mortality than misplaced attempts to "jugulate" the disease, or than
a completely negative treatment.
General treatment of uncomplicated cases. — In a case of primary pneu-
monia in a young subject our first care should be to keep him cool by
light covering, cradles under the bedclothes, and frequent sponging with
cold or tepid water. He has no appetite, and there is no necessity to
force food upon an unwilling and often flatulent stomach. If the patient
will drink two pints of milk, or one pint of milk and one of broth, in the
twenty-four hours, he will not starve. Stimulants should not be given
untU required by some special indication.
The thirst, the parched tongue, the fever, the scanty and con-
centrated urine, and the hot, dry skin all call for drink; and the
patient should be allowed to take as much cold water as he pleases. It
relieves his thirst, it moderates the sensation of heat, it flushes the
kidneys, by inducing perspiration it relieves discomfort, and by evapora-
tion it helps to lower the temperature. If patients prefer effervescing
drinks they may have them, and milk with soda water is often the
pleasantest mode of supplying nourishment ; but it must be remembered
that milk is food, and to keep a pneumonic psitient on milk and beef-tea
without water is a practice as unphysiological as it is disagreeable. The
exception is when a child refuses nourishment and will only drink
milk when compelled by thirst. Toast and water, barley-water with or
without a slice of lemon, tamarind or red-currant water may be given
according to the patient's preference; and, although the cold and
unadulterated element is as a rule most grateful, some patients, particu-
larly if troubled by gastric disturbance, much prefer to drink hot water.
There is no reason for withholding tea as a beverage ; but this and other
indulgences the patient will probably enjoy the more if not given imtil
asked for. Oranges or grapes are more pleasant in convalescence than
PNEUMONIA 123
during the height of the disease; but there is no objection to their
use at any time.
With regard to drugs, though an uncomplicated case of pneumonia
will do well without them, yet long and wide experience shows that
solutions of neutral salts are of service in diminishing the sense of
heat and tension, and in promoting secretion. Mtre is perhaps the best
of these ; but citrate or acetate of potash or acetate of ammonia act in
a similar way; the potash salts are supposed to act most on the
kidneys, and those of ammonia on the skin. They may be given with
chloroform or peppermint, or in any bitter infusion such as serpentary,
orange, or quassia. They are not necessary, but beside their un-
doubted, though slight, physiological effects, an occasional draught of
medicine is liked by most patients, and it helps to keep up the attention
of the nurse.
It is an old custom, and perhaps a wise one, to administer a purge
at the beginning of any acute disease. The furred tongue, the headache,
and the customary constipation seem to caU for it; and it helps to
prevent flatulence and so to favour respiration in the course of pneu-
monia. A blue pill, followed by a black draught — or, what is much
pleasanter and nearly as eflScient, by sulphate of magnesia with bicarbonate
of soda in a carminative vehicle, or some other natural or artificial
solution of purgative salts, are the best ways of meeting this indication.
An efficient action of the bowels on the first day of the disease has the
important advantage of setting the mind of the patient and of his nurses
at rest, and of preventing luiseasonable purging afterwards.
From the first day constant attention should be directed to the chart
of temperature, to the pulse and respirations, and to the auscultatory signs.
The chest should be thoroughly examined on the first or at least on the
second day ; and, when the diagnosis and seat of the disease are thus
made clear, the frequency and minuteness of subsequent examinations
may depend upon the patient's condition. It is often wise to refrain
from rousing a patient from sleep for this purpose, or from exciting the
resistance of a child. In such cases, or when delirium or extreme weak-
ness forbids a thorough physical examination, we may generally judge of
the condition of the lungs by counting the number of respirations, by
noticing the colour of the face and lips, and by observing the action of
the nostrils and muscles of forced respiration. By gently rolling the
patient on his side, first one and then the other, we can obtain sufficient
evidence of the state of the lung, by means of the flexible stethoscope,
without raising him in bed.
Treatment of special symptoms. — We now come to the treatment of
symptoms, ordinary or extraordinary.
The temperature is always or almost always high, and hyperpyrexia is
frequently met with ; but it is less common than in rheumatism, typhus,
or scarlatina, and its danger is certainly less than in rheumatism. A
temperature of 104° demands attention, but in children and young adults
does not in itself require interference. When it rises above this point
124 SYSTEM OF MEDICINE
a tepid bath for a child, and sponging the body with cold -water in an
adult are indicated. In some cases it 'is more convenient to put bladders
or india-rubber bags filled with ice in a man's armpits and between his
thighs. If the temperature rise above 105°, frequent sponging with ice-
cold water, rubbing with ice, or immersion in a bath at a temperature
of 80° is called for.
In some cases wrapping the patient in a sheet wrung out of cold
water is more convenient or less unpleasant, and it is an efficient means
of relieving moderate pyrexia ; or Leiter's tubes may be carried in coils
round the head and placed over the great blood-vessels, above the collar-
bones, in the armpits, and in Scarpa's triangle.
In children a high temperature is more frequent and less injurious
than in adults; whereas in elderly patients a temperature above 103° is
a serious matter, and cooling measures must be sedulously and yet
cautiously employed.
Whatever the temperature which appears to call for interference (and
in this we must be guided not only by the thermometer, but also by the
mental condition and the state of the pulse), direct application of cold
should be the treatment adopted. Antipyretic drugs are either in-
efficient or their action is transient; and they often cause dangerous
depression of the heart's action or complete collapse. SaHcyl-compounds
are only indicated when pneumonia occurs as a complication of rheumatism;
and full doses of quinine only in the case of persons who have sufiered
from malaria. Antipyrin or phenacetin is sometimes useful for rehev-
ing severe headache ; but even then they must be used cautiously.
When headache is troublesome, the application of ice to the head often
gives the greatest relief. A dose of bromide is sometimes efiicient, or
the aromatic spirits of ammonia, or a strong cup of coffee.
The pain of the pleurisy which always accompanies pneumonia
varies greatly in its severity and duration. Often it is so slight that a
warm poultice, or an ice-bag, or rubbing with menthol is enough to
allay it. In severer cases two or three leeches are sometimes of striking
benefit ; or, if there be no counter-indications, the sixth or the fourth
of a grain of morphia may be injected under the skin. When the
pain is persistent, a blister relieves it more certainly than any other
remedy.
The efiusion of pneumonic pleurisy is seldom large enough to demand
special treatment. If it should be considerable, it is best to aspirate at
once ; if it be small, it will often disappear of itself after the crisis, or
may be dealt with during convalescence by blisters and diuretics or, -if
these fail, by paracentesis.
Empyema is the most important sequel of pneumonia. When its
presence is discovered, it should be tapped at once, and afterwards
incised and drained. It is said that if the diplococcus of pneumonia
be present alone in the exudation, the pleura will recover without
fresh secretion of pus ; whereas if colonies of staphylococcus or strepto-
coccus are found, it is better not to aspirate but to incise at once, or the
PNEUMONIA I2S
pus is sure to form again : that the latter rule is true, at least for adults,
is supported by general experience ; the former statement is more
disputable.
One of the most formidable complications of pneumonia is pericarditis.
It is most common in cases of double pneumonia with well-marked
pleurisy, and may be chiefly fibrinous, or accompanied with large effusion
of serum, or occasionally purulent. Its recognition is often far from
easy. Marked orthopnoea, an irregular or intermittent pulse, and pre-
cordial distress are each of them valuable signs of pericarditis, but they
are neither constant nor infallible. In every case of pneumonia the apex
and base of the heart should be examined each day : from the former
to learn the strength and character of the first sound of the heart, from
the latter to detect the earliest sign of pericardial friction. This is
difficult to make out when noisy and frequent breathing obscures the
cardiac sounds; and the difficulty is often increased by the restlessness
and distress of the patient. When it is impossible to obtain even a
momentary pause in breathing, close attention to the pulse will impress
the cardiac rhythm on the ear ; and when this is once done, the practised
auscultator can neglect the bronchial riles almost as much as the noises
going on in a room. At least we may say whether the sounds are normal
or accompanied by a murmur; and in the latter case, if we know that they
were normal on the first day of the illness, the murmur is most likely a
pericardial rub.
It is sometimes impossible to detect a large pericardial effusion by
percussion. We must depend upon the situation and force of the cardiac
impulse, on the faintness of the cardiac sounds, and on the signs of down-
ward pressure of the left lobe of the liver. If called for the first time
to a case of acute pneumonia with pericarditis we may find the diagnosis
extremely difficult.
Our treatment of pericarditis, when recognised, is unfortunately not
yet very efficient. There is no reason to believe that bleeding, leeching,
or mercury has any effect on the inflammation. A blister, however,
over the cardiac region will often relieve the precordial oppression ; and
twice I have seen it signally and demonstrably successful in removing the
signs of friction and of efiiision. In a severe ease of pneumonia, however,
blisters are undesirable; and if we believe that pericardial effusion is exten-
sive it is probably better practice to introduce a hypodermic sjrringe at
once and draw off a few drops of the fluid : if serous, the pericardium may
then be aspirated ; if purulent, it should be incised and drained like an
empyema. I have repeatedly tapped the pericardium, and have never
seen harm to follow the practice ; on the other hand, I have been unfor-
tunate in not witnessing the marked relief which many physicians have
recorded. Several most successful cases of draining the pyo-pericardium
have been published.
The most imminent danger in pneumonia is dyspnoea from extensive
consolidation of the lung, overloading of the right side of the heart, and
arterial anaemia. We are at present powerless, or nearly so, to limit the
126 SYSTEM OF MEDICINE
spread of hepatisation ; all we can do is to help the patient to outlive the
stress of the disease.
For this purpose frequent feeding with sraall quantities of nutriment
is necessary. The most useful forms of nourishment are milk, raw eggs,
beef-tea, and meat jelly, or one of the various meat extracts in the market.
Food should not be given oftener than every two hours. When there
is vomiting, or when the patient refuses food— as sometimes occurs in
a child or in an adult who is delirious — it is best to abstain altogether
from feeding by the mouth, and to use instead a nutriment enema
or nutrient suppositories, after the rectum has been washed out.
In cases of secondary pneumonia, and in primary cases occurring in
later life with few exceptions, alcohol is indicated, and in all cases when
the pulse is irregular or very rapid, and the first sound of the heart weak.
It may be given in the egg-and-brandy mixture of the Pharmacopoeia, or
diluted with water as a beverage. Its effect should be watched, and the
amount and frequency of its administration regulated by its effects. It
often improves the pulse and soothes the brain ; when these effects are
apparent, it should be pushed freely. Half an ounce given every four
hours is suitable for an uncomplicated case of pneumonia in a patient
over fifty years of age. Six or eight ounces in the twenty-four hours are
needed in severe cases with feeble circulation ; and as much as twelve
ounces when by the patient's symptoms he seems to demand it, and his
state to improve under the remedy. In some cases champagne is better
tolerated than brandy, whisky, or rum, and has as good or perhaps a better
effect. Sometimes, however, we find that any form of alcohol causes
excitement and discomfort without strengthening the pulse ; in such cases
it is best to omit it for a time, and to rely upon strong beef-tea and
strychnine.
As the pulse affords the chief indication for the administration of
brandy, so the state of the patient's breathing guides our use of ammonia.
This admirable drug acts not only on the heart, but also on the respiratory
centre, stimulating the reflex action of coughing, and so clearing the air-
passages. Like other alkalies, its action on the bronchial secretion is
to make it thinner and more easily got rid of. In all cases of pneumonia,
except those affecting a single lung in children or healthy young adults,
carbonate of ammonia should be given in four or five-grain doses combined
with syrup of tolu, liquorice, or treacle, to soften its pungency. Com-
pound tincture of cardamoms or lavender may be added with advantage ;
or the drug may be given dissolved in peppermint or chloroform water.
It should be repeated every four hours or more frequently, up to five
grains every hour, if dyspncea and cyanosis threaten imminent danger.
There is always some bronchitis with pneumonia, and this may add
considerably to the dyspncea ; but bronchitis is most serious when in a
case of unilateral or extensive pneumonia it affects the healthy lung or
the healthy part of one. It is in such cases, perhaps, that carbonate of
ammonia is most signally useful.
In addition to brandy and ammonia, or in cases where one or the other
PNEUMONIA 127
seems to fail, we may use strychnine as an efficient stimulus of the
centres in the bulb. It is most valuable in cases of failure of the heart's
action, when alcohol seems useless or even mischievous to the patient ;
five drops of liquor strychninae may then be given with excellent effect,
and repeated should occasion arise. Strychnine is much more useful given
in one or two full doses than in smaller ones frequently administered.
Of course it must never be given with ammonia. When a pneumonic
patient is at the point of death, three or four drops of solution of strych-
nine injected under the skin of the arm are more effectual, and less liable
to lead to local abscess than brandy, ammonia, or ether administered in
the same way ; but each of these drugs thus exhibited has undoubtedly
saved life.
In severe cases of pneumonia, the rapidity of the pulse, its frequent
irregularity, and the low blood-pressure naturally suggest the use of
digitalis. It is generally prescribed along with other remedies, and it is
therefore difficult to estimate its individual effect ; but my own experience
has been disappointing, and my disappointment is shared by many
physicians who have used it since Traube recommended it fifty years ago.
In pneumonia its effect is incomparably inferior to that which we see
every day in mitral regurgitation, with dropsy and rapid, weak, irregular
pulse. The experiments of Drs. Brunton and Cash (8) indicate that the
effect of digitalis on the heart is greatly weakened by pyrexia. It has
been conjectured that the right ventricle, the cavity most burdened in
pulmonary obstruction, has not muscle enough to utilise the drug ; but,
if the objection were theoretically admissible, it is contradicted by the
fact that it is this right ventricle which we successfully stimulate and
control in cases of mitral regurgitation. Whatever the explanation,
digitalis would probably be seldom employed if our only experience of it
were in pneumonia. At the same time, it is right to add that some good
observers, both at home and abroad, have a much more favourable ex-
perience of this powerful drug in the disease. Dr. Petrescu of Bucharest
reports a remarkable low percentage of death in pneumonia treated with
large doses of the powdered leaves or of the infusion of digitalis.
An ancient stimulant, which had long fallen into disuse, has been
lately revived in cases of pneumonia, enteric fever, and other exhausting
diseases ; namely, musk, given in ten-grain doses, and repeated in three
or four hours. It is very expensive, and often it fails entirely ; but I
have seen it produce striking improvement for a time in severe cases of
bronchitis, pneumonia, and fever ; and in four or five of these instances it
probably saved the patient's life.
When dyspnoea is urgent, and the patient apparently djdng of
cyanosis, the inhalation of oxygen is a rational mode of treatment,
and has been advocated for many years past. It is now possible
to obtain the gas ready made in large iron cylinders much more con-
veniently and cheaply than before ; and it sometimes proves remarkably
useful. It seems never to do harm, and it is a matter of surprise that its
effects are not more uniformly and obviously beneficial. It is possible
128 SYSTEM OF MEDICINE
that we have yet to learn how to use it most efficiently. At present it
takes its place among the adjuvants of successful treatment.
Delirium is an important complication of acute pneumonia; this is often
best treated by an extra dose of brandy in the evening. In the case of an
intemperate patient digitalis is here a valuable drug. Bromide of potas-
sium, or full doses of henbane or chloralamide, may be used with good
effect. When coincident with high temperature, a wet pack or cold
sponging is often the best cure for delirium.
Sleeplessness is a frequent and trying symptom. In some degree it
is inevitable, and, when there is much bronchitis, to prolong sleep might
be dangerous to the patient ; but in other cases the insomnia is purely
injurious, and must be met by every means in our power. In ordinary
cases a cup of beef -tea with a spoonful of brandy is an excellent sedative;
and if, before this is taken, the patient has been well sponged, fur-
nished with a clean night-dress and a fresh pillow, if the head is kept
high and as cool as possible, and the room dark and quiet, natural sleep
will often follow. Nothing is worse at such times than meddlesome
nursing, movijig about on tip-toe, conversing in whispers, and smoothing
the patient's pillow. The administration of food or medicine may well
be omitted for three hours, or even longer. In cases where this would
be dangerous the patient is not likely to sleep too long.
The refreshment of sleep at some time of the day or night is of
primary importance in pneumonia as in other fevers; and when the means
above mentioned fail, and the patient has been sleepless for twenty-four
hours, the question arises of exhibiting our most powerful remedy, opium.
It has been forbidden lest its use should increase cyanosis, diminish
respiratory efforts, and lead to fatal coma. These fears are far from
groundless. When there is extensive consolidation or much bronchitis,
when the patient is becoming livid, and the expectoration scanty, it
would be bad practice to give this drug. Mustard plasters, strychnine
subcutaneously, and ammonia by the mouth are the remedies indicated
Often during a whole night the patient must be restless, must continue
to cough and expectorate, and must use every muscle available to keep
himself alive by forced breathing. The orthopnoea, the coughing, the
sleeplessness, the distress are all evidence of the struggle for life ; and
the worst sign is when a cyanotic patient lies low in bed, drowsy, with
weak and shallow breathing, the respiratory centre in his bulb poisoned
by carbonic acid. After such a restless night as we have just described
the patient will often find the breathing relieved when morning comes ;
and, after taking a cup of coffee or a glass of wine, he may sink into natural
slumber, and awake refreshed and ready to renew the struggle.
But in many cases of pneumonia the danger is not directly from
suffocation ; it is rather from the effects of a continued high temperature
upon the heart, the impending weakness of the respiratory muscles, and
exhaustion of the reflex activity of the nervous centres. In such cases
10 grains of Dover's powder, 5 grains of a compound soap pill, 15 or 20
drops of laudanum are often invaluable, and succeed when all other
PNEUMONIA 129
hypnotics are powerless. An additional -warrant for tte use of opium is
dilatation of the pupils. The presence of albumin, if only of pyrexial
origin, is no counter-indication j but if the patient be a subject of chronic
Bright's disease we must forgo the use of this valuable drug, or use it
at his peril, to escape a still more imminent danger.
There are two remedies which have fallen into general disuse, but
each of them worthy of being employed on occasion.
One is the use of emetics — antimonial wine, or ipecacuan in full doses,
or sulphate of zinc, or subcutaneous injection of apomorphia, or a
draught of mustard and water and tickling the fauces with a feather :
such drugs, in emptying the stomach, also get rid of accumulated bronchial
secretion, and produce deep and efficient respiratory effort. This method
of treatment is still much used with children suffering from broncho-
pneumonia, for in them vomiting is easy and expectoration difficult. In
adults a vomit and a purge no longer form a routine prescription ; and,
although no doubt an emetic is sometimes useful, it is an unpopular remedy,
and its effects are often disappointing. Not infrequently even large doses
of the emetic fail to excite vomiting, and the patient's condition is then
iincomfortable to himself and embarrassing to the physician. A full dose
should always be given, and in pneumonia and bronchitis stimulant
emetics like mustard and sulphate of zinc are more suitable than anti-
mony. Though often disappointed in this plan of treatment, I have seen
cases in which it was of undoubted benefit.
The other ancient remedy is that of bleeding. We saw that it was
once employed to subdue fever, and to cut short inflammation, and that iis
use for these purposes is deservedly discredited. Venesection is less
potent for good and also for evil than used to be thought, but it is not
to be forgotten or neglected. Its effect in relieving the pain of aneurysm
was insisted on by the late Dr. Hughes Bennett in the midst of his
attack upon its use in pneumonia. The same iconoclastic reformer also
recognised its value when used in the very first stage of pneumonia before
dulness had appeared. It is not often that a patient is seen in this stage,
which is usually very short ; but when pneumonia occurs as a primary
attack in a young and robust subject, with severe pleuritic pain, I would
advise bleeding, not as a cure, but as a means of relief. If the pulse
be full, strong and hard, and a great sense of prsecordial oppression
be present, the withdrawal of 6 or 8 ounces of blood from the arm,
by temporary lowering of the arterial pressure, will sometimes remove
distress better than any other remedy, and will leave, if not a beneficial,
at least no deleterious effect on the subsequent course of the disease.
In cases of cyanosis, with a small and feeble pulse, congestion of
the surface, and distension of the right ventricle, as shown by epigastric
pulsation and pulsation of the great veins, our object is not to lower
the arterial blood - pressure, but to relieve the over-pressure in the
right side of the heart and the systemic veins. The withdrawal of
10 or 12 ounces of blood under such circumstances is a rational pro-
cedure, and in practice is often successful in tiding over a dangerous
VOL. V K
SYSTEM OF MEDICINE
period of the disease. In my experience, however, venesection in the
cyanosis of pneumonia is less strikingly useful than in the corresponding
phase of bronchitis ; although it is more so than in the cyanosis of valvular
disease of the heart. '^
In the treatment of convalescence from pneumonia we have fortu-
nately little to discuss. Like typhus, and in striking contrast to enteric
fever and scarlatina, acute lobar pneumonia is a disease which either kills
the patient or leaves him much as he was before. When the crisis is past
the inflamed lung very seldom fails to clear up rapidly and completely.
As soon as the temperature falls, brandy and medicine should be
omitted or greatly reduced in amount and in frequency of administra-
tion. Sleep should be encouraged, and food given in accordance with
the patient's returning appetite. Wine is often useful during the first
days of convalescence ; or, if the patient prefer it, malt liquor may be
taken with at least equal advantage. There is no danger of catching
r;old, and the patient may go out of doors in favourable weather as soon
as he desires to do so.
Appendix of Cases
The statistics subjoined refer to 434 cases of (acute fibrinous) pneu-
monia collected from the following sources : 329 schedules were filled up
from the records of Guy's Hospital during years 1891-94 by the
medical registrar. Dr. J. H. Bryant, assisted by Mr. F. J. Steward, and to
both these gentlemen I am greatly indebted for this valuable help. I have
added 32 hospital cases of my own, admitted in 1895 and 1896; the
remaining 73 were private cases seen in consultation. The number of
cases is not large enough for all purposes, but it is, I hope, large enough
to be of service for others.
The facts tabulated in the schedules were : — (i.) the sex, and (ii.) the
age of the patient ; (iii.) the assigned cause, the antecedents, and initial
symptoms of the attack ; (iv.) the part of the lungs afifected ; (v.) some of
the chief symptoms, particularly the highest temperature attained, the
presence and characters of the sputa, the presence of herpes, and (vi.) any
important complications or sequels ; (vii.) the duration of the disease,
reckoned from the rise of temperature to the end of pyrexia, and, lastly,
(viii.) the result in recovery or death, with details of the fatal cases.
1. Sex. — Of the 434 cases, 320 occurred in male, and 114 in female
patients, a somewhat larger disproportion than usual. The difference is
most marked in early adult life, least in children, and disappears in the
statistics of prisons, where both sexes are imder similar external conditions,
and where epidemic pneumonia would affect both alike.
2. Age. — The following is the incidence of the 434 cases at the several
periods of life.
(a) Under five years. — Total, 29 patients. Of these, 6 were above four
years old; 9 were between three and four; 10 were between two and
^ See forty-nine cases of venesection in the Medico-Ohini/rgicaZ Fransactions for IJQl.
PNEUMONIA
131
three ; 1 was eighteen months old ; and 2 were under a year— one four
and the other seven months old.
Between fine and ten years there were 66 cases, making a total of 95
patients under ten years old.
Between ten and fifteen there were 45 patients, and between fifteen and
twenty 48, making a total of 93 between ten and twenty.
(J) Arranging the figures in perhaps a more instructive way, we have
3 cases in infancy, 26 in early childhood (two to five), and 159 between
five years old and adult age.
Between twenty and forty there were 149 cases.
Between forty and sixty there were 74 cases.
Between sixty and seventy there were 18 cases; showing a greater
frequency than between fifty and sixty, if we allow for the fewer possible
patients at the more advanced age.
Above the age of seventy there were 5 patients — 2 aged seventy-two, 1
seventy-three, and 2 seventy-five.
These numbers confirm what is a matter of general observation, that
lobar pneumonia is rare in infancy, very common between two years old
and twenty, gradually less common in adult life, more rare after fifty.
The cases in later life are mostly secondary.
(c) Arranged in decades the numbers are —
Between 3 months and 10 years 95
„ 10 and 20 years . . 93
„ 20 „ 30 „ . . 87
„ 30 „ 40 „ . . 62
Between 40 and 50 years .
. 54
„ 50 „ 60 „ .
. 20
„ 60 „ 70 „ .
. 18
., 70 „ 76 „ .
. 5
3. Opigin and onset. — In 38 cases only was the attack of pneumonia
explicitly attributed to a shortly precedent exposure to cold ; a " chill "
received more than a week before the illness began was not counted. In
14 cases the origin of the disease was imputed to an injury or "accident ";
but I have never seen a case in which this supposition was borne out.
In 3 cases only was there a probability of infection from another case
in the same house. Two of these patients were children ; the third was
a lady who was attacked with jmeumonia while nursing her child with
the same disease and while her husband was convalescent from it. Another
patient, whom I saw with Dr. Charles Addison at Colchester, was one of
no less than four cases of pneumonia in the same house ; but in each of
them the pneumonia had been preceded by influenza, so that the cases
should come under another heading.
In the hospital cases it is likely that many more had their origin in
influenza; but in only three was the sequence definitely recorded. Of
73 private cases, influenza had preceded the pneumonia in 8.
The onset of the disease was gradual in not less than 93 cases, an
unexpectedly large number — more than a fourth of the whole. In the
remaining 234, in which the early symptoms were clearly ascertained, the
onset was sudden ; it began with well-marked shivering in 95 cases, with
vomiting in 50 (chiefly children), with convulsions in only one case (a
132
SYSTEM OF MEDICINE
child), in the remainder with sharp pain in the side, or once or twice with
syncope.
A previous attack had occurred in 18 cases — in 3 within a year, in 3
within two years, in 1 three years ago, and in 3 so long as fourteen,
seventeen, and eighteen years before the second attack. One patient had
suffered five or six times from the disease, two had a fourth, and one a
third attack.
4. Locality. — The right lung was, as generally observed, more often
affected than' the left ; but the difference was due to the large excess of
right-sided over left-sided apical pneumonia. When the base only was
affected, there were in my tables rather more cases on the left than on
the right side.
Cases beginning in tlie right base
„ left „
,, right apex
„ left „
affecting the middle part of the lungs-
,, both lungs . , .
• ^5°! 291 basal.
• 20} 80 apical
-6 right, 2 left 8
55
Total number of cases affecting the right lung only ,
»j )j )) l®^t „ ,
„ ,, „ both lungs
434
206
173
55
434
Double Pnev/monia. — The 55 cases in which both lungs were affected
seem to deserve separate attention, particularly in their relation to age
and to prognosis. The table explains itself.
Sex.
Age.
Locality.
Complicated by
Complicating
Eesult.
M.
31
Both bases .
Tympanites .
Died
M.
43
B. base, L. apex ,
Chronic phthisis .
Died
M.
49
Both bases .
Chronic phthisis .
Died
F.
12
Both bases .
Gangrene . .
Spinal caries
Died
F.
4
Both bases .
Chronic otorrhoea .
Recovered
M.
36
Both bases .
Recovered
M.
49
Both lungs .
Morbus Brightii .
Died
F.
46
Both bases .
Gangrene, Endo-
carditis
...
Died
M.
6
Both bases .
Empyema . .
...
Recovered
M.
36
Both lungs .
Gangrene . .
Intemperance
Died
M.
21
R. base, L. apex .
Diarrhcea . .
Died
M.
15
Both lungs .
Recovered
M.
39
Both bases .
Recovered
F.
18
Both lungs .
Laryngitis . .
Recovered
M.
14
Both lungs .
...
Recovered
M.
22
Both lungs .
Empyema . ,
...
Died
M.
39
Both lungs .
Admitted moribund
Died
M.
8
Both lungs .
Empyema, Peri-
carditis
...
Died
M.
17
Both lungs .
Admitted comatose
Died
PNEUMONIA
133
Sex.
Age.
Locality.
Complicated by
Complicating
Result.
M.
32
Both lungs .
Intemperance
Recovered
M.
18
Both lungs ,
...
Intemperance
Died
F.
18
Both lungs .
Died
M.
4
Both lungs .
...
Died
F.
3^
R. base, L. apex .
..•
Died
M.
28
Both bases .
...
>.*
Recovered
F.
21
Both lungs .
• ••
Puerperium ■
Died
M.
30
Both lungs .
...
Recovered
M.
23
Both bases .
Pyopneumotho-
Intemperance •
Died»
F.
13
Both apices .
Recovered
M.
45
Both lungs .
Died
M.
37
R. base, L. apex .
Delirium tremens
Cirrhosis of liver .
Died
M.
52
Both lungs .
Intemperance
Died
F.
28
Both lungs .
Empyema . .
Recovered
M.
20
Both lungs .
Died
M.
19
Both lungs .
Recovered
M.
30
Both lungs .
Recovered
M.
6
Both lungs .
Empyema . .
Recovered
M.
7
Both lungs .
Empyema . .
Chronic otorrhtea .
Recovered
M.
18
Both lungs .
Empyema . .
Influenza
Recovered
M.
12
Both apices .
Recovered
M.
33
Both lungs .
Laryngitis . .
Died
M.
22
Both lungs .
Laryngitis . .
...
Died
F.
27
Both lungs .
Recovered
M.
20
R. and then L. base.
Recovered
F.
48
Both bases .
...
Died
M.
35
Both bases .
Intemperance
Died
M.
54
Both bases .
/Endocarditis, \
\ Meningitis /
Died
M.
17
L. base, then R. apex
...
Recovered
M.
35
L. base, R. apex .
Died
M.
48
Both bases .
...
Recovered
F.
43
Both bases .
...
Died
M.
20
Both bases .
...
Intemperance
Recovered
M.
9
R. base, i, apex .
• •>
Recovered
M.
12
Both bases .
Recovered
M. 20
Both bases .
Mania ....
Died
He left the hospital against advice.
Summary. — Deaths, 30 ; recoveries, 25. Only one recovery took
place among patients who were over forty years of age when attacked.
This was in the case of a man aged forty-eight with pneumonia of both,
bases.
5. Symptoms. — Those which I particularly recorded were the tem-
perature, the character of the sputa, and the presence of herpes labialis.
Albwninwria was frequently reported, and in cases when stated to be
absent an earlier or more frequent examination might often have found
it. Its presence from more or less latent Bright's disease, from acute
nephritis or renal embolism, and the occurrence of traces of albumin from
leucorrhoea, cystitis, spermatorrhoea, or gonorrhoea virulenta would also
disturb the results.
134
SYSTEM OF MEDICINE
Temperature. — In two cases this is recorded as subnormal ; both these
patients were admitted into hospital in a collapsed and moribund con-
dition, and died soon after being got to bed. In the rest the highest
point observed was as follows : —
Degrees Fahr.
100-100-4
101-101-8
102-102-8
103-103-8
104-104-8 :
105-105-8
106 {Us), 106-4, 106-6
107-8 .
109
5
22
55
114
164
421
4"
1»
13
408
Serpes. — A herpetic eruption was noted in only 53 patients. Of
these, 46 recovered and 7 died.
Sputvm. — Notice of this is not always explicitly made, and patients
may have died too soon for it to be seen. Of the 290 cases in which
definite statements were made, there were —
116 in which the sputum was "rusty."
7 „ „ „ "greenish."
24 „ „ „ mucous or muco-purulent
13 „ there was free haemoptysis.
130 „ no sputum was expectorated.
In 113 cases of children under fifteen expectoration was absent.
The only children who succeeded in coughing up their sputa were 4, aU
between eleven and fifteen years of age, who brought up rusty sputa ;
and 3 between six and eight years old, who coughed up blood-stained
mucus.
Of adults who did not expectorate at all during the whole attack of
pneumonia there were as many as 17. Three of these were between
fifteen and forty (out of 194); 5 were between forty and fifty (out of
52); 3 between fifty and sixty (out of 16); 3 between sixty and seventy
(out of 20) ; and 3 between seventy-two and seventy-five (out of 5).
, 6. Complications and sequels. — In five patients the pneumonia ended
in gangrene of the lung; one a case of chronic caries of the spine, one
complicated with pericarditis, one with ulcerative endocarditis, and one
with delirium tremens. All of these five- patients died.
Ulcerative, septic endocarditis occurred six times, and in three of
these meningitis was also present; while in two other cases meningitis
1 Of these forty-two, only four reached 105 '8°, and nearly half did not exceed (so far as
was noted) 105°.
" Two of these patients recovered after temperatures of 106° and 106-6°.
^ Both of these patients died.
PNEUMONIA
I3S
was found after death. Feriearditis was a complication in fourteen cases,
and in one of these there was abo endocarditis (in addition to the six
above mentioned).
Icterus occurred in four cases ; in three of these the right base, and
in one the right apex, was affected.
Delirium tremens complicated pneumonia in seven cases, and five of
these were fatal.
Otorrhea from tympanitis occurred three times, and pulmonary embolism
once, with recovery.
Many other complications recorded, as tonsillitis, gout, asthma, cardiac
and renal disease, and laryngitis, were no doubt accidental coincidences.
None of these occurred more than four times among the 434 cases.
In probably every case there was pleurisy ; but serous effusion was
only abundant enough to be noticed in 1 7 cases.
The most frequent sequel was emjpyema, which followed pneumonia
in 24 cases, one of them being circumscribed empyema of the right apex.
7. Duration. — This was measured by the pyrexia, which occasionally
preceded the evidence of hepatisation, and more often ceased before the
signs of consolidation had disappeared. In 118 cases the duration was
not ascertainable.
The shortest cases lasted three days ; and these mild, but certainly
not "abortive," cases occurred in children or youths, as the following
detailed statement shows : —
Duration of Pneumonia
Ages of Patients.
3, 5, 5, 5, 6, 8, 9, 12, 14, 22, 27
/5, 6. 7, 7, 7, 10, 11, 11, 12, 12, 13, \
1 14, 14, 17, 19, 19, 20, 21, 21, 22, 26/
Three
Four
Five
Six .
Seven
Eight
Nine
Ten
Eleven
Twelve (in four recovery delayed by complications)
Thirteen (fall of temperatnre by lysis)
Fourteen . . '.
Fifteen ......
Seventeen . . . . . ' .
Twenty-one (delayed by complications)
Above three weeks (delayed by complications)
Oases.
11
21
30
68
62
39
28
20
12
2
316
The most frequent duration of the disease was about a week; 32
patients were actually ill for only three or four days, 199 (nearly two-
thirds of the number) for five to nine days, and only 17 for more than
twelve days.
8. MoFtality. — The total number of deaths was 111, a high per-
136
SYSTEM OF MEDICINE
eentage (25'5) out of 434.^ But this general statement is of little value.
Hospital mortality in this as in most other diseases is higher than that
of private practice, because the previous habits and conditions of the
patient are less favourable. But again, general cases seen in consultation
are usually severe, and sometimes hopeless. Of 73 of the latter class
25 were fatal — more than a third.
Deaths among 362 Hospital Patients (86)
Highest
Sex.
Age.
pbserved
Herpes.
Locality.
Complications.
F.
Temp.
•
47
10°3-4
Absent
Right base .
Ulcerative endocarditis and men-
ingitis
M.
31
102-4
,)
Double
M.
43
104
Double
In course of phthisis
M.
49
103-2
Double
In course of phthisis
M.
37
100-4
Right apex .
Carcinoma of stomach
M.
43
101-4
Left base
Haemoptysis ; gumma of liver
M.
27
100-2
Left apex .
In course of morbus Brightii
F.
12
102-8
Double
Gangrene of lung ; chronic disease
of spine
M.
22
102-2
Right lung .
Ulcerative endocarditis
F.
51
104-4
Left apex .
Bronchitis
M.
43
104-2
Right apex .
Gangrene of lung ; pericarditis
M.
49
•Double
In course of morbus Brightii
M.
10
100-2
Right base .
Chronic basal meningitis
M.
39
103
Right base .
Marked delirium
M.
2
104
Right base .
Laryngitis
M.
33
104-6
Left apex .
Pleuritic effusion
F.
29
100
Right base .
Cancer of bowel
M.
42
Right apex .
Morbus Brightii (lardaceous)
M.
45
Left base
Morbus Brightii ; pericarditis ^
M.
66
Right apex .
Pericarditis ; delirium
M.
36
109
Right base .
Intemperate ; hyperpyrexia
M.
41
105-8
Right apex .
Intemperate
M.
35
103
Present
Left base
Delirium tremens
F.
46
103-6
Absent
Double
Gangrene of lung ; ulcerative
endocarditis
F.
42
101-8
?]
Left base .
Tumour of brain
M.
54
106-4
Right apex .
Intemperate ; ulcerative endocarditis
M.
34
104-6
Right base .
Delirium
M.
39
• Left base .
Delirium
M.
55
. •<
Left base
Pleuritic effusion
M.
58
102
Right apex .
Pericarditis
M.
27
103-2
Right base .
Delirium
M.
25
102-4
Right base .
Pericarditis ; thrombosis of pul-
monary artery
M.
33
103
,)
Left base
Delirium
M.
38
102-8
Present
Left base
Delirium tremens
' The total mortality for all ages and both sexes, without for the most part exclusion ol
secondary cases, was 191 in 1060 (Goll. Invest. Meport — private cases), 281 in 2618 (Huss —
hospital and private at Stockholm), and 192 in 1010 (Coupland — Middlesex Hospital).
PNEUMONIA
137
Deaths among 362 Hospital Patients — contimmd
Highest
•
Sex.
Age.
observed
Temp.
Herpes.
Locality.
Complications.
M.
42
10|-2
Absent
Left base
Intemperate
M.
36
106-8
jj
Double
Intemperate ; gangrene of lung
F.
63
102-4
3)
Right base
Pericarditis
M.
49
104
Left base
Intemperate ; gangrene of lung
M.
27
107-8
))
Left base
Hyperpyrexia
M.
21
102-4
IJ
Double
Delirium
M.
33
104-4
)J
Right apex
Intemperate ; pericarditis
M.
22
103-4
}]
Double
M.
39
97-8
})
Double
Admitted 7th day, moribund
M.
8
104
t)
Double
. Pericarditis ; empyema
M.
22
103-6
Left apex
Delirium tremens
M.
17
103-4
JJ
Double
Admitted comatose
M.
47
103-4
Left base
Diabetes
M.
48'
102-4
})
Double
Intemperate
F.
18
106
11
Double
M.
4
104-6
Double
...
F.
3
103-2
' ))
Double
...
M.
27
102-6
Present
Left base
Endocarditis
M.
45
103-6
Absent
Left base
Influenza ; pericarditis
M.
26
ii
Right apex
Delirium
M.
41
105
it
Right apex
...
F.
21
105-2
3t
Double
Pregnancy ; empyema
M.
29
103-4
Present
Right lung
Pericarditis
M.
15
100
Absent
Eight lung
Hodgkin's disease
F.
58
104-2
It
Left apex
Delirium
M.
48
103-6
It
Double
M.
63
101-2
It
Right base
M.
45
105-4
It
Right apex
Pericarditis ; delirium
M.
37
103-4
It
Double
Delirium tremens
M.
52
103-6
It
Double
Intemperate
M.
32
104-8
Left base .
'
M.
58
102-2
>»
Eight apex
Acute nephritis
M.
44
102
tt
Left base
Chronic nephritis
M.
20
104-2
Present
Left base .
M.
20
104
Absent
Double
M.
4ni.
104-4
tt
Right lung .
Pericarditis
M.
33
104-6
Present
Double
Delirium; laryngitis
M.
22
103
Absent
Double
Laryngitis
F.
29
104-2
It
Right lung
Intemperate
M.
62
101-4
tt
Left apex
Fatty liver
M.
36
102
It
Left base .
Intemperate
F.
18
105
)»
Eight lung
Empyema
M.
48
101-4
tt
Eight base
Pericarditis
M.
63
It
Eight base .
Morbus Brightii
M.
57
>t
Eight lung ,
F.
48
)f
Double
M.
35
It
Double
Intemperate
M.
54
»)
Double
Endocarditis ; meningitis
F.
24
tt '
Right apex .
M.
56
104
tt
Left base
Laryngitis
M.
36
104
Present
L. lung and R. apex
Intemperate
138
SYSTEM OF MEDICINE
Deaths among 73 Private Cases (25)
{Herpes absent in all)
Highest
Sex.
Age.
observed
Temp.
Locality.
Oomplioatians.
F.
39
103
Left base
Intemperate ; pregnant
M.
27
101
Right base
Intemperate
M.
48
Right base
Intemperate
F.
30
105
Right base
Delirium
F.
15
104
Left base
...
F.
43
104
Double .
...
F.
66
103
Right base
...
F.
43
102-5
Left base
M.
58
98
Left base
Chronic Bright's disease
F.
40
105
Left base
Pericarditis
M.
72
101
Right base
Phthisis
F.
45
104
Right lung
Icterus
M.
42
104-4
Right base
F.
45
108-5
Right base
Puerperium '
M.
57
103
Left base
M.
58
102
Left base
Diabetes
F.
68
104
Right apex
General bronchitis
M.
46
103-5
Right base
Intemperance
M.
75
101-5
Right base
Aortic valvular disease
F.
55
104
Right base
General bronchitis
F.
75
104-5
Right mid-lun
?
Delirium
M.
62
102-5
Right lung
Emphysema
M.
66
104
Left base
...
M.
20
104
Double .
Mania
M.
49
106
Left base
Delirium
vee
n 5 and 10,
1 death ,,
66
11
10 „ 15,
2 deaths ,,
45
jj
15 „ 20,
5 „ „
48
Death-rate of Pneumonia at several Ages
Under 5, 5 deaths out of 20 oases. Four months (pericarditis), 2J, 3 {donble)i
2 (laryngitis), 4 (double).
8 double, with pericarditis.
10 (meningitis), 12 (spinal diaeaise).
15 (general bronchitis), 15 (Hodgkin's
disease), 17 (double), 18 (double), 18
(empyema).
20 „ 25, 9 „ „ 45 „ 20 (double), 20, 20 (double), 21 (double),
21 (double), 22 (intemperance), 22
(double), 22 (endocarditis), 22
(double).
25 „ 30, 10 „ „ 38 „ 25 (perioarditis)^ 26, 27, 27 (endocar-
ditis), 27 (intemperance), 27 (tubal
nepliitis), 27 (hyperpyrexia), 29
(intemperance), 29 (cancer), 29
f X) 6T1C Sifd iijis ^
30 „. 35, 8 „ „ 29 „ 30, 31 (double), 32, 33, 33, 33 (doubleX
33 (intemperance), 34.
PNEUMONIA 139
Between 35 and 40, 13 deaths out of 33 cases. 35 (double), 35 (intemperance), 35
(double, intemperance), 36 (intem-
perance), 36 (intemperance), 36 (in-
temperance), 37 (cancer), 37 (double,
intemperance), 38 (intemperance),
39 (double), 39 (intemperance),
39, 39.
., 40 „ 45, 13 „ „ 27 „ 41 (pericarditis), 41 (intemperance), 42,
42 (intemperance), 42 (morbus
Brightii), 42 (tumour cerebri), 43,
43 (syphilis), 43 (double) Us, 43, 43
(pericarditis), 44 (morbus Brightii).
„ 45 „ 50, 18 „ „ 27 „ 45 (pericarditis), 45 (pericarditis), 45,
45 (intemperance), 45 (hyper-
pyrexia), 45 (morbus Brightii), 46
(endocajrditis), 47 (endocamitis and
meningitis), 47 (diabetes), 48 (peri-
carditis), 48 (double) Ur, 48 (in-
temperance), 49 (morbus Brightii),
49 (intemperance), 49 (double), 49
(hyperpyrexia).
„ 50 „ 55, 4 „ „ 5 „ 61 (bronchitis), 52 (double, intemper-
ance), 54 (endocarditis) Hs.
„ 65 „ 60, 10 „ „ 15 „ 55 (bronchitis), 55, 56 (diphtheria), 57,
57, 58 (morbus Brightii), 58 (peri-
carditis), 58 (double), 68 (dia-
betes), 59.
„ 60 „ 65, 5 „ „ 12 „ 62, 62, 63 (pericarditis), 63, 63 (morbus
Brightu).
„ 65 „ 70, 4 „ „ 6 „ 66, 66, 66 (pericarditis), 68.
Over 70, 3 „ ,, 5 ,, 72, 75, 75 (morbus cordis).
Causes of death. — That age is a grave element in the prognosis
■of pneumonia is clear from the last table. Excepting infants, there
are few deaths under 15. After this age, the mortality rises steadily
with the age of the patient, although even after 70 the prognosis is not
always fatal. It will also be noted that the deaths at the earlier ages
are generally accompanied by one of the untoward complications to be
mentioned presently ; whereas most of the fatal cases in the later decades
are uncomplicated.
In all cases, single or double, and at all ages, the important causes of
■death were as follows : —
Intemperance, with or without delirium tremens, was present in a
marked degree in 16 of the fatal cases, and this is probably below the
truth.
In 10 other fatal cases delirium, more violent and particularly more
diurnal than usual, was noted ; and although only 4 cases were distinguished
as well-marked delirium tremens, many of the other delirious patients were
intemperate.
Pericarditis occurred in 1 4 cases, all of which proved fatal : endocar-
ditis in 7, and meningitis in 5.
Bronchitis was fatal in only 3 cases, aU old people.
In 3 fatal cases there was pleuritic effusion, and in only 1 of these
was it purulent; so that aU the cases followed by empyema without
other complications ended in recovery except this one.
I40 SYSTEM OF MEDICINE
Hyperpyrexia — a temperature over 106° — occurred in 6 patients, of
■whom 2 recovered (under 107°), and 4 died.
Of fatal cases of secondary pneumonia 8 occuired in the course of
Bright's disease ; 5 in course of chronic tuberculosis ; 2 in diabetes, and
the 6 others happened in cases of cancer, lymphadenoma, tertiary syphilis,
cerebral tumour, and valvular disease of the heart.
REFERENCES
1. Addison, Thos. Ois. on the Diagn. of Pneumonia and on Pneumonia and its
Consequences, ISiS, 1837, reprinted in Collected Works, 1868. — 2. Andkal. "Hyper-
emia du poumon," Prids de Vanat. path, tome ii. p. 504 ; 1829. — 3. Attrelianus,
C^Lius. De Morb. Acmt. lib. ii. cap. xxv.-xxix. — 4. Ashbt and Weight. Diseases
of Children, pp. 214-233, 2nd ed., 1896. — 5. Baillib. "Lungs changed into a Sub-
stance like Liver," Morbid Anat. 1807.^ — 6. Balfour, Geo. JBdin. Med. Jour. Sept.
1858. — 7. Bennett, J. H. Sestorative Treatment of Pneumonia, 18S5 ; Clin. Lectures,
3rd edit. 1859, pp. 297-311.— 8. Beitnton and Cash. St. Barth. Reports, 1871.—
9. Oelsus. Lib. iv. cap. vii. — 10. Chomel. " Pneumonic," Legons de clinique iiiJd.
tome iii. 1840. — 11. Collective Jnvestigation Mecord, "Pneumonia: Analysis of 350
Cases," p. 93. Brit. Med. Assoc. 1883. — 12. Fox, Wilson. "Acute Pneumonia,"
Reynolds' System of Medicine, 1871. — 13. Idem. Diseases of the Lvmgs and Plevna,
pp. 285-377, posthumous work edited by Coupland, 1891. — 14. Feankbl. Congr. f.
innere Med. Berlin, 1884. — 15. Fribdlander. Virchow's Archiv, Ixxxvii. — 16.
Gamaleia. Annales de I'Inatitut Pastewr. Paris, 1888. — 17. Grisolle. TraiU de
la pneimionie, 2mo. ed., 1864. — 18. Hippocrates. Aphor. iii. 23, vii. 20, etc. — 19.
JuEGENSBN. " Croupose Pueumonie," Ziemssen's Rdbh. 1874. — 20. Klein. Micro-
organisms and Disease, 1896, p. 226. — 21. Klempbebk, F. and G. Perl. klin.
Woehenschr. 1891, Bd. xxviii. Nos. 34, 35. — 22. Labnneo. "De la P^ripneumonie,"
Ausc, mediate, 1819. — 23. Ibid, tome ii. p. 14. — 24. Osler. "Prognosis in Vnea-
monia,," American Jou/rnal of Medical Science, Jan. 1897. — 25. Powell. Brit. Med.
Assoc, in London, Aug. 1895. P.M.J. Nov. 9, 1895, p. 1149.— 26. Steenbeeg.
Lancet, 1889, vol. i. p. 474. — 27. SlOKES. Treatise on the Diagnosis and Treatment
of Diseases of the Chest, Sect. iv. "Pneumonia," 1837, pp. 267-348 of Syd. Soe. ed.
1882. — 28. Stueges. Nat. Sist. and Pelations of Pneumonia, 1876. — 29. Sturges
and COTJPLAND. Second edition, 1890.-30. Talamon. Progres mMical, Nov. 1883.
—31. Walshb. Diseases of the Lungs, 4th ed. 1871. — 32. Washbouen. Path.
Trans. 1895, and J. Path, and Pact. Jan. 1898. — 33. Wbichselbaum. Wiener med.
Jahrbuch. 1886.-34. White, W. H., and Peaece, A. C. Gfvy's Rosp. Pep. vol. Ii.
1894, p. 13.— 35. Weight, A. E. Brit, Med. Journ, 1895, vol. i. p. 303.
Catarrhal Pnexjmonia
Synonyms. — Pulmonary catarrh. Broncho-pneumonia, Lobular pneumonia.
Disseminated pneumonia, including Vesicular pneumonia.
Definition. — This disease is more difficult to define than is lobar
pneumonia. In some cases it closely resembles the latter both
clinically and anatomically, while in others the two diseases offer few
points of resemblance. Lobular pneumonia, as an anatomical lesion, in-
cludes such different conditions as acute pulmonary catarrh in a child
after measles, the chronic broncho-pneumonia of rickets, the hypostatic
Pneumonia hi
pneumonia of fever (in part), the caseating pneumonia of phthisis, and the
lobular suppuration of pysemia. The last two conditions form part of the
pathology of tuberculosis and of septic embolism respectively. Hypostatic
pneumonia is a secondary condition probably beginning in the bronchi,
certainly secondary to prolonged passive congestion, and made up of
lobular hepatisation, often confluent and sometimes primarily lobar, vrith
cedema, and collapse. The remaining kinds of pulmonary inflammation
which are included under the head of Catarrhal Pneumonia are better
dissociated from lobar or fibrinous pneumonia, and named acute or
chronic pulmonary catarrh.
Of the disease thus restricted we may say that it befalls children far
more frequently than adults ; that, though sometimes acute in its origin,
the signs of its invasion are never so abrupt or well marked as those of
lobar pneumonia ; that its course is either subacute or chronic, and that
it never terminates by crisis ; that it is accompanied by bronchitis, and
is probably always secondary. It is much more directly connected with
breathing cold air, or air laden with dust and other mechanical impurities,
than is lobar pneumonia, and seldom occurs in an epidemic form. It is
often secondary, not only to bronchitis, but also to measles and whooping-
cough, and to chronic conditions of iU health, particularly rickets. As
a rule it affects both lungs, and that in irregular patches, without pre-
ference for either apex or base. Although often accompanied by pleurisy,
this may be absent.
Anatomy. — As one of its names implies, catarrhal pneumonia affects
the lungs lobule by lobule, and these lobules are often found scattered
over both lungs, whence the name " disseminated pneumonia." More often
several adjacent lobules are affected together so as to form patches in
different parts of the lung. These patches again may coalesce, and thus
after death from pulmonary catarrh a considerable area of continuous
solid and hepatised lung is found which closely resembles the lobar
hepatisation of fibrinous pneumonia. Pulmonary catarrh does not affect
the base more frequently than the rest of the lung ; nor is there reason
to believe that it has a predilection for the apices, except when it is part
of the effects of tuberculous invasion. Occasionally only part of a lobule
may be affected ; smaller, separately inflamed areas may, in some cases,
be distinguished by the naked eye, and this kind of disseminated pul-
monary catarrh may be distinguished as "vesicular pneumonia."
Microscopic examination shows that the disease originates in a
catarrhal inflammation of the mucous membrane of the bronchi ; this
spreads to the last bronchioles, which open into the lobules — a condition
described as " capillary bronchitis." When the lobule is itself examined
it is found filled with epithelium and with smaller cells which have the
characters of leucocytes. There are no blood-discs, and fibrin is absent
or scanty. The larger epithelioid and smaller inflammatory cells fill
the air-vesicles and intralobular passages, and as they accumulate expel
the air and convert each infundibulum, and at last the whole lobule, into
a small solid mass.
142 SYSTEM OF MEDICINE
Along witk hepatised lobules there are almost always found, particu-
larly in young children, some lobules which have undergone coUapse;
they are airless, but not soft ; shrunken, not swollen ; and empty, that
is, not stuffed with inflammatory products. These collapsed portions are
seen as depressed, dark patches on the surface of the lung, and particularly
at its lower edges. They were formerly confounded with the patches of
lobular pneumonia which they so often accompany ; but from these
they are entirely distinct, and it is doubtful whether such collapsed
portions of lung are capable of undergoing the process of lobular
inflammation.
Baeteriology.^ — The encapsuled dipldcoccus (or pnemonocoecus) of
lobar pneumonia is often found in the alveolar contents of the affected
lobules 5 but it is often absent, and with it or in its stead may be seen
various other micrococci There is no reason to believe that pulmonary
catarrh depends upon, or even is constantly associated with the presence
of any one specific microbe.
Etiology. — ^CJatarrhal lobular pneumonia is almost always associated
with bronchitis, and is usually secondary to it. It is in children often
accompanied with signs of rickets ; and it is a frequent sequel of measles
and whooping-cough, less frequently of scarlatina, small-pox, or enteric
fever. It may follow as the result of burns, and complicate infantile
" dysentery." Why it is comparatively rare in adults is difiicult to say.
It does not appear to be a specific infective disease, and its relation to
true lobar or fibrinous pneumonia rather obscures the aetiology of the
latter than lights up its own.
Clinical symptoms.— The symptoms and signs of pulmonary catarrh
are far less striking than those of acute lobar pneumonia. There are no
rigors, no sudden rise of temperature^ to mark its onset ; we suspect
rather than ascertain its presence when a case of bronchitis in a child or
an aged patient is accompanied with fever; and comparatively slight
physical signs are sufficient to confirm our suspicions.
The onset of pulmonary catarrh is gradual ; the fact that bronchitis
is extending to the smaller tubes is not shown by any trustworthy
physical sign, although we may find a sonorous, deep-toned rhonchus
replaced or aecompamed in certain parts of the chest by a high-pitched
sibilus ; or the large, coarse, toneless rattles produced by mucus and air
in the trachea amd larger bronchi may be replaced by mucous rS.les of
the same qiuality, but smaller, that is to say with more numerous
explosions in each inspiration. These physical signs may or may not be
present. Our Tecognition of the presence of what is called capillary
bronchitis depends upon the symptoms of dyspnoea — ^upon cyanosis,
increased rapidity of breathing, and sucking in of the soft parts about
the thorax with each inspiration. When inflamm.ation has gone still
farther and affected the lobules, there is often, as we should expect from
the above anatomical account, no diminution of resonance on percussion ;
for the solidifiied lobules are scattered, and resonance spreads, while
dulness does not. If several infiamed or collapsed lobules are near
PNEUMONIA 143
enough to form an airless patch, -we may then recognise on light per-
cussion a note shorter, of higher pitch and of diminished tone, com-
pared with that afforded by the rest of the chest; but probably the
earKest physical sign of the presence of lobular catarrh will be a con-
sonating, more or less musical quality in the previously toneless inspiratory
rile.
If the affected lobules become so numerous and close as to form a large
solid area in one part of the lung, we obtain more decided dulness on per-
cussion ; and the riles become finer and more consonating imtil they
approach very nearly the characteristic fine crepitation of lobar pneumonia.
These last signs are not only slow in appearing, or absent throughout the
whole case, but they do not advance steadily from the base upwards.
They appear most often in the middle of the back, internal to one or the
other shoulder-blade, sometimes at one base, sometimes in the- armpit,
and occasionally at the apex ; but they frequently shift in position, and
are very seldom symmetrical on the two sides. This absence of definite
local distribution is an important element in distinguishing catarrhal
from fibrinous pneumonia, and also from phthisis ; but unfortunately
it affords no evidence against, the presence of diffused pulmonary
tuberculosis.
In a further stage of consolidation the dulness may be as marked
and extensive as in lobar pneumonia. Tubular breathing will then be
heard, and marked bronchophony, not with the child's ordinary voice but
with its cry.
The pyrexia which shows the presence of lobular and vesicular
pneumonia is usually moderate in degree, even in children ; and rarely
approaches the height seen in lobar pneumonia, in septicaemia, or in
tuberculosis. The course of the fever is irregular without constant
evening accessions, but remittent rather than intermittent.
The skin of a patient suffering from catarrhal pneimionia is often
dry and hot, but it never has the pungent feel characteristic of fibrinous,
pneumonia ; and in many cases, especially in children, it is covered with
sweat. This is particularly the case when the broncho-pneumonia is
tuberculous; but the symptom is not only inconstant in itself, it is
greatly mpdified by the use of poultices, steam-kettles, and other modes,
of treatment.
The urine is often scarcely affected, and when febrile in other
characters very seldom contains albumin.
The pulse is frequent and usually soft, more frequent in proportion
to the temperature than in lobar pneumonia.
The respirations increase in frequency in proportion to the extent of
the lungs involved. In mild cases they are not above thirty, but in
severe cases rise to fifty, and even considerably higher. The forced
muscles of respiration are usually brought into play, and the degree in
which they are used furnishes another valuable evidence of the severity
of the disease. The nostrils dilate with each inspiration, as in many of
the lower animals ; and the inspiratory movements of the diaphragm are
144 SYSTEM OF MEDICINE
followed by expiratory contractions of the muscles of the abdominal wall.
In young children, of whom we chiefly speak in this description, respira-
tion is mainly abdominal, and in dyspnoea the muscles which move the
thorax have less play than in adults ; but in these patients the want of
resistance of the tissues causes much earlier and usually more marked
movement of the soft parts than in adults. With inspiration a deep
depression is seen to form above each clavicle, and another between the
trachea and the manubrium. The epigastrium is drawn in, and even
the lower ribs and ensiform cartilage yield to atmospheric pressure, parti-
cularly when the bases of the lungs are collapsed and airless.
Orthopncsa may be seen when extensive catarrhal pneumonia affects
an adult, but is less common than in dyspnoea from cardiac disease,
bronchitis, or lobar pneumonia; and in children it is decidedly less
common than in dyspnoea from laryngitis or from empyema.
The important symptom of insufficient aeration of the blood, which
consists of blueness of the surface, is present in all severe cases of
pulmonary catarrh. It is usually first seen in the lips and the ears,
then in the fingers and toes, next in the face, and finally over the whole
surface of the body and the mucous membrane of the mouth. While the
frequent and forced respirations show the want of air, the cyanosis
just described shows how ineffectual these forced and frequent efforts
are in supplying the want. Thus the rapidity of the pulse indicates
the increased efforts of the heart to keep up the pulmonary circulation,
and the paleness of the skin proves the deficiency of supply to the
systemic capillaries, and gives us a hint of the similar failure of circula-
tion in the lungs.
In adults affected with catarrhal pneumonia the expectoration is
usually scanty, and consists of thin mucus without much admixture of
air. In most cases, however, there is already present the frothy muco-
purulent expectoration of precedent bronchitis. The rusty sputum of
fibrinous pneumonia, whether prune-juice, or saffron, or greenish in tint,
is probably never seen in cases of lobular pneumonia. In cases with the
symptoms and course of catarrhal, not fibrinous, pneumonia, I have occasion-
ally observed scanty and nearly airless sputa, of a pinkish colour from the
presence of blood ; and streaks of blood probably derived from the veins
of the trachea or upper air-passages may sometimes be seen, as in
ordinary cases of bronchitis which do not extend to the lobules. True
rusty sputa are as nearly pathognomonic of fibrinous pneumonia as any
symptom can be ; and pure hsemoptysis under similar circumstances is
almost as characteristic of phthisis ; but the expectoration ofiers us no
help in the often difficult question between uncomplicated pulmonary
catarrh and disseminated tuberculosis of the lungs.
In children, not only in infants, but often up to the age of eleven
or twelve, there is a remarkable inability to expectorate. Phlegm is
coughed up into the larynx and then swallowed ; and though some
children as young as seven or eight (once a boy of only five) have learnt
how to get rid of it, and others may be taught the art, we must reckon
PNEUMONIA 145
upon the absence of this valuable help in diagnosis. When by natural or
forced vomiting a child empties its air-passages of accumulated secretion,
mucus and muco-purulent matter may be seen in the vomit ; some of
it perhaps lately swallowed, and some ejected directly from the largei"
bronchi. In such cases the presence or absence of rusty sputa may be
observed.
In aged patients it is not uncommon to find the same inability to
expectorate as in children.
As the disease goes on, the patient's appetite suffers ; he becomes
pale and thin ; his nights are constantly disturbed by cough, and his
strength gradually fails.
Course, complications, and prognosis. — The duration of acute pul-
monary catarrh is undetermined. Infants may die in a few days from
want of power to get rid of the secretion which obstructs the air-passages;
and in aged persons catarrhal pneumonia, or so-called capillary bronchitis,
often occurs as the last stage of chronic bronchial catarrh, and proves fatal
in two or three days. But, with the exception of the two extremes of life,
patients suffering from catarrhal pneumonia seldom die within a week or
even a fortnight from the date of recognition of the disease. Most often
its special symptoms and signs gradually disappear, and the condition of
simple bronchitis in which the disease began remains at its conclusion.
In children, particularly, this also gradually subsides, as a rule, and com-
plete convalescence is established.
Of the complications to be feared, the most frequent and formidable
is tuberculosis, either in its generalised form or in that of chronic phthisis.
A large proportion of cases of bronchitis and broncho-pneumonia in
children are associated with the presence of caseous lymph-glands,
cervical, mesenteric, or mediastinal ; and the bacilli which already exist in
the lympharia may readily infect the lungs and other organs.
Another important complication of catarrhal pneumonia, in children
is empyema, and this must be sedulously looked for, or it may escape
notice. In infants the most frequent complication is extensive collapse
of the lung, which, as above stated, almost always accompanies lobular
pneumonia at an early age, and often determines a fatal event.
On the whole the prognosis is most affected by the age of the patient.
Broncho-pneumonia in little children and broncho-pneumonia in the aged
are very fatal diseases. In children above two or three years old the
forecast is much better, but it is still decidedly worse than in cases of
lobar pneumonia occurring at the same age. In adults uncomplicated
pulmonary catarrh is rare, and usually dependent upon some special form
of irritation. In such cases the prognosis depends upon the nature of
the irritant and the probability of its being withdrawn.
Pulmonary catarrh, which is secondary to measles or whooping-
cough, is more serious than that which occurs without these precedents.
Again, when it occurs, as is so often the case, in a child affected with
rickets, it is more likely to be intractable or fatal than when this con-
dition is absent. Of the symptoms of the disease, the extent of lung
VOL. V L
146 SYSTEM OF MEDICINE
involved in inflammation or collapse, the frequency of the pulse, and
above all the degree of dyspnoea estimated by the symptoms above
detailed, are the most important elements of prognosis.
The most dangerous symptoms are those of suffocation, and this is
the most frequent immediate cause of death. ,
Next in importance to the lividity and the forced and rapid breathing,
which show pulmonary obstruction, are the weak and frequent pulse and
pallor which point to failure of the heart.
In little children pulmonary collapse is often as extensive as pulmon-
ary catarrh. After the second year is passed, this complication is less
frequent and dangerous, and in adults it scarcely occurs except at the
posterior edge of the lower lobe. The most serious complication of all
is the presence of tubercle.
Diagrnosis. — The recognition of broncho-pneumonia in most cases is
not difficult ; but certain mistakes are apt to occur, and in some cases
it is impossible to decide upon the exact nature of the pulmonary inflam-
mation present, except by the progress of the case.
From lobar pneumonia the diagnosis, founded on the onset and
course, as well as on the symptoms above enumerated, is only difiicult
when many inflamed lobules coalesce to form a single large patch
towards the base of the lung. Here dulness on percussion, tubular
breathing, and crepitant r^les will simulate primary lobar inflamma-
tion ; and when such a case is seen for the first time it is almost
impossible to avoid the mistake. In children we have not the help
afforded by the sputum, and the physical signs are not so definitely
localised as in adults.
On the other hand, true fibrinous pneumonia in children is sometimes
called lobular merely because of the patient's age. The shortness of its
course will correct the error. In elderly people the difficulty is to dis-
tinguish broncho-pneumonia from " capillary" bronchitis — ^from bronchitis,
that is, affecting the smallest bronchioles, but leaving the lobules free.
Probably the two affections are often present together. When rhonchus
and sibilus are present over the whole of both lungs, with little or no
elevation of temperature, and with marked cyanosis, it is unlikely that
the bronchitis is complicated by pneumonia. When one lung is decidedly
more affected than the other, and particularly if partial dulness, bron-
chial breathing, or crepitation appear in patches which shift their position,
and if these symptoms are accompanied by pyrexia, we may be sure that
lobular pneumonia is present.
The most common and important difficulty of diagnosis is between
lobular pneumonia and acute tuberculosis of the lungs — not phthisis,
for in its symptoms and localised physical signs this disease is almost
always characteristic] if it be overlooked or mistaken in its early
stages, it is not confounded with lobular pneumonia. No doubt, a
chronic broncho-pneumonia confined to one apex would be difficult or
impossible to distinguish from early phthisis ; but the existence of such
an affection, apart from the actual presence of tubercle, is extremely rare
PNEUMONIA 147
in an adult. Acute broncho-pneumonia of one apex with pyrexia,
frequent pulse, sweating and general bronchitis, may, however, closely
simulate phthisis in a child. When the previous condition and mode
of onset are unknown, it is difficult if not impossible to distinguish this
from phthisis ; in fact, the physical signs are the same. The far more
frequent difficulty is to decide upon the presence of disseminated tubercles
in the case gf children who do not throw off a pulmonary catarrh, but
week after week grow paler and thinner and more feverish ; or, again,
in the case of adults who, long subject to bronchitis, begin to show
the pyrexia and physical signs of broncho-pneumonia in addition. In
such cases the bronchitis and lobular pneumonia are actually present
whether tubercle be there or not. The presence of the latter must be
recognised by other than auscultatory signs. In adults there is no likeli-
hood at this stage for blood and nummular sputa and fragments of elastic
tissue to be present in the sputa, but we may find tiie bacilli of
tubercle — a discovery which at once decides the question. In children
this means of diagnosis is absent ; and we depend rather on the height
and irregularity of the pyrexia, on the rapidity and degree of emacia-
tion, and the amount of sweating. The same symptoms help us in
the recognition of acute miliary tuberculosis in an adult. In the
latter case, however, the question more often lies between tuberculosis
and bronchitis.
A disease which not infrequent mistakes warn us to be watchful
against confounding with broncho-pneumonia in children, is empyema.
In both cases we have pyrexia, dulness on percussion, and cough, with
dyspnoea and without expectoration. In both the child may be pale
and thin, and the fingers clubbed ; in both its voice may be too
weak and high pitched to help us by yielding bronchophony or tactile
fremitus ; and, lastly, the small area of an infant's chest, the loudness
of its breathing, and certain conditions which favour conduction of
bronchial breathing through effiised liquid, even in an adult, may all com-
bine to obscure the diagnosis of empyema. On the other hand, a
knowledge of this danger will sometimes lead even an experienced
physician to suppose that dulness at the base of the lung vrith no vocal
resonance or crepitation must be due to pleuritic eflFusion, whereas it is
really a patch of inflamed and collapsed lobules.
The height of the temperature is often a guide, but, on the one
hand, this does not distinguish empyema from broncho-pneumonia
associated with tubercle ; and on the other hand we sometimes, though
rarely, meet with empyema in which, even in a child, the temperature is
scarcely above normal. One help we may gain in doubtful cases by
listening to the chest when the chDd is crying ; we may then often obtain
both bronchophony and fremitus ; and, after a prolonged scream, so deep an
inspiration is taken that crepitation or tubular breathing, before unheard,
becomes distinctly audible.
In doubtful cases of the kind the use of a grooved needle or a hypo-
dermic syringe is most valuable. It will decide a question which cannot
148 SYSTEM OF MEDICINE
be settled by the most careful and repeated auscultation ; and this is
its only legitimate use.
Beside tuberculosis, another general disease is not infrequently
mistaken for broncho-pneumonia, both in children and adults, namely,
enteric fever. Here we have pyrexia, often of irregular .course, and
usually, sooner or later, accompanied with pulmonary congestion,
bronchitis, or hypostatic pneumonia. The bowels are not infre-
quently constipated, an enlarged spleen cannot always be felt, and in
children the characteristic rose spots are sometimes absent. When seen
for the first time, and with an imperfect history of the case, a decision
is sometimes impossible. The points to look for are the early or later
occurrence of pyrexia or cough, the course of the temperature, the presence
of headache, delirium, or apathy, and the fulness of the abdomen. If
enterica be present, a few spots, after repeated searches, will generally
be found on "the back and loins, if not on the abdomen and flanks;
and repeated trial will seldom fail to decide whether the spleen be en-
larged or not. In doubtful cases pulmonary catarrh is more probable in
the case of children, and enteric fever in the case of adults.
Treatment. — In the early stage of pulmonary catarrh the treatment
is that of bronchitis. We endeavour to relieve cough, pain, and oppres-
sion of the chest, to promote secretion in the affected parts, and to
favour action of the bowels, the kidneys, and the skin. For this piu:pose
confinement to bed is usually desirable ; but with little children it is
sometimes better to cover the chest with a cotton-wool jacket, and allow
them to lie in the nurse's arms, or to sit up when they cough. In cold
dry weather a steam kettle is a useful help in addition to an open fire ;
and an adult patient will find still greater relief by inhaling steam from
boiling water to which compound tincture of benzoin, eucalyptus, turpen-
tine, terebene or some other aromatic oleo-resin has been added. When
the air is warm and moist there is no object in making it moister. The
same applies to protection by curtains, screens, canopies, and tents. In
the winter season, in large wards or draughty rooms, these appliances are
most valuable ; but when there is too free a secretion of mucus, when
the patient is sweating, feverish and restless, a close, hot and damp air
is not the best for the patient to breathe.
As soon as febrile symptoms have subsided and the patient may be
considered convalescent, it is most important for him to breathe the open
air when the weather is at all suitable. Even in winter a child well
wrapped up and carried out for a quarter of an hour at a favourable
time will often show by improved appetite and better sleep the benefit
of fresh air. This is particularly important in the case of children
suffering from broncho-pneumonia after measles or whooping-cough.
When the temperature is high and the sMn is very hot, tepid spong-
ing is called for, and the child should be put in a warm bath every
evening. If fever should run high, repeated lukewarm baths are the best
means of reducing it. A mustard plaster on the front of the chest is
often extremely useful in the early stages of the disease ; afterwards a
PNEUMONIA 149
jacket poultice of linseed is a common and for the most part a good
application : it relieves pain, promotes action of the skin, moderates the
cough, and comforts the patient. For infants, however, its weight and
tightness are as a rule undesirable, and it may be better replaced by a
jacket of cotton-wool worn next the skin.
The food of a patient with broncho -pneumonia should be liquid,
given in comparatively small amount and more frequently than in health.
To young and weakly children a little milk or broth should be given
every two hours ; but in other cases there is no need for such frequent
feeding, and four hours is not too long a time to elapse between each
meal ; even this is sometimes too short an interval for the digestive
powers of an older patient, and it is better to be content with three or
four meals in the day.
Diluents should be taken freely ; cold water, soda water with milk
or fruit syrup, thin barley-water, toast and water, tamarind water, or
lemonade made with cream of tartar ; this " imperial drink " is grateful to
the patient, and is also diuretic and slightly laxative.
Stimulants are not to be prescribed as a matter of routine. Brandy
should be given if the pulse be very rapid and the action of the heart
weak and irregular.
The most useful drugs in the early stages are ipecacuan, squill and
nitre, sweetened with syrup of tolu or oxymel. Occasionally ■ in the
early stage of the attack a few drops of antimonial wine are efficacious in
promoting secretion in the bronchial tubes and skin. In serious cases
with urgent dyspnoea no drug is so valuable as carbonate of ammonia,
given in doses of one grain for an infant to five for an adult ; its pungency
may be covered by liquorice, treacle, or syrup.
When there is marked cyanosis, with a small and weak radial pulse
and distension of the jugular veins and epigastric pulsation, bleeding to
six, eight, or even ten ounces is indicated ; and may often save a patient's
life. In the case of children, two or three leeches on the sternum may
be applied in similar circumstances.
As soon as the temperature is normal and the physical signs abated,
the patient should be removed to another room, and allowed to sit by an
open window, if the weather be favourable. Beside drives in an open
carriage, it is often desirable that removal to the south coast of England
or to the shores of the Mediterranean should follow an attack of bron-
chitis with broncho-pneumonia. Children should be removed as soon as
possible to the seaside, or at least to pure country air.
Chronic Pneumonia
It is doubtful whether acute lobar pneumonia ever ends in a chronic
inflammatory process. At any rate, in the great majority of cases, if the
patient recover, the inflamed lung recovers also, and completely. I once
had the opportunity of observing the state of a lung in a patient who
died accidentally about a fortnight after recovery from acute fibrinous
ISO SYSTEM OF MEDICINE
pneumonia. The previously inflamed part of the organ was still dis-
tinguishable ; its consistence was firmer, its colour darker, and it
contained less air and more serum than the rest of the lungs : but no
other traces of hepatisation were present, and it was no doubt functionally
active.
Chromk lobar hepatisation. — Addison, however, described a condition of
persistent consolidation of lung following acute lobar pneumonia, in
which the section is no longer soft and granular but homogeneous, smooth
and tough ; though still solid and airless. • He believed that recovery
from this condition might take place. He called it " uniform albumin-
ous induration" (la, p. 28). Charcot and some other modern writers
admit the existence of a similar condition, but regard it as a coales-
cence of inflamed lobules; and due therefore to catarrhal, not fibrinous
pneumonia (7). We cannot doubt the existence of an anatomical state
such as is described ; but it must be extremely rare, and its true nature,
origin, and event are at present undetermined.
Chronic broncho-pneumonia. — That lobular pneumonia may pass from a
sub-acute to a chronic form is no doubt true if we regard the question of
time alone without reference to acuteness of symptoms ; but there is no
evidence that an inflammatory process of a catarrhal kind will continue
and spread after the temperature has become normal. The broncho-
pneumonia which follows measles, whooping-cough, or diphtheria in
children, and the much rarer broncho-pneumonia of adults, or that again
which is caused by inhalation of dust (pneumoconiosis), have, so far as at
present known, only one event if the patient neither dies in the acute
stage nor recovers ; and that event is infection by the baciUus of tubercle
and the establishment of pulmonary phthisis.
Chronic interstitial pneumonia. — There is, however, another form of
disease of the lung to which the name of chronic pneumonia is often
given. It is that which was described by Cruveilhier as "induration
■ardoise," by Addison as " iron-gray consolidation " (la, p. 28), by Corrigan
■&S " cirrhosis of the lung " (8), by some French writers as " scUrose puhnorir
■aire." ''■ The origin and limits of the disease are still matters of dispute,
.and its clinical history does not appear tobe precisely correlative with its
anatomy. On the one hand, it has often been confounded with the more
chronic forms of phthisis; on the other, it is usually associated with
dilatation of the bronchi, although the two conditions are not always
coincident. It appears sometimes to be a sequel of bronchitis or
broncho-pneumonia, and sometimes to begin in successive attacks of
pleurisy. Lastly, a similar anatomical condition is occasionally foimd in
cases of syphilis, associated with gumma and probably originating in
specific peribronchitis of the trachea and bronchi ; this last group of
cases is precisely analogous to those of so-called syphilitic cirrhosis of the
liver. Clinically it may simulate (tuberculous) phthisis, and was formerly
' Bayle probaWy described this condition (as others have done since) under the title of
phthisis with melanosis : Auenbmgger earlier still as scirrhus (that is, induration) of the
lung. Corvisart and Chomel also described its anatomy independent of phthisis.
PNEUMONIA 151
described as a variety of phthisis. The fact that this form of lues does
not affect the apices of the lung and thence travel downwards, that it is not
associated with other tuberculous lesions and is with those of syphilis, and
the absence of bacilli from the sputum are the chief diagnostic points which
usually guide us aright, even when hectic, emaciation, haemoptysis, and the
phthisical signs of phthisis are most misleading (Path. Tr. 1877, p. 313).
The resemblance, however, which Corrigan justly remarked between
his chronic indurating fibrous process in the lung and that which was
described by Laennec as cirrhosis of the liver, is an anatomical one.
Anatomically we may put the two conditions together, and may compare
with them the chronic interstitial nephritis of Bright's disease, which is
often styled cirrhosis of the kidneys. We may even extend the com-
parison to the chronic indurating process in the nervous centres which is
now named sclerosis ; but in their origin these similar anatomical results
differ greatly. By far the most frequent and characteristic fprms of
cirrhosis of the liver are due to intemperance, but there is no correspond-
ing alcoholic cirrhosis of the lungs.
Morbid anatomy. — Pulmonary cirrhosis is most often limited to a
single lung. It may begin in any part ; but most frequently it starts
from the root of the lung and spreads along the peribronchial connective
tissue so as to cause on section a radiating appearance of fibrous bands.
In other cases it spreads inwards from a patch of local pleuritic thicken-
ing. Occasionally it affects the base or the whole lower lobe, or the
middle lobe of the right lung ; while the rest of the organ remains
unaffected. The new fibrous tissue is white, dense, and often so
extremely tough as to cut like tendon, or even like cartilage. It is
sometimes confined to broad septa or patches, leaving the rest of the lung
free ; but often it penetrates extensively between the lobules, mapping
them out and giving a marbled aspect to a section. The pulmonary
tissue itself is darker than the healthy 'parts of the lung, and varies from
a. slate colour to an almost black tint. It is firm, and contains less air
than usual, but does not sink in water. On microscopical examination,
the fibrous tissue is as dense as that of a tendon, though the course of
the fibres is less parallel. The pulmonary tissue within a lobule is
Altered by collapse of some of the air-vesicles, by the lining epithelium
being more visible and thicker than normal, by the capillaries being more
■or less obliterated, and by the thickening of the alveolar wall.
The process is not, therefore, a purely interstitial inflammation as
■defined by Virchow : it is parenchymatous also. Some pathologists,
indeed, consider the intralobular changes as primary and essential ; and
the interlobular and peribronchial fibrous growth as secondary. But if
it be trile that pulmonary cirrhosis is seldom the consequence of broncho-
pneumonia, and most often takes its rise in peribronchitis or pleurisy, it
seems probable that the primary seat of the disease, as of the correspond-
ing changes in the liver, the kidneys, and the spinal cord, is in the
interstitial connective tissue.
The affected lung on section shows cavities which can readily be
152 SYSTEM OF MEDICINE
traced to the bronchial tubes, of wliicli they are certainly dilatations.
These saccular pouches were regarded by Corrigan as the result of traction
of the cicatrising fibrous tissue ; and, although an opposite opinion has
been ably defended by other pathologists, from Laenneo downwards, it
seems probable that the Dublin physician was correct. There are, no
doubt, many cases of primary bronchiectasis, such as those which follow
whooping-cough or bronchitis in children, and lead to uniform cylin-
drical dilatations without consequent fibrous thickening ; and, again, such
as form the bronchial pouches which have been described as retention-
cysts in fetid bronchitis. The saccular dilatations in cirrhosis are often
extremely irregular, and in some parts so closely packed together that
scarcely any pulmonary tissue is left between them.
The result is contraction with diminution in bulk of the affected
parts of the lung. There may be emphysema in the parts unaffected
by cirrhosis, and sometimes large subpleural bullae are seen. On the
whole, however, the process is that of contraction. The afifected lung
becomes smaller as well as denser ; and, when one side only is affected,
the opposite lung may be hypertrophied and the mediastinum dragged '
over by the diseased lung.
Beside bronchiectasis, emphysema is also very frequently present, and
shows its characteristic signs during life and anatomical appearances after
death. Sometimes the hypertrophic pleurisy which has been the starting-
point of pulmonary cirrhosis is only part of a general chronic inflamma-
tion with thickening of the whole pleuro-peritoneal cavity ; and lungs,
heart, and abdominal viscera are all affected by a similar process {Path.
Tr. 1882, p. 172).
Symptoms. — These are often obscure and difficult of interpretation.
They are chiefly of a physical kind. More or less dulness on percussion
will be present, due probably to thickened pleura rather than to the
pulmonary cirrhosis itself. Bronchial breathing may be heard, although
this is far from constant ; more often the pulmonary murmur is obscured
by rhonchus and sibilus ; but perhaps the most frequent auscultatory
sign is the presence of rales, medium or large, and sometimes gurgling,
accompanying inspiration and expiration. Not infrequently deficiency
of breath-sounds, combined with the dulness, may raise a doubt whether
there be an effusion of pus or serum in the pleura.
Expectoration is commonly abundant, muco-purulent in quality, and
often nummular. Hsemoptysis is not unknown, even when cases of
chronic phthisis are carefully excluded.
On inspection the affected side moves less freely than the sound one,
and is ascertained by the cyrtometer to be the smaller. Owing to the
same process of contraction the cardiac impulse may be displaced towards
the affected side, or may be higher than usual.
There is often no pyrexia; the temperature is never high unless,
as occasionally happens, septicsemia ensues from ulceration of dilated
bronchial cavities. There is dyspnoea, increased on exertion, and the
fingers may be clubbed.
PNEUMONIA ' 153
Natural history. — Cirrhosis of the lung may come on at any age ; but
the majority of the patients are under fifty. It is rare in children,
but not very rare between 15 and 20. The disease is more common in
men than in women. It is often associated with intemperate habits, and
sometimes with a similar interstitial fibrosis, degeneration, and shrinking
of the kidneys or the liver; or with chronic peritonitis as well as pleurisy.
Diagnosis. — Some definitions of this disease would include all cases
in which the physical signs denote a contracted, indurated, and com-
paratively airless condition of one or both lungs, due to fibrous degenera-
tion of the pulmonary tissue, with the presence of numerous cavities
containing pus and mucus. In the majority of such cases, however, this
condition is due to tuberculous infection. The tuberculous disease
affects both lungs ; it begins in the apices and travels downwards. The
cavities are excavations due to ulceration — vomicae in the technical sense
of the word. In fact the disease is chronic, and sometimes obsolete,
tuberculous phthisis. Many of the earlier cases recorded by Andral,
Corrigan, and Addison were undoubtedly tuberculous ; and the same
criticism applies to a majority, at least, of the cases which have been de-
scribed by the late Sir Andrew Clark and other writers as "fibroid phthisis."
The long controversy as to the degree in which the names pulmonary
tubercle and phthisis are coextensive in signification may now be re-
garded as settled ; and the final verdict is in favour of the doctrine
originally taught by Laennec, and against that which distinguished
between tuberculous and non - tuberculous phthisis. All phthisis is
tuberculous ; but, along with tubercle, catarrhal pneumonia, congestion,
ulceration, bronchitis, pleurisy and fibrosis are always present. Phthisis
of rapid course, with extensive ulceration and congestion, may still be
called " pneumonic " ; and cases which are long protracted, and perhaps
at last cured, with abundant cicatrisation, may still be called "-fibroid," or
rather " fibrous " ; but these are forms of essentially the same disease.
If all cases of cirrhosis of the lung were, as the late Dr. Moxon put
it, "phthisis in the preeter-pluperfect tense," there would be no need for
the name ; or, if retained at all, it would merely denote an anatomical
condition present in various degrees in all cases of chronic phthisis.
There is, however, abundant evidence that cirrhosis may be independent
of tubercle from beginning to end; and the problem is to distinguish
this non-tuberculous disease from the much commoner cases of chronic
phthisis which simulate it, as well as from the fibrous degeneration
which accompanies syphilis of the lung.
In the first place, phthisis almost always affects both lungs, cirrhosis is
as a rule confined to one. Either disease may follow chronic bronchitis
or repeated pleurisy; but in phthisis other organs, sooner or later,
partake in the disease. Accordingly the presence of laryngitis with
hoarseness or aphonia, diarrhoea, symptoms of tubercle of the testes or
kidneys, of joints or of lymph-glands, is good evidence that the disease
of the lung, however chronic, is tuberculous phthisis. Cirrhosis, on the
other hand, is confined to the chest. It is a purely local condition ; and
154 SYSTEM OF MEDICINE
its symptoms, in nature and degree, depend entirely upon the physiological
eifects of the local lesion. No doubt the diagnosis, comparatively easy
as it is in the dead-house, is sometimes difficult at the bedside ; but the
presence or absence of the bacillus of Koch should be decisive.
Next to chronic phthisis, empyema is perhaps the affection most
likely to be confounded with cirrhosis of the lung. In both cases the
symptoms may be similar, namely, cough, wasting, pallor, pyrexia,
dyspnoea; and in both there may be dulness at the base of one lung.
In empyema the breath-sounds are usually absent over the dull area, and
there may be no expectoration ; but bronchial breathing is occasionally
heard through pleuritic effusion, and if an empyema have opened into
the lung, the expectoration may be of much the same kind as that which,
in a case of cirrhosis, proceeds from a bronchial pouch. Moreover, in
empyema some amount of contraction of the affected side of the chest is
often present. The physical conditions are so similar that it is not
surprising to find the physical signs also similar. The diagnosis depends,
in most cases, upon a knowledge of the origin and progress of the
patient's illness. In this, as in so many other cases, a right decision does
not depend upon a single so-called pathognomonic symptom, but upon a
wide survey of probable alternatives, and weighing of the course and
probabilities of the individual case along with the actual physical signs
present.
After all, in some cases puncture alone can decide the matter, and
the test is readily applicable.
Prognosis. — Cirrhosis of the lung is always a grave but rarely a hope-
less condition. The forecast varies with the amount of lung involved,
with the duration of the disease, and, most of all, with the degree of general
disturbance ; loss of appetite, ansemia, wasting, sweating, vomiting, or
diarrhoea are unfavourable circumstances. When the patient's weight is
kept up, and he eats and sleeps well, we may hope that even extensive
cirrhosis of the lung may gradually lead to contraction and obliteration
of cavities, and final cicatrisation of the affected parts with hypertrophy
of the opposite lung. Such a complete cure is no doubt exceptional ;
more often the disease passes into a permanently chronic condition, and
the patient dies at last from bronchitis affecting the sound lung, or from
some intercurrent affection.
Among the complications to which the patient with cirrhosis is liable
may be mentioned — first, dilatation of the right side of the heart and
anasarca; next, septicaemia from ulceration of one of the bronchial
cavities ; more rarely, abscess of the brain from pyaemia of a similar origin ;
or lardaceous disease, the result of prolonged suppuration.
Treatment. — From the nature of the case, the treatment must be
tentative and expectant, following the indications of the patient lather
than of the local disease. We endeavour to keep the expectoration from
becoming fetid, and to check its amount, to relieve cough, particularly at
night, by paregoric and other anodynes, and to hasten the process of
cicatrisation by occasional counter-irritants, or by strapping the affected
PNEUMONIA I5S
side with plaster. Inhalations of turpentine, thymol, terebene or
creasote are often useful in lessening the secretion and correcting foetor.
At the same time, by help of mineral acids and bitters, particularly
quinine and nux vomica, we try to improve the patient's appetite ;
with the same object we give him varied and abundant food, consulting
rather his own caprice than ordinary rules of diet : of stimulants, by
far the most useful, if the patient can bear it, is malt liquor, particularly
porter. If this cause cough, constipation, or headache, ale or light
German beer may be taken with advantage at the mid-day meal. Some-
times wine is better relished and proves more useful ; in most cases it is
certainly superior to alcohol in the form of spirits ; if given at aU,
brandy is, as a rule, most useful when given as a sedative at night.
Whenever the weather permits it, the patient should be taken out of
■doors. When this is impracticable, he may sit before a widely open
window, warmly wrapped up, and breathing through the nostrils with
the mouth persistently closed. Fresh air often proves the most powerful
promoter of appetite and of sleep.
Cases of cirrhosis of the lung are greatly benefited by climatic treat-
ment ; removal from dust-laden workshops and from foggy towns to pure
air is the first step to improvement, and may often cut short the disease
in its early stage. A mild and equable climate, such as that afibrded by
the south-west coast of England and many parts of Ireland, is the best
ior these patients.
There is no doubt that these cases are among those that derive most
benefit by spending successive winters and springs on the Eiviera, at
Palermo, Corfu, Cairo ; or in islands like Madeira, the Canaries, or those
of the Southern Pacific. If the patient's means are ample, this arrange-
ment is the best than can be made for his advantage. \Vide art. " Climate
in Disease," vol. i. p. 247.]
P. H. Pye-Smith.
REFEEENCES
Broncho-pneumonia (Pulmonary catarrh) : 1. Eox, Wilson. Disease of the Lungs,
"Broncho-pneumonia," p. 378. — 2. GooDHAKT. Diseases of Children, chap. ii.
"Pneumonia.." — 3. Jukgenson. Ziemssen's Hwadbuch. — 4. Walshb. Dis. of
Limgs, 4th ed. 1871. — 5. Smith, Eustace. Disease in Children, ohap. v. "Catarrhal
Pneumonia." — 6. West, Chas. Diseases of Children, lectures xviii.-xx. "Capillary
Bronchitis. " — 7. VoN Ziemssen. Pleuritis u. Pneumonie in Kindesalter.
Interstitial pneumonia (Cirrhosis, of the lung) : 1. Addison. Guy's Hasp. Pep,
1843. — la. Collected works. N. Syd. Soc. — 2. Andral. Clinique mid. — 3. Bastian.
Reynolds' System, toI. iii. ; and Path. Trans, vol. xix. — 4. Biekmee.. " Bronchieuer-
weiterung, " FisVcAow's ^rcAw, vol. xix. — 5; Du Castbl. 1884. — 6. Coats. Manualof
Pathology, p. 536.^ — 7. Chakoot. "Pneumonie ohronique," ThAse du concours d'agrdga-
tion, 1860, quoted in Science. — 8. Cokkioan. Dublin Sosrp. Gazette, 1857 ; Dublin
Med. Jowrnal, 1838, vol. xiii. — 9. Fagge. Path. Tr. 1868, vol. xx. — 10. Fox, Wilson.
Disease of the Lungs, p. 412. — 11. Shatttjck. "Cirrhosis of the Lungs," Eoston
Med. amd Surg. Journ. cvii. 1882. — 12. Stewart, Thos. Gkaingek. Edin. Monthly
Journ. 1866. — 13. Sutton, H. G. "Fibroid Degeneration of the Lungs," Med.-
Chir. Tr. 1865, with 34 cases. — 14. WiLKS. Path. Trans, vol. viii. 1866, p. 40; and
Lectures on Path. Anat. 3rd ed. 1889, p. 352.
P. H. P.-S.
1S6 SYSTEM OF MEDICINE
PHTHISIS PULMONALIS
Causes. — The causation of ptthisis pulmonalis is a matter of far-
reaching importance to the human race, inasmuch as statistics show that
one-seventh of the total death-rate of the world is attributable to this
disease.
Phthisis was known to Hippocrates (460-377 B.C.) ; and in all prob-
ability it has existed from the earliest times.
Geography. — Laborious and careful research has established the fact
that the geographical distribution of phthisis is coextensive with the
habitable regions of the globe. We have the high authority of Hirsch
for the statement that pulmonary consumption is " a disease of aU times
and countries."
But although it cannot be admitted that any part of the world
manifests a complete immunity from this disease, Lombard's maps show
that it is all but absent in certain Arctic regions, deserts, and places
situated at great altitudes ; in other words, as pointed out by Dr. Ransome,
just where the population is most scanty. If we survey the statistics of
various countries, a special incidence on certain districts and towns comes
out in the clearest manner. It is perhaps doubtful, as Hirsch remarks,
whether a comparison of the statistics of different countries possesses the
same value as a study of the returns of individual towns or districts,
which ensure a greater degree of accuracy.
Climate. — The influence of climate has been much discussed. Some
writers hold that phthisis is commoner in hot than in cold countries ;
others again consider that it is of more frequent occurrence in tem-
perate climates. But a review of the information at present available
leads to the conclusion adopted by Hirsch, that " the mean level of the
temperature has no significance for the frequency or rarity of phthisis in
any locality." A few examples will illustrate this point. The mortality
from this cause in Iceland is very low, whereas in North Greenland phthisis
is one of the commonest causes of death. On the north coast of Africa,
Morocco and Algiers are distinguished by a remarkable freedom from
consumption ; but at Tunis, and at Alexandria and Damietta on the sea-
coast of Egypt, the disease is very prevalent : in the interior of Upper
and Lower Egypt, on the other hand, phthisis is decidedly uncommon.
Other discrepancies equally striking might be quoted to prove that places
sharing a similar climate may widely differ in their phthisis death-rate.
Consumption seems to follow in the wake of advancing civilisation,
especially where men congregate together in large numbers. All accoimts
agree as to its extraordinary prevalence in New Caledonia, Hawaii,
Tahiti, and other South Pacific Islands. There is a strong consensus of
opinion that phthisis has become far more rife in these parts, and also
among the Maoris of New Zealand, since the date of the European
PHTHISIS PULMONALIS 157
immigration ; when, as Hirsch says, " the natives began to adopt the
manners and habits of the Europeans." Until recent times the mortality
from this disease among the troops of the British Army, in the most widely
separated parts of the world was deplorably high, more particularly in
times of peace ; and often considerably exceeded the mortality of the
resident population. Improved hygienic arrangements in the barracks,
especially as regards overcrowding and ventilation, have reduced the
death-rate from phthisis in the most remarkable manner.
Such facts cannot be reconciled with the belief that climate is an
important etiological factor. But while the evidence negatives the
opinion that hot climates favour phthisis, all authors are agreed that
the disease in tropical countries assumes a most acute and virulent type.
Moisture. — A maleficent influence has been ascribed to moisture of the
atmosphere and soil. In America, Bowditch was led to believe, by an
inquiry into the incidence of phthisis on the inhabitants of certain places,
that the disease is most prevalent in areas where the sott is impregnated
with moisture. He found in certain localities that efficient drainage was
followed by a diminution of phthisis. Dr. Milroy's investigations
in Scotland gave similar results. Working out the same idea in England,
a few years later. Sir George Buchanan made the discovery that in several
towns the phthisis death-rate had undergone a notable decrease since the'
introduction of an improved system of sewerage — a result which he
attributed to draining of the subsoil water. He accordingly expressed
the opinion that the mortality from consumption is directly related to the
degree of dampness of the soil. But there are certain considerations
which make it difficult to regard this conclusion as one of general applica-
tion. For example, in one of the towns investigated by Buchanan the
mortality from phthisis rose remarkably after carrying out the drainage
work; moreover, in Berlin, and some other towns in Germany and in
England, improvement in draina,ge has not been followed by the good
results anticipated by Buchanan. Lastly, in some of the districts quoted
by Buchanan in support of his hypothesis, subsequent investigation by
Dr. Kelly has elicited the fact that the diminution in the phthisis rate
noted at first has not been sustained in recent years ; and, as Dr.
Payne remarks, although the subsoil of London is becoming drier
every year, owing to the large area covered by houses and almost
impervious pavements, there is no corresponding decrease in the amount of
phthisis in this town. It is indeed a significant fact that in so wet a
country as Holland the death-rate from phthisis is rather low. From
these considerations we are driven to admit with Hirsch that other
etiological factors beside the influence of soil are probably concerned —
factors that " serve to neutralise the benefits even of the most favourable
conditions of soil."
Altitude. — Observations made in divers parts of the world have left
no doubt of the infrequency of phthisis at higher altitudes, though
instances of the disease are not wanting even at the very highest points.
The sparseness of the population at such levels may account to some
IS8 SYSTEM OF MEDICINE
extent for their relative immunity, but not entirely ; for in some large
commercial and not very sanitary to'vms in Mexico, and on the Andes,
situated at an elevation of from 7000 to 13,000 feet, the extreme rarity
of phthisis is generally admitted ; a proof, as Hirsch writes, " that the
influences "which go with very considerable altitudes have the power to
overcome those detrimental things that arise from a bad kind of hygiene
and social life, in so far as they tend to produce consumption."
Statistics from Switzerland strongly confirm the opinion that a
great elevation affords some protection, though they supply no proof of
anything like complete immunity. The explanation of the beneficial
action of altitude is by no means clear. The extreme freedom of the
air from impurities of all kinds and the dryness of the atmosphere
have been alleged as the principal causes. But in the case of the un-
sanitary towns on the Andes above referred to, the absence of organic
atmospheric impurities cannot be assumed ; and that dryness of the air does-
not in itself confer any protection is clearly shown by the returns from the
towns on the sea-coast of Egypt to which attention has already been directed.
Hirsch makes the suggestion that people living at great elevations and
breathing rarefied air are obliged to make deeper inspiration, and acquire
in consequence a more vigorous development of the respiratory organs,
which are thus enabled to offer a more powerful resistance to external
influences. The bearing of this view on the baciUary origin of the
disease will be discussed further on.
No ram is exempt from the ravages of consumption. Hirsch states
that among the Kanakas— the natives of New Caledonia^— two-fifths of the
total mortality is due to phthisis. And Dr. Osier states, on the authority
of Surgeon Kennedy, that the mortality from this cause in a tribe of
Red Indians of the Rocky Mountains living in a splendid climate amounts
to 23 per cent of the total death-rate. The Negro appears to be
extremely Vulnerable, especially when removed from his own country;,
and in this race phthisis runs a very acute course.
The evidence with regard to the Jews is somewhat ambiguous. There
is a general impression that Jews are less afflicted with tuberculosis than
Christians. This has been accounted for by the more careful selection of
carcases in Jewish slaughter-houses, and by the more frequent house-
cleanings practised by the Hebrews. There is some reason to believe
that this favourable estimate applies only to the well-to-do members of
the community. Further investigation must decide whether the current
opinion is correct or not.
Sociological. — ^We have now to consider another class of etiological
factors ; the density of population, and certain injurious influences con-
nected with trades and occupations, particularly those which involve an
indoor life.
As the general result of statistical inquiry in different countries, it is
clearly proved that the mortality from phthisis is lower in the country
than in the towns ; and that in the case of towns the mortality on the
whole increases with the population. The proneness to phthisis manifested
PHTHISIS PULMONALIS 159
by dwellers in towns seems to be largely connected with overcrowding
in rooms badly ventilated and lighted. Numerous investigations have
attested the high death-rate from phthisis in convents, sisterhoods,
military barracks, and above all in prisons. These institutions have been
notorious for overcrowding and defective ventilation. In jails and
convents insuflBcient food and indoor confinement have no doubt militated
also against the health of the inmates ; but these factors cannot be said
to have been operative in the case of military barracks. Happily the
hygienic reforms of recent times have effected an enormous reduction
in the mortality from phthisis in such institutions.
Sedentary occupations, whether in town or country, appear to dispose
to the disease. Certain trades, particularly those which are associated
with much dust, enjoy an evil distinction on account of the prevalence of
consumption among their workers. Attention was chiefly directed to
this point by Greenhow's excellent reports, in which he traced the influence
of dusty occupations in originating diseases of the lungs.
It is generally believed that the sharper particles of dust are most
injurious. Flint workers, needle - polishers, file-cutters, grinders and
potters supply the largest contingent of pulmonary diseases. It is still
undecided whether most cases of this sort attributable to dust (" pneu-
monoconioses " of Zenker) are of a tuberculous nature or not. Some
authors, among whom is Hilton Fagge, have asserted that practically all
these affections of the lungs are tuberculous. Others, including physicians
who have seen much of this form of disease, refuse to admit the truth of
this statement. It seems to be a fact that in some, perhaps in most of
such cases manifest tuberculous lesions are found after death ; but even
then it may sometimes be difficult to decide whether tuberculosis con-
■stitutes the substantive disease, or whether it has implanted itself, as a
secondary process, in lungs already the seat of fibroid changes. The
researches of Zenker, Virchow, and others leave little doubt as to the
occurrence of circumscribed non-tubercular fibroid lesions of the lungs,
in consequence of the irritation of finely divided particles of iron and
other metallic or mineral substances. But it remains to be proved that
massive induration of the lung can be produced by this cause alone
without the coexistence of tuberculous disease. This much, however, is
certain, that pulmonary affections in persons following dusty occupations,
if not always in the first instance tuberculous, are very liable to become
so ; the chronic inflammation of the bronchi and lung being favourable to
the development of this infection.
The comparatively small post-mortem experience in this variety of
pulmonary disease which has fallen to my share has almost invariably
revealed the presence of chronic tuberculous lesions associated with
excessive blackish pigmentation of the lungs. In one or two cases
where no evidence of, tuberculosis could be detected the lesions consisted
of scattered patches of fibrous induration in the peribronchial districts.
For a full account of pneumonoconiosis the reader is referred to the
article on the subject in the present volume (p. 242).
i6o
SYSTEM OF MEDICINE
No age is exempt from pulmonary tuberculosis, though it is less
common at the two extremes of life.
The view, which prevailed until recent times, that infants and children
under two years of age are scarcely ever attacked, has been proved to be
incorrect. Landouzy found that in several fatal cases of broncho-pneu-
monia in children under two years, some of which during life were ascribed
to measles or cold, tubercle bacilli were present in the broncho-pneumonic
patches ; although the naked-eye appearances of tuberculosis were not
recognisable. These observations were made at an infant asylum in
Paris, in which institution one-third of the deaths among the children
proved to be the result of some form of tuberculosis.
Sex. — The following statistical account by Dr. W. Ogle, formerly
Registrar-General, deals with the subject of age and sex on a very large
scale.
"There is practically no difference between the two Sexes in their
respective liabilities to death from phthisis when all question of age is
put aside. For the mean annual mortality of males on an average of
thirty years from this cause is 2418, and of females 2428 per million
living. . . . But when instead of taking the aggregate rates, that is, the
death-rates of each sex en bloc, irrespectively of age, we take the rates at
each successive age period, there are found to be very remarkable differ-
ences between the sexes. In the first quinquennium of life (0-5) the male
and female rates are pretty nearly the same, the male being only very
slightly the higher. In the next five age periods, covering between them
the interval between the ends of the fifth and thirty -Tifth years of life,
the female rate is in marked excess of the male rate, the excess being
especially notable in the periods from ten to twenty years of age. After
the thirty-fifth year the reverse is the case, and the male rate becomes
the higher, and remains so in each age period to the end of life.
Table A
(Slightly abridged)
Mean Annual Mortality from Phthisis (1851-80) per 1,000,000 living at aU
ages, and at twelve successive age periods.
All
Ages.
0
6
10
15
20
25
35
46
65
65
76 and
upwards.
Both sexes .
Males .
Females
2423
2418
2428
1013
1034
993
461
432
491
838
616
1061
2549
2088
3008
3742
3676
3798
4060
3941
4165
3954
4097
3826
3313
3850
2812
2648
3274
2075
1687
2112
1322
613
730
523
PHTHISIS PULMONALIS
i6i
Table D
Mean Annual Mortality (1861-80) per 1,000,000 living of Children in each
Year of the first Quinquennium of Life from Phthisis, Males and Females.
Under 1
1
2
3
4
All under
5 Years.
Males .
Females
1589
706
13il
1295
634
655
394
409
339
360
880
842
" It appears from this table that the male death-rate from phthisis in
the first year of life is more than twice as high as the female rate ; in the
second year it is also the higher, but only to the extent of about i\ per
cent ; while in the third, fourth, and fifth years of life the female rate is
slightly the higher; namely, 3'3 per cent in the third year, 3'8 per cent
in the fourth year, and 6 '2 per cent in the fifth. These percentage
differences are slight ; but they run in an ascending series, and, in
combination with the figures in Table A, seem to justify the statement
that the female liability to phthisis begins to exceed the male liability in
the third year of life, and continues to be in excess till somewhere alaout
thirty-five years of age — the maximum of excess being in the ten to
twenty years of age period, when the excess reaches 50 per cent."
Dr. Ogle expressly states that the contrast between the male and
female mortality described above characterises pulmonary phthisis ; and
that no similar contrast is observable in the death-rate from other tuber-
culous diseases.
It is not easy to account for the great excess of the male rate in the
first year of life. But as regards the decided excess of the female
mortality over the male between the ages of ten and twenty, Dr. J. F.
Payne points out that it is at this period of life that the difference
between the outdoor life of boys and the indoor life of girls begins ; and
he suggests that the excessive female mortality at this age is connected
with the existence of unfavourable conditions in the house. But, as he
further remarks, " the greater liability of the male sex to phthisis after
thirty-five years of age seems to be quite unexplained by such considera-
tions."
Dr. Ogle's Tables show that the excess of the female death-rate is not
related specially to the child-bearing period, as the excess over the male
rate begins to decline after the age of twenty ; and after thirty-five the
rate has fallen below that of the male sex.
In connection with differences of sex we may now briefiy consider
the influence of menstruation, pregnancy, parturition and lactation.
Menstruation. — There is no clear evidence that this function, whether
at its commencement or subsequently, exerts any definite causative
VOL. V M
i62 SYSTEM OF MEDICINE
influence. Irregularity or arrest of the catamenia seems at times to be
connected witli the onset of haemoptysis ; but the nature of this associa-
tion is probably less intimate than at first sight it appears to be. For it
may be safely conclude'd that a considerable pulmonary haemorrhage at the
outset of the phthisical symptoms is a sure sign that the disease is already
of long standing, although perhaps hitherto quite latent. Arrest or dis-
order of the menstrual flow may occasion reflex vascular disturbance, and
so give rise to haemorrhage from lungs already diseased ; but the occur-
rence is not by any means common.
Tregnancy. — -The influence of pregnancy has been much debated.
The disease not infrequently appears to extend during this period ; but
the impossibility of fixing the date at which the disease begins renders
the question a difiicult one. Wilson Fox considered that the rapid in-
crease of phthisis in woman between the ages of twenty and thirty-five
points somewhat strongly to the influence of pregnancy in the develop-
ment of the disease. The force of this argument is weakened by the fact
that the increase in the male rate (see Ogle's Table A) in the same period
is almost as pronounced. Dr. R. E. Thompson, as the result of a statis-
tical inquiry into the subject of phthisis in women, concludes " that the
susceptibility of single women is rapidly diminished after thirty years of
age, while that of married women maintains its intensity between twenty-
five and forty years of age (that is, during the child-bearing period)."
Parturition. — It is not common to find that symptoms of phthisis
set in directly after parturition, though this event has generally an
accelerating effect upon pre-existing disease.
Lactation, by its debilitating influence on weakly women, may no
doubt act as an indirect cause. Dr. Pollock states that the periods of
puberty, of gestation, of parturition, and of lactation are fraught with
danger to persons disposed to phthisis.
The influence of these conditions on the established disease will be
considered in a subsequent section.
General depressing influences. — Among the remoter causes of phthisis
may be reckoned all conditions that tend to lower the standard of
health ; such as insufficient food, anxiety, grief, excessive mental work,
want of exercise, fresh air, and sunlight. Among diseases that have the
same general effect diabetes mellitus must especially be named — a point
on which all authorities are now agreed. It is interesting to note the
liability of diabetics to another disease of microbio origin, namely,
carbimcle.
Concerning the etiological importance of chronic alcoholism, malig-
nant disease, and syphilis, agreement is less general. Both clinical and
post-mortem experience alike support the view that topers are prone to
tuberculous affections. The frequent association of peritoneal tubercu-
losis with cirrhosis of the liver is generally recognised by pathologists.
It has been urged that alcohol has a preventive action; and that it
tends to promote fibroid changes if tuberculosis should be contracted :
both statements are at variance with my own experience.
PHTHISIS PULMONALIS 163
The association of pulmonary tuberculosis and malignant disease of
various organs is by no means rare, though it is very uncommon to find
evidence of simultaneous activity of the two diseases. Mr. Eoger
Williams' statistical investigations appear to him to justify the conclusion
that the proclivity to cancer is closely allied to the tuberculous diathesis.
A history of syphilis is not rarely obtained from phthisical patients ;
but if the former disease be possessed of any etiological influence it can
only be of an indirect character.
Rheumatism, gout, insanity, chlorosis, dyspepsia have also been
regarded as etiological factors ; but their connection with phthisis is not
intimate.
The frequency with which pulmonary tuberculosis appears after
measles, influenza, and, to a less degree, after whooping-cough is well
known. Although these diseases cannot be regarded as immediate
causes, it must be admitted, more particularly in the case of influenza
and measles, that they are apt to precipitate an eruption of tuberculosis ;
whether it be in consequence of the attendant pyrexia, or of some other
action of their specific virus. There is more to be said in favour of the
view that a latent tuberculous focus is lighted up, than that tuberculosis
is initiated by the presence of another disease. On the other hand, it is
possible that influenza and measles may cause certain changes in the
bronchial and pulmonary epithelium which result in a lowering of their
power of resistance, and thus lay them open to the invasion of tubercle.
Pneumonia. — It is an old belief that croupous pneumonia may ter-
minate in phthisis ; but it is now quite certain that this sequence of
events is infinitely rare. Two principal fallacies have been concerned in
the origination of this erroneous opinion : in the first place, certain
rare cases of pulmonary tuberculosis begin with severe constitutional
symptoms, and with signs of extensive infiltration of the lung, simulat-
ing acute pneumonia ; secondly, delayed resolution, or the exceptional
supervention of chronic pneumonia, may give the impression that croupous
pneumonia has terminated in phthisis. Patients suffering from the
latter disease often declare that their illness began with " inflammation
of the lungs " ; but such statements will seldom stand the test of a
critical examination.
Bronchitis not uncommonly appears to have been the starting-point
of phthisis, and there is nothing improbable in such a belief ; but, more
often, careful inquiry will elicit the fact that symptoms of phthisis pre-
ceded the attack of bronchitis. In many instances where the tuber-
culosis appeared to have supervened on chronic bronchitis, an autopsy
has demonstrated that the bronchitis was itself symptomatic of chronic
pulmonary tuberculosis. The fact that many phthisical persons attribute
their illness to a simple catarrh possesses little scientific value ; for what
ailment do patients not put down to catching cold ?
Pleurisy. — The oft-repeated observation that an attack of pleurisy is
frequently followed by phthisis, led to the belief that the latter disease is
the result of pleurisy. But there is no doubt that, under such circum-
i64 SYSTEM OF MEDICINE
stances, the original pleurisy has itself been of a tuberculous nature ; and
secondary, as a rule, to tuberculosis of the lung. There is no reason to
think that simple pleurisy disposes to phthisis. In metapneumonic
pleurisy, whether sero-fibrinous or purulent, where the effusion is directly
due to the pneumonic process, recovery is generally complete and per-
manent. It is believed by Koch and others that pleuritic adhesions, by
impeding the movement of the chest walls and lung, may dispose to
phthisis. But patients suffering from deformity of the chest — as the
result of kyphoscoliosis, rickets, or caries of the spine — wherein the thoracic
movements are greatly restricted — so rarely acquire pulmonary tuber-
culosis that Eokitansky came to the conclusion that the two affections
are antagonistic.
Traumatism has been supposed to play an important part in the
causation of phthisis. Mendelssohn has published nine cases of his own,
with a reference to seventeen other recorded cases, in which injuries to
the chest, of various kinds, were followed by pulmonary tuberculosis.
In some instances hsemoptysis occurred at the time of the injury or soon
afterwards ; in others cough and symptoms of pleurisy ensued within a
few days or weeks. In one or two cases an interval of a few months,
and, in one case, of two years, separated the accident from the appear-
ance of definite symptoms. Mendelssohn ascribes the occurrence of
phthisis in such circumstances to laceration or contusion of the lung, and
infiltration of its tissues vnth blood or inflammatory products, favouring
the entrance and germination of the tubercle bacilli, which he assumes
to be more or less ubiquitous. From the rapidity with which pulmonary
symptoms appeared in most of these instances, it seems more reasonable
to suppose that injury to the chest wall may rouse into activity some
latent tuberculous focus, possibly by laceration or loosening of its fibrous
capsule. As the result of direct questions put to many hundred
patients suffering from phthisis, I have met with but a comparatively
small number who referred their complaints to an injury of any kind. In
one or two instances, when the patient gave a history of injury to one side
of the chest, physical signs of disease were confined to the opposite side.
Antagonism of other diseases. — Ague has been said to confer a protec-
tion against phthisis, but investigations in malarious localities in various
quarters of the world have proved that no such antagonism exists.
An attack of erysipelas has been followed by arrest of the pulmonary
disease in a few recorded instances.
Disease of the heart. — Eokitansky taught that all conditions which
induce a state of venosity of the blood impart an immunity from tuber-
culosis. Among the affections included in this category he placed
cardiac dilatation and hypertrophy, whether primary or the result of
valvular disease, congenital malformation of the heart and great vessels,
aneurysms, deformity of the chest depending on rickets, lateral curva-
ture or caries of the spine, pleural effusions, chronic bronchitis, emphy-
sema, bronchial dilatation, pregnancy, or of any other condition tending
to obstruct the passage of venous blood through the right side of the
PHTHISIS PULMONALIS 165
heart. The relation of some of these affections to phthisis has been
already mentioned ; but the influence of cardiac disease must now be
considered. It is undoubtedly uncommon to find phthisis and disease
of the heart in the same patient, but this association is by no means so
rare as Rokitansky's statement would imply. Most writers agree in
saying that mitral stenosis is scarcely ever met with in this association :
this combination is rare, but I have seen at least a dozen clinical ex-
amples ; and in five other cases the two conditions were found on post-
mortem examination to be associated.
Eokitansky's view that the antagonism of the two affections depends
on the venosity of the blood has been objected to by Lebert and others,
on the ground that the subjects of congenital stenosis of the pulmonary
artery are exceedingly prone to contract tuberculosis. But in such
persons, as Lebert himself admits, the lungs are often small and unde-
veloped, and their nutrition must be below the average. And, although
the bronchial arteries are abnormally developed, in order to supplement
the pulmonary circulation, the lungs are still very inadequately supplied
with blood, and are less capable than normal lungs of resisting the
action of the tuberculous virus. It appears then that, in the case of
pulmonary stenosis, increased venosity of the blood is not the sole or
perhaps the . chief influence at work ; and Lebert's objection is possibly
not so fundamental as it has been held to be. Dr. Pollock considers
that hypertrophy and dilatation of the heart retard the progress of
tuberculosis, and that imder such conditions a prolonged duration may
safely be anticipated. This observation is a very true one, and affords
support to the theory of antagonism^
It seems, then, that Eokitansky's doctrine is true, though true in a
more limited sense than that in which he intended it to be taken. All
diseases of the heart which bring about a passive congestion of the lungs,
and consequently an increased venosity of the blood, confer a certain
degi'ee of protection against pulmonary tuberculosis ; but, in the words of
Peacock, "this opposition certainly in no degree amounts to an incom-
patibility."
Gout. — In the rare instances in which gouty persons acquire tuber-
culosis the disease runs a very chronic course.
Infection. — The doctrine of the infectious nature of tuberculosis, pro-
mulgated by Villemin in 1865, was verified by Robert Koch's discovery
in 1882 of the immediate cause of the disease, the tubercle bacillus.
After much difficulty he succeeded in isolating and cultivating the
microbe. In artificial nutrient media the bacillus was found to grow
with extreme slowness. Pure cultures inoculated into healthy animals
produced tuberculosis with unfailing certainty. From the fact that the
micro-organism can only be cultivated within certain narrow limits of
temperature (82° to 105° F., the best temperature being that of the
interior of the human body), Koch regarded the bacilli as true parasites,
" that is, as finding the conditions necessary to their existence only in
the animal or human organisms."
l66 SYSTEM OF MEDICINE
These facts have been confirmed by many observers, but Sir H.
Beevor, by means of the method of cultivation introduced by Nocard and
Eoux, claims to have obtained a very slow growth at a temperature of
60° F. If this observation should be confirmed, the tubercle bacillus
could no longer be considered to be an obligatory parasite. The experi-
ence of all investigators supports Koch's statement that the microbe
resists prolonged drying for months ; though when exposed to the action
of putrefaction it loses its virulence much sooner. The presence of
oxygen is necessary for the growth of the bacillus ; sunlight has been
said to retard or prevent it.
Persons suffering from tuberculous disease of the lungs are con-
stantly expectorating tubercle bacilli in enormous numbers. That the
sputa are infectious has been abundantly proved by experiments on
animals. Koch and many others consider that tuberculous sputum is
the chief source of the parasite. The extreme tenacity of life which
characterises this bacillus warns us that the sputum is dangerous long
after it has been expelled from the lungs of a phthisical patient. In
many well-authenticated cases accidental inoculation of human beings
with sputum or other material derived from tuberculous persons has been
followed by local or generalised tuberculosis. In one case, a patient
dying of gangrene of the leg was inoculated with tuberculous sputum,
and at his death three weeks later a few recent tubercles were found in
one lung.
Accidental inoculation of the skin, mostly of the hands, has occurred
in different ways ; for instance, from washing soiled linen of tuberculous
people ; by a scratch from a broken spittoon used by a phthisical
patient ; from wearing the earrings of a person that had died of phthisis ;
by the prick of a morphia syringe ; by post-mortem examinations of
tuberculous men or animals. In most of these cases the tuberculosis
remained localised, and, in some instances, the disease was cure'd by
timely excision of the affected parts. Eitual circumcision in Jewish
infants has been followed in several cases by tuberculous ulceration of the
prepuce and swelling of the inguinal glands : in some instances it was
proved that the operator, himself tuberculous, had sucked the wound to
stop the bleeding ; in one case where a phthisical operator had not
employed suction, he had squirted wine from his mouth over the wound.
Bacteriological examination of the ulcer and enlarged glands of the
infant, and of the sputum of the operator, was carried out in some in-
stances, and established the infective and tuberculous nature of the proaess
beyond all doubt. But while the inoculability of tuberculous sputum can
no longer be denied, it is nevertheless apparent that direct inoculation is
a rare occurrence in man, and in no way accounts for the great mass of
human tuberculosis. The rarity of this mode of infection is explained
by Baumgarten's discovery that tuberculosis cannot be induced by
inoculation of the superficial layers of the skin, subcutaneous puncture
being required to ensure a successful result.
The fact that the disease, in the great majority of cases, appears to
PHTHISIS PULMONALIS 167
begin in the lungs suggested to Koch that the tubercle bacilli enter the
body by the air passages. He further expressed the belief that the
bacilli were derived from dried sputum which had become pulverised,
diffused in the atmosphere, and inhaled into the lungs. This view has
been adopted by most subsequent writers. It may be objected that this
mode of infection is insusceptible of direct proof; a striking example,
however, has been recorded.
Tappeiner, by spraying tuberculous sputum into a cage where dogs
were confined, succeeded in inducing pulmonary tuberculosis in some of
the animals. In spite of repeated warnings, Tappeiner's servant, a very
robust man aged forty, and free from hereditary taint, insisted on going
into the cage, and contracted acute pulmonary tuberculosis from which
he died in fourteen weeks. It may be freely admitted that the condi-
tions in this caSe were not strictly parallel to those that obtain under
ordinary circumstances where the amount of tuberculous dust inhaled
must be very small ; yet the case demonstrates the possibility of man
acquiring tuberculosis by inhalation. All observers have admitted the
difficulty with which tuberculosis can be communicated to animals by
means of inhalation, a fact which Baumgarten maintains is opposed to
Koch's conclusions. After the discovery of the tubercle bacillus the
view was very generally expressed that the parasite is ubiquitous, and
that every one, especially in towns, must be frequently inhaling the
microbe. But a careful and extensive research, conducted in Berlin by
Cornet, proved that the bacillus is not so widely distributed as had been
assumed. The plan which Cornet adopted was to collect dust with
sterilised instruments from the walls of hospitals, prisons, asylums, and
private houses, and from the public streets. The dust was mixed with
sterilised broth and injected, with full antiseptic precautions, into the
peritoneal cavity of guinea-pigs. Many of the animals died rapidly of
septic peritonitis ; others remained in good health, and a certain
number contracted tuberculosis. The specimens of dust which communi-
cated tuberculosis to the animals were obtained from private rooms or
wards that had been inhabited by phthisical persons ; whereas in surgical
wards, out-patient departments, and in quarters not occupied by such
persons, the dust, as regards tuberculosis, gave negative results.
In the course of experiments made, after Cornet's method, by Dr.
Heron and Dr. Chaplin with dust from the Victoria Park Chest Hospital,
only two out of a total of a hundred guinea-pigs inoculated were attacked
by tuberculosis. In both these cases the particular specimen of dust
came from the main ventilating shaft, which had not been swept for
forty years. Dust taken from the wards, out-patient waiting-room, and
pathological laboratory failed to cause tuberculous infection in a single
instance.
Dr. C. T. Williams succeeded in detecting a few tubercle bacilli in
the air of the Brompton Hospital. His method consisted in the exposure
of glass plates, smeared with glycerine, in the ventilating shafts of a ward
set apart for phthisical patients. After some days the plates were
1 68 SYSTEM OF MEDICINE
examined microscopically and a few bacilli were found. It is very prob-
able that in this case the microbes were conveyed to the glass plates
with dust.
Dr. Eansome, by condensing the breath of consumptive people in a
glass globe surrounded with a freezing mixture, was able to discover a
few tubercle bacilli in two cases. But in such experiments it must be
difficult to prevent patients from coughing and expectorating minute
quantities of sputum or saliva which may contain bacilli. Numerous
workers have failed to verify these observations, and we may assume
that the bacillus is not exhaled from the lungs during ordinary respira-
tion. Cornet believes that the great majority of cases of pulmonary
tuberculosis are the result of inhalation of dried sputum in association
with dust.
Others think that the alimentary canal is a more important channel
of infection. Experiments on animals have proved that tuberculous
material when swallowed may induce tuberculosis of the mesenteric
glands and intestine. Considering that tubercle bacilli may lie dormant
amid the dust of houses inhabited by phthisical people, it is not
improbable that children may accidentally contaminate their food and
thus acquire abdominal tuberculosis. Milk and butter from tuberculous
cows, and the flesh of oxen, pigs, and fowls, when imperfectly cooked,
may also communicate the disease.
For a detailed discussion of this topic the reader is referred to the
article "Tuberculosis" (vol. ii. p. 29). The preponderance of primary
disease of the lungs, however, seems to support Koch's view that the
virus in most instances enters the body through the respiratory system.
The difficulty found in producing tuberculosis in animals by inhala-
tion may seem to oppose this view. But the pulmonary affection in
man, as compared with the artificially induced disease in animals like
guinea-pigs and rabbits, is always a chronic process. If an animal after
inoculation fail to show evidence of disease in a few weeks or months, the
experiment is generally regarded as unsuccessful ; whereas, to make the
parallel complete, continued observation for a much longer period would
be required. For in man the period of latency of pulmonary tubercu-
losis is generally one of months, or even perhaps of years. The success
of infection is largely a matter of dose ; a very small dose producing a
chronic affection or no result at all, a large dose, on the other hand,
causing an acute infection. Moreover, variations in the virulence of the
bacillus may be evidenced by corresponding differences in the type of
disease. Bacilli subjected to the action of desiccation for months are less
capable of active growth than when freshly removed from the animal
body or from artificial cultivations.
That Cornet's injections of dried tuberculous dust proved fatal to
guinea-pigs in a comparatively few weeks does not constitute a serious
objection to this conclusion; injections of such dried matter under the
skin or into the peritoneal cavity is a much stronger measure than its
introduction by inhalation ; for in the latter case the ciliaiy movement
PHTHISIS PULMONALIS 169
of the epithelium and the vital resistance of the cells of the respiratory
tract represent a powerful defensive mechanism that cannot be claimed
for the subcutaneous tissue or the serous membranes. The existence of
such a mechanism is well shown by the history of anthracosis and other
dust affections of the lungs. Children and animals living in the dusty
atmosphere of towns, as Baumgarten remarks, seldom show any of the
pigmentation of the lungs and bronchial glands, which is never altogether
absent in adults living under similar conditions. It seems as if the
ciliary action of the epithelial cells can remove all the foreign particles
introduced with the air up to a certain point and for a certain length of
time ; but after a time the carbon and other particles enter the lymphatic
vessels and become deposited in the lungs and in the neighbouring
bronchial glands.
It is very probable that tubercle bacilli entering the mouth are taken
up by the tonsils and carried to the cervical glands ; thence they may
pass into the large lymphatic vessels, and thus ultimately reach the
lungs.
Sonse infection. — A considerable number of observations have now
been recorded in support of the view that the tuberculous virus clings to
certain dwellings.
Dr. Eansome's investigations in Manchester and Salford have shown
that tuberculosis is. especially apt to haunt houses situated in close
courts, narrow streets, and, above all, houses built back to back, where
ventilation is necessarily defective. Similar observations have been
made in America and Germany. In some of the cases published the
evidence is very strong, as, for instance, in the following by Engelmann.
A newly-built flat, in a fairly sanitary condition, but badly lighted and
ventilated, had been occupied for eight years by three families in succes-
sion ; all of them had presented a clean bill of health until the family
X took up their residence in the same quarters. In this family the
mother was consumptive when she came, and died in the flat. Shortly
afterwards the family left, having lived there for one year only. The flat
was next occupied by the family Y, of seven persons, all healthy ; after
a year's stay they left, and some years later the father, mother, and one
son died of phthisis, and a boy of chronic peritonitis. A third family, Z,
all healthy to begin with, next took the rooms : one child died of menin-
gitis, another of marasmus, and a third contracted hip disease : subse-
quently the father died of phthisis, another child of meningitis, the mother
acquired consumption, and a child became scrofulous. A fourth healthy
family, W, next came into residence ; after a time the mother became
phthisical, and two children died of meningitis. In reference to these facts,
Dr. Payne remarks : " Summing up the history it appears that for eight
years the dwelling was free from tuberculous diseases. Then came one
year's tenancy by a person already tuberculous. After this, in a period
of twelve years, at least twelve cases of tuberculous disease were traced
to this source. It is noted that the dwelling was never vacant, the new
tenants entering while it. was, so to speak, still warm from the last ; and
■I70 SYSTEM OF MEDICINE
during the whole period it was never painted or cleaned." In other
parts of the same house, where cleaning was not neglected, but the con-
ditions were otherwise the same, no cases of tuberculosis could be traced.
The facts point strongly to infection in the case of the third and fourth
families (Z and W) ; but in respect to the second family (Y) the
evidence is not so convincing, as according to Engelmann's statement
some years elapsed between the tenancy of the infected house and the
deaths of some of the members from tuberculosis. The hypothesis that
the virus is air-borne, and intimately connected with dust, helps us to
understand how house-infection may come about. In most of the
instances recorded the victims lived in small, ill-ventilated rooms, so that
the chances of infection were thereby much increased. The smaller the
room the less the likelihood of adequate ventilation, and the greater the
opportunity for the accumulation of dust.
An important side light is thrown on this part of the subject by the
returns of the mortality from phthisis in the male and female sex among
certain agricultural populations in England and Germany, which show a
marked excess of the female over the male death-rate. In other words,
the males who lead an outdoor life suffer much less from consumption
than the females, who spend most of their time indoors. Although, as
Payne points out, this disparity in the phthisis death-rate may be ex-
plained on the ground that the open-air life of the men is healthier, it
is quite as logical to say that the indoor life of the women exposes them
to some injurious influence derived from the dwellings. We know that
the tubercle bacillus is apt to cling to ill-ventilated and insufficiently
cleaned rooms inhabited by phthisical persons, conditions only too well
fulfilled in the houses of the poor. It is hard to resist the conviction
that these facts are most readily to be explained by the more prolonged
exposure of the women to the risk of house infection. In towns the
male death-rate from phthisis exceeds the female. The difference here,
no doubt, depends on the unfavourable conditions under which men
commonly work in rooms badly ventilated and dusty.
The great preponderance of the phthisis rate on the female side
between the ages of ten and twenty, as shown by Ogle's tables, corre-
sponding, as it does, with the period in which the outdoor life of boys
and the indoor life of girls differ most widely, points in no uncertain
manner to the dwellings as the source of the mischief.
Contagion. — The contagious nature of phthisis, long an article of
popular belief in parts of Southern Europe, appears then to derive con-
firmation from Koch's discovery.
Since 1882 many cases have been published in support of this
doctrine. In most of these the parties concerned were married couples ;
and the disease seems to have been communicated from husband to wife
more frequently than in the reverse direction. We may briefly consider
the ways in which contagion may possibly occur.
(i.) By the skin. Direct inoculation has been already discussed and
shown to be a very exceptional occurrence.
PHTHISIS PULMONALIS 171
(ii.) By the alimentary canal. Tubercle bacilli might be accidentally
introduced into the mouth, as by kissing ; or less directly, by the use of
knives, forks, spoons, or drinking-vessels. The great rarity of primary
disease of the tongue, oral cavity, and alimentary tract generally, and
the comparative 'infrequency of primary tuberculosis of the mesenteric
glands, except in children, negative this mode of infection.
(iii.) By the respiratory system. Although the bacilli are not given
off in the breath, the possibility of their being expelled by coughing
with small quantities of mucus or saliva must be admitted ; but this
accident cannot be regarded as playing an important part.
(iv.) By the generative system. Where the generative organs are
tuberculous, it is possible that contagion may take place during sexual
intercourse, in either direction ; but the occurrence of primary tubercu-
losis of these organs in either sex is extremely rare. Direct contagion
must be very uncommon, and it can have little bearing on the causation
of the disease. It is possible that the bacillus or its spores may pass with
the sperm cell to the ovum without infecting the moflier, as is believed
to occur in syphilis. This question will be again referred to under the
head of heredity.
If the views already expressed as to the part played by dried sputum
and tuberculous dust be correct, there is no necessity to invoke the
supposition of direct contagion, which, in truth, stands on no firm
foundations. Husband and wife living in the closest relationship and in
the same rooms, are necessarily exposed to the same risks ; although the
member who spends most time in the infected rooms is more likely to
contract the disease. If husband or wife be already tuberculous a fresh
dwelling may be converted into a focus of infection, and the healthy one
may indirectly acquire phthisis by inhaling tuberculous dust.
Heredity. — Phthisis has always been accounted one of the most
hereditary of all diseases. Numerous statistics, dealing with this point,
are at hand ; but, seeing that some refer to parental inheritance only,
while others include collateral influence also, and in view of the fact that
information concerning collaterals is less likely to be precise, we may
confine our attention more particularly to parental inheritance.
The extent to which parental heredity is manifested in the subjects
of phthisis has been very variously stated, Portal rating it as high as 66
per cent, Louis as low as 1 0 per cent. We may, perhaps, regard 30 per
cent as about the proportion in which, according to most investigators,
a history of parental heredity can be obtained. It has been maintained
that fathers transmit to sons more frequently than to daughters, mothers
to daughters more frequently than to sons. But the statistics of Walshe,
R. E. Thompson, and Wilson Fox do not support this assertion.
Heredity is generally but not universally regarded as playing a more
important part in females than in males. It is stated that more female
than male patients give a history of phthisis in the parent ; and that
among all hereditary cases maternal is in excess of paternal inheritance.
In some cases inheritance seems to have been derived from grand-
172 SYSTEM OF MEDICINE
parents or great -grandparents, the parents having played the part of
silent carriers of the disease. According to several observers, phthisis
is manifested at an earlier age in those that evince an hereditary taint.
After the age of twenty-five the acquired cases equal the inherited, and
ultimately out -number them. According to Dr. E. E. Thompson, a
greater severity of form and a shorter duration of life characterise the
hereditary cases ; but the experience of Dr. C. T. Williams does not
confirm this conclusion.
Enough has now been said to show that, after all the labour expended
on this subject, no general agreement has yet been reached.
It is evident that the investigation of this question is exposed to
many fallacies, a few of which may be mentioned. In the first place,
many deaths of parents and grand-parents may have been wrongly
attributed to bronchitis, pleurisy, or pneumonia when the affection was
really tuberculous. Against this, of course, in other cases death may
have been erroneously ascribed to tuberculous disease. In dealing with
a large number of cases these opposing fallacies will to some extent
neutralise each other. A more important source of error depends on the
undoubted fact that many ancestors reputed healthy have been the
subject of arrested tuberculosis. Again, parents may not manifest signs
of phthisis till after the death of some of their offspring from this
cause.
In the case of heredity among collaterals — brothers and sisters, uncles
and aunts, cousins — ^the same fallacies must arise, but with an important
addition. In all families, but especially among the poor, the mortality
of infants and young children is very high ; and there can be no doubt
that the existence of tuberculosis at this age is very largely overlooked,
death being ascribed to marasmus, diarrhoea, bronchitis, or broncho-
pneumonia. On the whole, it seems that the tendency of the fallacies
referred to would be to underestimate rather than to exaggerate the
influence of heredity. The heredity of phthisis has received two widely
different explanations. According to the prevailing opinion, it is not
the disease itself that is inherited, but a disposition or tendency to
acquire the disease when exposed to the necessary influences ; the other
view is, that the germ of the disease is directly communicated from the
parent to the embryo.
The doctrine of hereditary predisposition has been assailed on more
than one ground. In the first place, the existence of a peculiar bodily
conformation in the children of phthisical families, the tuberculous and
scrofulous diatheses so much insisted upon by some writers, has been
called in question. It is admitted that some of the features described
are often seen in persons suffering from phthisis, though it is believed
that to a considerable extent they are attributable to wasting of the
muscles and adipose tissue, or to enlargement of external lymphatic
glands, and are, therefore, manifestations of existing disease. These
objections seem to be justified ; but the hypothesis of hereditary proclivity
does not necessitate the assumption of a special bodily habit, and
PHTHISIS PULMONALIS 173
the abandonment of this postulate does not materially weaken the
position of those who hold to the doctrine of predisposition. It has been
objected that the percentage of family inheritance reckoned up from
phthisical patients does not truly represent the influence of heredity,
and that the percentage should be compared with the incidence of the
disease in healthy families. Moreover, it is suggested that what is
inherited is not a special disposition to tuberculosis only, but a general
delicacy or vulnerability to adverse conditions of all kinds. According
to Beneke this vulnerability is connected with the relatively small
size of the heart in such persons. Others again would explain the
prevalence of the disease in certain families by the greater opportunities
of infection that exist in the dwellings of such persons. The first objec-
tion may be admitted as valid ; but in order to arrive at accurate con-
clusions on this basis the subject would require investigation on a much
larger scale than has been hitherto attempted. As Dr. Kingston Fowler
points out, it is obviously misleading to work back from the consumptive
member of a family to the parents, and to deduce the influence of
heredity from a comparison of the percentage incidence of phthisis in the
children of the phthisical and non-phthisical — a method adopted by some
investigators in this field. For this practically assumes that there is a
consumptive in every family, and takes no account of the families in
which, in many unselected series, no member is phthisical.
With regard to the explanation of heredity on the hypothesis of
family infection, it seems that although this may account for many cases
it will not explain all. Instances are not wanting where several members
of a family, widely separated from one another, have manifested the
disease in succession. If, however, the extreme latency of the tubercle
bacillus postulated by some writers could be substantiated, the question
of heredity would at once assume a new aspect altogether. Before pro-
ceeding to discuss the doctrine based upon this hypothesis, it may be
pointed out that the existence of a family susceptibility to other infec-
tious diseases — as to typhoid fever, scarlatina, and diphtheria — has long
been recognised by epidemiologists.
To Cohnheim we owe the suggestion that heredity depends upon the
direct transmission of the tuberculous virus to the embryo — a view which
has been further developed by Baumgarten. This author holds that
infection of the respiratory and digestive tracts will only account for a
small proportion of the cases of tuberculosis ; and by a process of
exclusion he is led to the belief that heredity is the most potent factor in
the continued existence of the disease. After rejecting the notion of
hereditary predisposition mainly on the strength of arguments derived
from the results of the experimental inoculation of animals, Baumgarten
embraces the doctrine of the direct inheritance of the tubercle bacillus or
its spores. According to his view the microbe may either be introduced
through the placenta and thence infect the foetus through the umbilical
vein ("placental infection"), or it may find access to the ovum itself
either in the ovary or after its passage into the Fallopian tube (" germina-
174 SYSTEM OF MEDICINE
tive or conceptional infection"). In the latter case the microbe would
mostly be conveyed by means of spermatozoa, though an observation of
Jani's suggests that the bacilli may enter the Fallopian tube from the
peritoneal cavity. The possibility of germinative infection from paternal
sources cannot be denied in view of the discovery, by Jani and Weigert,
of tubercle bacilli in the healthy testes and prostate glands of phthisical
men. Virchow objects to the view that germinative infection plays an
important rdle in heredity, on the ground that the presence of the bacillus
must interfere with or arrest the development of the ovum ; but Baum-
garten urges that this argument is negatived by the history of congenital
syphilis, and by the analogy of the pebrine disease of silkworms. In the
case of syphilis, although miscarriages may occur, it commonly happens
that the child is apparently healthy at birth, and signs of the disease do
not appear for some weeks ; a period of latency, therefore, undoubtedly
ensues between infection of the ovum or foetus and the first few weeks
of extra-uterine life. In the pebrine disease, which is caused by a psoro-
spermial organism, Pasteur has shown that the ova of the silkworm
become infested with the spores of the parasite ; but in spite of this the
eggs are hatched normally, though the caterpillars ultimately succumb
to the growth of the parasite in their bodies.
Baumgarten would explain the latency of the pebrine disease, con-
genital syphilis, and inherited tuberculosis by the supposition that the
actively growing embryonic cells inhibit the development of the respective
microbes.
Some interesting researches by Maffucci have an important bearing
on this question. Tubercle bacilli from a tuberculous fowl were intro-
duced into fertilised hen's eggs and incubation was allowed to proceed.
Maffucci found that the bacilli did not multiply, but underwent a regres-
sive change into granules exhibiting the staining reactions characteristic
of the normal bacilli. The chick was hatched out in the usual way, but
after about the twentieth day the bacilli began to develop, and a typical
tuberculous infection ensued, the liver being conspicuously involved. If
the dose of the bacilli introduced be small no visible tubercles form, but
the chicken nevertheless dies of extreme marasmus and bacUli are found
in the organs in small numbers. The analogy suggested with congenital
syphilis, the pebrine disease, and congenital tuberculosis of fowls is both
interesting and instructive.
Placental or germinative infection may explain the rare cases in which
tuberculosis is fouiid in the foetus or new-born infants ; and also perhaps
the less uncommon instances where the disease arises during the first
few months of life. But there seems to be no sufficient reason for the
belief that the tubercle bacillus or its spores may remain dormant from
the time of conception of the ovum to adult or middle life. Baum-
garten would go even farther, for he applies his hypothesis to explain
atavism occurring in tuberculous families ; and would trace the inherit-
ance of the microbe to a grand-parent or even more remote ancestor,
when the parents have remained health--. The evidence in favour of
PHTHISIS PULMONALTS 175
Baumgarten's hypothesis is not strong, and is mainly drawn from
observations on animals. Foetal tuberculosis has now been demonstrated
in several cases in calves, but in man such an occurrence is extremely
rare. Landouzy and Martin have published a case where the apparently
healthy foetus of a phthisical mother proved capable of infecting animals
with tuberculosis, to show that tubercle bacilli may be present in the
tissues without exciting any manifest lesion. The hypothesis of direct
inheritance does not appear to be reconcilable with the facts disclosed by
Ogle's statistics. A reference to his table shows that the mortality from
phthisis declines greatly after the completion of the second year until the
tenth year, when it begins to rise again, attaining its maximum from
twenty-five to thirty, but maintaining a high level up to the age of sixty-
five. Moreover the marked difference in the incidence of the disease on
the two sexes between the ages of ten and twenty is quite inexplicable on
Baumgarten's theory.
The only conclusion at present warranted is that direct inheritance is
of decidedly subordinate importance to extra-uterine infection, however
acquired.
Pathological Anatomy. — Tuberculosis is in its origin a local disease
depending on the lodgment and growth of the. tubercle bacillus; but in
virtue of its infective character it not only extends by continuity from
the primary lesion, but it tends also to invade other parts of the body.
Fever and other constitutional effects of tuberculosis are often out of
all proportion to the extent of the local disease, and must be ascribed to
the circulation in the blood of some as yet unrecognised chemical poison
produced by the bacillus.
We have now to consider the changes in the lungs that result from the
invasion of the tubercle bacillus. The initial lesions exhibit certain
differences according to the manner in which the microbe is introduced
into the organ. Excluding the comparatively few cases in which the
pulmonary disease is due to direct extension from neighbouring lymphatic
glands, or from the osseous parietes of the thorax, it may be said that the
bacillus gains entrance in one of two ways, through the blood-vessels or
through the bronchial tubes. In the former case the entry of a large
number of bacilli into the circulating blood gives rise to an eruption of
miliary nodules disseminated through the whole lung, and through many
organs of the body. In such cases, as was first pointed out by
Buhl, a caseous focus will almost invariably be found in some lymphatic
gland; or, possibly, in the lung itself. It is probable that the intro-
duction of a small dose of the bacilli may have as its result a circumscribed
lesion of the lung. In either case infection is brought about by an embolic
process, the microbe being arrested in the alveolar capillaries. The
presence of the bacilli in the first instance provokes a specific cellular
growth in the capillary wall, but the process soon extends into the cavity
of the air sacs, where a similar cell growth develops. If the microbes
enter the lung through the air-passages they appear to become arrested in
176 SYSTEM OF MEDICINU
the terminal bronchioles or alveoli, in which parts the epiLuuiiiiiu is not
ciliated. From the bronchiole the cell growth invades the peribronchial
sheath and alveolar cavities, the result being an islet of peribronchitis and
broncho-pneumonia. Tuberculous growths, wherever situated, are devoid
of blood-vessels. In generab'sed miliary tuberculosis the pulmonary changes
are but a part of a general infection of the body, though the lung may
suffer most. As death results in a few weeks at the latest the tubercles
in the lungs have not time to go through the usual cycle of changes
manifested in the cases which run a more chronic course.
Inasmuch as the lesions of chronic tuberculosis differ in degree father
than in kind it wiU be convenient to study the process in the chrtjnic
form. We have seen that in primary tuberculosis of the lung the bacilli
are probably introduced as dust with the air. Since the time of Louis
the preference of tuberculosis for the apex of the lung has been universally
recognised ; the earliest lesions are found about one to two inches below
the extreme apex. In rare instances the disease begins in other parts of
the lung, as at the base of the lower lobe ; but in adults a primary basic
origin is exceedingly rare, and is probably not found in more than one in
400 or 500 cases : in children it is relatively less infrequent, but this is
due to the fact that in them primary tuberculosis of the bronchial glands
is more common and attains to greater proportions than in adults. Many
cases of tuberculosis in children apparently basic in origin are really due
to direct extension from caseous bronchial glands. In rare cases of
irregular localisation, whether in children or adults, the disease has
originated in the vertebrae. The special proclivity of the apex of the lung
to tuberculosis has been variously explained : this part of the lung
undoubtedly possesses a smaller range of movement than the lower
portions in consequence of the greater rigidity of the upper ribs, and this
condition must favour the retention of foreign matter in the bronchial
tubes and alveoli, and will thus favour the lodgment of the bacilli. More-
over, Dr. R. E. Thompson points out that the comparatively fixed
position of this part of the thorax tends to keep the bronchial tubes of
the apex widely open, whereby the entrance of dust and other extraneous
matter is promoted. But in generalised miliary tuberculosis also, where
the bacilli enter the lung through the blood-vessels, the lesions are often
most advanced at the apex, a fact which points to the existence of a
special vulnerability of this part of the lung itself. It has been stated
that the circulation in the apex is less vigorous than in other parts of the
lung, and that this part of the lung being drier is more susceptible, but
of these opinions there is little direct proof. At an early stage of the
disease the lesion will be found to consist of one or more small grayish
nodules, the centre of which corresponds to a bronchiole ; as these nodules
increase in size they tend to acquirfe a racemose shape owing to the
growth of miliary granulations at the periphery. In man it is not easy,
as a rule, to trace the earliest steps of the process in the primary nodule,
as before the patient's death regressive changes have already set in ; but
from a study of the secondary nodules developed in similar cases we may
PHTHISIS PULMONALIS
177
conclude, as Eindfleisch has long taught, that the process begins in a
terminal bronchus and thence spreads to the corresponding lobule — that
is to say, the lesion is essentially broncho-pneumonic. In the early stages
^sMMm^^'
Fig. 6.— Composite photograph taken from three different sections, illnstrating the development of the
tubercular process. (Low power.) 1. Islet of tubercular peribronchitis, a bronchiole with sur-
rounding tubercular infiltration. 2. Patch of tubercular " pneumonia " : a, Early stage— alveoli
stuffed with large pale epithelioid cells (not recognisable with so low a power) ; 6, Later stage-
alveoli contain granular necrotic masses, the outlines of the cells having disappeared. 8. Fibro-
casi' 'US tubercular nodule, showing a pale amorphous caseous centre embedded in concentrically
arranged fibro-cellnlar connective tissue, which contains a few giant cells in its inner zone. Coarse
black carbon particles in places.
we find the mucous membrane of the bronchiole swollen and infiltrated
with cells, and the surface more or less denuded of epithelium. The
cavity of the tube contains mucous secretion mixed with pus cells.
Tubercle bacilli may sometimes be recognised in the secretion as well as
VOL. V N
178 SYSTEM OF MEDICINE
in the cellular infiltration. A similar cell growth, with a varying number
of bacilli, is found in the peribronchial sheath and in the corresponding
alveoli. The tuberculous gi-owth, whether in the bronchiole or in the air-
sacs, is seen to consist at first mainly of cells of an epithelial type — epi-
thelioid cells. In some cases the nodule seems to be composed exclusively
of small round cells. Subsequently large multinucleated cells ("giant
cells ") appear singly here and there in varying numbers. At the peri-
phery of the tuberculous area a zone of small lymphoid cell can generally
be recognised. In the last-named region the cells are entangled in a scanty
meshwork of delicate fibres ; but in no cases, save the most chronic, is
fibrillation visible at the centre of the tubercle. By degrees the cellular
growth extends to neighbouring lobules, where the same process is
enacted ; and thus the original nodule may become more or less lost in a
diffuse infiltration or tuberculous pneumonia. The direct propagation of
the disease is brought about by the spread of the tubercle bacilli along the
lymph spaces and vessels in the interstitial tissue of the lung. In the
course of the tuberculous process the walls of the alveoli and, in a lesser
degree, the coats of the small arteries and veins become involved in the
cell growth. Perforation of the wall of a pulmonary vein and entrance of
the bacilli into the blood is, as was first shown by Weigert, one of the
commonest modes of general infection of the body in cases of pulmonary
tuberculosis. A small artery may be affected in like manner, and a
localised eruption of miliary tubercles take place in the lung in the area
of distribution of the affected vessel ; but in most cases extra-alveolar
lesions are of quite subordinate importance to the changes occurring
within the air-sacs. In the most chronic varieties of tuberculosis the
development of fibrcms tissue is the predominant feature ; and this leads to a
thickening of the interalveolar, peribronchial, interlobular and subpleural
connective tissue. Tubercle hacilli are found in and among the epithelioid
cells, in the giant cells, and occasionally in the small-celled area ; but not
in the fibrous tissue itself. Except in miliary tuberculosis, and in certain
instances of acutely spreading disease, the number of the microbes that
can be demonstrated is generally small, and contrasts strongly with the
large numbers met with in the artificial tuberculosis of animals. The
paucity of the bacilli in the former case agrees with the far more chronic
course of the disease in man ; but it may be, as Ehrlich suggests, that in
certain stages of their growth the bacilli cannot all be successfully stained
by our present methods.
The destiny of the tuberculous growth is twofold. In the first place,
the cells undergo necrosis; their outline becomes indistinct, the nucleus
disappears, and the cell is converted into a finely granular or hyaline
mass, which then becomes fused with neighbouring cells in a similar state
of degeneration. As a result of this change large areas of the affected
wgan become transformed into opaque, yellowish white material, re-
embling cheese — a result known as caseous degeneration, or necrosis.
The cause of this change is uncertain, but it may depend, as Professor
Watson Cheyne suggests, on some chemical poison elaborntid by Ihc
PHTHISIS PULMONALIS 179
bacilli. Caseation is regarded by Weigert as an instance of coagulative
necrosis. Cheesy foci may remain unaltered for a considerable time ;
but they are very liable to undergo liquefaction, and when a communica-
tion is established with a bronchus the softened material is evacuated
and a cavity or vomica is formed. In some cases the process of softening
and excavation originates in a small bronchus. Tubercle bacilli are found
in immense numbers in the cavities, but in caseous material they are
generally very scanty. Cavities also contain various pyogenetic cocci ;
but, according to some observers, suppuration may be excited not only by
such cocci, but also by the tubercle bacillus. A caseous or necrotic
change is probably never altogether absent at some period in the develop-
ment of any tuberculous forhaation, and, as a rule, this is the prevailing
feature ; but at the same time, in most cases of pulmonary tuberculosis in
man, and in all chronic forms without exception, another process of a
conservative or reparative character is recognisable in the shape of a
growth of connective tissue. This change begins at the margin of the tuber-
culous area, where it constitutes a species of fibrous capsule. It is doubtful
whether this be a direct result of the tuberculous process, or whether it
be attributable to reactive inflammation around the tubercle. In some
cases the central caseous mass becomes thus shut off from the surrounding
parts and complete arrest of the disease is effected. The cheesy matter
may subsequently become calcified, or it may be gradually permeated by
connective tissue and converted into a solid fibrous knot. Fibrosis and
encapsulation are the natural mode of healing. The well-attested
frequency with which old fibrous tubercles or calcareous nodules are
found in the lungs at post-mortem examinations of patients dying of
other diseases, shows that recovery from tuberculosis is by no means so
rare .as was formerly supposed. In the great majority of cases, however,
the fibrous change is more limited, indications of a capsule can scarcely
be recognised, and fresh islets of tuberculous disease spring up on the
confines of the original patch. These secondary foci, which depend on
the spread of the bacilli along the lymphatic spaces, go through similar
stages of ceU growth, necrosis, and connective tissue development. Ac-
cording as the necrotic or fibrous change preponderates, the case assumes
an acute or chronic complexion ; but the combinations of the two processes
are subject to infinite variety. Thus a case originally of a marked fibroid
type may be complicated by the occurrence of acute destructive disease
in other parts of the lung ; or, again, though this is far less common,
rapidly progressing tuberculosis may undergo partial arrest and pass into
a chronic fibroid stage. In ordinary cases we find some indications of
healing at the apex, while in the more recent lesions necrosis is the
predominant factor.
Histogenesis. — The origin of the cells constituting the tubercle has
long been a matter of dispute ; some authors maintain that they are the
result of the proliferation of fixed tissue cells, others regard them as
leucocytes that have escaped from the vessels.
An important experimental research by Baumgarten has gone far to
i8o SYSTEM OF MEDICINE
prove that the specific tubercle cells are epithelioid in type, and are the
offspring of the epithelial, endothelial, and connective tissue cells of the
body. In miliary tuberculosis of the lung the process begins with
swelling and nuclear division of the endothelium of the alveolar capillaries,
of the epithelial cells lining the alveoli and bronchioles, and, in a minor
degree, of the interstitial connective tissue cells. For a fuller considera-
tion of this point and for further histological details the reader is referred
to the article " Tuberculosis " (vol ii. p. 6). Although in the case of
miliary tuberculosis the bacilli reach the lung through the blood-stream
and become arrested in the capillaries, yet the earliest lesions consist
predominantly of an accumulation of epithelioid cells within the air-sacs ;
and miliary tuberculosis of the lungs has not inaptly been designated a
miliary pneumonia.
For simplicity's sake the development of the disease has been sketched
as it affects individual sections of the lung ; but as a matter of fact the
process is far more complicated. While separate foci of tubercle go
through the stages, just described, various secondary changes of a congestive,
inflammatory, and cedematous nature commonly ensue in the intervening
portions of lung. These conditions are partly the result of compensatory
hypersemia ; but in the main they depend on obstruction of the smaller
bronchi and on the lobular collapse that follows.
Collapse soon passes into hroncho-pneumonia, which, if not from the first
actually tuberculous, soon becomes so. In such cases scattered caseous
spots are seen embedded in reddish, solidified lung. The pneumonic
condition, at first, is usually patchy or lobular in distribution ; though
from the coalition of numerous individual foci the consolidation may
ultimately involve the greater part of one lobe. On section the surface
is moist, flat, and glazed ; seldom dry and granular, as in croupous
pneumonia : this difference depends on the fact that the exudation is
mainly composed of cells and cedematous fluid, and contains little fibrin.
In some instances the consolidation has a pale pinkish gray gelatinous
appearance, the " gelatiniform infiltration" of Laennec. This condition
seems to be due to the existence of marked ansemia and cedema in
addition to the alveolar catarrh and collapse. In such infiltrations it is
not uncommon to discover small specks of caseous necrosis, which stamp
the process as essentially tuberculous. Sometimes a large area or even
a whole lobe presents a more or less uniform grayish or yellowish con-
solidation known as caseous pneumonia. In such cases, as a rule, old
caseous foci, or a cavity, will be found at the apex, suggesting the second-
ary nature of the diffuse infiltration.
Acute croupous or lobar pneumonia is stated by many authors to be a
common termination of pulmonary tuberculosis. I am convinced that this
is an error. An experience of some thousand necropsies of cases of this
disease has not furnished me with more than one undoubted instance in
which progressive tuberculosis of the lung was complicated by acute
fibrinous pneumonia. During the first influenza epidemic, two or three
cases, in patients who succumbed to an acute pneumonia of more or
PHTHISIS PULMONALIS l8i
less lobar dimensions, revealed an oedematous, ill-defined consolidation,
consisting microscopically of cells and oedematous fluid without any
fibrin ; these may have been modified instances of acute lobar pneu-
monia, but with these few exceptions the above statement holds good.
Phthisical patients are indeed often cut off' by acute intercurrent
disease of the lower lobes ; but this is essentially broncho-pneumonic, and
probably depends on the inhalation of septic microbes from ulcerative
cavities in the lung.
In the more chronic cases a localised emphysema is not uncommon,
especially where contracting lesions are separated by tracts of unaltered
lung. This condition, which is most pronounced towards the apex and
anterior margin of the upper lobe, may be so extensive as almost to mask
the original disease. The affected lung may present the appearance of
large superficial bullse, or the form of emphysema may be more diffuse.
The surface of such portions is often puckered from the contraction of
subjacent fibrous patches or cavities. Emphysema in these circumstances
is compensatory, and results from obliteration of adjacent alveoli. It is
necessary to distinguish clearly between true emphysema, which is a
degenerative atrophy of the alveolar walls and capillaries, and what may
best be described as pulmonary distension. When one lung is contracted,
the opposite lung undergoes vicarious enlargement, the alveoli becoming
uniformly enlarged without being otherwise altered ; the expanding lung
passes across the middle line of the sternum and encroaches upon the space
formerly occupied by its fellow. The efi'ect of this enlargement is an
increase of alveolar surface, and consequently an improved aeration of the
blood. This condition has been named "hypertrophy of the lung," a
description which implies increased function, and is therefore strictly
correct. It is possible, however, that this condition may, in time, pass
into true emphysema.
Cylindrical dilatation of the smaller bronchi is not uncommon, and may
be found in any part of the lung, whether its texture be spongy or
indurated. Bronchiectasis is to be attributed mainly to the positive
expiratory pressure of cough acting on the bronchial walls softened by
inflammatory or other changes. The existence of contracting fibrous
tissue in the surrounding lung, by drawing apart the walls of the bronchi,
will further contribute to the dilatation.
In all chronic cases 'pigmentation is a more or less marked feature ; it
.depends mainly on the deposit of particles of carbon derived from the
atmosphere. Old fibroid lesions . have a blackish or slaty colour, which
contrasts sharply with the red, yellow, or grayish tint of other parts of
the lung.
The process of softening of the caseous material and the formation of
cavities have been already briefly alluded to. The liquefaction which
occurs has been likened by Duclaux to the ripening of cheese ; but the
nature of the chemical transformation is still unknown. The shape of
pulmonary cavities varies greatly. They may be rounded or oval ; but
more often they are sinuous or anfractuous, in consequence of the
i82 SYSTEM OF MEDICINE
coalescence of separate vomicse, and of the irregular extension of the
excavating process. Cavities are often traversed by tough septa and
bridles, and are then described as trabeculated. The trabeculae were
formerly said to consist of persistent bronchi and blood-vessels, but
they have been shown by Dr. William Ewart to be chiefly composed of
condensed airless lung, representing the remains of collapsed alveolar
tissue originally separating discrete cavities. The ridges and stumps
■often observed on the walls of vomicse are relics of trabeculse destroyed
by ulceration.
In acutely developed and extending cavities the wall is ragged,
and formed by soft caseating or necrotic material. Such cavities are
commonly filled with thick pus, their walls softened and in a state of
purulent infiltration. Chronic and quiescent vomicse are lined with a
definite pyogenetic membrane like that of a chronic abscess. The lung
tissue around may be indurated or simply collapsed ; less frequently
spongy or emphysematous. Extension usually takes place by slow
ulceration of individual cavities, which tend ultimately to coalesce ; but
in some cases acute suppuration and sloughing cause rapid destruction
of the lung. Excavation sometimes begins as a tuberculous bronchiolitis,
ulceration subsequently extending through the thin bronchiolar wall
to the surrounding alveoli. In other cases a dilated bronchus may
undergo secondary ulceration and become sacculated. It may be very
difficult to decide whether such cavities were originally bronchiectatic or
pulmonary. True bronchiectatic cavities are seldom very large, whereas
those of pulmonary origin may involve the greater part of a lobe, or even
the whole of one lung. Excavations of this magnitude are always the
result of fusion of several cavities. In the great majority of cases exca-
vation originates in the lung, and is not bronchiectatic. A fuller treatment
of this subject is to be found in the article on " Bronchiectasis " in the
present volume [pp. 59 and 74].
In the course of excavation the bronchi become ulcerated and eaten
away, so that ultimately their wall passes insensibly into the lining mem-
brane of the vomica. Cicatrisation may cause narrowing or virtual
obliteration of the bronchial orifices. Chronic cavities not uncommonly
undergo a considerable reduction in size, as the result of contraction of
their capsule or of the neighbouring lung. It has even been asserted
that they may close completely, but there is no proof of this, and such an \
event, in view of the imperfect removal of the secretions effected through
the bronchi, must be regarded as highly improbable. A vomica resembles
a chronic abscess discharging externally through a narrow sinus ; now
unless the abscess can be freely opened it will not granulate up thoroughly,
and will continue to secrete for years. Contraction of a cavity is, how-
ever, promoted by a spongy yielding condition of the adjacent lung.
Fibrosis is an essential feature in all chronic excavation, and, as wo
tave seen, the same change is always present in chronic tubercular con-
solidation. In the most pronounced examples of this condition fibroid
induration is associated with excavation. In either case fibrosis causes
PHTHISIS PULMONALIS 183
shrinking of the lung, the upper lobe as a rule being most affected ; but
at times the whole lung becomes uniformly contracted. In extreme cases
the lung may be reduced to the size of a man's fist. Contraction of the
lung is followed by elevation of the diaphragm and of the abdominal
viscera, displacement of the heart and mediastinum to the affected side,
and a varying amount of depression of the chest wall. When the lung is
not too firmly adherent to the ribs, a contracting cavity at the apex may
shift slightly outwards and backwards towards the fixed point, the root of
the lung, as shown by Dr. C. T. Williams.
The primary cavity is situated at the apex of the upper lobe.
Secondary cavities may be formed in any part of the lung, but Dr. William
Ewart pointed out that excavation is especially prone to attack a definite
region, the apex of the lower lobe, and at a date anterior to the implica-
tion of the lower part of the upper lobe. The base and anterior border
of the lower lobe are least prone to excavation, just as these parts are the
last to be involved by the disease.
It remains now to consider the mode in which the tvhercidous process
extends through the lungs. In generalised miliary tuberculosis, where
infection, for the most part, is derived from a caseous lymphatic gland —
that is, from a source external to the lungs — the pulmonary blood-vessels
are flooded with bacilli, and the lungs become stuffed with miliary granu-
lations from apex to base. In chronic pulmonary tuberculosis the lungs
become gradually but progressively invaded by a process of auto-infection,
the primary focus being situated at the apex of one upper lobe. In a
moderately advanced case we find one lung more diseased than its fellow,
and towards the apex of the former a cavity or cavities with tough walls,
the tissue around being pigmented and fibroid, and often containing some
caseous nodules. In the lower part of the same lung we see scattered
tuberculous nodules and masses, some softening to form small cavities.
The other lung presents lesions of a similar appearance and localisation,
but in a less advanced stage. It sometimes happens that the disease
becomes partially arrested in the lung first attacked, while in the lung
secondarily involved it extends progressively from apex to base.
It cannot fail to strike the observer that the secondary lesions in the
lung are not the result of direct extension by continuity from the apex,
for the individual foci are separated by tracts of healthy lung tissue. Nor
is it possible to believe that tuberculosis spreads exclusively or mainly by
lymphatic or vascular channels ; for, in cases where the disease is not too
advanced, the lesions often consist solely of a cavity at the apex of the
upper lobe surrounded by a zone of tuberculous infiltration, and some race-
mose masses of tubercle at the apex of the lower lobe ; the rest of the lung
being unaffected. Extension to the lower lobe is evidently effected
through the bronchial tubes, infective secretion being inhaled from the
apical cavity into the bronchi of the lower lobe. This view is in harmony
with the results of the " inhalation tuberculosis," artificially produced by
exposing animals to a spray of tuberculous sputum. It also accords with
the fact that the prevailing lesions in man are broncho-pneumonic in char-
i84 SYSTEM OF MEDICINE
acter. Dr. Ewart explains the marked proclivity of the apex of the lower
lobe to secondary excavation by the fact that the bronchus supplying this
part is a wide, straight tube coming off horizontally from the main
bronchus, a condition which appears to favour the inhalation of infective
secretion from cavities in the upper lobe. Dr. J. K. Fowler also has
pointed out that the distribution of tuberculous disease follows a very
definite path. From the initial lesion at the apex the process spreads
downwards in the upper lobe. Excavation of this region is followed by
secondary disease of the apex of the lower lobe on the same side, and of
the apex of the upper lobe of the opposite lung. Dr. Fowler states that
the former district is involved before the latter ; but in my experience the
apex of the opposite lung is quite as often the first point to be affected
with secondary disease, though the apex of the lower lobe of the hmg
primarily attacked is almost always implicated at an early date. The
lower part of the upper lobe is then gradually infiltrated, and simul-
taneously the disease extends from the apex of the lower lobe forward
and downward along the interlobar septum. The base and anterior
border of the lower lobe are the last parts to be affected.
In the process of destruction blood-vessels for the most part become
obliterated as the result of thrombosis ; but when rapid excavation is taking
place, ulceration may extend into large vessels and cause severe haemor-
rhage. In cases of a more chronic nature it is not uncommon to find
aneurysmal dilatation of branches of the pulmonary artery lying in the
walls of a vomica. In my post-mortem examinations aneurysms were found
in 15 per cent of all cases of pulmonary tuberculosis; these aneurysms
consist of a lateral expansion of the vessel on its exposed side. In rare
instances an artery crossing a cavity becomes uniformly dilated to form a
fusiform aneurysm. In either case the dilatation is to be attributed to two
causes : (i.) to arteritis and softening of the arterial coats, the result of
extension of inflammation from the cavity ; (ii.) to withdrawal of support
from the wall of the exposed vessel. Pulmonary aneurysms vary in size
from that of a pin's head to that of a plum, but they are seldom larger
than a cherry. It is usual to find only one aneurysm ; though, at times,
several may be discovered in the same cavity or in diJfferent parts of the lung.
In one extraordinary case I found twenty-two aneurysms in one lung.
Rupture of the sac is a common event, and is by far the most frequent
cause of profuse haemorrhage. In a series of eighty cases of fatal haemo-
ptysis, examined by myself, a ruptured aneurysm was found in seventy.
When rupture does not occur, thrombosis is apt to ensue. Thrombosed
aneurysms are often met with in cases where no haemorrhage has taken
place. Observation shows that aneurysms after leaking for some time
may become ultimately cured by coagulation of their contents. When
the cavity containing the aneurysm is small, the pressure of the effused
blood may be sufficient to prevent further haemorrhage. If the i patient
live long enough, the healed aneurysm in time undergoes necrosis, and
may entirely disappear.
Localised gangrene occasionally takes place in connection with rapidly
PHTHISIS PULMONALIS 185
spreading excavation. It is, however, a remarkable fact that, in spite of
the existence of numerous profusely secreting cavities, putrid changes are
very rarely met with as a result of tubercular disease.
Pleurisy is a well-nigh constant accompaniment of the pulmonary
disease, and is mostly due to extension. Pleurisy may also be consecutive
to peritonitis, the virus being transmitted from one serous cavity to the
other through the lymph spaces of the diaphragm. Primary tuberculosis
of the pleura is said to occur, but of this there is some doubt. In cases
of apparently primary pleural origin the disease may have started in a small
caseous bronchial gland which has escaped detection.
Fibrinous exudation is the commonest form, but sero-fibrinous effusion
often ensues. Empyema is uncommon in adults, though less rare in
children. Hsemorrhagic exudation is occasionally met with, and may be
attributed to rupture of the newly-formed capillaries of the inflamed
pleura. In many cases tuberculous granulations and, less frequently, caseous
nodules can be recognised in the serous membrane. But it is not infre-
quently impossible to discover any naked-eye signs of tubercle, whether
in cases of fibrinous, sero-fibrinous, or suppurative pleurisy. In some
instances of this description the microscope may reveal the presence of
isolated miliary tubercles in the thickened pleura. There can be little
doubt that the granulations in the pleura, as in the peritoneum, may
undergo complete fibrous transformation. It is not improbable that in
some instances pleurisy may have a non-tuberculous origin. In any case
the ultimate result of pleurisy is to cause more or less thickening and
adhesion of the pleura. The former may attain to considerable dimensions
in chronic cases, especially at the apex of the lung, where the pleural
investment may measure as much as an inch in thickness.
Eapid softening and excavation of the peripheral parts of the lungs
are apt to cause perforation of the pleura and entrance of air into the
serous cavity, if the pleural space at the affected spot have not previously
been obliterated by adhesions.
Pneumothorax causes collapse of the lung, and is followed in most cases
by effusion of serous or, more often, -of purulent fluid in consequence of
the entrance of tubercle bacilli and pyogenetic cocci from the lung.
It is not unusual to discover more than one perforation of the pleura.
The opening may be situated at any point where the pleural surfaces are
not adherent. The middle third of the lung corresponding to the lower
part of the upper lobe and upper part of the lower lobe is the most fre-
quent site of perforation. Occasionally the air escapes into the sub-
cutaneous tissue of the chest wall or into the mediastinum, and surgical
emphysema is produced. At times a cavity in the lung may extend out-
wards through the pleural adhesions and give rise to emphysema, or to an
abscess in the chest wall communicating with the lung. Pneumothorax was
found in 11 per cent of the cases of phthisis which I examined after death.
The bronchial, mediastinsil, and tracheal glands are very often the seat
of secondary tuberculous deposit. They may also be primarily affected,
and, as already mentioned, the disease may extend thence to the lung or
l86 SYSTEM OF MEDICINE
pleura. The extreme frequency with which arrested tuberculous lesions,
in the shape of calcareous nodules, are found in these glands is well known
to all who are in the habit of making necropsies.
Stenosis of a main bronchus is occasionally caused by enlarged glands
in children; but this very seldom occurs in adults, as their bronchial
tubes are much firmer. The smaller bronchi may be compressed in adults
as in children. Marked obstruction entails some degree of collapse of the
lung, and sometimes gives rise to bronchial dilatation beyond the seat of
pressure. In one case I found that a large calcareous bronchial gland had
perforated the bronchus and set up ulceration, wliich had extended at
another point into a larger branch of the pidmonary artery.
Suppurating caseous bronchial glands may perforate the trachea,
bronchi, lung, cssophagus, or pericardium. Sudden death has more than
once resulted from the entrance of a caseous gland into the trachea. In
cases where a fistulous communication is established between the oeso-
phagus and the air-passages a septic broncho-pneumonia ensues, and
pulmonary gangrene has been a relatively frequent complication.
From the foregoing sketch it will be seen how manifold are the lesions
of phthisis pulmonalis. The unity of phthisis, that is to say, the essen-
tially tuberculous nature of the disease first advocated by Laennec, was
long and vehemently disputed ; but the truth of this doctrine was at
length removed from the sphere of controversy by Koch's discovery of the
tubercle bacillus. The presence of the specific microbe in miliary granu-
lations, caseous nodules, caseous pneumonia, and pulmonary cavities
supplies a positive demonstration of the pathological identity of these
apparently different manifestations. Hence such distinctions as tuber-
culous, pneumonic, tuberculo-pneumonic, catarrhal and scrofulous phthisis,
always artificial and unworkable, are now entirely superfluous. Phthisis
is tuberculous disease of the lungs.
Symptoms. — The manner of invasion of pulmonary tuberculosis
varies somewhat in different cases. From the slowness of growth mani-
fested by the tubercle bacillus we might expect the invasion of the
disease to be gradual. In the great majority of cases this is the case,
and certain general or constitutional symptoms often precede those of
local disorder of the respiratory organs. But as in a considerable number
of cases the disease begins more or less abruptly, we must distinguish
(A) acute, and (B) chronic tuberculosis.
A. Aeute pulmonary tuberculosis. — Three forms of the acute disease
may be recognised.
I. Ldbar-pnewmonic form. — In this form — -the rarest of the three — the
whole of one lobe, nearly always the upper lobe, or the greater part of
one lung becomes converted into a solid gelatinous or caseous substance.
The consolidation, though massive, usually presents some scattered foci
of older date, suggesting that the diffuse pneumonia is secondary to an
originally localised form of tuberculosis.
This sequence of events is well illustrated by cases where, a cavity
PHTHISIS PULMONALIS 187
ejdsts in the apex or other part of the lung, under which circumstances
the diffused infiltration may be attributed to the inhalation of infective
secretions from the cavity. But in a few recorded instances the caseous
infiltration has been perfectly uniform, which observations support the
belief that the affection was, from the first, lobar and acute, all parts
having been simultaneously and equally attacked. In some of these
cases there was a cavity in the lung which may have been the starting-
point of the pneumonia. Miliary tubercles may sometimes be discovered
in the lower lobe or in the opposite lung ; caseous nodules are more
common. Tuberculous pleurisy, mostly of the dry variety, is a constant
accompaniment.
The disease may begin sharply with a rigor, high fever, dyspnoea,
pleuritic pain, and a short cough with mucoid, tenacious sputum, which
may be rusty or may contain florid blood. Occasionally the attack begins
with haemoptysis. Herpes labialis is not uncommon. The patient often
attributes his illness to a chill.
The foregoing mode of invasion closely simulates acute pneumonia.
In other cases the onset may be less abrupt, the patient experiencing a
malaise, aching in the back and limbs, and slight cough and expectoration,
before the onset of marked pyrexia and other pneumonic symptoms.
Physical examination discovers signs of consolidation, dulness, tubular
breathing, crepitant or subcrepitant riles, bronchophony and increased
tactile vocal fremitus. The breath-sounds may be merely weakened, and
no tubular breathing may be heard for some time. Pleuritic friction is
frequently met with ; signs of effusion are somewhat rare. The whole
picture is that of acute pneumonia, for which the disease is almost invariably
mistaken at first. But no crisis appears, and the fever persists for weeks.
In a few instances the temperature becomes lower, and after a few days
the symptoms abate somewhat ; but the improvement is only short-
lived, and the patient relapses into his former condition. The fever for
the first two or three weeks manifests a remittent character, the evening
temperature being one or two degrees higher than . the morning, and
ranging from 103° to 104° F. Later the temperature falls somewhat
and assumes a hectic character. From the first the patient wastes rapidly
and exhibits extreme prostration, sometimes passing into a typhoid state
with dry tongue, subsultus, and mild delirium. In the less rapidly fatal
cases signs of excavation of the lung gradually come on. The sputum
becomes mueo-purulent, and is found to contain tubercle bacilli, and perhaps
elastic tissue. A fatal termination may be reached in less than a fort-
night ; more often life is prolonged for six weeks or two months. Now
and then the disease gradually loses its acute character and assumes the
form of chronic pulmonary tuberculosis.
The diagnosis during the first week or ten days presents great diflS-
culties. In some instances the invasion is less sudden, and the severity
of the symptoms less pronounced than in cases of acute lobar pneumonia.
But these distinctions are often wanting. In the tuberculous form the
fever is less continuous, and is generally marked by irregular remissions.
SYSTEM OF MEDICINE
The pulse-respiration ratio, again, is less deranged than in acute pneumonia ;
for the pulse-rate is greatly increased, often reaching 130 to 140, with
a respiration of 30 or 40.
It has been said that in tuberculous cases the breath-sounds over the
affected lobe are more often weak and suppressed than tubular, but this
sign is by no means constant ; moreover, this sign is not very rare in
croupous pneumonia. From acute pneumonia with delayed resolution
the disease may be discriminated by the progressive wasting and prostra-
tion, as well as by the fluctuating high temperature which accompanies
it ; for in the former complaint, in spite of the persistent pulmonary con-
solidation, the general condition mends and the temperature falls. In
doubtful cases the appearance of signs of excavation, and, above all, the
detection of tubercle bacilli in the sputum, are the only facts on which
a positive diagnosis can be based. The complications of this form of
tuberculosis do not differ materially from those attending the chronic
variety, under which head they will be discussed ; but it may be said
that complications are much less frequent in acute cases, owing to the
rapid termination entailed by the severity of the pulmonary lesions.
II. Broncho-pneumnnic fwm. — This form, which is much less uncommon
than the last, represents what has been called galloping consumption or
phthisis fiorida. The special anatomical features consist of disseminated
tuberculous foci, of various sizes, which may be soft, yellowish white,
and cheesy ; or grayish, slightly pigmented, of racemose shape, and
somewhat indurated. Miliary tubercles are seldom to be seen. In most
cases rapid softening and excavation of the nodules is a very prominent
feature. Small suppurating cavities with soft ragged walls are scattered
through both lungs. In the apices of the upper lobes the cavities are
generally larger, and in some cases the apex is the seat of old fibrosis
and excavation. The lung tissue separating the nodules is often hyper-
inflated, especially towards the anterior borders ; in other parts the
nodules are embedded in tracts of grayish red consolidation, more par-
ticularly towards the back. This fusion of the individual foci may
ultimately result in a diffuse infiltration of lobar dimensions. The bronchi
are always deeply injected and contain abundant purulent secretion. The
localisation of the lesions is essentially broncho-pneumonic and lobular,
and depends on the inhalation of tubercle bacilli from a cavity in the
lung or from external sources. Pleurisy in some form, whether dry,
sero-fibrinous, or sanguineous, is always present. The larynx and large
air-passages are more prone to tuberculous ulceration than in the lobar-
pneumonic form, in consequence of the more profuse secretion discharged
from the cavities and bronchi in the present variety.
The mode of onset is subject to considerable variations. Occasionally
without any early period of ill-health the patient is suddenly seized with
rigors and other symptoms of acute pneumonia : more often the disease
begins insidiously with a cough, which, after the lapse of a few weeks,
is succeeded by fever, malaise, and other constitutional symptoms. Haemo-
ptysis is occasionally the first symptom. In some instances the disease
PHTHISIS PULMONALIS
189
begins with symptoms of gastric disturbance, loss of appetite, furred
tongue, and vomiting ; and the real nature of the malady is not recog-
nised until the chest is examined.
In recent years this form of tuberculosis has not uncommonly followed
an attack of influenza. Whatever the mode of invasion, marked wasting
and loss of strength soon appear. Hsemoptysis is not very common, and
is seldom profuse. The sputum at first is muco-purulent, but it soon
becomes more puriform, and sometimes acquires a greenish yellow colour ;
in some cases it has a reddish brick-dust colour for weeks. Tubercle
Pig. 7. — Diagram illustrating the localisation of tuberculous lesions in the lungs. P, Primary lesion
(double shading) ; P^, local extension from primary lesion (single shading) ; S, secondary lesions.
bacilli and elastic tissue are generally recognised before long. Night
sweats are frequent, and often are very profuse. The temperature ranges
high, reaching 104° F. at times; the fever is fluctuating, being marked
by morning remissions of one or two degrees : as the disease proceeds, the
teniperature becomes more hectic. Anorexia, vomiting, aphthous stoma-
titis, a dry red tongue, and diarrhoea are very common, and the patient
is apt to pass into a typhoid state. In the worst cases death ensues in
three or four weeks, but the end is more often deferred for three or
four months. Very occasionally the acute progress of the disease is
stayed, and the patient lingers on for eight or nine months.
190 SYSTEM OF MEDICINE
Physical examination at first reveals nothing more than signs of
general bronchitis ; but subsequently pleuritic friction and patches of
dulness on percussion, more particularly at the apices, make their appear-
ance, and signs of excavation may ultimately be discovered. In some
instances the signs may predominate at the base of the lower lobe. In
the most acute cases no cavernous signs can, as a rule, be recognised, as
death takes place before the cavities have reached suificient size to permit
of their detection. Moreover, the patches of distended lung tissue which
separate individual foci tend to obscure the existence of extensive disease.
The diagnosis at first rests on the discovery of physical signs of broncho-
pneumonia, accompanied by great prostration and loss of flesh. But the
detection of tubercle bacilli in the sputum may alone enable us to decide
whether the disease be tuberculous or not. In the case of young children
the differences are greatly enhanced, for no sputum is obtainable, and
death commonly .takes place before softening and excavation can be
recognised.
III. Acute miliary tuberculosis. — In this form the pulmonary condition
is frequently dwarfed by the symptoms of general infection. This con-
dition, from its resemblance to typhoid fever, is sometimes described as
the typhoid form of acute tuberculosis. In other instances the disease
manifests a special incidence on certain organs, and types have been dis-
tinguished varying with the parts of the body principally affected ; for
instance, the cerebral, the abdominal, and the pulmonary.
It has been the custom to draw a sharp distinction between acute
miliary tuberculosis and phthisis on account of the marked difference in
the clinical symptoms of the two affections ; but an eruption of miliary
granulations in the other organs is a fairly common complication of chronic
pulmonary tuberculosis, and is to be attributed to the entrance of a large
number of tubercle bacilli into the pulmonary circulation. Moreover,
many cases, clinically indistinguishable from the typhoid or disseminated
type of acute tuberculosis, are found after death to present old circum-
scribed tuberculous lesions of the hmg, which had escaped recognition
during life. In fact, the acute miliary form differs from chronic tuber-
culosis of the lung only in the acuteness of its course and in the more
widespread infection of the body. In the pulmonary type, which alone
will be considered here, the disease may advance in an acute or subacute
manner without any premonitory symptoms. In a large proportion of
cases a period of ill-health, of variable duration, precedes the onset of the
disease. The symptoms first noticed are cough, expectoration, dyspnoea,
and occasionally pleuritic pain. Dyspnoea, as a rule, soon becomes the pre-
dominant feature, and is often accompanied by marked cyanosis. Haemo-
ptysis is uncommon ; but now and then it is the earliest symptom. The
temperature is generally high, reaching 103° to 104° F., and the morning
remissions are less pronounced than in the broncho-pneumonic form.
Some cases have been known to run their course without any definite
elevation of temperature. The pulse, from the first, becomes rapid and
weak. Examination of the chest reveals signs of general bronchitis, fine
PHTHISIS PULMONALIS
191
bubbling rS,les, and rhonchi on both sides. At first no dulness on per-
cussion can be elicited, but the anterior parts of the lungs are found to
be rather hyper-resonant, the change depending on compensatory dis-
tension of the alveoli — the so-called " acute emphysema." As the disease
progresses, pleuritic friction sounds are often heard ; and patches of
dulness pointing to secondary broncho-pneumonia may sometimes be
recognised. In these parts the breath-sounds may be tubular, but more
often become muffled. This difference does not depend on the prepon-
FiG. 8. — Photograph of a section of the lung from a case of acute miliary tuherculosis, showing the
mode m which general infectitm occurs through branches of the pulmonary veins. (Low power.)
V, Small puhuonary vein ; T, tubercular growth from intima, projecting into the lumen of the vein ;
B, small bronchus showing tubercular infiltration of its wails.
derance of consolidation or pleural effusion ; for, in the absence of
pleuritic exudation, the vesicular breathing may be greatly diminished
by the concomitant bronchitis and lobular collapse. Lobar pneumonia is
an occasional complication. The patient rapidly loses flesh and strength,
dyspnoea and cyanosis increase, the cough grows more troublesome, and
the sputum — which at first was mucoid — now becomes muco-purulent.
It is rare to find tubercle bacilli in the expectoration, and when this
happens, a cavity, often a very small one, will generally be found in some
part of the lung. The spleen is more or less enlarged, and may some-
times be recognised by ipalpation.
192 SYSTEM OP MEDICINE
The diagnosis is occasionally easy, but more often difficult. In the
presence of general bronchitis, associated with marked dyspnoea, cyanosis,
pyrexia, and rapid emaciation, the diagnosis presents little difficulty. But
in cases where the evidence of bronchitis is slight or absent, the dispro-
portionate amount of dyspnoea is a diagnostic point of considerable value.
Tubercles may occasionally be recognised in the choroid by means of the
ophthalmoscope, and tubercle bacilli have, in a few instances, been found
in the blood ; but unfortunately such evidence is rarely to be obtained.
B. Chponie pulmonary tubereulosis. — The following modes of inva-
sion may be recognised in their order of frequency : —
(i.) Insidious. — The commonest prodromal symptoms are loss of flesh
and strength, accompanied, in some cases, by a slight evening rise of
temperature. Less frequently the disease is ushered in under the guise
of anaemia, or of a functional derangement of the digestive system.
(ii.) Brimchitic. — After frequent attacks of bronchial catarrh, or with-
out any previous tendency to bronchitis, the " disease begins with cough
and expectoration, which are attributed at first to a common catarrh ; but
after a few weeks or months pyrexia and other constitutional symptoms
make their appearance. In some instances careful inquiry will establish
the fact that a period of ill-health existed before the appearance of the
cough. Many cases with such a story have originated in influenza.
(iii.) Pleuritic. — The first definite symptom is pain of pleuritic type,
increased by cough or deep inspiration. The pleurisy is generally of the
dry form, but effusion may take place. Pyrexia and other symptoms of
phthisis may follow hard on the pleuritic seizure, or the pleurisy may
gradually disappear, and the patient make a temporary recovery, only to
fall ill again later, with pronounced symptoms and signs of pulmonary
tuberculosis.
(iv.) Hxmoptoic. — In this class, the " phthisis ab hsemoptoe " of the old
authors, the first symptom to attract attention is haemoptysis. When
the haemorrhage is profuse, it almost certainly indicates rupture of an
aneurysm in a vomica, that is, old-standing disease ; even when no other
evidence of a pulmonary lesion is forthcoming.
(v.) Laryngeal. — Phthisis occasionally begins with laryngeal symp-
toms ; hoarseness, loss of voice, hypersesthesia, or paraesthesia of the
throat being the most common.
Symptoms. — A constant and perhaps the most important symptom
from the diagnostic point of view is cough. At first dry, short, and in-
frequent, it is accompanied, sooner or later, by expectoration, and may
become so incessant as to prevent sleep and to set up vomiting, whereby
the patient's strength becomes reduced in the most serious manner.
There is no direct relation, however, between the gravity of the disease
and the severity of the cough. Some patients, with extensive pulmonary
lesions, have little or no cough ; whilst in others, with comparatively
slight disease, cough may be the predominant symptom. Cough is
generally most troublesome in cases of progressive disease, and where
the larynx, trachea, and large bronchia are actively engaged; but it
PHTHISIS PULMONALIS 193
depends to a considerable extent on the excitability of the nervous
centres. When the larynx is extensively affected the cough is peculiarly
muffled and hoarse. In some cases, especially when large cavities form
in the base of the lung, it assumes a paroxysmal character. Coughing
fits occur most frequently in the early morning, owing to the accumula-
tion of secretion in the larger air-passages during the night. In some
cases an irritable cough is excited by the ingestion of food, and the fit
may end in vomiting. This occurrence is partly to be explained by the
mechanical compression of the stomach and abdominal viscera against the
diaphragm ; but vomiting so often follows slight fits of coughing that it
seems necessary to assume the existence of a neurosis of the vagus in
these patients.
Hxpecioration. — In the early stages expectoration is scanty and mucoid;
but it soon becomes muco-purulent, and is commonly very viscid. At
times it is thin and watery, from admixture with saliva. As the disease
progresses, the sputum collects into small thick lumps of a dirty white or
yellowish colour; this " nummular sputum" is more common where cavities
have formed in the lung, but it may be met with in cases of simple
bronchitis and of bronchiectasis. It is not uncommon in the same specimen
to find small yellowish spots or streaks mixed with frothy mucous secretion
— the mixture representing bronchial secretion and pus from cavities in the
lung. At times, especially in advanced cases, the sputum becomes uni-
formly opaque and thick, and may assume a greenish colour. Expec-
toration is sometimes markedly paroxysmal, especially where cavities
exist in the lower part of the lungs. Blood is often discharged with the
sputum. The blood-stained sputa may be bright red, or, when blood-
clots have been retained in cavities or bronchi for some time, the colour
may be dark purple or blackish. In certain instances the sputum presents
a brownish or chocolate colour from decomposition of blood in the cavities
or bronchi. In other instances it may be of a brick-red tint, especially
when active ulceration of the lung is going on ; but it seldom has the
rusty, tenacious character of acute pneumonia. Foetor is practically
unknown in the absence of such complications as bronchiectasis or gan-
grene. In the more chronic forms of phthisis small particles of calcare-
ous matter, consisting mainly of phosphate of calcium, are coughed up
from time to "time. These pulmonary calculi represent caseous
material that has undergone calcification, and has become loosened in the
process of excavation. Sometimes they show a tendency to branch,
so that some think that they may come from the small bronchia. I
have found them on many occasions in the recesses of old cavities in
the lung. Calcareous bronchial glands occasionally perforate the air-
passages and are expectorated. The discharge of pulmonary calculi
implies ulceration of the lung or air-passages, and is a sign of chronic
disease ; but no further diagnostic value can be assigned to it.
As regards the importance of the sputum of phthisis, it must be
allowed that the naked-eye appearances alone possess no certain and
pathognomonic significance, if we except the presence of blood and cal-
■\'0T,. ^■ 0
194
SYSTEM OF MEDICINE
Pig. 9. — Sputum showing pus corpuscles and tubercle
bacilli ; some of the bacilli are beaded, x 550.
careous matter. The former will be considered under the head of haemo-
ptysis. It is doubtful whether chalky masses are expectorated in any
disease other than tuberculosis of the lungs or bronchial glands ; conse-
quently this event has a certain
diagnostic significance. Micro-
scopic examination of the sputum,
is a most valuable method of
diagnosis. By this means we
recognise various forms of ceUs
— squamous, flattened, spheroidal,
columnar and ciliated epithelium,
blood corpuscles, pus cells, mucin,
crystalloid products of chemical
change, such ascholesterine, leucine
and tyrosine, fatty acids and drops
of myeline, carbon particles, elastic
tissue from the lungs, and microbes
of different kinds. Of all these
constituents of the sputum two
only are pathognomonic, elastic
tissue and tubercle bacilli. The
presence of the former is a positive proof of destructive disease of
some portion of the respiratory apparatus, though it does not enable
us to distinguish the precise nature of the disease ; but as tuberculosis
is by far the commonest ulcerative affection of the lung, the presumption
is in favour of this being the process at work. When the elastic
tissue shows an alveolar arrangement we may be certain that it is derived
from the lung ; but isolated fibres may possibly come from the larynx,
or from the trachea and bronchi ; though, unquestionably, their main
source is the lung.
Elastic tissue. — If the opaque whitish particles seen in the sputum be
teased out with needles and examined in a drop of water, branching
elastic fibres with their curled-up ends, oi portions of the more char-
acteristic alveolar framework of the lung, may be recognised under a
low power. Sometimes, in cases of chronic excavation, the fibres are
encrusted with minute particles of lime salts. The persistent presence of
elastic tissue with alveolar grouping is a sign of progressive destruction
of the lung. A better and more certain method is that devised by Dr.
Fenwick. The sputum is mixed with an equal quantity of a solution of
caustic soda of the strength of 20 grains to the ounce, and boiled for a
few minutes until the mixture becomes clear. The fluid is now allowed
to stand in a conical glass for a few hours, when the elastic fibres fall to
the bottom. A drop of the sediment is then withdrawn with a pipette
and examined for elastic tissue under a low power (90 to 100). It is
important not to continue the boiling too long, as the elastic fibres them-
selves ultimately become much altered.
Microbes — Tubercle bacillus. — The sputum voided in the early morning
PHTHISIS PULMONALIS
195
should, if possible, be chosen for investigation, as it contains no particles
of food, and as, being composed of the secretions accumulated during the
hours of sleep, it represents a mixture
of the products of the various sections
of the respiratory tract. The ex-
pectoration is poured out into a fiat
glass dish, and examined against a
dark background. The small opaque
specks and streaks, or, where the
sputum is uniformly opaque, the most
curdy portions, are the most suitable
for examination. A small portion
should be removed with a scalpel,
needle, or platinum wire and transferred
to a perfectly clean cover-glass. A
second cover-glass is pressed gently on
the first, so as to distribute the sputum
in as thin a layer as possible ; and
the two glasses are then separated by
a sliding movement and allowed to
dry. When quite dry, the cover-slips
are seized with a forceps and passed
three times quickly through the ilame
of a Bunsen. burner or of a spirit-lamp
to coagulate the albumin. Various
methods are in use for staining
the bacillus. Ziehl's modification of
Ehrlich's method gives excellent results and will alone be described. The
following reagents are required : — (a) Ziehl's solution of carbol-fuchsine,
consisting of 10 c.c. of a saturated alcoholic solution of fuchsine, added to
90 c.c. of a 5 per cent watery solution of carbolic acid. (J) A 25 per
cent solution of sulphuric acid, (c) A concentrated aqueous solution of
methylene blue. The staining fluids should be filtered before they are
used. The cover-glasses are placed in some of the fuchsine solution (a)
in a watch-glass or porcelain dish, which is then heated carefully over a
spirit-lamp or a sand-bath until bubbles are given off. The staining fluid
is then set aside for two or three minutes to cool. Next, the cover-glasses
are removed with forceps and passed through some of the acid solution
(J) for a few seconds, until the red colour changes to a yellowish gray.
The preparations are then washed in a gentle stream of water running
from a tap for eight or ten seconds, when the sputum again turns red.
Lastly, the slips are stained with a drop of the blue dye (c) for half a
minute to a minute, washed again in a stream of water for a few seconds,
and the excess of water allowed to drain away. The cover-glasses may
now be left to dry ; or rapid drying may be effected by pressing them
gently between two pieces of clean blotting-paper. When they are quite
dry the preparations are mounted in a drop of Canada balsam, dissolved
Fig. 10. — Elastic tissue from the lung, with
well-marked aveolar arrangement. Per-
pared from sputum by Fenwick's method.
(Low power.)
196 SYSTEM OF MEDICINE
in xylol or benzol. If the illumination be good, the tubercle bacilli can be
recognised with a magnifying power of 300 ; but in order to obtain
satisfactory results it is well to use Abba's substage condenser and a one-
twelfth oil immersion lens.
With the above mode of staining the tubercle bacilli appear as deli-
cate rods of a red colour, in length from a quarter to a half the diameter
of a red blood corpuscle, often straight or slightly curved, and in many
cases presenting a finely-beaded appearance. This beading, supposed by
some to depend upon the presence of spores, possesses no special clinical
significance. The number of bacilli in the sputum is very variable.
They may be scattered singly through the preparation, or they may be
found in groups. In some instances the sputum seems to be an almost
pure cultivation of the bacilli. Many other microbes, pyogenetic and
putrefactive, the nuclei of pus and epithelial cells and threads of mucin
are stained blue by this process, but no definite importance can at present
be assigned to any microbe but the tubercle bacillus. The detection of
tubercle bacilli in the sputum is a certain sign of tuberculosis of some
part of the respiratory tract.
Instances of primary tuberculous ulceration of the larynx or pharynx
are infinitely rare, but the number of bacilli shed from the surface of
such ulcers is insignificant when compared with the enormous masses
discharged from cavities in the lung. When the sputum contains a large
number of bacilli we may reckon on the existence of a vomica, whether
large or small.
Hmmoptysis is one of the most striking symptoms of the disease.
Streaks of blood may be seen in the expectoration of many other affec-
tions, and are the result of capillary hsemorrhage from the lungs or air-
passages : such streaks are seldom of much importance ; nevertheless,
they occasionally herald the approach of a more profuse hsemorrhage.
When the amount of blood brought up is considerable, the significance is
far greater.
Hsemorrhage from the lungs may occur as the result of hypersemia
and rupture of capillaries, or of gross pulmonary lesions involving per-
foration of vessels of considerable size. Slight attacks of hsemoptysis are
mainly due to capillary hsemorrhage from the lungs, less frequently from
the large air-passages, and are indicative of inflammatory or congestive
states. When, however, the blood expectorated can be measured by
ounces, the bleeding must be attributed to rupture of an artery or vein of
some size. Perforation of vessels, generally of an artery, may be effected
in three ways : — (a) The walls of the small pulmonary arteries and veins
may become infiltrated with a tuberculous growth. The usual consequence
■of this change is thrombosis of the affected vessel ; but in the case of the
arteries, softening of the vascular wall may lead to rupture, and some of
the small haemorrhages of phthisis are probably thus produced. (/3) The
ulcerative process associated with excavation of the lung may perforate
an artery of considerable size, and occasion alarming hsemorrhage. It
soems strange, at first sight, that this does not happen more often ; but
PHTHISIS PULMONALIS 197
the tendency in all but the more rapid forms of tuberculous destniction
is towards thrombosis of vessels. This is a more important cause of
haemoptysis than the preceding, but it is very much less common than
the next (y), namely, rupture of an aneurysm in a cavity in the lung :
this is by far the most common cause of profuse hsemorrhage.
Haemoptysis may prove directly fatal from cerebral anaemia, though a
termination by syncope is uncommon. The usual cause of death is
asphyxia, which results from flooding of the bronchia with the effused
blood. Ruptured aneurysms may become closed by thrombosis and the
patient recover. There is every reason to believe that most cases of pro-
fuse haemoptysis which 'end in recovery are due to the rupture of an
aneurysm, and that ulceration of large vessels is a much less frequent
cause.
The old view that the extravasation of blood can set up inflamma-
tory and destructive changes in the lung — " phthisis ab h^moptoe " — is
no longer entertained.
One of the points adduced by Memeyer in support of this notion,
namely, that pyrexia often appears a few days after the haemorrhage, is
more easily explained by the aspiration of infective cavity secretions,
mixed with blood, into other parts of the lung, leading to tuberculous
broncho-pneumonia. An attack of haemoptysis is occasionally determined
by some obvious cause of vascular excitement, such as mental agitation,
muscular exertion, straining at stool, or menstruation; but more often
the patient suddenly begins to cough up blood without any warning,
often while in bed. Haemoptysis is generally repeated frequently, and
may last for hours or days with intermissions. The blood expec-
torated is generally bright and frothy; but when it has gathered
slowly in cavities or in the bronchial tubes it may be dark and clotted.
The quantity lost varies considerably ; as much as two or three pints
may be brought up in a short time. When the flow is not excessive
the blood is often mixed with sputum, a point of considerable diagnostic
importance ; and in most cases expectoration of blood-stained secretion
continues for a day or two after all active haemorrhage has ceased. The
bleeding may manifest a marked tendency to recur at intervals for some
time ; in such cases the rent in the walls of the aneurysm has undergone
only partial repair, and leaking goes on from time to time. The patient
is almost always greatly alarmed by the supervention of haemorrhage.
The face is pale and bedewed with sweat, the extremities cold, and the
pulse is feeble ; the bodily temperature sinks below the normal. Blood is
brought up with a frequent short cough, and is often swallowed. "When
the haemorrhage is arrested the temperature returns to the normal range,
and on the third or fourth day may rise three or four degrees. After the
attack, patients are much exhausted and depressed ; partly in consequence
of the loss of blood, but still more as the result of nervous shock.
Some patients show no serious deterioration of health after the
immediate debilitating effects of the haemorrhage have passed away ; but
in not a few instances, under the influence of repeated attacks of haemo-
igS SYSTEM OF MEDICINE
ptysis, chronic disease assumes a subacute, progressive character, a result
attributable to the violent inspiratory efforts provoked by the presence of
blood in the bronchia and the consequent insufflation of infective secretion
into healthy lung.
Some vrriters have described a special variety of phthisis under the
name " hsemorrhagic," but there does not appear to be any sufficient
reason for the subdivision. Cases beginning with a sudden haemoptysis,
repeated, perhaps, at intervals for a considerable time, may subsequently
run the ordinary course of chronic phthisis without any further haemor-
rhage. Other patients presenting the usual form of disease may succumb
after a succession of attacks ; or their first hseraorrhage may prove fatal.
Haemorrhage is an accident which may complicate any case of the disease,
and is not a satisfactory basis for classification.
Dyspncea. — A subjective sense of dyspnoea is seldom complained of,
save in the later stages of the disease ; though most patients with pro-
gressive phthisis exhibit increased frequency of respiration, especially on
slight exertion. The rate of respiration rises slightly in the evening.
The absence of dyspncea is explained by the tolerance acquired during
the slow, insidious progress of the pulmonary affection, and also, as has
been suggested, by the low standard of respiratory requirement due to
the reduced volume of blood.
When chronic lesions are complicated by acute tuberculosis, especially
in its miliary form, and when pneumothorax occurs, urgent dyspncea
may arise.
Pain in the chest. — Many patients have pain in the chest, mostly in
the axillary or mammary regions, varying in degree from a slight aching
sensation to the agonising stitch of pleurisy. Severe pain is nearly
always referable to the implication of the pleura, in which case tenderness
to percussion is often met with. Vague rheumatoid pains in the chest
have been regarded as very significant ; but in the absence of other
symptoms more directly pointing to the lungs, little importance can he
attached to them. They are, not infrequently, of muscular origin, and
may be attributed to the violence of the cough. Dragging pain over
chronic cavities, associated with retraction of the chest wall, is sometimes
a persistent symptom depending on stretching of the adjacent pleura and
intercostal nerves. The muscles of the chest wall in some cachectic
patients are extremely tender to percussion, and the slightest tap may
promote muscular contraction ; but this increased excitability of the
muscles is not peculiar to the disease.
General symptoms. — Pyrexia is a symptom hardly less significant, from
the point of view of diagnosis, than cough ; and of infinitely more value
as a measure of the activity of the disease. The cause of the elevation
of temperature must be ascribed to the presence in the blood of some
soluble poison produced by the bacillus. It is generally agreed that the
pyrexia of tuberculosis attains its maximum, and may often be exclusively
present, in the post-meridian hours of the day. A slight evening rise of
temperature may be one of the earliest symptoms. Some observers have
PHTHISIS PULMONALIS 199
noted a persistently subnormal temperature as the first definite indication
of the disease. Accordingly careful thermometric observations, night and
morning, should be made in all cases of obscure ill-health, especially in
young persons.
The onset of fever is sometimes accompanied by slight shivering, but
a marked rigor is seldom observed except in acute cases. The maximum
temperature is found from 2 to 10 p.m., and the minimum from 2 to 8
A.M. In exceptional cases the order is reversed, the morning tempera-
ture being higher than the evening — the " inverse type." This may be
only temporary, or the same relation may be preserved throughout the
vrhole course of the case.
Two main forms of pyrexia may be distinguished, the intermittent
and the remittent. One or other form may predominate or prevail
exclusively for weeks or months, but various combinations are apt to
arise ; in fact, one of the characteristics of tuberculous fever is its
fluctuating and irregular course.
In the first or intermittent type the temperature is normal or slightly
subnormal in the morning, and reaches 100° to 103° F. in the evening.
In the higher grades of this form the fall is still more pronounced, and
may amount to 7° or 8° F., the thermometer sometimes registering a
temperature as low as 94° or 95° F. The second or remittent type
shows a maximum temperature of 103° to 104° F., the minimum tem-
perature being 2° to 3° lower, but not reaching the normal level. A
slight degree of intermittent fever, where the maximum, for the most
part, does not exceed 101° to 102° F., is often found in the early phases
of the complaint ; but a similar temperature curve may be recorded at
any stage. When the range of temperature is greater, and more particu-
larly when the morning reading is below normal, profuse sweating is
very common, and the resemblance to the hectic fever of pyaemia is very
close. The remittent form of fever commonly betokens active tuber-
culous infiltration, and is more often met with in the acute varieties
of tuberculosis, but may also appear temporarily in chronic phthisis as
the result of acute exacerbations or of intercurrent disease. In acute
miliary tuberculosis, uncomplicated by suppuration in the lung or else-
where, the type of fever is generally remittent, a fact which would point
to this being the form of pyrexia peculiar to tuberculosis.
Pulmonary phthisis never runs its whole course without fever, but in
many chronic cases there may be no appreciable rise of temperature for
long periods of time. Observations by Dr. 0. T. Williams have shown
that pyrexia may be absent even when the disease is making rapid pro-
gress. But this is a very unusual course, and it may be stated as a
general principle that activity of the disease is indicated more surely by
pyrexia than by any other symptom or sign.
A high evening temperature vrith a markedly subnormal morning
temperature (95° to 97°) is a common feature of advanced and progres-
sive disease, though in such cases the fever may assume the remittent
type at any time. Towards the close of life the temperature generally
SYSTEM OF MEDICINE
tends to fall. The very low temperature registered in pneumothorax, in
some cases of excessive pulmonary haemorrhage, and in the comparatively
rare instances where perforation of the intestine occurs, must be attri-
buted to the effects of shock. When we consider the various processes
of infiltration, necrosis and suppuration occurring in the lungs, as well
as the numerous complications that may arise, we cannot be surprised at
the great variations exhibited by the temperature chart.
It is necessary to mention the assertion of Peter, that the temperature
of the skin differs on the two sides of the thorax, the higher reading
being found on the side corresponding to the lung more affected. Most
observers have failed to verify this statement, and a similar want of
symmetry in the temperature of the two armpits has occasionally been
observed in other conditions.
Sweats. — Profuse perspiration is a common symptom in pyrexia!
cases, though it has no constant relation to the fever. Sweating is most
pronounced in the early hours of the morning, when the temperature of
the body is at its lowest ; but it also occurs sometimes while the fever is
continuously high. Night sweats may occasionally occur in apyrexial
periods, in which case they seem to be due to fits of coughing.
Dr. Lauder Brunton has suggested that sweating is the result of
exhaustion of the respiratory centre in the medulla, and consequent
accumulation of carbonic acid in the blood ; the effect of this being to
stimulate the sweat centres. This symptom is certainly more prevalent
in advanced cases, associated with excavation and suppuration of the
lung ; but it is not uncommon in early and circumscribed disease, in
which case Brunton's hypothesis seems less applicable.
Emaciation is one of the most frequent and important symptoms, and
may proceed to an extreme scarcely reached in any other disease ; hence
the names phthisis and consumption.
The greatest loss of weight is witnessed in chronic cases, but although
sometimes at first comparatively slight in the acute type which termin-
ates in a few months, it is never absent altogether. Wasting affects all
the soft parts, but especially the fatty and muscular tissues. It has
been said that the liver does not share in the general wasting, but this
statement is probably to be explained by the great liability of the liver
to congestion and to fatty and amyloid degenerations, conditions which
involve enlargement of the organ. The loss of flesh is mainly, though
not exclusively, due to the increased metabolism inseparable from the
febrile process. Patients with a high temperature lose weight as long
as the fever continues ; and, as a rule, when the heat of the body becomes
normal, wasting ceases. Moreover, a certain correspondence between the
degree of the fever and the loss of weight can often be recognised. At
the same time a considerable degree of fever is not incompatible with an
actual increase in weight, if an adequate supply of food can be taken,
and if digestion and absorption be unimpaired. In apyrexial cases the
weight of the body may remain stationary for months, or even years;
but when pyrexia appears, loss of flesh soon follows.
PHTHISIS PULMONALIS
The early emaciation, which not uncommonly precedes any appreci-
able rise of temperature or other signs of disease, cannot be thus
explained. In the absence of any definite knowledge on this point we
may adopt the provisional hypothesis that the toxins of tuberculosis
may cause a general failure of nutrition apart from any febrile move-
ment. Functional derangements of the stomach and diarrhoea, by their
interference with digestion and assimilation, are potent causes of wasting.
Debility. — A sense of weakness and loss of energy, both of mind and
body, are commonly felt at a very early date, and not infrequently
appear to be out of all proportion to the extent of the disease.
Anmmia. — In certain patients the complexion acquires a peculiar
faded yellowish tint, which has been well likened to a dead leaf. On
examination the blood shows the changes of chlorosis — a considerable
reduction of the haemoglobin with a relatively slight diminution in the
number of the red corpuscles, and also a diminution in mass. In active .
pyrexial disease a moderate degree of leucocytosis is common.
The pulse in all progressive cases is rapid and of low pressure ; some-
times it is full, but more often small. The frequency of the heart's
action is not invariably determined by the degree of fev-er, but seems
rather to stand in direct relation to the extent and activity of the disease,
and to the strength of the patient; consequently the pulse is a most
valuable index of the gravity of the case. The pulse is generally some-
what more frequent in the evening, but exceptions to this rule are met
with. Some authors have regarded a persistent rapidity or ready excite-
ment of the heart as important premonitory symptoms ; and there is no
doubt that cardiac erethism is often present at a very early stage of the
disease.
Cyanosis is seldom a marked symptom, except as the result of serious
pulmonary or cardiac complications, though the fingers, toes, lips, ears
and nose often present a slightly dusky or livid hue, in marked contrast
to the general pallor. Coldness of the extremities and extreme sensitive-
ness to trifling depressions of temperature are a common complaint, and
further testify to the feebleness of the circulation.
Skin and hair. — In connection with the subject of nutrition reference
must be made to the state of the skin and hair. The skin of tuberculous
patients is generally very oily, and the sweat has a peculiarly pungent
garlicky odour. In some emaciated subjects, on the contrary, a dry
branny condition, "pityriasis tabescentium," may be observed. The
texture of the skin in one type of patients is delicate and thin, and the
complexion transparent ; while in another class the skin is coarse and the
complexion dull and muddy, — distinctions which are included in Sir
William Jenner's classical description of the tuberculous and scrofulous dia-
theses respectively. But in the majority of phthisical persons no such
peculiarity can be recognised, though in all cases of long standing some
degree of pallor is wont to appear. Pigmentation of the skin may become
so marked in certain chronic cases that Addison's disease may be simulated ;
but the patchy pigmentation of the tongue and buccal mucous membrane.
SYSTEM OF MEDICINE
SO characteristic of the latter affection, does not occur. The cause of this
pigmentation is unknown. " Pityriasis versicolor " is observed rather fre-
quently on the chest and back, but no special significance can be assigned to
this parasitic complaint. Lupus is only occasionally found in phthisical
patients. The terminal phalanges of the fingers and toes frequently show a
curious bulbous enlargement associated with incurvation of the nails ; the
swelling is believed to be due to thickening of the subcutaneous tissue, but
it is possible that the bony structures may also be involved. This clubbing
of the fingers and toes is not peculiar to tuberculosis, and it is found in
empyema, in chronic pneumonia, in certain forms of heart disease, and in
emphysema — conditions in which impediment of the pulmonary circulation
and consequent engorgement of the systemic veins are a common factor.
The hair, participating in the general malnutrition, may become thin
and straight ; but this change is by no means constant, as in some persons
the hair of the head and beard remains very thick, and the trunk may be
unusually hirsute. In children and young persons the body is sometimes
covered with a growth of fine downy hair.
Physical diagnosis. — Certain abnormal forms of chest are met with
in many phthisical subjects. Two special varieties may be mentioned on
account of the frequency with which- they occur. In the first, named
alar or pterygoid by Galen and Aretaeus and in our own day by Dr.
Gee, the angles of the scapulae project like wings, the ribs are unduly
oblique, the shoulders fall, and the length of the thorax from above
downwards is increased, but the antero-posterior diameter is small. In
the second or flat type the chest in front is flat instead of being rounded,
and the sternum may even be depressed below the level of the costal
cartilages, which lose their curve and become straight. These peculiari-
ties are certainly common in tuberculous persons, but they are frequently
met with also in persons who remain free from the disease. Moreover
many phthisical persons have large and well-formed chests. It cannot
be said, in other words, that there is any type of thorax peculiar to
phthisis, although the chest, in common with the muscles and bones, is
often ill developed. Much more importance is to be attributed to
partial deformities of the chest walls, the result of pulmonary disease.
Before discussing the' physical diagnosis of the disease in its early
stages, it may be well to recall briefly a few anatomical facts. The
initial lesion consists of a small nodule or group of nodules situated
somewhat below the extreme apex of the lung. The nodule is broncho-
pneumonic ; that is, it consists of a localised bronchitis with surrounding
lobular consolidation. The neighbouring parts of the lung at first
remain spongy and practically unaltered, so that the nodule is enclosed
in a shell of healthy pulmonary tissue.
Physical examination of the lungs at this period may yield a com-
pletely negative result, especially wheh the focus of disease is small, and
the layer of spongy lung around is fairly thick. As long as the surround-
ing lung is crepitant, percussion gives no dulness. The earliest signs are
almost exclusively discovered by auscultation, though at times, on
PHTHISIS PULMONALIS 203
inspection and palpation, a slight diminution of respiratory movement
may be recognised in the subclavian region. Owing to the persistency
of the apical catarrh, and to the consequent lobular collapse, the entry of
air into the corresponding section of lung is diminished, and the breath-
sounds become weakened. Jerky, interrupted, or wavy breathing — the
" respiration saccadic " of the French — is not very uncommon, but is not
pathognomonic, and may often be heard in neurotic or hysterical, or even
in healthy persons. Weakness of breathing at the affected apex is
often associated with increased loudness of the vesicular murmur on
the opposite side — a condition known as compensatory or puerile breath-
ing, which is sometimes erroneously regarded as an indication of disease.
Another important and early sign is furnished by harshness of the
breath-sounds affecting the expiratory sound to a greater degree, and at
an earlier date than the inspiratory. The expiratory murmur at the
same time acquires a higher pitch, and becomes so prolonged as to equal
or exceed the length of the inspiratory sound. This change is an early
indication of consolidation, the character of the breath - sounds being
modified, without having actually attained to the bronchial or tubular
type. It is necessary to distinguish this condition from mere prolonga-
tion of the normal expiratory murmur, which may be the result of
bronchial obstruction, as in bronchitis, emphysema and asthma, and is
then generally associated with a weak vesicular inspiration. At this
period the vocal resonance and tactile fremitus may be slightly increased,
or there may be no recognisable alteration.
It will be convenient at this point to make a passing reference to
what may be called the physiological dissimilarity of the right and left
apices. In the large majority of healthy persons, especially in thin sub-
jects, the breath-sounds are louder, the expiratory murmur more audible
and prolonged, and the vocal resonance and fremitus more pronounced
at the right than at the left apex. Occasionally the breathing may even
be tubular at the extreme right apex. This difference probably depends
upon the following facts : the right main bronchus is slightly wider and
more vertical in direction than the left ; the bronchus to the upper lobe
is given off higher up, that is, nearer to the trachea; and the apex of
the lung lies slightly closer to the trachea on the right side. The
general effect of these conditions is to favour the conduction of the
glottic sounds to the right apex. Accordingly we must bear this in
mind in estimating the importance of any slight want of symmetry of
the auscultatory signs at the apices.
In some instances a slight impairment of the inspiratory expansion of
the affected apex and some flattening below the clavicle may be the only
physical indications of disease. The want of mobility may be recognised
by inspection, but is more easily detected by palpation ; the hands of the
observer being placed on the subclavian region on each side, and the
patient directed to breathe deeply meanwhile. At this time also fine
crackling or subcrepitant rales may be heard over the affected area.
These rales, which are less fine than the true crepitant rale of Laennec,
204 SYSTEM OF MEDICINE
are mostly heard during inspiration, and are probably caused by the
separation of the moist surfaces of the small bronchi. In some cases
where the bronchial obstruction is more pronounced no adventitious
sounds are audible during ordinary respiration, but when the patient
coughs, a shower of crackling riles is produced by the explosive separation
of the swollen bronchial walls. At times subcrepitant riles can only be
elicited during the deep inspiration that follows cough.
Persistent rhonchi at one apex may sometimes be the only adven-
titious sounds. A systolic murmur, heard beneath the clavicle, was
thought to indicate consolidation of the apex of the lung, and was attri-
buted to the effects of pressure of the infiltrated lung on the subclavian
artery ; or, with greater probability, to contraction of the thickened
pleura at the apex. Similar murmurs may be heard in anaemic and
other persons, and are not any certain guide to disease of the lungs.
Thus far physical signs give evidence of bronchitis confined to the apex
of the lung, the character of the breath -sounds possibly suggesting the
existence of a small patch of consolidation surrounded by spongy lung.
As the infiltration is often massed at several centres, islets of spongy
tissue separate the individual nodules, and for a time mask to a great
extent the signs of consolidation. Thus when the lobules around the
tuberculous patches are hyper-inflated the percussion may be slightly
higher pitched than normal, tympanitic, or even hyper-resonant.
As the disease extends, the lung becomes more airless, and adhesive
pleurisy is set up. The inspiratory expansion becomes decidedly
restricted, vocal fremitus is increased, and the percussion resonance
xmdergoes progressive impairment. The breath -sounds assume a more
definitely tubular or cavernous quality ; bronchophony or pectoriloquy
appears, and the riles become larger and more ringing or metallic. This
complete assemblage of signs is by no means generally, or indeed often
presented, except in fairly advanced cases. Tubular breathing may
appear at a comparatively early period, but this is unusual; and with
marked dulness, bronchophony, and coarse crackling rales, the respira-
tory murmur may remain simply weakened with slight prolongation of
expiration.
The comparatively late appearance of tubular breathing is mainly due
to the obstruction of the bronchi, which is so generally present, and to
the irregular composite nature of tuberculous consolidation.
Dulness appears first at the supraclavicular and supraspinous fossse,
and thence extends downwards over the front of the chest. For the
recognition of slight degrees of dulness light percussion and careful atten-
tion to the sense of resistance are required. Increased conduction of the
heart's, sounds to the corresponding apex generally accompanies and
sometimes precedes loss of resonance to percussion. Increasing size of
the riles, with a sharply conducted or ringing character, is generally
described as marking the presence of softening ; but the same signs may
be furnished by profusely secreting bronchi of considerable size situated
in solid lung.
PHTHISIS PULMONALIS 205
Ehonchi of a croaking or metallic quality are not uncommon at this
period, this peculiarity being imparted to them by the adjacent solid lung
or cavities. Dulness gradually extends over a considerable portion of
the upper lobe, and rtlles become audible at the apex of the opposite
lung, and at the infraspinous fossa on the same side ; that is, at the apex
of the lower lobe.
The date at which signs of excavation can be recognised varies greatly.
In some cases a cavity may be detected almost as soon as consolidation
can be diagnosed, whereas in others it may be months or even years
before this is possible.
S«(/MS of excavation. — Over a cavity of considerable size the percussion
is generally more or less impaired, and it may be markedly dull in con-
sequence of the surrounding infiltration and of the pleuritic thickening
which so often coexist. As excavation proceeds, the dulness may
diminish. The resonance is often of tympanitic, tubular, or amphoric
quality, as well as slightly dull, resembling the note produced by per-
cussion of the trachea in the neck. Percussion may elicit the cracked
pot sound where a cavity communicates freely with the bronchus, and its
walls are suflSciently elastic. This sign is not pathognomonic of a cavity,
as it may often be obtained by percussing the chest of a healthy infant
while crying, and is sometimes found in. cases of pneumonia and pleural
effusion. The bell sound — "bruit d'airain" — is occasionally heard over
large cavities.
According to Wintrich, the pitch of the tympanitic percussion sound
over a cavity becomes raised when the patient opens his mouth. An
alteration of pitch may sometimes be recognised when the patient changes
from the sitting to the lying position, or conversely (Gerhardt) ; but
these changes are seldom pronounced, and give little practical assistance.
It is, however, to auscultation that we must mainly trust for the diagnosis
of pulmonary excavation. In well-marked cases the breath-sounds are
tubular or cavernous — the term " tubular " is used here as synonymous
with "bronchial."
Some writers maintain that there is no difference between tubular
and cavernous breathing, unless it be in the greater intensity and hollow-
ness of the latter. Flint makes the relative pitch of the inspiratory and
expiratory sounds the basis of distinction. According to this author,
cavernous breathing is generally of lower pitch than tubular, and the
expiratory sound is of lower pitch than the inspiratory ; whereas the
pitch of tubular breathing is generally higher than that of cavernous
respiration, and expiration is higher pitched than inspiration.
The breath-sounds over a cavity may be very weak, or even absent
when- the bronchial opening is small or obstructed i'n any way, as by pro-
fuse secretion or by cicatricial contraction. If the vomica be separated
from the chest wall by a zone of spongy lung the respiration may be
simply blowing, with prolonged expiration.
The " metamorphosing " breathing of Seitz consists of an inspiratory
sound, harsh or rough at its commencement, becoming hollow or tubular
2o6 SYSTEM OF MEDICINE
towards the end of the act of inspiration. This sound is supposed to be
due to the removal of a partial obstruction of a bronchus as inspiration
proceeds. It is not a common sign, and it is not certain that it is
exclusively a cavernous sign. Amphoric breathing is pathognomonic of
a large air-containing cavity with smooth walls. Large gurgling rSles
are often heard where cavities contain abundant secretion, and this may
be the only auscultatory evidence available at times. Wnen such sounds
are audible in regions like the apex, which contains no bronchi of large
size, they are very significant of cavities. Auscultation of the cough
gives valuable, perhaps the most valuable, evidence of excavation. In a
cavity containing fluid and air the agitation produced by cough often
gives rise to rales of a splashing character, resembling on a small scale
the succussion sound of pneumothorax. Bales of this description are
very suggestive of a cavernous origin. A metallic or amphoric echo of
the cough is less common but is quite characteristic.
PosWussic suction is another highly significant sign ; it consists of
a high-pitched, sucking, inspiratory sound, immediately following the
forced expiration of cough, and is due to the elastic recoil of the cavity
walls. This has been well named the "india-rubber ball soimd" by
Dr. Mitchell Bruce.
Metallic tinkling is occasionally heard over large smooth-walled
cavities. The vocal resonance is generally increased, bronchophony
or pectoriloquy being very common ; but the latter is not so decisive a
test of excavation as is generally believed. In rare cases an amphoric
quality is imparted to the voice when other metallic phenomena are
present. In some cavities, where the breath - sounds are feeble, the
resonance of the -voice may be diminished, especially if the bronchus be
obstructed. Cardiopulmonary systolic murmurs are sometiines heard
over large thin-walled superficial cavities lying close to the heart, mostly
in the left upper lobe. These murmurs are caused by expulsion of air from
the cavity through a bronchus by the impact of the heart on the lung.
Similar oardio-pulmonary murmurs may be occasioned in the absence
of any cavity in the lung, if the heart's action be much excited. In cases
of contractile disease of the left upper lobe, a systolic murmur is not
uncommonly audible in the second left interspace close to the sternum,
the bruit being due to traction of 'the lung on the pulmonary artery.
In one case of this sort there was also a marked systolic thrill in this
region, which suggested the possibility of stenosis of the pulmonary
artery ; but an autopsy showed that it was due simply to contracting
lung.
A few instances have been recorded in which a systolic murmur was
produced by an unsupported and dilated branch of the pulmonary artery
crossing a cavity. It should be mentioned that the chest wall may be
markedly retracted over the site of a chronic contracting cavity.
Some writers, following Sir Andrew Clark, recognise "fibroid
phthisis " as a peculiar variety. Most of these cases are but pulmonary
tuberculosis in a very chronic form. There is little in the physical
PHTHISIS PULMONALIS 207
signs to distinguish them from non-tuberculous chronic pneumonia, except
that in the former the disease is nearly always most pronounced in the
upper lobe, and the apex of the other lung is often involved. In the
fibroid or contractile form of pulmonary tuberculosis, signs of excavation
are generally to be recognised at one apex, associated with much dulness
over the upper lobe or over the whole lung, together with displacement
of neighbouring organs. When the left lung is affected the heart is
drawn outwards and upwards, and pulsation may be felt as high' as the
second rib or clavicle; or the apex beat may be discovered in the
axilla. In such cases the shock of the second sound may often be
recognised in the upper intercostal spaces by palpation. In two of the
most extreme instances of displacement of the heart in this disease I
found the heart beating under the angle of the left scapula.
When the right lung is contracted the heart is drawn over and may
lie wholly to the right of the middle Hne, the pulsation sometimes
reaching as far out as the right axilla. The diaphragm and abdominal
viscera are raised by the contracting lung, especially when the upper lobe
is principally involved. On the left side the tympanitic resonance of the
stomach may extend as high as the fourth or fifth rib. In extreme con-
tractile cases the opposite lung is always considerably enlarged, and may
pass beyond the middle line of the sternum into the opposite half of the
thoracic cavity. It is often extremely difficult to detect any signs of
disease in a lung thus distended, though a post-mortem examination in
these circumstances will nearly always reveal the existence of deeply-
seated tuberculous lesions. The fact cannot be too strongly insisted upon,
that in the presence of distension or emphysema of the lung extensive
foci of disease may escape recognition altogether.
Ippegular forms. — It seems advisable, at this point, to make a few
remarks concerning the physical diagnosis of certain irregular forms of
the disease.
Emphysematous form. — In this variety the history as well as the
physical signs are those of bronchitis and emphysema. In addition to
hyper-resonance on percussion, together with weak inspiratory and pro-
longed expiratory murmurs, careful percussion will sometimes elicit slight
comparative dulness at one supraspinous fossa, and perhaps above the
clavicle. There may be no further deviation from the normal type of
emphysema. In other cases, on coughing, a few muffled rales may be
audible at one apex. If, as often happens, diffused rhonchi are also
present, the difficulties of diagnosis are much increased. The shape of
the chest is often flat instead of being rounded, a matter of some
importance. In emphysematous people with such a formation of thorax,
especially if there be much wasting or if haemoptysis have occurred at
any time, the possibility of tuberculosis should be carefully considered,
and the' sputum should be repeatedly examined for tubercle bacilli.
Pleuritic form. — Reference has already been made to the onset of
pulmonary tuberculosis with symptoms of pleurisy. Signs of fluid
effusion, thickened pleura, or dry pleurisy in one axilla or at the base,
2o8 SYSTEM OF MEDICINE
may be the only recognisable signs. It is of the utmost importance in
all cases of pleurisy to keep in mind the close relation of this aifection to
tuberculosis. Double' pleurisy, whether there be eifusion of fluid or not,
is nearly always tuberculous — the principal affections that have to be
excluded being renal disease, acute rheumatism, and intra - thoracic
growths. Where a large effusion occupies the whole of one pleural
cavity, no evidence of tuberculosis can be obtained from physical ex-
amination of the affected side.
At times rales or other morbid signs may be detected at the apex of
the other lung, but too much importance must not be attributed to such a
discovery, as in cases of this description the unaffected lung is often the
seat of compensatory hyperaemia and oedema. Similar evidence of
apical disease in cases of basic dry pleurisy, on the contrary, has a very
definite and positive value. But the sputum may be the only trustworthy
evidence of the tuberculous nature of the complaint.
It is commonly said that an insidious onset characterises tuberculous
pleurisy, Avhereas an acute invasion is more suggestive of the simple
idiopBjthic variety. No reliance can be placed on such statements.
Tuberculous pleurisy may commence in the most acute manner ; and a
chronic insidious onset is not rarely witnessed in cases of a comparatively
harmless nature. In any case of pleurisy, marked wasting, or a history
of haemoptysis, should arouse suspicion.
Anomalous distribution of physical signs. — When signs of infiltration or
excavation are confined to one base, or predominate there, an accurate
diagnosis may be very difficult, in view of the extreme rarity of primary
tuberculosis of this part. The fact that physical signs of disease are
confined to or predominate at the base, by no means proves that there is
not, at the same time, older disease of the apex of the upper lobe, a point
which I have several times established on post-mortem examination.
This depends on the fact that when the lesions are covered by a shell of
healthy lung considerable masses of tuberculous disease, or even cavities,
may exist towards the central part of the upper lobe without giving any
evidence of their presence.
Disease confined to the base of one lung in most cases is not tuber-
culous, and we have, in such instances, to exclude various affections, the
most important of which I may here enumerate : — chronic pneumonia
with or without bronchial dilatation, localised pleurisy, abscess of the
liver, new growths, hydatid cysts of the lung or liver, and hypophrenic
abscess. Examination of the sputum is of the utmost value under such
circumstances.
It is well, at the same time, to remember that these diseases may be
complicated by a secondary tuberculosis, and the discovery of tubercle
bacilli may divert attention from the primary affection. Chronic con-
tracting lesions of the apex of the upper lobe, particularly on the right
side, may so uncover the great vessels at the base of the heart as to cause •
pulsation to be felt in the upper intercostal spaces, and thus aneurysm
may be simulated. This is more likolv to occur on the rie;ht side,
PHTHISIS PULMONALIS 209
where, on more than one ■ occasion, I have known the association
of dulness, pulsation, systolic murmur, and accentuated second sound
to give rise to considerable suspicion of aortic aneurysm in middle-
aged men.
Larynigeal form. — ^Where laryngeal obstruction exists the entry of air
into the lung may be so greatly diminished that auscultation may give
no trustworthy indications of the actual condition of the lungs. The
amount of pulmonary disease, without any corresponding auscultatory
signs, which may exist under such circumstances is surprising, and can
only be appreciated by those who have been able to compare the post>
mortem appearances with the results of physical examination during the
patient's life. Percussion sometimes gives more valuable assistance than
auscultation ; but the most certain information is often afforded by the
sputum test.
Diagnosis. — The diagnosis rests, in the first place, on the presence
of chronic disease of the lung, affecting mainly or exclusively the apex of
the upper lobe. Signs of persistent catarrh, consolidation, or excavation
of this part are, for practical purposes, conclusive evidence of tuberculous
disease.
The existence of tubercle bacilli in the sputum is an absolute proof of
tuberculosis of some part of the respiratory tract. In the absence of
tuberculous ulceration of the larynx, pharynx, or oral cavity, the lung
may be regarded as the source of the bacilli, even if auscultation and
percussion give no indication of any pulmonary lesion, or if physical signs
of disease be found in aberrant situations.
Most writers consider the subject of physical diagnosis under three
stages — the first, second and third stages of phthisis. Such a division of
the subject implies that physical examination may be trusted to decide
at which of these stages the disease has arrived — an assumption by no
means warranted by the facts. As a description of the history of
individual tuberculous foci, there is not much fault to be found with the
time-honoured division into three stages of consolidation, softening, and
excavation ; but these distinctions are, to some extent, misleading. In
the first place, as soon as the stage of softening is reached excavation has
begun ; in other words, the two processes are, more or less, concomitant ;
moreover, the rule is to find in the same lung — often in close proximity
— solid nodules, softening caseous masses and fully formed cavities : in
other words, all three stages are run simultaneously.
On the clinical side of the question auscultation and percussion enable
us to recognise consolidation with no little accuracy, and in many cases
the existence of a cavity is revealed by certain physical signs ; but there
is no distinctive sign of softening whatever. In the majority of cases,
where, as the result of physical examination, the patient is said to be
suffering from phthisis in the first stage, cavities already exist. This is
frequently proved to demonstration by the detection of elastic tissue and
numerous bacilli in the sputum of cases in which auscultation and percus-
sion point only to catarrh, or to slight consolidation of one apex. It is a
VOL. V P
SYSTEM OF MEDICINE
matter of everyday experience that cavities in the lung may escape detection
during life ; and I have known the most experienced physicians diagnose
excavation where post-mortem examination showed that none existed.
The efiects of this artificial classification on the patient's mind have, in many
instances, been most pernicious. For, knowing that there are three stages,
and hearing that he has a cavity in his lung, he concludes that, as he is in
the last stage, his days are numbered. As a matter of fact, many persons
in whom a cavity can be diagnosed are in a better condition, and have far
more favourable prospects, than others in whom there are only signs of
the first stage. It is time that the three stages were consigned to a well-
merited oblivion. I make these remarks in no wish to detract from the
importance of physical examination ; my object is rather to recognise the
limitations of this valuable method, and to give a caution against the
overweening confidence still reposed by some physicians in auscultation
and percussion, to the exclusion of other means of diagnosis.
The eomplieations.of phthisis are mostly referable to the transmission
of the tubercle bacilli to other parts of the body. In the case of the
pharynx, larynx, and trachea, tuberculous changes are mainly produced
by the direct inoculation of these parts with the sputum which is con-
stantly passing over them. But in secondary tuberculosis of the genito-
urinary, nervous and osseous systems, infection is conveyed by the blood —
the microbes, for the most part, effecting an entrance into the circulation
through branches of the pulmonary veins.
Laryngeal tuberculosis is almost always secondary to the same disease
of the lungs, though in a few well-authenticated cases the limgs have been
found on post-mortem examination to be unaffected. The larynx is very
frequently implicated ; according to my post - mortem statistics this
happened in 50 per cent of all cases of pulmonary tuberculosis. In
many cases the lesions were recent, and were evidently due to late
infection of the larynx. If we exclude all patients in the last stages, it
may be said that laryngeal tuberculosis is clinically recognisable in from
20 to 25 per cent. The lesions consist of infiltration or swelling and
ulceration. The localisation is a matter of great diagnostic importance.
Tuberculous affections show a marked preference for the posterior part
of the larynx, the hinder extremities of the vocal cords, the interary-
tsenoid fold, and the laryngeal surface of the arytaenoid cartilages. The
epiglottis is less frequently implicated, and the ventricular bands are
seldom involved, except in widespread disease of the larynx. The
progress of tuberculosis is slow, contrasting strongly with the relatively
rapid course of tertiary syphilitic ulceration. The early symptoms are
those of chronic laryngitis; hoarseness, tickling, a sense of fatigue on
using the voice, and various other parsesthesise referred to the throat.
Pain on swallowing is a far more important symptom, and is generally
associated with swelling or ulceration of the epiglottis or arytsenoid
regions. Inspiratory stridor and dyspnoea depend for the most part on
massive swelling of the epiglottis and aryepiglottic folds ; but in certain
cases extreme stenosis occurs from mechanical fixation of the cords in the
PHTHISIS PULMONALIS
median position, in consequence of infiltration around the crico-arytsenoid
joints.
In the obstructive form of laryngeal tuberculosis difficulties in
physical examination of the chest frequently arise ; for when the entry
of air into the lungs is much curtailed auscultation may discover nothing
more than weakness of the breath-sounds. Hence the importance of an
accurate laryngoscopic diagnosis, and repeated examination of the sputum
cannot be too strongly insisted upon. For an account of the laryngo-
scopic appearances, and for further details of this important affection, the
reader is referred to the article " Larynx." It should not be forgotten
that aphonia in phthisical persons is not uncommonly the result of
functional paresis of the adductor muscles of the vocal cords. The trachea
is rarely affected except in advanced cases of pulmonary tuberculosis, and
the larynx nearly always shows similar and more extensive disease.
Bronchial glands. — ^The bronchial, mediastinal, and tracheal glands are
very prone to tuberculous disease. In adult cases this adenopathy, as the
French style it, scarcely ever gives rise to definite symptoms or physical
signs. The glands most affected are the anterior or pretracheal,
and the subtraeheal which lie beneath the fork of the trachea. In
children the enlargement of the glands may be so pronounced as to
cause obstruction of the large bronchial tubes, or even of the trachea.
Bronchial obstruction, if pronounced, leads to pulmonary collapse; in
which case dulness on percussion and weakness of the breath-sounds, or
tubular breathing, will be found over the affected area. When the upper
lobe is concerned the similarity to phthisis may be very close. In some
cases the continued absence of adventitious sounds may suggest the
glandular origin of the lesion, as in some cases under my care which
ended in recovery. Dulness and tracheal breathing over the manubrium
may occasionally be found when the pretracheal glands are greatly
enlarged. It is said that dulness may be recognised in the upper inter-
scapular region ; but I have never met with this myself ; and it seems
unlikely that enlarged glands in the fork of the trachea and, therefore,
lying in front of the spine, should occasion dulness in the situation
indicated. The subjects of this complaint sometimes suffer from a
spasmodic cough like whooping-cough, and from attacks of dyspnoea,
attributable to pressure on the vagus trunks.
Compression of the recurrent laryngeal nerve, more particularly on
the left side, may cause paralysis of the corresponding vocal cord.
Perforation of the oesophagus by a suppurating caseous gland, when
the abscess opens into a bronchus, is apt to give rise to septic broncho-
pneumonia, and gangrene of the lung may follow. Rupture of a glandular
abscess into the trachea may cause fatal asphyxia. In many instances
caseous glands undergo calcification, and the disease is thus arrested.
Pneumothorax is one of the most serious and fatal complications,
statistics proving that the patient rarely survives this accident by more
than one month at most ; though exceptions to this rule are to be met
with. It is at first sight remarkable that pneumothorax does not occur
SYSTEM OF MEDICINE
more frequently, considering the tendency of pulmonary cavities to extend
outwards towards the pleura. Dr. Samuel West's experiments enable us
to understand why perforation of the visceral pleura is not necessarily
followed by pneumothorax, even when there are no adhesions. For, as
he shows, before the elastic recoil of the lung can assert itself, the
normal cohesion of the two layers of the pleura must be o.vercome, and
this requires considerable force ; in other words, the force of cohesion
considerably exceeds the elasticity of the lungs. He concludes that
"pneumothorax, in its initial stage, must be an active process. Some
force will be required to overcome the normal cohesion between the two
layers of the pleura, and to separate them. This must be obtained by
expiration, and pneumothorax, therefore, in its initial stage, is an
expiratory process, and not essentially different in its production from
surgical emphysema. As soon, however, as separation has been effected,
the elasticity of the lungs will come into play, and air will enter the
pleura until its retractility is completely satisfied " {vide p. 335).
Inasmuch as perforation of the pleura is always succeeded by inflam-
mation the force of cohesion may soon be supplemented by adhesive
pleurisy, and the entry of air into the pleural sac may be thus prevented.
In cases where the opposite lung is extensively diseased the dyspnoea at
first is very great, and death may occur in a few minutes ; but the
immediate consequences of the perforation are almost invariably recovered
from. Physical examination on the affected side shows absence of move-
ment, increased fulness of the intercostal spaces, diminished tactile
fremitus, and hyper-resonance or tympanitic percussion note. On
auscultation the breath-sounds are absent or feeble — at times amphoric,
and the vocal resonance is diminished ; occasionally amphoric echo of the
voice may be obtained. Percussion by means of coins, or with a
pleximeter and percussion hammer, while the stethoscope or naked ear is
applied to the chest, yields a clear metallic sound, the bell sound, or hruiff
d'airain. Metallic tinkling and amphoric echo of the cough may also be
heard. The hippocratic succussion splash can often be detected when fluid
effusion has occurred, if the ear be placed on the chest and the patient be
shaken sharply. The heart is displaced to the opposite side, except in
the rare instances where it is fixed to the sternum by adhesions, or where
the opposite lung is solidified or completely adherent.
This displacement is not due to the pressure of the pneumothorax as
is commonly assumed; for in such cases, as shown by Sir R. Douglas
Powell, manometric measurements may indicate no positive pressure in
the pleural cavity ; and his experiments have demonstrated that the
dislocation of the heart is due to the unopposed elastic traction of the
sound lung. The diaphragm and the abdominal viscera on the corre-
sponding side, being no longer held up by the elasticity of the lung, sink
downwards. In some cases depression of the liver or spleen may be
detected by palpation. Although effusion nearly always ensues, it may
be difficult to obtain clear evidence of its presence. Sometimes there is
a small area of dulness at the base, shifting, to an unusual degree, with
PHTHISIS PULMONALIS ■ Z13
the position of the patient. In other cases there may be no signs of fluid
except the succussion splash, which, however, is quite decisive. The
absence of dulness is to be explained by collection of the fluid in the
cup-shaped space formed by the depressed diaphragm. In more chronic
pneumothorax a copious exudation may occur, and the air gradually
become absorbed. Under these circumstances there will be marked
dulness and other signs of simple pleural effusion, from which the case
can only be distinguished by the history. The effused fluid is generally
purulent, but may be sero-fibrinous.
Instances of complete recovery after pneumothorax have been re-
corded by many observers. In most of these the perforation of the
pleura occurred without any previous evidence of pulmonary disease ;
and, although it is probable that many of them were tuberculous, this
cannot be stated with certainty. In a much smaller number of cases,
where pneumothorax appeared in the course of manifest pulmonary
disease, life has been prolonged for months or years. The occurrence of
pneumothorax seems, in some instances, to exercise an inhibitory effect
on the disease in the affected lung — a result probably to be attributed
to the diminished blood-supply consequent on the pulmonary collapse.
Pleurisy.— A. certain degree of pleurisy occurs in every case, although
it may be unaccompanied by any symptoms. Signs of dry pleurisy,
without any evidence of effusion, are often met with. When a dry rub is
heard over a considerable area — usually the lower part of the chest— it not
uncommonly indicates progressive disease ; but there are many exceptions
to this rule. Pleural effusion occurring in the course of pronounced
phthisis is seldom very profuse, perhaps, because the pleural cavity has
been already partly obliterated by adhesions. The fluid is generally
sero-fibrinous, sometimes purulent, and occasionally sanguineous. Cases
have been recorded where rapid absorption of an effusion was followed by
acute generalised tuberculosis. This, however, is a very rare sequence of
events, and the relation may be accidental. Some cases of tuberculous
empyema have originated in pneumothorax, where the opening has been
closed by inflammation, and the air has been gradually absorbed.
Empyema is much more unfavourable than sero-fibrinous effusion, as
absorption cannot be expected, and treatment by incision is rarely
successful. Small empyemas very occasionally undergo inspissation and
arrest. Sanguineous effusion is less common than the statements of
writers would lead one to suppose. Pleural effusion, like pneumothorax,
exercises a retarding influence on the pulmonary disease in virtue of the
collapse of the lung which ensues.
Pneumonia. — As already stated in the section on Pathology, croupous
pneumonia occasionally attacks phthisical patients ; but this is very
uncommon. Most of the authors who mention this subject consider
that the course of phthisis is not materially influenced by intercurrent
pneumonia. In the only instance of this accident that I have met with,
the pneumonia ended favourably with a well-defined, crisis, and the old
apex lesion was left in the same condition as before the acute attack.
214 SYSTEM OF MEDICINE
Tuberculous persons are apt to acquire more or less acute broncio-
pneumonia from time to time ; but most of these attacks represent acute
exacerbations of the tuberculous process. Influenza, attacking the subjects
of phthisis, may set up pneumonia of the broncho-pneumonic kind, less
frequently the lobar.
Circulatcyry system. — The heart of phthisical persons is small, and
shows atrophic changes, occasionally slight fatty degeneration, and very
rarely solitary tuberculous masses in its muscular walls. ' It is rarely that
such lesions give rise to any functional disturbance. In some of the
most chronic cases dilatation of the right ventricle may occur.
Endocarditis is not very uncommon, and is sometimes attributable to
previous attacks of acute rheumatism, but by no means always. Some
French observers state that they have discovered tubercle bacilli in the
valvular vegetations in such cases; but the relation of endocarditis to
tuberculosis is still in need of investigation. Dilatation of the heart,
whether due to valvular defects or myocardial disease, exercises a retard-
ing effect on the progress of pulmonary tuberculosis. Attacks resembling
pseudo-angina pectoris may be encountered ; and it is said that they
occur more often where the left upper lobe is contracted and the
heart much exposed. It is doubtful whether this association amounts
to anything more than a coincidence.
Periea/rditis is generally due to extension of tuberculosis from the
pleura or anterior mediastinal glands, or occasionally from the peritoneum.
In a few recorded cases a pulmonary cavity has perforated the pericardium,
and produced pyopneumopericardium. Tuberculous granulations or
caseous nodules may be seen in. the serous membrane ; or the tuberculous
nature of the affection may only be demonstrable by the microscope.
The effusion, as a rule, is scanty and sero-fibrinous in character;
occasionally purulent or hsemorrhagic. There is always much fibrinous
exudation, and usually more or less adhesion of the two layers.
Tuberculous pericarditis generally escapes recognition diuing the patient's
life ; though, from its weakening effect on the muscular wall of the heart,
it must be regarded as an important complication.
Pulmonary embolism, from detachment of thrombi formed in the right
ventricle or auricle, is an occasional occurrence. When hsemorrhagic in-
farction of the lungs ensues the condition may generally be diagnosed.
But if no infarction be produced embolism may pass unrecognised,
especially in moribund patients. Thrombosis of branches of the
pulmonary artery may take place in the last stages, but this is not a
common event. In some advanced cases we find great oedema of one
leg from thrombosis of the large veins. Tenderness and induration can
generally be discovered in the course of the affected vessel. Purpuric
spots may appear on the lower extremities in conditions of cardiac
debility.
Alimentary canal. — Tuberculous ulceration of the lip is extremely
rare, but the tongue and other parts of the oral cavity are more often
affected. Ulceration of the tongue appears most commonly on the dorsum,
PHTHISIS PULMONALIS 2 1 S
but it may attack the sides, and occasionally the fraenum. In cases of
extensive tuberculosis of the soft palate and pharynx ulceration sometimes
invades the buccal mucous membrane and the gums. The soft palate,
uvula, and the pillars of the fauces are more often attacked ; the prevail-
ing lesion consisting of diffuse submucous infiltration and swelling, with
shallow serpiginous ulceration. Miliary nodules m^y be seen in the base
of the ulcer at times. Tuberculosis attacks the posterior wall of the
pharynx less frequently than the palate. The usual lesions are circular
ulcers with raised edges and granulations in the base, and superficial
ulceration extending from the posterior pillars of the fauces. In some
instances the larynx also is extensively aifected, and the tuberculous
disease appears to have originated there. But ulceration of the pharynx
or tongue may occur without any laryngeal complication, and is
generally due to infection from the sputum ; but it may be part of a
generalised tuberculosis.
Tuberculous ulceration of the oral cavity may be occasionally mistaken
for syphilis, or for malignant disease. Herpes of the pharynx simulated
miliary tuberculosis of the soft palate for a time in two tuberculous
patients who came under my notice. For the diagnosis of such cases
reference should be made to the article "Pharynx" (vol. iv. p. 745). In
tuberculous affections of these parts pain is always a prominent symptom,
and interferes greatly with the act of deglutition ; in consequence of which
the nutrition of the patient suffers seriously. Aphthous stomatitis is a
fairly common complication in the terminal stages, and may occasion
great discomfort.
The tongue presents no special features in phthisical patients, and its
condition varies with the state of the oral cavity and alimentary canal.
In cases of intestinal ulceration it is sometimes red, glazed and raw-
looking ; but similar appearances may be observed where no ulceration of
the stomach or intestine exists. The red line on the gums, to which
much attention was paid formerly, is by no means characteristic, and,
moreover, is not very frequent.
Isolated instances of oesophageal tuberculosis have been recorded, but
the gullet rarely shows any morbid change. Tuberculous ulceration of the
stomach is extremely rare. A mammillated condition, pointing to chronic
gastritis, is not uncommon. Chronic interstitial gastritis, atrophy of the
glandular cells, and dilatation of the stomach have been found in some
cases, but, as a rule, no morbid appearances are presented ; the gastric
symptoms are mostly dependent on functional derangements. Symptoms
of dyspepsia, such as loss of appetite, cardialgia, flatulence, and constipa-
tion, are very common. Vomiting is often a very troublesome symptom :
sometimes it is associated with a red irritable state of the tongue and
epigastric pain, and is attributable to gastric catarrh ; but more frequently
it is unrelated to any affection of the stomach, and is excited by fits of
coughing, which are apt to arise after meals and are possibly a result of
hypereesthesia of the vagus. Attention to the state of the stomach and
digestion is of great importance in the treatment of all cases.
2i6 SYSTEM OF MEDICINE
The intestine is more often the seat of secondary tuberculosis than any
other organ. In my post-mortem examinations the intestine was involved
in 70 per cent of all cases of phthisis. The lesions are mostly situated
close to the ileo-csecal valve ; the last few feet of the ileum, and the caecum
being most frequently attacked : but tuberculosis may show itself in any
part of the alimentary canal from the duodenum to the anus. The fact
that the process begins in Peyer's patches and the solitary follicles, where
the lymphatic system is most highly developed, suggests that the virus
is absorbed from the intestine ; and it is probable that the bacilli are
conveyed by sputum, which has been swallowed.
In the small intestine the ulcers are at first more or less rounded,
and extend laterally, the edges and base being thickened, and the latter
often studded with granulations or small caseous foci. On the peritoneal
surface groups of miliary tubercles are often seen, with localised peri-
tonitis ; and on this surface whitish beaded cords, representing lymphatics
filled with tuberculous material, may be traced from the ulcer towards the
mesentery. In the colon the ulcers are more elongated in a transverse
direction, and often partially or wholly encircle the gut. Thickening is
less conspicuous than in ulceration of the small intestine, and subserous
tubercles and localised peritonitis are seldom seen. Partial cicatrisation
of tuberculous ulcers is not uncommon, and at times stenosis may result.
Owing to the thickening of the base of the ulcers, and the marked tend-
ency to the formation of adhesions between neighbouring coils of intestine,
perforation is generally prevented ; but this accident is less rare than is
generally supposed : the peritonitis which ensues will be restricted or
general according to the presence or absence of adhesions. Circumscribed
purulent peritonitis is by no means rare ; and, when occurring in the caecal
region, is very liable to be mistaken for simple perityphlitis. The
symptoms of intestinal tuberculosis are few and uncertain ; they may be
indicated as diarrhoea, localised pain and tenderness in the abdomen;
but, unfortunately, none of these can be depended upon. Cases of the
most severe ulceration of the small intestine or colon may run their
course without any definite pain or tenderness, and may be accompanied
by obstinate constipation from paralysis of the muscular fibres of the
gut. Diarrhoea may be due to other causes, especially enteric catarrh
and lardaceous disease. In the case of ulceration the stools may have a
pale yellow or drab colour, but they commonly present no characteristic
features. Local tenderness is more common with the diarrhoea of
ulceration. In some instances the discovery of tubercle bacilli in the
motions will put the diagnosis beyond all doubt. The presence of pus in
the stools cannot often be detected, and is generally symptomatic of
ulceration, in which case bacilli are likely to be found ; but an abscess
communicating with the intestine will have to be excluded : a large
amount of pus would be in favour of an abscess. Small quantities of
blood may be discharged with the motions, but copious haemorrhage is
very rare : however, in two patients under my care death resulted from
profuse bleeding. In one case only could a post-mortem examination be
PHTHISIS PULMONALIS 217
obtained, and here a tuberculous ulcer of the colon was found to be the
cause of the haemorrhage. In severe cases of ulceration the activity of
the process in the lungs seems, at times, to become arrested.
Fistula in ano can sometimes be traced to a burrowing tuberculous
ulcer of the rectum ; but it is not uncommon, in cases of this description,
to iind the lower part of the bowel free from ulceration or obvious
It is by no means certain that ischio-rectal abscess is always or indeed
generally of tuberculous origin.
In two female patients who came under my observation, with advanced
tuberculous ulceration of the intestine and rectum, the muco- cutaneous
margin of the anus 5nd the neighbouring skin were affected with a
superficial serpiginous ulceration of similar nature.
The diagnosis of lardaceous disease of the intestine can only be arrived
at when there are signs of similar disease of the liver, spleen, or kidney.
Enlargement of the spleen or liver, with albuminuria, casts in the mine
and polyuria, coexisting with diarrhoea, would strongly suggest lardaceous
disease ; but it must be remembered that lardaceous degeneration and
tuberculous ulceration may exist in the same patient and in the same
intestine. A marked degree of anaemia is very general in cases of
lardaceous degeneration. Transient diarrhoea is mostly attributable to
simple catarrh, the diarrhoea of ulceration and amyloid disease being very
persistent.
The liver tsx&j contain miliary tubercles, large caseous nodules, and
occasionally tubercular abscesses ; but, as a ride, these affections are
clinically unrecognisable. In one case that I examined a hypophrenic
abscess was caused by a perforating tuberculous abscess of the left lobe of
the liver. Enlargement of the organ is most frequently caused by fatty
and amyloid degeneration. The presence of a large spleen, albuminuria,
and diarrhoea would be in favour of lardaceous disease, especially if the edge
of the liver be thick and very firm. Cirrhotic enlargement is relatively
of frequent occurrence in cases of chronic tuberculous peritonitis. It is
possible that cirrhosis may be causally related to peritoneal tuberculosis.
Miliary tubercles and extensive fatty degeneration are commonly associated
with the cirrhosis of tuberculous subjects.
Enlargement of the spleen is a frequent symptom of lardaceous disease,
and is only likely to be confounded with the secondary splenic tumour of
hepatic cirrhosis. In both cases the spleen is very firm. In acute
generalised tuberculosis, as in other specific fevers, the spleen may be
enlarged, whether it contain miliary tubercles or not ; but its consist-
ency is soft. Caseous nodules are often found in the spleen, especially in
children, but they possess no clinical importance.
Tuberculous peritonitis may be part of a general tuberculosis, or it may
be due to extension from the abdominal organs — intestine, lymphatic
glands, and female generative organs ; or it may be the result of infection
from the pleura or pericardium, the bacilli being transmitted through the
lymph spaces of the diaphragm.
2i8 SYSTEM OF MEDICINE
Miliary tuberculosis of the peritoneum is often unaccompanied by any
symptom whatever ; but it may give rise to ascites, in which case some
degree of chronic peritonitis will be found. In another form the tuber-
culous lesions consist of large nodules or masses, which are generally more
or less caseous, but may at times be mainly or entirely fibroid. Caseous
and fibro-caseous nodules may coexist in the same case. When the
individual nodules coalesce large masses are formed which may be recog-
nised by palpation during life. The great omentum is frequently much
thickened, shortened and rolled up, forming a thick transverse band just
above the umbilicus ; but omental growths may be situated in the lower
part of the abdomen also. The omentum may also undergo a general
tuberculous infiltration, giving it the appearance of a thick apron hanging
down in front of the intestine.
Eetraction of the thickened mesentery, fixing the intestine against the
spine, sometimes gives the appearance of a tumour. Large tuberculous
masses may be found in the pelvis or in any part of the abdomen.
When the pelvis is involved the disease has commonly originated in the
female generative organs, the bacilli passing from the Fallopian tubes into
the peritoneal cavity ; but, at other times, the pelvic peritonitis may be
secondary to disease in the upper part of the abdomen, the virus having
apparently gravitated to the pelvis. In these cases the intestines are
always much matted together, and patches of soft lymph, with crops of
miliary tubercles, may be found, showing that the disease is still in pro-
gress. The fluid exudation is often purulent, but it may be sero-fibrinous
or sanguineous. Softening of the caseous masses sometimes leads to
perforation of the hollow viscera — intestine or bladder.
Partial or complete arrest of tuberculous peritonitis is by no means
rare. Where cicatrisation takes place contraction may ensue and cause
stricture of the intestine.
In cases of peritoneal tuberculosis the mesenteric and other lymphatic
glands of the abdomen are always more or less enlarged and caseous.
The glands may be the only abdominal organs affected, but intestinal
lesions are very frequently present. Enlargement of these glands in
adults is seldom so extensive as to admit of their being felt through the
abdominal walls ; but I have known caseous glands in the iliac and
umbilical regions to form tumours as large as an orange. The tuberculous
glands of children attain to a relatively larger size, and are more often
susceptible of palpation ; but even in children, and stiU more in adults, it
may be difiicult during life to decide whether a tumour be glandular or
omental ; though a deep situation and greater fixation of the tumour
would be rather in favour of the former. The designation " tabes mesen-
terica " has been shown by Dr. Gairdner and others to comprehend not only
tuberculosis of the mesenteric glands, but also tubercular peritonitis and
other morbid conditions associated with wasting ; and the name has conse-
quently fallen into disuse.
Urogenital system. — Miliary tubercles and small tuberculous foci in
the kidney may be accompanied by slight albuminuria, or may cause no
PHTHISIS PULMONALIS 219
symptoms. In the important variety known as scrofulous or tuberculous
pyelitis, large areas of the kidney undergo caseous necrosis, and in most
instances softening and ulceration ultimately ensue. Inasmuch, as the
process predominantly involves the pyramids and calices, disintegrated
tuberculous material and pus are discharged with, the urine from time to
time. Tuberculous infiltration may ultimately involve the whole kidney,
which then generally becomes enlarged, and may be converted into a
loculated thick-walled cyst, containing soft putty-like caseous material ;
the dilatation of the pelvis being attributable to obstruction to the flow
of urine. Both kidneys are affected as a rule, though one is usually in
a more advanced stage of the disease. The infiltration and ulceration
may extend from the pelvis of the kidney to the ureter, and thence to
the bladder, prostate, vesiculse seminales, vas deferens and epididymis.
The symptoms of this form of renal tuberculosis are mainly the result
of the pyelitis which constitutes the most salient feature of the affection
— ^lumbar pain, mostly of dull character, but at times paroxysmal and
colicky, when the ureter becomes obstructed, pus with a corresponding
quantity of albumin, caseous debris, renal epithelium, and, at times, blood
in the urine. Tubercle bacilli may be recognised in the urinary sediment,
and are a conclusive proof of tuberculosis. If tuberculous disease of the
bladder, prostate, and vesiculae seminales can be excluded, the existence
of renal tuberculosis would amount to a certainty. Occasionally a definite
renal tumour can be made out by palpation, but this is the exception.
In addition to the foregoing affection phthisical patients may acquire
acute or chronic nephritis, lardaceous disease, and granular kidney. The
commonest of these lesions is lardaceous disease. Slight degrees of this
degeneration may need the application of iodine for their recognition, and
in such cases no clinical symptoms would be presented. The higher
grades of this disease are always combined with a varying amount of
chronic nephritis, the kidneys in such cases being large, pale, and trans-
lucent, with yeUowish opaque patches in the cortex. The surface is
generally uneven, and the capsule adherent.
The amyloid disease affects principally the glomerular capillaries, but
also the small arteries, the vasa afferentia and vasa recta. Degenerative
changes in the convoluted tubes are due partly to the obstructive effects
of the lardaceous disease of the vessels supplying these structures;
and partly to the blood state, in which the lardaceous degeneration itself
originated. In association with these changes a varying amount of
scattered cell infiltration and fibrosis is nearly always found ; these re-
present reactive inflammation secondary to parenchymatous degenera-
tion. The urine in such cases is abundant, of low density, and contains
albumin in considerable quantities, and hyaline casts. Dropsy is un-
common. The other forms of renal disease mentioned above present no
features to distinguish them from similar affections in non-tuberculous
subjects. Acute nephritis is uncommon, and is probably of haemato-
genous origin and attributable to absorption from ulcerative cavities in
the lungs. Granular kidney is not uncommonly met with in elderly and
SYSTEM OF MEDICINE
middle-aged persons, and is sometimes accompanied by slight degrees of
lardaceous degeneration. It is very doubtful whetlier there be any causal
relation between granular kidney and pulmonary tuberculosis. In cases
where albuminuria supervenes a fall of temperature and a diminution of
the activity of the pulmonary disease are not uncommonly observed.
Phosphaturia is said by Sir R. Douglas Powell to be an early indication
of phthisis. Ehrlich's diazo reaction is found in febrile progressive forms
of tuberculosis, but no diagnostic significance can be attached to it.
Tuberculous ulceration of the bladder is not very common, and is mostly
associated with similar disease of other parts of the genito-urinary system.
The symptoms are those of cystitis. Tubercle bacilli may be found in
the urine. Tuberculous disease of the epididymis is much less uncommon,
but this affection and tuberculosis of the prostate and vesiculae seminales
come rather within the sphere of the surgeon.
Tuberculosis of the uterus is decidedly rare. The disease, which
attacks the lining membrane of the fundus, consists of tubercular infiltra-
tion, which is soon succeeded by caseous necrosis and ulceration. The
uterine cavity commonly contains thick cheesy pus, and is apt to be
somewhat dilated. There is rarely much enlargement of the organ.
The Fallopian tubes are much more frequently attacked, and are seldom
spared where the uterus is affected. In tuberculous salpingitis similar
lesions are found in the mucous membrane ; but the thickening and
dilatation of the tubes attain to much greater proportions.
Tuberculosis of the ovary is one of the rarest occurrences : the only
case I have seen is recorded by Dr. Habershon. In this case both ovaries
contained tuberculous abscesses which communicated with the Fallopian
tubes and intestine.
Tuberculous peritonitis is not uncommonly attributable to extension
from the Fallopian tubes or uterus. It is probable that genital tuber-
culosis may also be caused by infection from the peritoneum ; but more
often the disease is communicated through the blood. The possibility of
direct sexual infection cannot be denied.
Some writers have contended very strongly that pregnancy exercises
a retarding influence on the disease ; others hold that phthisis is aggravated
by this condition : on the whole, pregnancy seems more often to intensify
the symptoms of pulmonary tuberculosis. There is little doubt as to the
injurious effects of parturition. It is a common experience that after
confinement the pulmonary disease makes rapid progress, and is apt to
terminate fatally in a few months. Hanau believes that this is to be
explained by the inhalation of infective material from cavities into
healthy parts of the lungs during the forcible inspirations that accompany
expulsion of the foetus. The exhausting influence of lactation is
notorious. Menstruation is nearly always much deranged, apart from
any definite lesion of the generative organs. Amenorrhoea, or scanty,
infrequent menstruation, is the rule in this disease, and may be one of the
earliest symptoms of it. Very occasionally menorrhagia occurs, but is
seldom persistent.
PHTHISIS PULMONALIS
The suprarenal bodies occasionally contain isolated caseous nodules,
whicli cause no symptoms. Still more rarely both adrenals are converted
into firm caseous or caseo-calcareous masses, in which case bronzing of the
skin and other symptoms of Addison's disease supervene.
Osseous system. — Secondary tuberculosis of the osseous system and
joints is not very common, and may show itself, among other places, in
the vertebrae, sternum, and ribs, giving rise to chronic abscess in connec-
tion with the chest walls. This subject possesses more surgical than
medical interest.
Nervous system. — The mental attitude of many phthisical patients is
one of irrepressible hope, especially in the less chronic forms. Such
persons often asseverate that if they could but get rid of some par-
ticular symptom, such as cough or shortness of breath, they would be
perfectly well ; and they go on making plans for the future within a few
hours of their death. But in most cases presenting definite symptoms of
mental derangement depression is the prevailing feature. Melancholia,
stupor, delusions of suspicion or persecution, religious foreboding, insomnia,
hallucinations, a suicidal tendency, and refusal of food are among the
commonest symptoms. Maniacal excitement is much less frequent. For
further information the reader is referred to the section on Insanity in
the last volume of this work.
Tuberculosis is much less liable to afiect the nervous system in the
course of chronic phthisis than in acute tuberculosis. It is also of much
more frequent occurrence in children than in adults. In most cases the
tubercle bacilli are conveyed through the blood. Th'e cerebro-spinal
meninges are the parts most commonly attacked, the tuberculous process "
being grouped especially along the small vessels. The growth of tubercles
is soon followed by fibrinous exudation, in consequence of which the pia
mater becomes much thickened.
Meningitis nearly always predominates, or is exclusively localised at
the base of the brain, and extends thence to the Sylvian fissures, the
ventricles, the surface of the cerebellum, the pons Varolii, and the medulla.
The ventricles are often much dilated and filled with turbid fluid —
" acute hydrocephalus " of the old writers, the convolutions becoming
flattened by pressure. The cortex of the brain and the walls of
the ventricles are often much softened, from extension of the inflamma-
tion of the pia mater, so that the process is more correctly described as
a meningo-encephalitis. Tuberculous nodules or masses may grow in
the brain tissue, and sometimes attain to a considerable size. These
solitary tubercles or tuberculous tumours are found most frequently in the
cerebellum and cerebral hemispheres, but they may arise in any part of
the brain and are often multiple. Small tuberculous nodules are not infre-
quently found in the cortex, extending inwards from areas of chronic
tuberculous meningitis.
Lastly, meningitis, encephalitis and myelitis may be due to extension
from neighbouring bones of the cranium or spine.
The symptoms of meningitis are many, and can only be briefly
SYSTEM OF MEDICINE
enumerated : — ^headache, irritability of temper, fretfulness, coma, convul-
sions, marked retardation, acceleration, or irregularity of the pulse, Cheyne-
Stokes respiration, vomiting, retraction of the head and abdomen, rigidity
and weakness of Umbs, paralysis of cranial nerves, optic neuritis. Reten-
tion of urine is very common towards the close, and pyrexia is nearly
always present. Headache is perhaps the most common symptom in the
more chronic form. Tuberculous tumours of the brain give rise to
symptoms not diifering from those of other cerebral tumours. For a full
account of this subject reference must be made to the appropriate articles.
Peripheral neuritis has been observed in a small number of cases in
the form of extensor paralysis of the arms or legs. The cause of the
neuritis is uncertain. It may be the result of toxines, elaborated by the
tubercle bacilli.
Some of the pains and tenderness affecting the limbs in phthisical
patients may possibly be of neuritic origin. Beau grouped these together
under the name "melalgia." It is difficult at present to discriminate the
pains which many patients in advanced phthisis complain of. Some are
probably neuritic, others myalgic ; while, in some instances where pains
fly about from one part to another and affect the joints, the resemblance
to rheumatism is very close. In these last the rheumatoid pains are
possibly a septicsemic symptom, depending on absorption from pus-
secreting cavities in the lung. Suppurative otitis media is not very un-
common, but it is seldom that tubercle bacilli can be discovered in the pus.
Course. — The course of pulmonary tuberculosis is essentially variable
and fluctuating,' intervals of quiescence or apparent arrest alternating
with prolonged periods of fever and other constitutional symptoms. In a
large percentage of cases the disease is for the most part slowly progres-
sive, and death ensues in a few years at the latest. The average duration
of phthisis has been variously estimated. Louis found that in more than
half the eases observed death occurred in less than nine months. The
mean duration has thus been stated : — ^twenty-three months (Louis and
Bayle) ; two years (Laennec and Andral) ; four years (C. J. B. Williams and
Sir J. Clark) : Dr. C. T. Williams, from analysis of a thousand cases
among private patients, put it at seven years and three-quarters. On
account of the great difficulty so frequently met with in attempting to fix
the date of onset of the disease such calculations are fraught with
uncertainty. Those physicians who have had much experience of the
disease at special as well as general hospitals, will probably agree that
statistics derived from the latter source exclusively would give a very
erroneous impression of the duration of phthisis. Patients admitted
into general hospitals are either exceptionally ill, or are suffering from
some serious complication. The mortality among such patients is natur-
ally very high, and the duration of the disease may often be measured
rather by months. Most valuable are the statistics collected by Dr. J. E.
Pollock from 3500 cases of phthisis attending the out-patient department
of the Brompton Hospital.
" Here (among the out-patients)," as he truly says, " are seen indi-
PHTHISIS PXJLMONALIS 223
viduals of all classes, excepting the highest, and of all ages and occupa-
tions. The necessities of home cares and of continuing the daily work
are but little interfered with by a visit once a fortnight to their physician ;
but these urgent claims of domestic life shut out large numbers from the
possibility of availing themselves of indoor treatment in a hospital. The
large class affected with chronic slow phthisis are, therefore, found chiefly
among the out-patients.
" The average duration, while under observation, of all the cases taken
together was two years six months and three-fifths nearly, but this repre-
sents only a part of the period of the affection, and in it are included
cases of the most acute and rapid form as well as those which have
become chronic."
The actual duration of the cases must have been considerably longer,
and the whole average duration of the disease, as Dr. Pollock says, must be
raised beyond four years. An experience of twelve years' out-patient
work at the Brompton Hospital has convinced me that Dr. Pollock is far
nearer the mark than those who would limit the average duration to two
years.
The complexion of the malady, while running a chronic or slowly
advancing course, is liable at any time to undergo a complete change,
depending on acute exacerbation of the pulmonary disease. Fever and
other constitutional symptoms often herald renewed activity of the tuber-
culous process before physical examination gives any decided indication of
extension. In other instances we find the signs of disease slowly extend-
ing for some time without any corresponding aggravation of the patient's
symptoms.
The lines along which the disease spreads in the lungs have been
described in the section on the pathology. It is very important not to
be satisfied with exploration of the front of the chest only, but to examine
with care the back also, more especially the supraspinous fossa — that is,
the posterior aspect of the upper lobe — and the interscapular region just
below the spine of the scapula, which corresponds to the apex of the
lower lobe, a part specially prone to secondary tuberculosis. And, as Dr.
J. K. Fowler quite rightly insists, search should be made for signs of
disease extending from behind forwards from the apex of the lower lobe
along the upper border of the same lobe, the position of the septum dividing
the upper and lower lobes being roughly indicated by the "vertebral
border of the scapula, when, with the hand upon the spine of the opposite
scapula, the elbow is raised above the level of the shoulder."
The upper part of the axilla is another region that must be carefully
investigated, as it is in this space alone that the outer aspect of the upper
lobe is accessible to examination ; and signs of excavation may sometimes
be found at the apex of the axilla only.
Towards the close of life bubbling r&les are generally heard over the
whole of the chest, and are an indication of pulmonary oedema, the result
of cardiac failure. It is usual to find resonance to percussion over the
lower part of one or both lower lobes up to the very end ; a fact which
224 SYSTEM OF MEDICINE
is to be explained by the persistence of patches of spongy lung between
the tuberculous masses.
Where the fatal termination is not directly or indirectly dependent on
complications, but is the result of slowly extending disease, death most
frequently occurs from exhaustion. Asphyxia is seldom the -cause of
death except in acute forms of tuberculosis. In most chronic cases death
is preceded by profound emaciation and debility, which steadily increase
in spite of the considerable quantity of nourishment the patients often
continue to take. Bed-sores may form if the nursing be not vigilant,
and oedema of the legs is not uncommon. The pulse becomes more rapid
and feeble, the temperature gradually falling often becomes subnormal,
tracheal rales appear, and the end comes quite peacefully. In the com-
paratively few cases in which complete arrest of the disease takes place,
the constitutional and local symptoms gradually subside, and the patient
regains his health. The physical signs at the same time undergo certain
modifications, or occasionally disappear entirely. In most cases, although
rales and other adventitious sounds cease to be heard, signs of consolida-
tion and contraction of the apex persist, and some degree of localised
emphysema is often developed.
Prognosis. — Of the many complicated problems presented to the
physician the prognosis of pulmonary tuberculosis is one of the most
difficult. An accurate prognosis would involve full knowledge of the
parasite and its host, as well as of their environment. At present little
is known concerning variations in the virulence of the tubercle bacillus as
it occurs in the body of man.
Still less information is forthcoming as to the histo-chemical and
biological conditions of the human organism which retard or favour the
development and activity of the parasite. Certain facts concerning the
external conditions that appear to exert a salutary or injurious influence on
the disease have been discussed under its causation. A complete under-
standing of these points is intimately connected with the question of
immunity, a most difficult subject, which is only just beginning to be
studied. For practical purposes we have to estimate the prognosis, in the
first instance, by a careful consideration of the effects of the disease,
immediate and remote, in each patient. By these means we are able to
gauge, approximately, the severity of the malady and the resisting power
of the individual. Furthermore, an acquaintance with the natural history
of tuberculosis, including the influence of heredity, of previous or con-
current diseases, and of various conditions of life, and lastly, the know-
ledge of the effects of treatment, will be required if we would forecast the
probable course of pulmonary consumption. The symptoms of the
patient, representing the result of disordered function, are of the first
importance. Of all the general symptoms fever is the most important.
A markedly intermittent or remittent pyrexia, in the absence of acute
intercurrent affections, is very significant of progressive disease, and is,
therefore, of bad augury. At the same time it must be remembered that
a considerable degree of fever is not incompatible with gain of weight and
PHTHISIS PULMONALIS 225
other signs of improvement. Moreover, after periods of severe pyrexia
the temperature may fall, and the disease enter upon a chronic phase.
Nevertheless, it may be accepted as a general principle that the existence
of marked pyrexia always necessitates a very guarded, though not
necessarily an entirely unfavourable prognosis.
A slight evening rise of temperature, with a fall to normal or slightly
below normal in the morning, is not uncommonly present in comparatively
favourable cases. The supervention of fever in the course of a mild
chronic case is often one of the first indications of renewed activity of the
tuberculous process, which may prove intractable. The absence of fever
does not in itself justify the expression of a hopeful opinion, for, as we
have seen, an apyrexial temperature may accompany advanced and active
disease. Subnormal or collapse temperatures have a very ominous
import. Emaciation signifies deficient alimentation (whether due to
insufficient feeding, digestion, or assimilation), or profound constitutional
intoxication. In the first case the pause is more amenable to treatment,
and the outlook is consequently less unfavourable. A persistently rapid
or easily excited pulse is indicative of debility, or of a state of general
nervous erethism, both of which are very undesirable features. Anaemia
and debility are also an evidence of profound constitutional impression,
and must therefore darken the prognosis.
Among the more important symptoms of local disorder we must
reckon dyspnoea depending on diffuse or acutely extending pulmonary
changes. When these changes consist in disseminated miliary tubercles,
or in lesions of the broncho-pneumonic or pneumonic type, the gravity of
the symptom can hardly be exaggerated. Expectoration, profuse, puru-
lent, and containing numerous elastic fibres, implies progressive destruction
of lung. Absence or scantiness of expectoration is, at times, a marked
feature in severe cases : this is mostly, but not exclusively, seen in
children and women, who often swallow their sputum. But while no
great importance can be assigned to the quantity of the sputum, scanty
or moderate expectoration is on the whole a good sign.
The expectoration of pulmonary calculi is never met with except in
very chronic cases.
The significance of foetor varies with its cause. When the odour has
a sickly or slightly fishy character, due to the retention of secretion in
cavities, it is of less moment than when it possesses the penetrating odour
of bronchiectasis : in the latter case the dangers of septic broncho-pneu-
monia and other accidents are added to those already existing. The
supervention of gangrene renders the prognosis quite hopeless.
The number of tubercle bacilli in the sputum is no accurate measure
of the extent or severity of the disease, and is largely a question of dis-
charge. In some acute cases the bacilli may be very scanty, whereas in
other cases, quiescent and circumscribed, the sputum may teem with them ;
complete and permanent disappearance of the microbes is a most hopeful
sign ; but their continued presence in the sputum does not preclude a
protracted and favourable course.
VOL. V Q
226 SYSTEM OF MEDICINE
An incessant and intractable cough, especially when it interferes witk
sleep and causes vomiting, adds greatly to the exhaustion of the patient.
Some of the most irritable coughs depend on catarrhal affections of the
upper air-passages, and can often be relieved ; but cough associated with
signs of persistent diffuse bronchitis is often indicative of widely dis-
seminated tubercialous lesions.
The state of the digestion is of the greatest importance. Where the
symptoms of gastric disorder, or of faulty absorption or assimilation, prove
rebellious to treatment the prospects of improvemeot are small indeed.
In attempting to weigh the indications of physical examination of the
lungs, the two chief points requiring attention are the character and the
extent of the disease. An acute onset is commonly followed by pro-
gressive invasion of both lungs, and has the gravest significance. An
insidious, bronchitic, or hsemoptoic onset is more favourable. Rapidly
extending disease is always of ominous significance. Riles and other
morbid signs scattered widely over a large part of both lungs, especially
in pyrexial cases, point to disseminated lesions, a most unfavourable type
of disease ; but similar physical signs, without much fever, may sometimes
persist for months or years in cases where the disease takes the form of
discrete fibro^caseous or fibroid processes. Cases with severe symptoms,
and relatively slight physical signs are to be regarded with suspicion, for
the true extent of the pulmonary disease is generally masked by other
conditions ; on the other hand, the presence of marked signs of consolida-
tion or excavation of one upper lobe is not inconsistent with a chronic
and favourable course so long as the lower lobe and the opposite lung
remain comparatively free.
Signs of contraction are a sure index of chronieity. Localised and
stationary disease is a good element in prognosis. The disappearance of
rMes is, in general, a favourable feature.
After what has been said in a previous section about the stages of
phthisis, it is futile to base the prognosis on considerations which are so
apt to be fallacious. If, in a chronic case, we could be sure, which we
cannot be, of the absence of softening and excavation, the prospects of
arrest would be better than if cavities had already formed, for the
existence of a cavity carries with it the risk of extension by means of
inhalation of infective secretions into distant bronchi. Moreover, there
is no evidence that a vomica can become obliterated by cicatrisation j
whereas we know that tuberculous nodules often undergo healing by
encapsulation, calcification, or fibrous transformation.
Among the most ominous complications are meningitis and pneumo-
thorax. Pleurisy with effusion sometimes appears to exert a retarding
influence on the pulmonary affection. Empyema is unfavourable. Dry
pleurisy is regarded by some authors as a very unfavourable sign ; but
this is by no means generally true. The appearance of the diffuse
infiltrating form of laryngeal tuberculosis, with its tendency to produce
dysphagia and stenosis, betokens a speedy termination. Oft repeated
haemoptysis depresses the patient morally as well as physically ; and
PHTHISIS PULMONALIS Z27
under such circumstances the possibility of a sudden and fatal issue has
always to be reckoned with.
Tuberculous peritonitis and intestinal ulceration cause great wasting
and prostration, and generally hasten the patient's end. Tuberculosis
of the abdominal lymphatic glands and generative organs tends to
aggravate the general condition, and is commonly a sign of generalised
disease.
Pronounced lardaceous disease of the viscera is a most serious complica-
tion of chronic cases, pointing, as it does, to profound derangement of
nutrition. A combination of diabetes and phthisis is also a most grave
condition.
The presence of cardiac hypertrophy and dilatation, or of marked
emphysema, justifies the opinion that the duration of the disease will be
long.
The environment is a matter of much importance. A patient living
in a healthy country place, under suitable climatic conditions, has better
prospects than one who is compelled to dwell in a large town, especially
if his Ufe be spent in dusty or smoky rooms. Again, pecuniary means
have a direct bearing on the prognosis : those who can procure, not only
the necessaries, but also the luxuries of Ufe, and can afford to rest, are in
a better position to battle with the disease than those who must work
hard for a living. Nevertheless, among poor hospital patients we see,
not very infrequently, persons who have been suffering from phthisis for
ten years or more, and who still go on working under the most adverse
circumstances. A history of previous good health is a hopeful featiu-e,
as a greater capacity of resistance may be expected where the general
health has not been already undermined. The influence of age has been
much disputed. As a general rule, pulmonary tuberculosis runs a more
rapid course in children and young adults than in older persons, among
whom the chronic form is rather the rule. Cornil and Herard suggest
that tuberculosis is more chronic in old people, because heredity has
abeady weeded out those of least resistance. Nevertheless, acute disease
may occur in elderly patients, and, conversely, the phthisis of children
may be chronic. Each case must be estimated on all the data ; and
the influence of age can only be credited with a very subordinate
importance.
It has been said that the duration of the disease is shorter in women
than men. If we exclude the cases associated with pregnancy and
parturition, it is doubtful whether this statement be true.
The influence of heredity is undoubtedly an important one. It is a
common belief that this factor determines the earlier manifestation of
ijhe disease. A strong predisposition is an unfavourable element, as in
such cases there often appears to be a general lack of vitality and
resistance. But, although this is generally true, hereditary influence
cannot be ranked on a level with considerations derived from a careful
estimation of the efiects of the disease in the individual patient. The
best results may be expected in cases presenting the following features :
228 SYSTEM OF MEDICINE
— apyrexia, or a subfebrile temperature ; weight stationary or increasing ;
signs of disease confined to one lung or to limited portions of both lungs
(especially if associated with contraction) ; a quiet pulse and nervous
system; a good digestion; absence of serious compKcations; a good family
and personal history, and favourable hygienic surroundings.
Treatment. — A. Preventive. — If, as our present knowledge appears to
show, the sputum of tuberculous persons be the main source of the disease,
it is obvious that the complete destruction or disinfection of this secre-
tion should be our first duty. In many hospitals this is effected by
means of special destructors, or furnaces, in which the sputum is burnt.
In private houses, where this method is difiicult of application, the
expectoration, after previous disinfection, maybe discharged into the drains.
For general purposes carbolic acid in a strength of 5 per cent is the best
disinfectant; experiment shows that' the infectiveness of the bacilli is
completely removed after exposure of the sputum to this solution for a
short time. Sputum should not be thrown on the diist-bin, where the
contents may dry and become a further source of danger. In all cases,
whether in hospitals or private houses, patients should be directed to use
spittoons containing a suitable disinfectant. If, in spite of advice
to the contrary, patients use handkerchiefs for receiving the sputum,
these should be burnt ; or at any rate should be scalded before being
sent to the wash.
Persons suffering from phthisis should be warned not to spit about
the streets, or the house, or into any vessel which does not contain
some disinfectant. Underclothing, linen, sheets, and pillow-cases should
also be scalded before being washed, especially in the case of bed-ridden
patients, when the chances of contamination are greater. Phthisical
persons should occupy separate beds. Bedrooms and sitting-rooms so
occupied must be carefully cleaned with a damp cloth, so as to avoid
raising a dust ; and should be well aired and exposed to light every day.
Eooms that have been inhabited by such patients should be thoroughly
cleaned, and, if possible, white-washed, painted, and re-papered before
being used by other persons.
It is desirable that patients should be provided with separate sets of
knives, and forks, and spoons ; but, in default of this precaution, all
table utensils, as well as plates, cups, glasses, should be scrupulously
cleaned.
Milk is undoubtedly a vehicle of disease, and should be carefully
boiled ; particularly when intended for children. For the principles on
which slaughter-houses and dairies should be regulated, and for further
information on the general question of prophylaxis, the article " Tuber-
culosis " (vol. ii. p. 30) should be consulted.
In persons threatened vrith tuberculosis, and in others with a strong
family predisposition, the importance of a good general hygiene can
hardly be over-estimated.
Abundance of fresh air in the dwelling — especially in bedrooms —
secured by suitable methods of ventilation, a large amount of outdoor
PHTHISIS PULMONALIS 229
life in pure country air, a generous diet, including a large proportion of
fatty constituents, daily cold sponging of the body, and the use of flannel
or similar underclothing, are amongst the most necessary conditions. In
the case of children the throat needs special attention ; enlarged tonsils
should be removed, and catarrhal affections must not be neglected. The
opinion is gaining ground that the tonsils are frequently the portals by
which tubercle bacilli enter the body ; at any rate, in primary tubercu-
losis of the cervical lymph glands. The question of the removal of
caseous glands, and the surgical treatment of tuberculous disease of bones
and joints, are matters of great importance, but cannot be discussed here.
[Fw^e vol. iv. p. 599.] Tuberculous mothers ought not to suckle their
infants.
The choice of a profession or trade is a matter of no small con-
sequence. Occupations in which life is mainly or largely spent in the
open air are the most favourable ; but, in the case of the poor, out-
door work generally implies more or less heavy labour, which is often
prohibitive under the circumstances. Many people, in whom tuberculous
affections of bones, joints, or lymphatic glands have been cured or
partially arrested, manage to carry on successfully various sedentary
trades or professions. Dusty occupations, as in the case of millers,
bakers, knife-grinders, stone-masons, and the like, are fraught with special
dangers to vulnerable persons. Free ventilation of dusty workshops is
all-important, and serves to minimise, to a large extent, the dangers of
the aforesaid trades.
There can be no doubt whatever that persons suffering from pro-
gressive disease ought not to marry. In cases of quiescent or apparently
arrested tuberculosis there is room for difference of opinion. When all
symptoms of disease have disappeared, the sputum no longer contains
bacilli, and the general health remains good, marriage, in the case of
men, may be undertaken after the lapse of two or three years without
any great risk. Women incur far greater danger in connection with preg-
nancy, parturition, and lactation •■ for it is well known that, under the
influence of such conditions, quiescent tuberculous lesions are apt to
prove the starting-point of active disease. If, however, the tuberculous
process can only be regarded as quiescent, and bacilli continue to be
expectorated, marriage ought to be forbidden in either sex. Most
writers agree on this point as regards women ; but some have urged that
men, under these circiunstances, may be allowed to marry on the ground
that their lives are thereby made happier ; and that, if children should be
begotten, they tend to die off early, and the race does not appreciably
suffer. The morality of such advice need not be discussed here ; but the
possibility of a phthisical husband directly or indirectly infecting a
healthy wife cannot be disregarded; and the risk of adding to the
already high tuberculous death-rate is one that no medical man should
willingly countenance. However, as all writers point out, the question of
marriage is seldom decided, solely or even mainly, on medical grounds.
B. Specific treatment. — It has been well said that where the number of
230 SYSTEM OF MEDICINE
remedies recommended for any disease is large, there is good reason for
the belief that none of them is possessed of much efficacy. Of no disease
may this more truly be said than of tuberculosis. Tuberculin, a glycerine
extract of pure cultures of tubercle bacilli, deprived of the bacilli by a
special method of infiltration, and injected under the skin, was found by
Koch to exert a marked influence on tuberculous lesions. The local
action of the remedy consists in an inflammatory swelling and disinte-
gration of the diseased foci. Constitutional reaction is indicated by
fever, malaise, headache, pains in the limbs and trunk ; and occasionally
by nausea and vomiting. The effects of the remedy were most con-
spicuous in cases of lupus, where the changes in the skin could be
readily followed.
Although Koch's statement that- tuberculin had a specific influence
on tuberculous lesions was speedily verified, his claim that the action was
curative was not so generally admitted. Pathological evidence was soon
brought forward by Virchow and others to show that the use of tuber-
culin was often followed by the development of acute inflammatory
changes in the lungs ; and that under its influence quiescent disease may
spring into activity and lead to generalised tuberculosis. Space wiU not
admit of a detailed discussion of this matter. The prevailing opinion at
the present time is that the administration of tuberculin in cases of
pulmonary tuberculosis is dangerous, though some surgeons still regard
it as a useful adjunct to other methods of treatment in surgical forms of
tuberculosis.
Klebs and Dr. W. Hunter, working independently, claimed to have
succeeded in separating the fever-producing and toxic elements from the
direct curative constituents of tuberculin ; but their extracts failed when
put to the test by other observers. Quite recently Koch has described a
new method by which he was able to prepare an improved tuberculin.
Dried cultures of the tubercle bacillus were thoroughly triturated in a
mortar, then mixed with distilled water and centrifugalised. The sedi-
ment was again dried, triturated, suspended in distilled water, and centri-
fugalised. This procedure was repeated until no sediment remained.
The liquid separated by the first centrifugalisation contains the active
principles of the original tuberculin, while the fluid obtained at sub-
sequent stages of the process is believed to contain the debris of the
disintegrated bacilli themselves. This solution has the great advantage
that it produces no constitutional disturbance beyond a slight rise of
temperature. The new tuberculin was found to confer immunity on
guinea - pigs, and its use in the human subject in cases of lupus and
early pulmonary tuberculosis was followed by improvement Further
experience can alone decide as to the therapeutic value of the new
preparation ; but it is no exaggeration to say that in a further develop-
ment and improvement of Koch's method lies our best hope of arriving
at a successful treatment of tuberculous disease.
The number of drugs that have been vaunted as specifics for tuber-
culosis is legion. In recent years iodine, iodoform, carbolic acid, corro-
PHTHISIS PVLMONALIS 231
sive sublimate, creasote and one of its constituents, guaiacol, have been
most largely used, im virtue of their antiseptic properties. These have
been administered by t'he mouth, by inhalation, subcutaneous injection,
inunction, and direct injection into the lung ; and sulphuretted hydrogen
gas has even been pumped into the rectum. The results have not
differed greatly in respect of any of these methods. They have all
passed through successive stages of exaggerated and hasty laudation,
half-hearted approbation, and contemptuous neglect. The history of
guaiacol is a good illustration : at first it was advocated as a specific ;
now the only claim seriously made in its favour is that it has a beneficial
■effect on cough and expectoration.
As we have no specific remedies, our aim must be to increase, as far
as possible, the resisting power of the patient, so as to put him in the
best condition to withstand the inroads of the disease.
In order to maintain the nutrition of the body at as high a level as
possible, the dietary must be liberal, and should include a, large amount
•of fat in the shape of milk, cream, butter, fat bacon, and the Kke, in
addition to a due proportion of nitrogenous and carbohydrate constituents.
A special distaste for fatty foods is manifested by some patients, but this
.aversion is by no means so general as certain writers would have us
believe. Cod-liver oil is a valuable adjxmct to the diet, but is possessed
■of no specific virtues. This valuable food is sometimes prescribed in
& manner calculated to bring it into discredit, that is, when it is
administered in too large quantities. Two to four drachms twice
or thrice in the day is as much as most patients can digest, and it is
frequently necessary to begin with even smaller- doses. It usually agrees
best when taken soon after a meal ; but some people prefer a single dose
at Ijedtime. In all cases of dyspepsia, and whenever the taste of the oil
keeps rising into the mouth, it should be withheld. If persevered with
Tinder these circumstances it seldom fails to derange the digestion. It is
better for the patient to enjoy his food without the oil, than to persist in
its use and lose his appetite.
The taste of the oil may Ije disguised with peppermint, lemon juice,
ginger or orange wine, cognac, liqueurs, and other flavourings. Many
patients prefer to take the oil in the form of an emulsion, or in combina-
tion with malt extract. Malt is much used at present in England, and
no doubt it possesses some digestive value ; but it is no substitute for
cod-liver oil or fats. Glycerine, in doses of three to four tablespoonfuls
daily, has been recommended as a substitute for the oil by Jaccoud, but
it has not found much favour with other physicians. Alcohol is not to
be ordered in all cases indiscriminately ; where the disease is quiescent,
nutrition fairly well preserved, and the appetite good, it is not required ;
in conditions of debility, deficient appetite, and, above all, in pyrexial
cases, alcohol is of great value.
The particular form in which stimulants are to be administered is
largely a matter of taste. Ale and stout are preferred by many patients.
In pyrexial cases brandy, whisky, or some form of spirit, seems often to
232 SYSTEM OF MEDICINE
suit best ; and the quantity that can be taken 'with advantage under
these circumstances may be very large. Alcohol has no influence in
promoting repars,tive sclerotic changes, as some have asserted. In cases
of obstinate anorexia forced feeding by means of the stomach-tube has
been found useful by Debove and others. Massage is occasionally useful,
especially where debility is a prominent symptom, and is unaccompanied
by pyrexia.
In addition to the utmost attention to the matter of food the rules
of -general hygiene must be carefully observed. The patient's house
ought to be well drained, builfron a light porous soil, and, if possible, it
should face the south. The rooms, and especially the sleeping-apart-
ments, must be well ventilated and suitably warmed. It is hardly
possible to over-estimate the value of fresh air and sunshine. Regular
exercise, walking, riding, outdoor games of the less violent kind, such as
golf, cycling, shooting, and fishing, may all be practised with moderation
if the patient's general condition be good, and if there be no pyrexia.
Where this is not possible, the patient, in favourable weather, may go
out in a bath-chair or in a carriage ; or he may sit out of doors in a
suitably arranged shelter. Even when he is entirely confined to bed
with fever, wasting, night sweats, and symptoms of progressive disease,
much benefit may still accrue from wheeling the patient's bed out of
doors into a sheltered spot, or into a sunny balcony, as is done at
Falkenstein and other places ; bed-ridden persons may, in this manner,
spend the greater part of the day in the open air with great advantage.
The clothing should be warm and yet light, and woollen garments should
be worn next the skin. Comforters for the neck and chest-protectors,
which encourage hypersemia and increased sensitiveness of the skin to
changes of temperature, are unnecessary and unadvisable. Woollen
socks or stockings and thick boots are required to prevent the feet from
getting chilled. Respirators worn over the mouth are not now so much
in vogue as formerly. If the patient breathe through his nose, as he
ought to do, a respirator is superfluous. When a strong, cold wind has
to be faced, a light shawl or thick veil may be wrapped round the face for
temporary protection.
The skin may be rendered less sensitive to changes of temperature
by the daily use of the cold shower bath or douche in the morning ; but
in the case of more delicate patients, with feeble circulation, a warm bath
followed by cold sponging is preferable. Early hours, the avoidance of
crowded rooms, theatres, and smoking-rooms, a life free from excitement,
and occupation for the mind, such as reading, drawing, chess, billiards, and
other indoor games, are to be recommended. Instrumental music may
be practised, but singing is not advisable, except for the more robust
patients, in whom the disease is quiescent; though Walshe gives in-
stances of singers continuing to take leading parts in the opera while
suffering from pronounced pulmonary disease. Medical direction is most
desirable ; and the success of some Continental health resorts is doubtless
attributable in a large measure to the careful and strict superintendence
PHTHISIS PVLMONALIS 233
of the physicians in charge. But the majority of English patients find
such a rigid supervision irksome and disagreeable; and hitherto such
establishments have not been in much request in this country.
In selecting a suitable climate we must be guided by certain general
principles. Purity of the atmosphere, and especially freedom from dust
of all kinds, and abundant sunshine, are the fundamental requisites.
Questions of altitude, temperature, and moisture of the air, and geo-
graphical considerations in general, are still matters of dispute, and are
discussed elsewhere in this work.
If the patient's surroundings satisfy the requirements just indicated,
it is unnecessary, in many instances, to advise a permanent change of
residence. In the case of wealthy people it may be desirable to send
them away to some health resort, where they will be more ready to
submit to strict medical supervision and direction than at home. When
the patient lives in a large town he should be recommended to remove
into purer air, if his means permit. It is useless and cruel to send
patients with advanced disease to a distant health resort. To such
persons the fatigue of a long journey may have disastrous consequences,
and the loss of home comforts cannot be compensated even by the best
of climates.
If the general health be well maintained, and the pulmonary disease
be neither very active nor extensive, great benefit may be obtained by
spending the winter, or better still, by continued residence at the high
alpine stations, such as St. Moritz, Davos, and the like. Better results
are generally obtained in men than in women, as che tastes and the
habits of men impel them to take a fuller advantage of the oppor-
tunities of outdoor life and exercise presented by an alpine climate.
Under similar conditions of health, emigration to Colorado, the Rocky
Mountains, and the high levels of South Africa offers good prospects to
young men.
Emphysema, laryngeal tuberculosis, and manifestations of nervous
erethism are generally regarded as contra-indicating residence at the
high alpine stations. Such cases are more adapted for Egypt, the
Eiviera, Madeira, the Canaries, or the south coast of England. For
a detailed discussion of this subject the reader is referred to the article,
" Climate in the Treatment of Disease," vol. i. p. 247. »
C. Symptomatic treatment. — In combination with the general hygienic
measures that have been briefly sketched the exhibition of certain tonic
drugs is often very useful. The most valuable are strychnine or nux
vomica, arsenic, and quinine. Opinions differ as to the relative value
of these, but strychnine appears to deserve the first place. Arsenic has
no specific influence on the disease, but it may do good service in
its capacity of a nervine tonic ; the same may be said of quinine.
Iron has still a great reputation with some physicians ; but it does not
suit all patients, especially the large class that suffer from a tendency
to gastric catarrh ; and it has little eff'ect on the ansemia of phthisis.
In persons who can take a fair amount of exercise, and have a good
234 SYSTEM OF MEDICINE
digestion, a short course of iron, either alone or in combination with
arsenic, is sometimes attended with good results. The hypophosphites
of lime and soda have been largely tried, and are still much used in this
country. They are certainly not possessed of any direct action on the
tuberculous process, and their tonic efifects have been greatly over-
estimated.
Fever. — Quinine has been extensively used for the purpose of
reducing fever, especially on the Continent ; but it is generally allowed
that in order to obtain this result 20 to 30 grains must be given in a
single dose, or divided into four or five doses, to be taken at short
intervals some hours before the temperature begins to rise. Even
when administered in such quantities the antipyretic action of quinine
is but slight, and the stomach is often deranged by the drug. The
combination of quinine, opium, and digitalis, known as Niemeyer's Pill,
has long enjoyed a great reputation in pyrexial cases ; but, although
its general effects are sometimes salutary, it is rarely very efficient in
the reduction of temperature.
Of late no small number of antipyretic drugs have been employed —
salicylic acid, salicylate of soda, antipyrin, thallin, phenacetin, anti-
febrine, and many others. The most effectual seem to be antipyrin and
antifebrine, which, when given in sufficient doses, undoubtedly effect a
considerable fall of temperature. Antifebrine is a very powerful
remedy, but its action is somewhat uncertain. It is never advisable to
prescribe larger doses than two or three grains to begin with : in these
quantities it may be repeated at short intervals till eight or ten grains
have been taken. Unfortunately the reduction of temperature produced
is but temporary, and no further effect on the disease is produced.
Moreover, the prolonged use of antifebrine and antipyrin is extremely
depressing, an 1 causes profuse sweating. Wilson Fox believed that the
continued use of small doses of these remedies and of salicylate of soda
had a beneficial result on the general condition, although the range of
temperature was not appreciably affected.
Tepid sponging during the pyrexial periods sometimes gives con-
siderable relief, even if it fail to reduce the temperature of the body to
any great extent. The use of the cold or tepid bath finds few advo-
cates on account of the further depression which, in the prostrate con-
dition of such patients, is apt to follow its use.
Sweats. — Atropine in doses of xoir*^ *o -rtrt^ of a grain, given at
bedtime, is the most effectual agent we possess for checking sweats. A
combination of extract of belladonna and oxide of zinc is also useful,
but it is inferior to atropine. Picrotoxin, roTr*^ *o w^h of ^ grain
(Murrell); strychnine, 10 TT|^ of the liquor (Lauder Brunton) ; and
agaricin may also be employed with advantage in some cases. In the
slighter cases, to sponge the skin with toilet vinegar and water may
be sufficient. Arsenic is recommended by some authors, but when the
sweats are profuse it has little influence.
Cough. — A moderate cough is the natural consequence of pulmonary
PHTHISIS PULMONALIS 235
disease, and needs no special treatment; moreover, where secreting
■cavities exist, effective cough is most desirable. But when the cough is
very violent, spasmodic, or incessant, and the patient becomes much
exhausted thereby, it is necessary to treat this distressing symptom
directly. In order to do this with success we must first discover the
source of the cough. The more violent the fits of coughing, the more
likely are we to find that the cause is situated in the larynx or main air-
passages. "When the larynx is the seat of ulceration or inflammation
local treatment is indicated. Among the most useful sedative remedies
we may mention an intra-laryngeal spray of cocaine (2 per cent solution),
an inhalation of 10 drops of oil of peppermint, or of a 20 per cent
alcoholic solution of menthol in an orinasal respirator, and the use of
1 drachm of glycerine of carbolic acid, with 10 drops of chloroform
added to half a pint of boiling water in a steam-inhaler. Creasote or
•carbolic acid, diluted with rectified spirits, or spirits of chloroform, may
also be used for inhalation in an orinasal respirator. In similar
affections of the trachea and large bronchial tubes the same treatment
may be applied ; but the cocaine spray can only reach the upper part
■of the trachea at farthest.
Where the cough depends on bronchitis of the smaller tubes the
treatment is that of ordinary bronchitis ; an alkaline mixture contain-
ing bicarbonate of soda, or citrate of potash, with a few minims of
ipecacuanha wine, may be prescribed ; and, if expectoration be difficult,
3 or 4 grains of carbonate of ammonia may be added. In some cases
5 TTL of antimonial wine may be substituted for ipecacuanha for a few
days with excellent efiect. Similar drugs may be prescribed in an
effervescing mixture. Iodide of potassium in small doses, squill, and
senega may also be given when secretion is tough and difficult of
removal. Warm drinks, like tea, cocoa, or milk, or a steam-kettle to
moisten the air, may often be used successfully for the same purpose,
and may be tried before resorting to expectorant remedies. But in
many cases all the above-named measures fail to give more than tem-
porary relief, and sedative drugs are required. A linctus containing
tincture of belladonna, spirits of chloroform, and glycerine may some-
times prove useful ; but in the worst cases opium in some shape is
indispensable. A combination of morphia and hydrocyanic acid with
glycerine, spirits of chloroform, or syrup of wild cherry, forms an
effective linctus, which, however, must not be used too freely lest the
digestion be deranged.
Codeia may be substituted for opium, as it interferes less with the
appetite ; but its sedative effects are not equal to those of morphia.
In some cases of early disease, associated with a troublesome cough,
much relief may be obtained from a small blister applied to the sub-
•clavicular region on the affected side.
Expectoration. — When the expectoration is very profuse, the
administration of purified creasote or guaiacol in capsules is sometimes
•effectual in diminishing the excessive secretion of the bronchi and
236 SYSTEM OF MEDICINE
pulmonary cavities. Turpentine and various resinous drugs are some-
times given for the same purpose ; but the expectoration is symptom-
atic of broncho-pulmonary disease, and rarely requires direct treatment.
DyspncBa, though seldom a prominent feature, is occasionally very
distressing. When due to acute miliary tuberculosis and rapidly
advancing pulmonary disease it admits of little relief, and we must be
content to administer stimulants ; such as ammonia, ether, and brandy.
Attacks of dyspnoea, depending on violent and ineffectual attempts
to remove tenacious secretion from the bronchial tubes, may be miti-
gated by the judicious use of expectorants, the best being ammonia and
senega. Steam inhalations of carbolic acid may render good service.
In some cases dyspnoea has been lessened by inhalations of iodide of
ethyl, as suggested by Dr. E. E. Thompson. Dyspnoea arising from
cardiac failure, with attendant oedema of the lung, must be treated by
diffusible stimulants and hypodermic injections of strychnine. The
dyspnoea of pneumothorax will be referred to presently.
Haemoptysis. — The pulmonary haemoptysis of tuberculous disease
may be due to capillary haemorrhage, ulceration of vessels, or aneurysm
of the pulmonary artery. The loss of blood in the first case is never
extensive, and direct treatment is not required. In the second and
third cases haemorrhage is the result of gross lesions of comparatively
large vessels, consequently the amount of blood lost may be consider-
able ; yet even under such circumstances spontaneous cure is not infre-
quently effected by the formation of a thrombus, which seals up the
ruptured vessel.
In our treatment of haemoptysis we endeavour to imitate nature's
method, that is, to promote thrombosis by lowering the pressure in the
pulmonary artery.
It is important to recognise that the faintness which often attends
the attack is a symptom of cardiac depression — a condition in itself
favourable to thrombosis. In all cases, whether the haemorrhage be
profuse or slight, absolute rest must be insisted upon. The patient
must keep in bed in a cool airy room, and should maintain a semi-
recumbent position. Talking, movement, or excitement of any kind
must be avoided. Nothing more than iced milk, meat jelly, and small
sandwiches of bread and butter should be given for the first few days,
and alcohol in any form must be expressly forbidden. The cough, which
is rarely absent, may be relieved by sucking ice ; but when it cannot thus
be checked some preparation of opium must be administered. Small
and frequent doses of morphia may be given by the mouth, or one-third
of a grain may be injected under the skin. This remedy not only exerts a
valuable local effect on the injured vessel by the rest which it gives to
the lung, but it helps also to allay the restlessness and agitation of the
patient. At the same time, seeing that in most fatal cases of haemoptysis
death occurs from suffocation rather than from the amount of blood lost,
it is clear that the indiscriminate use of morphia is not without its
dangers.
PHTHISIS PULMONALIS 237
When from flooding of the bronchial tubes with blood dyspnoea is
very pronounced, cough should not be checked by sedative drugs. With
the view of reducing the blood-pressure, sulphate of soda or magnesia,
in doses of 60 grains, should be given every three or four hours to
begin with. Saline purgatives cause determination of blood to the
intestine, and thus relieve vascular tension, but, unfortunately, their
action is rather slow. Aconite has been recommended by Dr. Andrew, on
the strength of experiments by Dr. Bradford and Mr. Dean which show
that it causes a fall of pressure both in the carotid and pulmonary arteries.
This method seems worthy of trial, but I have not had sufficient experi-
ence of it to express an opinion as to its merits. Astringents, like gallic
acid and lead, are still extensively used, but it is difficult to see what
effect they can have on aneurysms or ulcerated vessels. Ergot is per-
haps the most popular drug at present, but, according to Bradford and
Dean, it causes a rise of blood-pressure not only in the aortic but also in
the pulmonary circuit ; a result which must aggravate rather than check
haemorrhage from the lungs. , Clinical experience shows that the effect of
ergot is as uncertain and unsatisfactory as those of gallic acid and lead.
The constipation which is produced by the last two remedies must
tend, moreover, to raise blood-pressure, which is injurious. Oil of turpen-
tine in large doses sometimes does good service, probably in virtue of
the cardiac depression which it causes. Nauseating doses of ipecacuanha,
recommended by Trousseau, seem to act in the same way ; but the risk
of vomiting is a serious one, and the remedy is now seldom employed.
The application of ice to the chest appears to be of very doubtful utility,
and in this country is little used.
The artificial induction of pneumothorax to cause collapse of the
lung and pressure on the ruptured vessel was unsuccessfully employed
by Dr. Cayley in one case of persistent haemoptysis. Under similar
circumstances it would be worth while, in conjunction with other
measures, to try Prof. A. E. Wright's plan of administering chloride of
calcium in 15-grain doses three times a day, for a few days, to increase
the coagulability of the blood. In any case great care is needed in the
management of the patient after the haemorrhage has ceased. The diet
should be very sparing, and the patient should not rise from bed for
three or four days at least. Free action of the bowels should be secured
by the continued use of saline laxatives. Alcohol should be avoided
altogether for some weeks.
Pleurisy. — For the relief of the pain of dry pleurisy Dr. F. T.
Eoberts's plan of strapping the affected side gives excellent results, and
can be strongly recommended. But in cases where one lung is exten-
sively diseased, and pleurisy attacks the opposite side, it may not be
possible to apply strapping without dangerously curtailing the already
restricted respiratory surface. Under such circumstances we must be
content with counter-irritation, a few leeches, and poultices; if these
fail, a hypodermic injection of morphia will be required.
Eoberts's method is specially adapted for the treatment of pleurisy
238 SYSTEM OF MEDICINE
affecting the lower part of the chest, where the ribs are more yielding
and their movement easily restrained. Pleurisy in the region of the
upper three or four interspaces seldom causes such acute pain, as the
range of movement of the upper ribs is limited ; here counter-irritation
is generally sufficient. In cases of sero-fibrinous or heemorrhagic effusion
paracentesis should not be resorted to unless the quantity of fluid be so
great as to cause embarrassment of the respiration. Experience shows
that the pressure resulting from pleuritic efiusion promotes arrest of the
tuberculous process in the corresponding lung. As a rule the fluid is
slowly absorbed.
In the comparatively few instances of advanced phthisis in which
empyema occurs, the pleura should not be opened unless the abscess
point externally, or unless the effusion be so large as to constitute a
mechanical hindrance to respiration. In the latter case aspiration is
preferable to free incision. The empyema once opened will rarely close
again ; and free incision appears rather to hasten the patient's end.
In cases of early or limited pulmonary disease empyema must be treated
on ordinary lines. It occasionally happens that the pus spontaneously
becomes inspissated, and undergoes a caseous change.
Pneumothorax. — When pneumothorax arises acutely, with severe
dyspnoea and symptoms of shock, stimulants in the form of brandy,
ether, or ammonia should be given at once. Morphia has been recom-
mended by some writers to minimise the effects of shoct, but in the
presence of marked dyspnoea an opiate is contra-indicated. Where the
opening is valvular, and air accumulates in the pleural cavity under great
pressure, paracentesis may be necessary in order to withdraw a sufficient
quantity of air to relieve the pleural tension. Sir E. Douglas Powell
advises that the side be afterwards strapped to prevent reaccumula-
tion of air. Paracentesis is sometimes followed by subcutaneous emphy-
sema. In the event of sero-fibrinous effusion, tapping may be success-
fully employed, but seeing that spontaneous recovery may ensue, it is
well to wait for a time before resorting to this measure. In pyopneumo-
thorax incision is generally considered to be unadvisable, and this, no
doubt, is true of advanced cases. But the practice of early drainage is
worthy of further trial, where the general condition of the patient is
fairly satisfactory and the lung is presumably not much affected.
Laryngeal tuberculosis. — The treatment of this complication may
be general and local. The general treatment is practically that of
pulmonary tuberculosis, with certain reservations as to climate. The
best atmospheric conditions are a temperate climate, a moderate degree
of moisture in the air, and an absence of dust. At the same time, it
may be admitted that many cases do well in such a dust-laden and
apparently undesirable atmosphere as that of London and other large
towns. Tobacco-smoking requires a brief notice. Many patients have
no desire to smoke, but some have a craving for tobacco : if so, the
patient may be allowed to smoke once or twice a day after meals, pro-
vided it be out of doors or in a large, well- ventilated room ; the object
PHTHISIS PULMONALIS 239
of these restrictions being to prevent the inhalation of smoky air into
the larynx and lungs. The practice of inhaling tobacco smoke should
be forbidden. Strong alcoholic drinks, spices, and highly seasoned
dishes irritate the pharynx and epiglottis, and are to be avoided. The
local treatment is fully described in the chapter on " Tubercle of the
Larynx," vol. iv. p. 800.
I may say here that to palliate the laryngeal irritation we may
prescribe steam inhalations containing carbolic acid and chloroform ; or
at other times menthol or oil of peppermint on a respirator.
To soothe the pain so often present a 2 per cent spray of cocaine
may be used a few minutes before meals. The local application of
menthol, in the form of a 10 to 20 per cent solution in olive oil, some-
times gives relief ; or, again, the insufflation of one-sixth of a grain of
morphia with a little starch powder or sugar of milk. Some patients
find benefit from sucking ice. When, in spite of these measures, the
patient is unable to swallow, Dr. Wolfenden's plan may prove successful ;
the patient is directed to lie on his face, with his head over the edge of
the bed, and to drink through an india-rubber tube. It may ultimately
be necessary to have recourse to nasal feeding, which, at times, does
excellent service. The operation of tracheotomy is very rarely required,
the only indication being afibrded by the existence of severe laryngeal
stenosis and impending asphyxia. The treatment of tracheal tubercu-
losis can only be palliative.
Tuberculous ulceration of the pharynx, palate, and tongue must be
dealt with in the same way, and with the same reservations as in the
case of the larynx. Good results sometimes follow the use of lactic acid
when the ulceration is localised and the subjacent infiltration is not very
great. Granular pharyngitis and other non-tuberculous aifections of the
pharynx, which may give rise to troublesome cough and other symptoms,
must be treated on the principles laid down in the article " Pharynx "
(vol. iv. p. 729).
Gastro-intestinal symptoms. — Loss of appetite, cardialgia, and other
symptoms of dyspepsia may be treated by alkaline and acid tonics ; but
for general use nothing can excel an alkaline mixture consisting of
bicarbonate of soda (15 grains), tincture of nux vomica (10 minims), and
compound infusion of gentian (1 ounce), given before meals. If a sedative
action be desired, dilute hydrocyanic acid may be substituted for nux
vomica. The good efi'ects of this mixture are witnessed not only by
increase of appetite and relief of the dyspeptic symptoms, but at the
same time expectoration is facilitated, whereby the cough is indirectly
relieved.
In other cases, especially where flatulence is a prominent symptom,
better results are obtained by acids, with or without strychnine, given
after meals. In cases marked by irritative symptoms— such as vomiting or
pronounced epigastric pain and anorexia — a mixture containing bismuth,
hydrocyanic acid, tincture of belladonna, or, if necessary, a few minims
of liquor morphinse, given before meals, is to be preferred. Bismuth in
240 SYSTEM OF MEDICINE
powder, or in an effervescing draught with hydrocyanic acid, may prove
more successful in particular cases.
In all instances of dyspepsia the diet requires a careful survey. The
diet should be light and digestible, and the meals small and more frequent
than in health. In the comparatively uncommon form, distinguishable
by a red glazed tongue, vomiting and anorexia, liquid food, especially
milk with lime-water or soda-water, koumiss, veal or chicken broth, will
be required ; and complete rest in bed should be enjoined.
Inasmuch as this kind of gastric disorder mostly affects patients
suffering from pyrexia and other symptoms of progressive disease, the
outlook is very grave unless the gastritis can be speedily removed so far
as to enable the patient to digest an adequate supply of food. If the
symptoms resist the measures indicated, it may be necessary to rely
exclusively on peptonised nutrient enemas for a few days, giving only a
little iced water by the mouth, for the relief of thirst. Fortunately this
form of gastric disturbance is not of very frequent occurrence.
In most cases of obstinate dyspepsia mild purgatives are called for,
such as a small dose of calomel (half a grain to a grain at bed-time),
followed by a teaspoonful of Carlsbad salts, dissolved in half a pint of
warm water, in the early morning. Violent purgatives should be carefully
avoided altogether, owing to the risk of setting up intractable diarrhoea.
A tumblerful of hot water, sipped at bedtime for a few nights, often
gives great relief by washing out the stomach and removing remnants of
undigested food which are apt to undergo decomposition, and thus
to aggravate the catarrhal condition of the stomach. Dilatation of the
stomach occurs occasionally, and washing out may be required ; though
the cases in which this operation can be recommended are very few, as
the disturbance caused by the passage of the stomach-tube in feeble
patients may be attended with serious consequences. Gastric digestion
may be assisted by the administration of pepsin or papain, but, except as
a temporary expedient, little benefit is to be expected from this line of
treatment.
Diarrhoea is a symptom that should never be neglected ; it should be
treated by rest in bed and the application of warmth to the abdomen
and extremities. In many instances it depends on slight errors of diet ;
and in such cases regulation of the diet, and a mild purge to free the
intestine from irritating substances, may be all that is required in the
way of treatment. For this purpose we may prescribe 2 drachms to half
an ounce of castor oil with 10 minims of laudanum, or a small dose of
calomel. If the diarrhoea do not speedily yield, bismuth should be given,
in 20-grain doses, with a few minims of laudanum. In the far more
serious case where diarrhoea is the result of tuberculous ulceration or
lardaceous disease, powerful astringents, combined with opium, are indis-
pensable. A mixture containing aromatic sulphuric acid, tincture of opium,
and decoction of logwood, or again of subnitrate of bismuth, tincture of
catechu, and tincture of opium, will often suffice to keep the diarrhoea in
check. But in the most severe cases we must have recourse to stronger
PHTHISIS PULMONALIS 241
remedies, the best, perhaps, being a pill containing sulphate of copper
{\ grain) and opium (J grain), given once, twice, or three times a day,
as may be required. In cases where the ulceration affects the lower
end of the colon the enema opii (B.P.) gives more relief than anything
else. It will generally be necessary to revise the diet carefully ; the
most suitable food in the acute cases being milk, koumiss, or carefully
prepared beef-tea \ but when the diarrhoea lasts for weeks, boiled fish
and tender meat, freed from fat and pounded or finely minced, may be
given in small quantities. Digestion may be aided by peptonisation of
the milk, and by the use of pepsine or papain after meals. The slightly
bitter taste of peptonised milk may be masked by the addition of a tea-
spoonful of rum, cognac, or liqueur.
If the diarrhcBa be accompanied by much pain, hot fomentations
should be applied to the abdomen, and the warmth of the extremities
sedulously maintained. In the rare event of serious intestinal haemor-
rhage, an enema, consisting of a teaspoonful of oil of turpentine sus-
pended in two ounces of starch mucilage, should be administered at once.
Acute peritonitis must be treated on general principles by opium and
hot fomentations. In the yet rarer instances in which perforation can
be diagnosed the propriety of surgical interference must be considered ;
but the patient's general condition and the extent of the pulmonary
disease may not justify such measures.
In chronic tuberculous peritonitis with effusion, whether serous or
purulent, incision has, in several instances, been followed by arrest or
cure. A similar result may also ensue without any surgical measures ;
in these cases, no doubt, the effusion is serous. Some physicians believe
that the application of mercurial ointment to the abdominal wall promotes
absorption of the fluid.
When suppuration has occurred, incision should not be delayed.
Drugs seem to be of little use in this affection.
Eenal symptoms. Albuminuria, whether due to nephritis or amyloid
disease, is mostly found in advanced chronic cases. In such circumstances
active treatment, by rigorous milk diet and purgation, is quite out of
place. If possible, milk should be taken freely ; but it is not advisable
to prohibit a certain amount of meat and fish if the patient can take
them. The drug treatment may include digitalis and iron, mild saline
diuretics, and an occasional small dose of blue pill. But treatment
should be addressed primarily to the general condition rather than
to the renal disease, which is a local consequence of the constitutional
malady.
In the few instances where nephritis occurs at an early period of the
pulmonary disease, and where the health is not seriously affected, treat-
ment may be conducted on ordinary principles.
The tuberculous pyelitis and cystitis of advanced cases do not admit
of more than palliative measures. If the lung disease be slight, surgical
advice should be sought.
Nervous symptoms. — For the treatment of meningitis, tuberculous
VOT.. V R
242 SYSTEM OF MEDICINE
tumours of the brain, and nervous complications in general, reference
must be made to the proper articles.
It seems desirable, in conclusion, to sum up the general plan of
treatment suitable for an ordinary case. In the first place, attention
must be carefully directed to the rules of general hygiene ; to the
importance of spending as much time as possible in the open air, and
the necessity of an abundant supply of food. Excepting in the most
favourable instances, where the disease is quiescent, some form of tonic
medicine will be required from time to time, the best being an alkaline
bitter mixture, such as that already indicated. Narcotic and sedative
drugs generally should be employed with great caution, because of their
prejudicial influence on digestion ; and complications, as they arise,
must be treated on general principles.
Percy Kidd.
kefeeences
1. Battmgartbn. "TJeber Tuberkel u. Tuberkulose,"^c4fecAr./. M. Med. Bde. ix.
u. X. — % Idem. Lehrbuch der pathologischen Mykologie, n. — 3. Cornet. Ueber Tuber-
kulose, 1890. — 4. Ewaet, Wm. "On Pulmonary Cavities," Srit. Med. Joum. 1882.
— 5. FowLEK, J. K. T?ie Localisaiion of the Lesions of Phthisis, 1888. — 6. Fox,
"Wilson. Diseases of the Lungs and Flewa, 1891. — 7. H^^eakd, Cobnil, Hanoi.
La phthisie pulmonaire, 1888. — 8. Hiesoh. JBandbooTc of Oeographical a/nd Historical
Paihology, vol. iii. New Sydenham Society's Trans. 1886. — 9. Jani. "Ueber das
Vorkommen von Tuberkel -baoillen in gesunden Genitalapparat bei Lungensohwind-
sucht," Virchow's Archiv, Bd. ciii. 1886. — 10. Koch, R. "Die Aetiologie der Tuber-
kulose," Mittheilungen aus dem Gesundheitsamte, vol. ii. 1884. — 11. Landotjzy and
Qtteyeat. "Note sur la tuberculose infantile," Gaz. hebdomadaire, 1886. — 12.
Mabfucci. Baumgarten's Jahresbericht uber pathologischen Mikroorganismen, 1889.
— 13. Ogle, Wm. Quoted by Wilson Fox. — 14. Payne, J. F. "Tuberculosis as an
Endemic Disease," Transactions of the Epidemiological Society of London, 1892. —
15. Peipbe, E. " Znr Frage der TJebertragung der Tuberkulose durch die Vaccination,"
Inlernat. Min. Rundschcm, 1889, Nos. I. and II. (This article also deals with the
general topic of accidental inoculation.) — 16. Pollock, J. E. The Elements of Prognosis
in Conswmption. — 17. Powell, R. Douglas. Diseases of the Lvmgs amd Pletura. —
18. Ransomb, a. The Causes and Prevention of Phthisis, MUroy Lectures, 1890. — 19.
ViLLEMiN. Gaz. hebdomadaire, 1865. — 20. West, S. On Pneumothorax, Bradshaw
Lecture, 1887. — 21. Williams, C. J. B. and C. T. Puljnonary Gonsvmption.
P. K.
PNEUMOCONIOSIS
Pneumoconiosis, pneumonoconiosis, or, translated into English, " Dusty-
lung -disease," is a lesion that has attracted but little attention in this
country — a circumstance the more remarkable considering that Great
Britain has long held the first rank in manufacture, and that a large
proportion of its population is consequently engaged in dusty occupa-
tions. At the same time, credit is due to British physicians for the early
recognition of inhaled dust as a cause of lung lesion ; among them may
PNEUMOCONIOSIS 243
be mentioned Christison, Addison, Bennett, Corrigan, and Peacock, who
taught that inhaled dust can penetrate the lung tissue, and that its
presence can be demonstrated therein. This doctrine, however, had for
a long time numerous adversaries, who argued that the black granules ^
so frequently met with were derived from the carbonaceous materials of
the blood ; and it is only within the last half-century that this opinion
has been given up. That it held sway so long was owing to the
influence of the eminent pathologist Virchow. Without denying that
a black colour can be derived from the blood, it must be admitted,
nevertheless, that the pigmentary particles generally found in the lungs,
and especially in the lungs of persons engaged in dusty occupations, are
derived from inhalation of dust.
The opposite opinion derived great support from the notion long held
that the orinasal passages are so perfect and efiBcient as dust-strainers
that, in co-operation with the cilia lining the bronchi, no dust could reach
the deeper lung tissue. This opinion has been disproved both by experi-
ment and by observation, and is no longer tenable. Further, although it
is true that this conservative apparatus, so efficient in itself, is greatly
re-enforced by the strong expiratory act of the lung, yet it will fail to
arrest the ingress of particles if dust exist in large quantity or is breathed
almost without intermission ; or again, if the mucous membrane have
suffered damage such as to facilitate its entrance into the submucous
tissue. Under such circumstances the foreign matter enters the extra-
vascular lymph-current and lymphatics, pursues its course along the
pulmonary interspaces and connective tissue, and eventually reaches the
alveoli and bronchial glands. The last-named organs act as barriers
against its farther progress, and in consequence they become deeply
coloured and swollen, and occasionally suffer ulterior changes.
Consolidation by the excessive growth of fibrous tissue is the chief
pathological feature of pneumoconiosis. The pulmonary is transformed
into fibrous tissue ; the extent of change being dependent chiefly upon
the physical character of the dust inhaled, but in some degree also upon
accidental conditions of employment. The fibrotic change is almost
always associated with thickened pleura, and the degree of this change
bears some relation to the extent of fibrinous production in the lung
substance itself. Now and then the fibrotic change seems to start from
the pleura, and to spread in a branching, vein-like fashion ; or in bands
across and through the lung. The ramifying lines of fibrous growth for
the most part represent interlobular or interstitial spaces, and are white
in colour ; this, however, is no essential character, for not infrequently
' It is very gratifying to be able to refer to so admirable a collection of specimens ol
Pneumoconiosis as that in the museum of the Middlesex Hospital, — the result of long-con-
tinued pathological research made by the late Dr. Headlam Greenhow, physician to that
hospital. Moreover, we have the benefit of his history of many of the cases that furnished
those specimens recorded in the volumes of the Pathological Society of London. In no better
way can the morbid anatomy of pneumoconiosis be studied than by au inspection of this
collection ; I have accordingly introduced the numbers affixed to some of the specimens in
the proper places of this article.
244 SYSTEM OF MEDICINE
the marble-like venation is black or brown, and its colour is largely
dependent on that of the dust inhaled. The consolidation in question
evidently has its origin in an exudation of lymph consequent upon very
chronic inflammation of low intensity, due to the passage of dust into the
bronchial tubes. A very similar consolidation, though rarely so extreme,
follows the inhalation of tubercle bacilli ; and as there is no little resem-
blance in many particulars between pneumoconiosis and tuberculous disease
of the lung, there has been great confusion between the two — particu-
larly on the part of laymen, who have not inaptly called both the one
and the other by the common name of consumption. At the same time,
as it was observed also that consumption, in this wide sense, manifests
itself pre-eminently in certain occupations, further distinctions were made
between that of potters, of stone-workers, and of Sheffield grinders ; —
" grinders' rot," " miners' rot," and so forth.
The fibrosis in difi'erent cases varies greatly in extent, in density, and
in the degree to which the bronchial tubes and pleura are implicated.
The condensation in some instances does little more than destroy the
sense of crepitation under the fingers ; whilst in others the pulmonary
tissue, losing its sponginess, is transformed into a dense mass which, in the
most advanced specimens, shows no traces of normal structure, and in
hardness, and often also in colour, resembles india-rubber. On section,
moreover, this dense mass betrays at times an appreciable amount of gritti-
ness, particularly if the dust inhaled be of a siliceous or metallic quality.
The resemblance between specimens of pneumoconiosis and of tuber-
culous disease — especially where the latter has been very chronic — is
often so great that, to the eye, the two may be almost indistinguishable,
and the true nature of the disease a matter of doubt. In the eyes of
many persons the two diseases are inseparable, and the opinion is held
that the dust-made disease does not exist apart from tubercle. That
pneumoconiosis, however, does exist apart from tubercle is the conclusion
of a large number of independent observers. The determination of this
problem in particular cases will depend, therefore, upon the discovery of
the specific bacillus.
Sir Andrew Clark uses the name " phthisis " in a wide sense, and
recognises two forms of it : (i.) the tuberculous, and (ii.) the fibroid,
the former being characterised by the tubercle bacilli. Dr. Thomas
Harris of Manchester, in his able lectures on phthisis, makes a parallel
division of fibrotic pulmonary consolidation — under the appellation of
interstitial pneumonia — into "primary" and "secondary." The former
is represented by Corrigan's pneumonia, which makes its appearance
without evident cause ; the latter by pneumoconiosis, with an obvious
cause in the inhalation of dust.
The grounds for the distinction made by both these authors are well
set forth, by the former on clinical, by the latter on pathological data ;
both, however, agree that the non-tuberculous variety is of comparatively
rare occurrence. As pneumoconiosis is primarily local, and without
constitutional complications, all other viscera, except the lung affected.
PNEUMOCONIOSIS 245
may remain normal and carry on their several functions, until indeed the
long-persistent local derangement brings about secondary disturbance in
one or more functionally connected organs. AH such secondary disorders
are of late a])pearance among the phenomena of pneumoconiosis ; they
may even extend to heart disease, with a certain amount of general dropsy,
gastric and hepatic troubles, and secondary albuminuria. This being the
case, the sufferer with pneumoconiosis is enabled to undergo considerable
exertion for a long time, and is apt to look upon his earlier symptoms as
uo very important affair.
Although linked by its inflammatory characters to pneumonia,
pneumoconiosis is not an example of croupous inflammation ; it is rather a
bilateral peribronchitis. Not infrequently it sets up a nervous disorder
indicated by spasmodic breathing ; hence it is also often called asthma, a
name further distinguished by a noun indicative of the employment to
which it is due. It is, moreover, a non-febrile malady ; though there may
be an intercurrence of active disease, the product of chill, or of superven-
ing tuberculous deposit, with consequent elevation of temperature. In
either case hectic symptoms may appear, local softening, and now and
again a patch of ulcerative gangrenous decay. Pneumoconiosis is not a
disease of children, but of adults, and these for obvious reasons are
almost always of the male sex. The form of fibrosis which occurs in
children after attacks of measles and whooping-cough is quite different
from pneumoconiosis. Pleuritic thickening, as before said, is commonly
met with ; nevertheless it cannot be esteemed a necessary concomitant.
The like is true also with regard to chest deformity. This last incident
owns as contributory causes pleuritic adhesions and the shrinking of the
lung itself as a result of progressive contraction of the fibrotic tissue
diffused through its substance.
When once fibrosis has invaded the pulmonary substance, its tendency
is to advance ; chiefly because of repeatedly recurring bronchial attacks,
due to fresh bronchial colds and the continued introduction of dust, inten-
sifying the inflammatory action. For the most part both lungs become
affected, though in varying degree. This would seem to be a necessary
consequence of the entrance of the dust by the common channel of the
larynx; nevertheless, some further determining cause operates to vary
its diffusion, and to account for its predilection for the posterior and
middle portions of the lungs. The chronic interstitial pneumonia of
Clark and others is a unilateral disease generally due to a dry pleurisy.
Symptoms. — The disease is an extremely chronic one, and, beginning
as a non-febrile bronchitis, it attracts little attention until an area of the
breathing tissues of considerable extent is more or less disabled. The
augmented bronchial secretion is at first noticed chiefly on waking, or on
passing from a warm workshop into the open air. It is nothing more
than ordinary mucus, with minute particles diffused throughout it,
numerous" enough in many instances, when the dust is of a dark hue, to
give it a black colour ; it is glairy, and is coughed up with some effort.
As yet the affected workman does not suffer in his general health. He
246 SYSTEM OF MEDICINE
eats, drinks, and sleeps -well, and joins in active physical exertion. But
the conditions of employment, involving continuous exposure to dust
inhalation, cause recurrent bronchial attacks, each in its turn damaging
the lung more and more. Months and years may pass with but a slow-
increase of cough and spitting, though with an amount of dyspnoea
exceeding that which is met with in ordinary bronchitis, and out of
proportion to the severity of the evident organic changes. Constitutional
symptoms are, however, still absent, and as appetite and digestion are
good there is no wasting.
Continuance in the dusty occupation is soon attended by more and
more copious expectoration, which gradually acquires a yellowish gray tint
and the features of muco-pus. At length, however, the time arrives when
impeded respiration, oft-repeated cough, loss of rest and appetite, and the
discharge of muco-purulent fluid tell injuriously upon the general health
and strength. The sufferer loses ground in all directions, he cannot
pursue his work as heretofore, nor take outdoor exercise; he cannot even lie
comfortably in the horizontal position. He seeks hot rooms and qjiietude,
and becomes a valetudinarian, calling for medical treatment to relieve
his cough and yet more to relieve his breathing. And now it is that loss
of flesh and colour becomes apparent, whilst urgent and now constant
dyspnoea confines him to hishouse or to his chamber. At this stage of
the malady the name of consumption is applicable enough ; though, as
will presently be seen, sufficiently distinctive signs between the two
maladies are discernible.
The great dyspnoea suggests the existence of pulmonary emphysema
(1271), but the known pathology of fibrosis indicates that where emphy-
sema exists, it is vicarious and comparatively insignificant. The dyspnoea
is attributable to abridged respiratory area, to the choking of bronchial
tubes by secretions, and, it may be, to cardiac mischief ; and, as before
stated, certain dusts, by the possession of special properties over and
above the strictly mechanical, still further aggravate the difficulty of
"breathing, and assimilate it to the asthma of emphysema : an example
•of such properties is found in flax -dust. Moreover, the asthmatic
state is not conjoined with the barrel-shaped thorax of emphysema :
■on the contrary, the lungs shrink as the diffused fibrin progressively
■contracts, and the bronchi, as the tissues are compressed and solidified,
are distorted, dilated, and thickened (1274, 1279). The movements of
the chest walls are crippled by the fibrous bands which pass between the
costal and pleural surfaces. By other adhesions the lobes of the lungs
also are distorted, drawn together, and compressed ; and as a result their
freedom of action and air capacity are seriously curtailed. All these
conditions necessarily add to the difficulty of respiration (1274). If
pneumoconiosis be unilateral, the fellow lung expands, and indeed may
become truly emphysematous.
Pathology. — That a particle of dust, when it comes in contact with
mucous membrane, will cause great irritation is a fact of everyday
observation in the case of the conjunctiva. The irritation is immediate.
PNEUMOCONIOSIS 247
and so severe as speedily to produce injection of the blood-vessels, and
an outpour of tears from the lachrytnal glands ; if the disturbing cause be
not soon removed, the phenomena of inflammation will set in with sero-
purulent discharge, thickening of the conjunctival membranes, and
efi'usion of lymph as a fibroid film upon the transparent cornea beneath.
All these phenomena fall within the range of unaided vision ; and
we are fully justified in concluding that something of the sort occurs
when the mucous membrane of the respiratory passages is directly
irritated, modified, as it may be in some details, by the special histological
qualities of lung tissue.
The degree of irritation set up, and its consequences, will vary accord-
ing to the physical, chemical, and physiological properties of the offending
agent, the quantity introduced, the frequency of its introduction, and the
period during which its action continues. For instance, there are dusts
which are escharotic and damage at once the structures they fall upon.
This is true of dusts both of mineral and organic nature. There are
other dusts which damage by their chemical properties ; and, again, others
of animal origin which may inoculate or infect the system. Lastly,
the dust of poisons may enter the body and display their respective
efi'ects, not only locally, but on the whole organism also.
The dust that has entered within lung tissue can be detected by the
microscope ; and may often be seen, under appropriate tests, to preserve
both its physical and chemical properties. For instance, particles derived
from coniferous wood have been identified by their gland-bearing fibres,
and siliceous particles by their translucent appearance and their resistance
to acids other than hydrofluoric. But the particles of dust are for the
most part amorphous, and diffused sparsely in the tissue invaded by
them (1272); or they are arranged in linear fashion, or collected in small
masses, or in vein-like form marking out the lobules and alveoli within
the interior of some of which they may be seen (1279).
The permeating dust is usually of a black colour, though where it
possesses a distinctive hue of its own this peculiar tint pervades the
altered tissue. (In specimen 1276 the lung is stained with carmine.)
A blue black is frequently seen (12'71), and a yellowish or buff hue is
not uncommon ; deposit of the latter colour is mostly seen in thB lungs
of quarrymen, or sometimes in accumulated matter suggestive of caseous
transformation (1278). Yet even where the dust inhaled is itself of a
pale colour, the parenchyma infested by it is more or less black or slate
coloured ; frequently this deep colour is not wholly derived from with-
out, but owes its origin to some material collected within the living
tissue ; it is most likely a derivative from the blood.
The very clogged portions of black lung formerly met with in coal-
getters were proved by Christison and others to be due to a great
accumulation of coal-dust, the nature of which was demonstrable by
combustion.
The lung of a young child, until about eight years old, has a clear
pink colour ; but about this age black pigmentary spots or lines appear
248 SYSTEM OF MEDICINE
in lobar and lobular spaces, mapping out the surface in irregular areas,
and producing thereby a marbled appearance. As age advances, these
dots and lines multiply and enlarge, and mostly in adult life produce
a generally diffused dusky colour.
In persons engaged in a dusty occupation this coloration becomes
progressively more pronounced ; its tint varies according to that of
the inhaled dusts, but a black colour largely preponderates. In the
instance of workmen exposed to the dust of oxide of iron a reddish colour
prevails.
The fine impalpable dust most people breathe is not the cause of the
true pneumoconiosis we are concerned with. It blackens the lungs more
or less, but these organs appear to be very tolerant of it ; nevertheless,
it may be that a lung deeply charged with black pigment is less efficient
and less able to withstand inflammatory or other disease. When, how-
ever, a directly irritant dust is abundantly inhaled during some industrial
process, an active morbid process is the result, one ending in structural
lesions.
The source, form, and physical qualities of inhaled dust particles have
furnished the basis for the classification of ensuing morbid consequences
to lung tissue. Thus authors have described the results of inhaling
siliceous particles as chalicosis or silicosis ; of metallic particles as siderosis ;
of carbonaceous particles as anthracosis ; of cotton particles as byssinosis.
Other uncouth words have been suggested for difierent morbid varieties
of the same general kind. To multiply such words is undesirable ; what-
ever the kind of dust, the consequences of its presence are, pathologically
speaking, substantially the same.
Besides the form we have to recognise other differences of inhaled
particles, as, for instance, the density and the chemical qualitites which
affect their pathological influence. This last, in like manner, is modified
by the solubility, miscibility with fluids, and cohesiveness of the dust.
A very soluble dust will be got rid of by speedy absorption ; a miscible
one, like flour and other amylaceous substances, will collect in tenacious
masses and obstruct the bronchial tubes ; the fine dust of hydrate of lime,
unless highly caustic and breathed freely, seems more or less to be
disposed of in the parenchyma by absorption and the influences of
secretions upon it ; whilst that of lime salts — for instance, the carbonate
in the shape of chalk, and the sulphate in the form of alabaster in fine
powder — may be breathed with impunity for long periods of time.
In numerous cases mixed dusts are encountered ; as, for example, in
the Sheffield and needle-making trades, where siliceous and metallic dust is
intermingled in various proportions. In such instances this circumstance
of admixture is presumably attended by some variations in the conse-
quent symptoms. Yet even in this matter the form and dimensions of
the scattered particles play a more important part than chemical consti-
tution.
Again, speaking generally, the ill results of dust are more serious the
greater its departure from organic tissue in character.
PNEUMOCONIOSIS 249
When dust which has entered the respiratory system has reached
the alveoli it attaches itself in the first place to the walls, but sooner or
later penetrates them. The particles are borne along by mucous cells,
which, being destitute of walls, envelop them after the fashion of amoebae ;
but the foreign bodies soon prove a source of irritation, which in the case
of the more irritant kind advances to inflammation of low intensity, but
sufiicient to induce an outpour of some lymph and the generation of
granular matter and exudation cells. The first effects of the foreign matter
are the detachment of the normal epithelial cells of the alveoli and an
attendant thickening. The accession of the new material within the alveolar
cells causes their distension and functional derangement, and presently, by
the action of the exuded fibrin, their obliteration. When a group of such
altered cells is formed, the next phenomenon is the production of a piece of
more or less solidified lung tissue, manifested in the form of a granule.
The multiplication and cohesion of such granules, and the gradual con-
densation of the fibrin, transform the piece of lung into the fibroid
texture we know as pneumoconiosis ; whilst the transformation is
proceeding the blood-vessels become thickened, blocked, and impervious,
and the compressed lymphatics are merged in the morbid growth.
In their general features these structural changes, though chiefly peri-
bronchial, resemble the early stage of croupous pneumonia ; but their
development is so slow and inactive that no marked fever attends them.
However, they possess the faculty of extension ; the mucous and inflam-
matory cells make their way along the adjoining connective tissue, and
fibrosis continues to spread in the form of fibrous bands, veins, or streaks.
On section of the condensed portions of fibrotic lung the surface
commonly exhibits numerous raised points which give it a coarsely granu-
lated appearance. Most of these points, if closely examined, will be
found to be small bronchial tubes, cut across, and thickened and
obstructed by secretions and, frequently, by a yellowish matter, sugges-
tive of caseation, which imparts a speckled aspect to the specimen
(1254, 1255, 1256). The occlusion in its turn embarrasses the lung yet
more, and retrograde structural changes are precipitated.
The morbid phenomena just described are those of dust of distinctly
irritating qualities ; but when the dust is of a more innocent kind, they
are considerably modified. For example, where the dust is organic, but
devoid of acrid qualities, as in the cases of the flour of wheat and other
cereals, and of like mild substances, the primary irritation is of small
account; the dust then operates chiefly as an obstructive agent, clogging
the respiratory passages ; if any inflammation be present it is very slow.
Yet this clogging cannot go on without disabling the air-cells by pressure
and otherwise. Soot and very fine charcoal, too, disturb the respiratory
organs and their functions to a still less degree ; and, though very widely
diffused, and causing, it may be, much dyspnoea, they produce no well-
marked signs or symptoms of inflammatory action and condensation.
The intimate pathological processes associated with anthracosis
(coal-dust condensation) differ considerably from those dependent upon
250 , SYSTEM OF MEDICINE
the denser dusts of stone and metal, as is indicated by their morbid
anatomy. Nevertheless, indurated lobes are met with, and pulmonary
tissue may be so permeated by fine coal-dust as to be rendered friable,
and to exude on section and pressure a black, inky fluid ; moreover, the
expectoration at the same time gets similarly coloured, and acquires
the name of " black spit." In some such cases the production of fibrous
tissue gives place to a process of disintegration ; the pervading dust
being, we may suppose, so considerable in quantity as to destroy the
vascular supply and lead to a sort of necrosis (1274). In other words,
the dusty irritant fails to arouse active inflammation and fibrinous exuda-
tion. Examples of the extreme forms of the disease are at the present
time unknown, or almost unknown, in English mining districts, thanks to
the improved ventilation of mines and the operation of the Mining
Acts which limit the age of children admitted to pitwork ; for the
same reasons the inky expectoration, known in past days as "black
spit," is correspondingly rare. It is generally true, indeed, of all dusty
occupations, that indurated impervious lungs are becoming rare as
sanitary construction is improved, as appliances are used in factories to
convey away and disperse the dust, and as sanitary laws and observances
are better observed.
The pneumoconiosis due to the coarser dusts which arise from the
operations of stone- dressing and quarrying present some peculiarities
attributable to the form and composition of the particles. The sawing
and polishing of Aberdeen granite appear to be unattended by severe
lung irritation ; whilst, on the other hand, working with Edinburgh
building-stone proves most injurious, and kills the workers by fibroid
phthisis in relatively large numbers.
Another peculiarity of the dust of stone is that it tends to collect in
masses, forming concretions (pneumoliths) which, by producing softening
and ulceration around them, give rise to cavities with soft walls, though
now and again lined by membrane. This state of things occasionally
«nds in the detachment and expulsion of the concretion, as it pene-
trates into a bronchus of sufficient calibre. Another feature in the lungs
of stone-workers is that a yellowish or grayish hue replaces more or less
the blackness seen in most other workers (1276, 1285, 1286).
Dust often reaches the pleura and lines its pulmonic surface, impart-
ing a more or less black colour to it, and at other times collecting in
nodules upon it. Its transference is effected by the lymphatics.
The ultimate goal of much of the dust inhaled is the bronchial glands,
where it becomes imprisoned, causing enlargement and possible suppura-
tion of those organs, which acquire a black colour, often of great depth.
Occasionally the enlarged and softening glands adhere to a contiguous
organ, as, for example, to the oesophagus ; this may be followed by ulcera-
tion through its coats, and the contents of the abscess thus discharged.
Not only do diff'erences of dusts, in their origin, form, and composition,
modify the form of the lung diseases which are set up, but they variously
affect the health of the sufferers ; and as the various conditions under
PNEUMOCONIOSIS 251
which labour is carried on have also their respective influences, it becomes
evident that the symptoms and pathology of pneumoconiosis must exhibit
a great variety. Intemperate habits in the patient, for example, precipi-
tate the onset of the lesion, and accelerate its course.
Further, no doubt exists that persons of any age who inherit chest
weakness, if they follow a dusty trade, are more liable to suffer from
pneumoconiosis. One practical lesson is that such persons should not be
thus employed. This inference points to the utility of certifying factory
surgeons to pronounce upon the comparative fitness of all who engage in
such work, especially of children and youths, and to the care they should
exercise in following their occupation.
Again, the lungs of very young children, and of those born of parents
with thoracic lesions and damaged constitution, suffer more readily from
exposure to dusty occupations, and to heat, moisture, and confined or
Titiated air, their too frequent accompaniments.
Associated lesions are found with the fibrotic change in the shape of
emphysema, bronchiectasis, cell-collapse, and cavities ; morbid events
which are described and explained in other parts of this chapter : the
first-named change is for the most part vicarious or complementary. A
specimen of this vicarious emphysema is No. 1276. The emphysema is
not confined to the circumference of solidified segments of lungs, but
occurs elsewhere, particularly along the free anterior border; here the
■dilated cells are much larger, and the septa between them frequently
broken through.
Bronchial dilatation or bronchiectasis \mde chapter on " Bronchiectasis "
in this volume] is usually but not invariably associated with fibroid
•disease. As the bronchi are the first to suffer from the inhaled dust we
might well expect them to be prominent in their lesions. A primary
change, indeed, does occur in them in the shape of thickening of their
walls, with loss of elasticity, due to the infiammatory action proceeding in
and around them. Moreover, whilst losing elasticity they get plugged
and distended by mucus and inflammatory products ; and the growing
fibrous tissue about them, in course of its contraction, drags on their
walls, and causes irregularity of form and disturbance of position.
In this view of the causal relations of bronchiectasis we have the
support of Dr. Coats of Glasgow and of Professor Hamilton of Aberdeen;
but the former contends that both it and the formation of cavities are
consequences and not causes of pneumoconiosis. The latter puts forward
the following mechanical hypothesis : that " as the chest wall forms a
comparatively fixed point to which the shrinking lung tissue also is
attached by means of pleural adhesion, and as the tissue also is attached
to the walls of the bronchi, the result of the shrinking will be that these
two points will be approximated, the chest wall drawn in, and the
bronchial wall drawn out. The latter, however, being the more yielding
structure, will be more affected than the former. In this way we have
the formation of cavities by bronchiectasis. Such cavities have for the
most part well-defined walls, and are directly continuous with bronchial
252 SYSTEM OF MEDICINE
tubes of which they are flask-like dilatations. It is to be remembered
that the primary process, involving as it does the smaller bronchi, leaves
all but these capable of dilatation."
This explanation may hold good in some instances, but cases are not
uncommon where no connection by bands with the chest wall exists, and
others where cavities occur in crepitant lung tissue.
Pursuing his criticism of Professor Hamilton's hypothesis. Dr. Coats
affirms that in some cases cavities arise by accumulation of the secretions
and inflammatory products behind an occlusion of a bronchial tube. He
believes also " that cavities form by bronchial dilatation by a similar pro-
cess to that which leads to emphysema without any primary disease of
their wall. The dilatation, in fact, is complementary to the shrinking
which has taken place in some part of the lung." Continuing these
observations, he cites a case of " congenital non-inflation of the lung in which
the bronchi had become converted into a series of sacs. Here the non-
inflation without any active disease, implying as the chest enlarged an
excessive distensible force acting on the bronchi, caused a general bron-
chiectasis. In a similar way in fibroid phthisis, we may have bronchi-
ectasis and emphysema in an otherwise sound part of the lung, in
consequence of shrinking in another part" (p. 124). These secondary
changes are features so well marked in the later stages of pneumoconiosis
as to call for our attention ; but for further details as to the forms and
other varieties of bronchiectasis the reader is referred to the special
chapter on this disease (vide p. 53).
Cavities, not of bronchial origin, may perhaps arise in a portion of
pulmonary tissue deprived of function and nutrient vascular supply ; as,
for instance, in a mass of condensed tissue, whether from fibrosis or from
collapse. Again, the presence of a concretion may operate as a cause
of softening of the tissue around it, when the cavity may contain a
" pneumolith," or only pus and detritus should the stone have ulcerated
into a bronchus and made its escape outward (1278, 1279). This pheno-
menon is most common in the case of coarse mineral dust as found among
stone-workers. I have already remarked on the almost constant associa-
tion of pleuritic thickening with pneumoconiosis, but expressed my
dissent from the opinion of Sir A. Clark as to the direct causal relation
between the two lesions. For, according to that opinion, fibroid lesion
is the result of growth from without inwards. This, indeed, does take
place in some instances, as seems to be illustrated by a case described by
Clark; but when fibroid lung is due to dust inhalation, the develop-
ment of fibrous tissue passes from within outwards, and fibrous bands
do not extend from the pleura (1282). There seems good reason,
moreover, for supposing that a primary inflammatory process is not
universally necessary to the development of fibroid mischief ; but that
any condition which destroys or suspends pulmonary action for a long
time, by obstructing access of air and blood-supply, will lead to lung
collapse and infiltration, and eventually to fibroid degeneration. In a
word, loss of function is a prelude to fibrous degeneration ; and Eind-
PNEUMOCONIOSIS 253
fleisch surmises that obstruction of bronchi by accumulated cells and
mucus will cause collapse of air-cells in the rear, and ultimately fibroid
degeneration.
The notion that a constitutional proclivity lies at the root of pul-
monary fibrosis receives some support from Clark's own statement; namely,
that albuminuria is commonly associated with it. As regards the uni-
lateral interstitial pneumonia this may be true, but as regards pneumo-
coniosis, in almost all the cases examined no albumin was found. Albumin-
uria is, of course, not unknown in such cases, but its occurrence is in no
higher ratio than among an equal number of persons sufi'ering from
miscellaneous maladies. The concurrence of pneumoconiosis with pul-
monary phthisis is not infrequent, but there is not pathological identity
between the two maladies. Irritation may be a common starting-point
in both; but, whereas in tuberculous lesion the apparent cause is the
existence of tubercles and of bacilli, and the prevailing tendency is to
soften, break down, or ulcerate, in fibroid disease, on the contrary, there
is a chronic inflammation with fibrinous products which tend to contract
and transform lung tissue into a hardened mass unfavourable to tuber-
culous extension and softening. For it is known that a piece of fibrous
tissue in a softening tuberculous mass operates as an obstacle to the dis-
integrating process. Nevertheless, experience proves that the one lesion
is often engrafted upon the other and may replace it.
Diagnosis. — Dust -phthisis and pulmonary phthisis have been, and,
indeed, still are very frequently confounded. The pulmonary fibrosis of
metal-grinders, of stone-workers, of potters, miners, and some other
artisans is popularly known as consumption or phthisis, and its victims
are entered in death registers as dying of consumption. As already shown,
the inflammatory phenomena of deposited tubercle and of fibrosis affecting
the pulmonary organs diverge at an early stage ; the thickened alveoli
and their contents suff'er a degenerative process, ending in the former
case in softening and ulceration ; whilst in the latter an abnormal develop-
ment of fibrous tissue takes place rather prohibitive of ulceration, but
directly productive of condensation and shrinking.
However, this differential feature must not be pushed too far ; for, as
already asserted, a tuberculous lung presents more or less condensation from
excessive development of fibrous tissue, especially where life has been
greatly prolonged, and opportunity given for the conservative agency of
the fibrinous effusion to advance at a greater rate than that attained by
the disintegrating action of tubercle (1302, 1310). A very important
preliminary part of the diagnosis is to ascertain the presence or absence of
tubercle in the history of the patient's family, or of any organ of his own
body. The nature of the work followed, and the conditions and cir-
cumstances of employment, will likewise, of course, be ascertained. A
third point of importance is to get a correct account of the onset of the
malady, its course and its duration. Pneumoconiosis is compatible for
many months with capacity for physical labour and for adequate nutrition ;
tuberculous phthisis, on the other hand, within an equal period, will reduce
254 SYSTEM OF MEDICINE
^ s
the patient to a state of considerable debility and emaciation. Tuberculous
phthisis is rather a disease of youth and of early middle life, of consti-
tutional nature, and without obvious causal connection with the breathing
of dust ; whereas pneumoconiosis is a local lesion of middle life, directly
referable to dusty employment, and not associated with any marked
constitutional bent. Moreover, it is not only most prevalent in middle
life, but it is also almost peculiar to men. Nor is the previous history
of dust -disease that of acute or febrile thoracic maladies, such as
pneumonia or pleuro-pneumonia, but of smaller ailments, especially of
winter coughs recurring year after year, and disappearing in the warmth
of summer. Other divergent features are the rarity of laryngeal troubles,
the comparative infrequency of diarrhoea, and the little pyrexia and
sweating in the dust-produced lesion. Haemorrhage in notable quantity
is an infrequent incident in dust-disease, unless the lesion be provoked
by sharp particles as of iron and steel. Green purulent sputa are also less
common, though not unknown ; for in the far-advanced stage they occur.
The sputum for a long period is a whitish frothy mucus, which presently
gets lumpy and grayish yellow, and for the most part is in smaller
quantity, regard being had to the extent of lesion, than in tuberculous
disease ; speaking generally, the s3rmptoms of dust-disease are more like
those of chronic bronchitis, with which, in fact, it is usually confounded,
than of phthisis. Foetid bronchitis and gangrene are unusual, but not
unknown results.
The temperature is less elevated than in phthisis, and hectic fever,
if present, less pronounced. In the earlier stage emaciation proceeds and
may for a time pass unobserved, for usually the appetite and digestion
continue more or less good. Diarrhoea seldom appears.
Again, whilst anaemia and oedema are less prominent, dyspnoea is
more so, and often paroxysmal. Dyspnoea is greatly aggravated when
pulmonary embarrassment has long existed and secondary cardiac disease
been established ; and as in chronic bronchitis, the cough, expectoration,
and hard breathing are increased on first rising, or on passing out into-
the cold outer air, and are abated by warm drinks and warm atmosphere.
Phthisis particularly affects the apices of the lung, whereas pneumo-
coniosis prevails rather in the posterior and inferior segments. Moreover
it is distributed in separate patches, and gives rise to a greater or less
number of areas of dulness on percussion. Dulness under the clavicles,
when found, does not resemble that of tuberculous deposit or of pleurisy ;
it points rather to absence of respiration and bronchial mischief, and is
less accompanied by moist crepitus and rales, or by the " cracked pot "
sound of a cavity.
Iq those instances where pleurisy has played a prominent part the-
adhesions cause deformity of the chest wall and consequent displacement
of the heart. The same event happens where the lung itself has become
greatly shrunken or displaced by its fibrous transformation (1274).
Yet, notwithstanding differential features, tuberculous phthisis and
pneumoconiosis are separable by a somewhat shadowy line (1263, 1264);
PNEUMOCONIOSIS 255
and if the presence or absence of bacilli are to furnish the securest
foundation for making the distinction between the two, far more careful
and numerous researches are needed than, have as yet been made.
The intermingling varieties of fibroid and tuberculous disease are well
exhibited by Sir A. Clark, who describes two main forms as properly
distinguishable, namely, the tuberculo-fibroid and fibro-tuberculous, — the
main difference between the two being the order of succession of tubercle
and fibroid ; but a further examination of those problems would lead us
beyond the limits of a chapter on pneumoconiosis.
Of the many cases placed on record as pneumoconiosis by various
observers it remains doubtful whether all are true examples of the disease.
Some of them certainly are not, and unfortunately the opportunity for
stud3dng the disease is to a great extent denied to the bulk of medical
men. Indeed, I apprehend from my study of his able treatise on
Fibroid Diseases of the Lung that its distinguished author lacked material
for a thorough exposition of the morbid consequences of dust-inhalation,
apart from tuberculous complication.
Non-tuberculous fibroid disease, indeed, whether due to dust or not, is
an uncommon lesion, and it is becoming more uncommon day by day by
reason of the advances of hygienic knowledge and of its increasing
practical application to those employments wherein dust is an almost
necessary accompaniment.
Prognosis and Treatment. — From the account given of pneumo-
coniosis it is evident that when once established a permanent lesion will
remain, which cannot be undone by medicinal treatment. Nevertheless,
it is capable of great alleviation ; and, if not beyond a certain stage, its
symptoms will remain quiescent if the sufferer abandon his dusty occupa-
tion. Moreover, it scarcely need be said that whatever sanitary arrange-
ments can be provided, and whatever mechanical contrivances can be
invented to obviate the entrance of dust within the chest, so much less
severe and less frequent wiU be the disease.
Being a very chronic malady, it affords ample time and opportunities
for hygienic management, and for whatever medicinal treatment can be
suggested. The first indication, then, is to withdraw the sufferer from
his employment, or to diminish the production and diffusion of dust in
the work by mechanical and other devices to secure thorough ventilation
of shops. Eespirators should be worn, the workmen themselves should
carry on the technical details of their calling so as to produce the least
amount of dust, and observe the general rules of temperance and health
in their way of living. On the part of masters it is an imperative duty
to provide healthy workshops with efficient ventilating apparatus and all
sanitary arrangements calculated to protect their work-people from the
evils of the occupation they are engaged in.
Thus fibrotic patients may live many years, though they must be
accounted more or less invalid. At the same time it is to be remembered
that the dormant lung affection may be easily aroused into activity by
fresh exposure to dust, and become complicated or aggravated by bron-
2S6 SYSTEM OF MEDICINE
— i ■
chitis, broncho -pneumonia, and pleurisy, by depressing causes such as
cold and wet, and by irregular and intemperate habits.
Prognosis becomes highly unfavourable when symptoms arise indica-
tive of the development of tubercle in the already diseased viscus. This,
unfortunately, happens not infrequently, and is less to be wondered at
when we remember the prevalence of this hereditary disease, which
abounds in manufacturing populations. The occurrence of hsemoptysis is
thus of bad omen.
Of drugs I have found the iodide of potassium the most useful, some-
times, where additional alkali is needed, combined with bicarbonate or
citrate of potash ; or, where a spasmodic asthmatic state is present, with
ether or the ethereal tincture of lobelia. Where great weakness exists,
quinine is useful, and cod-liver oil may, when it can be. borne, "be ad-
ministered with great advantage to prevent wasting. Terebinthinate
inhalations, such as pinol, facilitate expectoration and relieve cough, for
which also vapor conii may be inhaled, or a linctus may be ordered con-
taining a minute dose of morphia with some preparation of squills and
tolu. But it is of the first importance to sustain nutrition, to encourage
exercise outdoors, and to promote action of the chest muscles by regu-
lated calisthenics. Further instructions in treatment will be found in the
other chapters on pulmonary disease in this work.
J. T. Aklidge.
REFEKENOES
1. Allbeecht. Handhich der pra/ctischen Gewerbehygiene, Part i. 1894. — 2.
Aklidge. "Diseases caused by the Inhalation of Dust," Brit, and For. Medico-
Chirurg. Beview, 1872. — 3. Mem. "Diseases of Occupations," 1892. — 4. Bastian,
C. " On Cirrhosis of the Lungs," Reynolds' System of Medicine. — 5. Bennett,
Hushes. "On Pulmonary Phthisis," Trans. Med.-Ghir. Soc. 1856. — 6. Catalogue
of Museum in the Middlesex Sospital, pp. 156-159. — 7. Glakk, Sir A., Bart., and
Hadley and Chaplin. Fibroid Diseases of the I/wngs, 1893. — 8. Coats, Joseph.
"On the Pathology of Phthisis Pulmonalis, " Lectures to Practitioners, by W. T.
Gairdner and Joseph Coats, 1888. — 9. Fox, Wilson. "On Chronic Pneumonia,"
Reynolds' System of Medicine. — 10. Greenhow, Headlam. " On Lungs of Colliers,
Potters, Mother-of-Pearl Cutters, and other Workers in Dust," Trans. Fath. Soc. Land.
vols. xTii.-xxi. 1865-1869. — 11. GussENBAUM. "On Mother-of-Pearl Workers,"
Langenbeok's Archiv. — 12. Hall, J. C. "Diseases of Shefiield Grinders," Lectures in
Brit. Med. Journal, March 1857. — 13. Harris, Thos. " On the Variations of Pulmonary
Phthisis," Reprint from the Lancet, 1889. — 14. Hasse. Works, New Sydenham Society.
— 15. HiRT, LuDwiG. Die StaubinhalationskranJcheit. 1871. — 16. Hirt. Merkel's
Handbuch der Sygiene, 1882, Zweite Theil. — 17. Holland, Calvert. Diseases of
Lungs from Mechanical Causes, 1843. — 18. Jubrgensbn. " Interstitial Pneumonia,"
Ziemssen's Cyclopaedia of Medieine. — 19. La yet, Albx. Hygiene des professions et des
industries, 1875. — 20. Lewin. "Die Inhalationstherapie," Krankheiten Bespirations-
organe, 1865.— 21. Mebkel and Pbttbnkoffer. Eandbuch der Hygiene, 1882. —
22. Peacock. "On Lungs of Millstone Workers," 5ri«. and For. Med.-Chir. Beview,
1860. — 23. Idem. "On Lungs of Cornish Miners," Trans. Path. Soc. Land. vol. xvi.
1865.— 24. Philip, R. W. On Pulmonary Tuberculosis, 1891.— 25. Purdon, C.
Memoir on the Mortality of Flax Worrlcers, 1875. — 26. Rindflbisoh. Works, New
Syilenham Society. — 27. Rokitansky. Works, New Sydenham Society. — 28. Sutton.
"On Fibroid Degeneration," Trans. Med.-Chir. Soc. 1865. — 29. Traoby, Roger.
Hygiene of Occupations. New York. 1889.
J. T. A.
PULMONARY ASPERGILLOSIS 257
PULMONARY ASPERGILLOSIS
Short description. — A destructive disease of the lungs due to tlieir
invasion by a fungus, the Aspergillus fumigatus. The disease depends on
the inspiration of the spores of the fungus, and occurs chiefly in those
whose occupation brings them in contact with infected grain. Clinically
the disease presents itself under two forms : (i.) like chronic pulmonary
tuberculosis ; (ii.) like emphysema and bronchitis.
Besides attacking the lungs primarily the aspergillus may become en-
grafted on pre-existing pulmonary lesions.
Histopieal. — Hughes Bennett, in 1842, described the first example of
pneumomycosis, in which the sputum and cavities of a phthisical subject
were found to contain a fungus. G-airdner, in 1853, showed a specimen
of a tuberculous lung which had given rise to pneumothorax, with small
circular white areas of fungoid growth on the pleural surface, penetrat-
ing very slightly (jij- inch) into the lung substance, and measuring \ inch
in diameter. Rayer eleven years before, in 1842, had met with a very
similar case. Bristowe in 1854 recorded the case of a woman who died
with signs of chronic bronchitis ; in the apex of the left lurig there were
two communicating vomicae containing no secretion, but on the septum
between them there was a powdery, velvety mass of mycelium ; although
there was no other evidence of tuberculosis : the vomicae were regarded
as being tuberculous. Virchow, in 1856, gave an account of several cases
of aspergillary broncho- and pneumomycosis in patients dying from other
diseases.
A number of other observers have recorded cases which, like the
preceding cases, were regarded secondary infections of pre-existing pul-
monary lesions.
In 1890 Dieulafoy, Chantemesse and "Widal described clinically as-
pergillary pneumomycosis in persons engaged in stuffing and fattening
pigeons for the Paris market, and struck out a new line in their view that
it is a primary affection.
In 1897 Renon collected all the evidence bearing on the subject
in his Mude sur I'asp&rgillose chez les animaux et chez Vhomme, to which
reference for an exhaustive discussion and account of the whole subject
may be made.
At first and for a considerable time the occurrence of aspergillus was
supposed to be no more than an accidental invasion of already diseased
lung tissue, the fungus being merely saprophytic. Thus in Bristowe's
case, although these was no sign of tubercle elsewhere in the lung, the
lesions were regarded as tuberculous and not due to the activity of the
fungus.
VOL. V S
258 SYSTEM OF MEDICINE
But lately the French school, and especially Eenon, whose conclusions
are based on extensive experimental research, have successfully argued
in favour of primary pneumo-aspergillosis ; while in England, Boyce and
Arkle and Hinds have within the last few years described cases of the
primary affection.
Aspergillary pneumomycosis may therefore be considered under the
two heads — (a) primary ; (J) secondary.
It is a difficult question, however, in many instances to settle whether
the aspergillary affection be undoubtedly primary, and the cause of morbid
lesions in a lung previously healthy ; or whether it be a secondary infec-
tion only. In former times there was a strong and general impression
that aspergillary occupation of the lung is essentially an accidental and
secondary phenomeiiDn.
Recently Max Podack has expressed doubts whether cases described
as primary by the French observers are in reality of this nature; on
the other hand, Eenon regards Wheaton's " case primarily of tubercle
in which a fungus (aspergillus) grew in the bronchi and lung" as being
an example of primary pulmonary aspergillosis. Thus different inter-
pretations are put upon the same case.
Etiology. — Pulmonary aspergillosis is a trade disease in Paris; it
occurs in persons whose calling is the artificial feeding of pigeons, and
in those who comb and sort hair. The essential factor is the intimate
relation to grain infected with the spores of the Aspergillus fumigatus.
The pigeon-feeder fills his own mouth with a watery mixture of canary
seeds and vetch seeds, and transfers the grain to the pigeon's mouth.
Spores of aspergillus attached to the seeds thus get into the trachea and
are conducted to the air-vesicles, through the walls of which they easily
pass. It is remarkable that the alimentary canal of man seems immune
to Aspergillus fumigatus. According to Eenon, there are only about ten
persons engaged in this trade in Paris.
The hair-sorters employ the flour of rye to enable them to separate the
hairs more easily ; this process impregnates the atmosphere in which they
work with dust, which may contain the aspergillus of the rye flour. The
atmosphere of their working-rooms is so poisonous that birds die after
being exposed to it for a fortnight.
Aspergillosis is a rare disease ; it appears more likely to occur in
millers, agricultural labourers, and those brought in contact with grain,
than in any other class of the community. Apart from the Paris cases a
few sporadic examples of the disease have been recorded.
Pulmonary aspergillosis belongs to a class of lesions which, though
comparatively little known, has been more studied in animals than man.
The lesions of the class pseudo- tuberculosis are granulomata, and
resemble those of true tuberculosis, except in respect of the causal
agents, which include baciUi other than those of tubercle, fungi of various
kinds, and even worms {wde Distomum Eingeri, vol. ii. p. 1027). The
close resemblance (to the naked eye) of the lesions of pseudo-tuberculosis
to genuine tuberculosis renders it very probable that they are often re-
PULMONARY ASPERGILLOSIS 259
garded as such ; and that, being rarely recognised, this form of lesion is
not so infrequent as our present experience would suggest. Systematic
examination of pulmonary lesions might prove that some conditions
generally dismissed as tuberculous are in reality pseudo-tuberculous, and
are due to quite a different cause. Flexner has recently described the
condition of Pseudo- tuberculosis hominis streptotrichia in a man who
died with the signs of pulmonary tuberculosis, and whose lungs showed
consolidation with early excavation.
The aspergilli are true fungi, and belong to the family PerisporiaceK,
order Asoomycetes. Of the varieties of aspergillus, two, A. fumigatus
and A. niger, are parasitic, and produce morbid changes in the human
body.
Pulmonary aspergillosis appears to be almost always due to A. fumi-
gatus ; A. niger has, it is true, been described in some instances, but
Renon throws doubt on the accuracy of the observations, and regards them
all as examples of A. fumigatus.
Both varieties have been described as attacking the external auditory
meatus, and the skin.
It should be remembered that in order to determine the species
cultures are necessary, and that without this no opinion as to the identity
of the form of aspergillus is valid.
Aspergillus fumigatus flourishes best at the temperature 37°-40° C,
while A. niger grows best at 25° C. ; and this might be thought to explain
the pathogenetic qualities of A. fumigatus ; but in Eenon's hands experi-
ments on frogs do not support the simple view that it is merely a matter
of the bodily temperature suiting the development of one species and not
of the other.
Primary pulmonary aspergillosis. — Symptoms.— The clinical features
presented by the recorded cases of primary pulmonary aspergillosis may
resemble either those of chronic pulmonary tuberculosis or those of
emphysema.
When the disease takes the first of these two forms there is recurring
hsemoptysis, cough, expectoration becoming green and purulent, and
signs first of bronchitis, and later of consolidation at the apex. Further-
more there is elevation of the temperature ; and pleurisy may supervene.
The resemblance, therefore, to pulmonary tuberculosis is so far exact ;
but if the sputum be examined, tubercle bacilli are absent, while the
mycelium of Aspergillus fumigatus is present. The course of the disease
is very slow and prolonged ; recovery takes place eventually by expectora-
tion of the aspergillus, but the afiected portion of the lung undergoes
marked fibrosis.
A patient affected with pulmonary aspergillosis offers a suitable soil
for tubercle bacilli, and a secondary infection may take place, tlie
aspergillus disappearing from the sputum and being replaced by tubercle
bacilli. Renon and Sargent have recorded a case of primary pulmonary
aspergillosis succeeded by tuberculosis, in which eventually both these
infections became obsolete : but so much chronic pneumonia resulted
26o SYSTEM OF MEDICINE
that death from failure of the right side of the heart terminated the
case. In another and similar case related by Eenon the sputum iirst con-
tained the aspergillus alone ; later very scanty traces of it were found,
but plenty of tubercle bacilli, and eventually no bacilli or aspergillus, the
patient surviving with evidences of chronic pneumonia.
In the emphysematous form the disease may run a rapid course, as in
the case recorded by Arkle and Hinds. Haemoptysis is infrequent, or
may not occur at all; there is loss of flesh and strength, frequent
cough and severe dyspnoea come on in attacks at night, and suggest
spasmodic asthma. The physical signs are chiefly those of emphysema
and bronchitis.
Intermediate forms between these two may occur, signs of apical
consolidation supervening in the emphysematous varieties ; and conversely
cases which appeared like chronic phthisis may be marked by attacks of
pseudo-asthma.
Morbid anatomy. — The data at our disposal are somewhat scanty,
but so far as they go they tend to show that the morbid appearances in
the lungs met with in the described cases of aspergillosis differ just as
do the lesions of acute and chronic tuberculosis. This difierence depends
on the resistance ofiered by the lung tissue to the inroads of the fungus.
It will be most convenient to describe the anatomical lesions in connec-
tion with the two chief clinical types of the disease to which attention
has already been called.
1. In cases where the disease has run a very chronic course, resem-
bling either chronic pulmonary tuberculosis or chronic pneumonia, the
aspergiUus may either (a) still be found on the lung tissue, or (6) it may
have been entirely removed, and then have left behind it a chronic inter-
stitial pneumonia which eventually proved fatal.
(ft) Our knowledge of the lesions existing in primary aspergillosis
when the aspergillus is still ptesent in the lung tissue is particularly
scanty. Eenon bases his description on two cases, those of Boyce and
Kohn. The lung tissue contains dilated bronchioles leading into cavities in
pneumonic areas, in which there are pseudo-tubercles composed of hyphse
so arranged as to resemble actinomycosis. There is much phagocytic
reaction in the pneumonic areas, showing that very active resistance had
been opposed by the lung tissue to the aspergillary invasion. Eenon
associates the actinomycotic form adopted by the aspergillus with the
active resistance of the tissues, and considers it as an indication of defen-
sive powers on the part of the tissue and of lowered vitality on the part
of the aspergillus. Hence this form of pneumo- aspergillosis is called
by Eenon "abortive." The cavities also contain the aspergillus. The
process is essentially the same as that in cases of aspergillosis ; its clinical
features are those of emphysema, namely, consolidation and destruction
of pulmonary tissue ; but it is a local process which has become arrested
at an earlier stage.
(6) In a case of primary pulmonary aspergillosis, described by Eenon
and Sargent, in which true tuberculosis supervened with disappearance
PULMONARY ASPERGILLOSIS z6i
of the aspergillus from the sputum, death took place from failure of the
right side of the heart, and examination of the lungs showed chronic
pneumonia ; but no trace remained either of the aspergillus or of tubercle
bacilli.
2. In cases where the symptoms have been those of emphysema
and dyspnoea the lungs contain patches of consolidation breaking down
into cavities, while there is compensatory emphysema which may be well
marked. The lesions in Hind and Arkle's case have some analogies with
Tooth's case of acute bronchiolectasis, though in the latter the causation
had nothing to do with aspergillosis.
Microscopically the walls of the small bronchi are thickened, and
both the lung substance and the alveolar cavities contain the aspergillus
mycelium. In places the lung tissue is so disorganised as to be un-
recognisable, and there is breaking down of the lung tissue leading to the
formation of microscopic cavities. The mycelium is in extremely intimate
relation with the lung tissue, and, as it is accompanied by phagocytic
reaction, the aspergillary invasion of the lung tissue appears to be the
direct cause of the lung lesions, not a merely accidental or post-mortem
event.
Since no toxin has been obtained either from the media in which the
Aspergillus fumigatus is grown (Kotliar), or from the fungus itself
(Renon), it appears probable that the large quantities of the fungus in
the lung tissue set up the inflammatory changes by mechanical irritation.
The absence of any toxin explains the comparatively mild character
of the disease ; but it makes it somewhat difficult to understand why
A. fumigatus is the chief if not the only variety of aspergillus pathogenetic
for pulmonary tissue.
Generalisation of aspergillosis does not occur.
Diagnosis. — The physical signs are not in any way characteristic, and
would point to bronchitis and emphysema or to chronic pulmonary
tuberculosis. In Wheaton's case there was a growth of the fungus at
first white, later black on the tongue and palate. But this is the only
help that ordinary methods of physical examination can be expected to
supply, and, unfortunately as regards diagnosis, this coexistence of oral
and pulmonary aspergillosis is almost unique.
The diagnosis depends on the presence of the fungus in the sputum,
and the absence of the tubercle bacillus. In cases where tubercle
becomes engrafted on primary pneumo -aspergillosis, both organisms
might be found in the sputum ; and, unless the patient had been under
observation from the beginning when the aspergillus alone was present
in the sputum, there would be no means at first of distinguishing
the primary form complicated by tubercle from secondary aspergillosis
occurring in the last course of pulmonary tuberculosis.
The fungus, derived from dust, is occasionally found in the mouths of
healthy persons.
Cultures of the aspergillus in appropriate media, such as Eaulin's fluid,
and inoculation of animals may be necessary to determine that the form
262 SYSTEM OF MEDICINE
of aspergillus is the pathogenetic Aspergillus fumigatus, and not the other
non-pathogenetic varieties, such as Aspergillus niger, glaucus, and so forth.
It must be distinguished from the streptothrix form of the bacillus
tuberculosis ; and, lastly, the lesions must be distinguished from other
forms of- pseudo-tuberculosis due to diflPerent factors such as bacteria,
streptothrix, actinomyces, or Distoma Eingeri.
The prognosis of pulmonary aspergillosis is less grave than that of
pulmonary tuberculosis, since the lesion is usually much slower, never sets
up a general infection comparable to generalised tuberculosis, and tends
to undergo a gradual and spontaneous cure. But there are several
reservations to this general statement. For, even if the aspergillus
disappear, the lesions of chronic interstitial pneumonia may lead to
dilatation of the right side of the heart, and so to a fatal result.
It need hardly be said that the development of genuine tuberculosis
renders the prognosis much graver.
The prognosis of the emphysematous form does not, from the few
recorded examples, appear to be nearly so favourable as that of the
more chronic variety which has been likened to chronic tuberculosis.
Treatment. — Although there is no specific remedy for pulmonary
aspergillosis, nor any drug that can be employed to kill the fungus out-
right in this situation, experiments on animals show that iodine, iodide of
potassium, and arsenic increase the resistance of the organism to the
invasion of Aspergillus fumigatus and inhibit its growth ; their employ-
ment is therefore reasonable in this disease in man. The general strength
should also be improved by good and generous feeding, cod-liver oil,
tonics, and fresh air ; thus we may guard against secondary infection
of tubercle, and assist the tissues in their struggle against the aspergillary
infection.
Symptoms should be treated as they arise. When haemoptysis
occurs the treatment is the same as in pulmonary tuberculosis. Attacks
of asthma may be relieved by iodide of potassium, tincture of lobelia, and
other appropriate remedies ; while creasote, terpene, turpentine, may with
other drugs be given for bronchitis.
Removal from the poisonous atmosphere is an important essential,
both in prophylaxis and in treatment.
When tuberculous infection has taken place, the course of treatment
is that of chronic pulmonary tuberculosis.
Secondary pulmonary aspergillosis. — Here the Aspergillus fumigatus
develops as a result of the inhalation of its spores ; and finds a suitable
nidus in lung tissue the resistance of which has been already much
lowered by pre-existing disease, or has actually undergone necrosis.
It has been found in the bronchi and in the lung substance. Thus
the aspergillus may be engrafted on bronchiectasis of old standing ; or may
take root on the walls of vomicaa due to tuberculosis ; or in the lung
under other conditions, such as malignant disease, pulmonary apoplexy,
chronic bronchitis, broncho-pneumonia, and gangrene of the lung.
In some of the cases where it has been described as secondary, it may,
EMPHYSEMA OF THE LUNGS 263
as already hinted with regard to Dr. Bristowe's case, in reality have
been primary.
In cases where there are multiple bronchiectases or vomicae in the
lungs, the absence of the fungus from some of them and its presence in
others are strong evidence in favour of the secondary nature.
It is remarkable that in gangrene of the lung associated with the
presence of aspergillus there is no foetor. It seems that the growth of
the micro-organisms of putrefaction is prevented by the aspergillus.
The actinomycotic form of the mycelium appears to occur where there
is considerable reaction and resistance on the part of the tissues, and it
is probable that it does not occur in secondary or terminal aspergillosis.
Clinically speaking, secondary aspergillary pneumomycosis, like thrush
in the mouth of adults, is probably a precursor of death, and is not likely
to be suspected or discovered unless the mycelium be found in the sputum.
It is in fact a terminal complication.
The treatment is that of the primary disease on which the asper-
gillosis has been engrafted.
H. D. ROLLESTON.
REFEEElirCES
1. Aekle and Hinds. Trans. Path. Soc. vol. xlvii. p. 8. — 2. Bennett, Hughes.
Trans. Boy. Soc. Edinburgh, 1842. — 3. Botob. Jowrnal of Pathology, vol. i. p. 163
with references. — 4. Bristowb. Trans. Path. Soc. vol. v. p. 38. — 5. Dibtjlafot,
Chantemesse, and Widal. Congress at Berlin, 1890. — 6. Dubkeuith. Archiv. de
mM. experiment et d'anatom. Path. 1891, p. 428.-7. Flexneb. Johns Hopkins Hospital
Bulletin, 1897, No. 75, p. 128.— 8. Gairdnee. Edinburgh Med. Journal, vol. xvi.
1853, p. 472.-9. KoHN. Deut. med. Woehens. 1893, No. 50.— 10. Kotliab. Ann.
de I'institut Pasteur, 1894, p. 479.— 11. Levi. Gas. des hdpitaux, 26tli June 1897.—
12. Podack. Virchow's Archiv, 1895, oxxxix. p. 268. — 13. Renon. itude sur
Vaspergillose. Paris, 1897. A full account of the whole subject with a bibliography.
—14. Renon and Sakgent. Soc. biolog. 27th April 1896.— 15. Tooth. Trans. Path,
Soc. vol. xlviii. — 16. Viechow. Virchow's Archiv, vols. ix. x. — 17. Wheaton.
Trwns. Path. Soc. vol. xli. p. 34.
H. D. R
EMPHYSEMA OF THE LUNGS
Definition. — K disease of the lungs characterised by over-distension of
the alveoli and atrophy of the alveolar walls.
It has been the custom to describe under this heading two essentially
distinct morbid conditions ; the one, corresponding in anatomical details
to the definition above given, having nothing in common with the othei
but the name. An account of this latter affection, interlobular or inter-
stitial emphysema, will be found at the end of this article.
The description of emphysema of the lungs given by Laennec, accurate
though it was as regards both anatomical characters and clinical history,
264 SYSTEM OF MEDICINE
remained incomplete until supplemented by the microscopical researclies
of Eokitansky and the clear exposition of its pathology which we owe to
Sir William Jenner. Our knowledge of the disease has been mainly
derived from their writings, and few additions of importance have been
made to it in recent years.
Pathogeny. — Various hypotheses have been advanced to explain the
origin of emphysema, some of which meet with but little support at the
present time. It would serve no useful purpose to enter upon a detailed
discussion of the problem, as it is exhaustively dealt with in the original
papers of Sir William Jenner, to which reference may be made. It will
be sufficient to mention those views which have at any time received
considerable support, and to discuss in greater detail that which is now
generally adopted.
Primary degeneration hypothesis. — The view that the general cause of em-
physema is a primary fatty degeneration of the alveolar walls was first stated
by Eainey, and subsequently received support from ViUemin. The latter
writer describes the changes as beginning in an excessive proliferation of
the intercapillary nuclei, followed by secondary fatty degeneration of the
nuclei and other structures, the result of pressure upon the capillaries.
It is now generally considered that the degenerative changes in the
alveolar walls are secondary to the distension of the air -vesicles and
interalveolar spaces, and to the diminution in the blood-supply thereby
induced.
It is possible, however, that in the form of emphysema met with in
old people, primary degenerative changes may play a more important part.
Eeference will be made to this point subsequently.
Inspiratory hypothesis. — The hypothesis that emphysema is due to dis-
tension of the lungs during inspiration was really first advanced by Laennec.
He believed that the air drawn into the lung in inspiration was retained,
being unable to escape during expiration, owing to the obstruction caused
either by catarrhal sweUing of the mucous membrane of the bronchi or
by accumulation of mucus in the tubes ; and that as a consequence the
lungs became over-distended with air.
Dr. Gairdner, in 1850, stated the inspiratory hypothesis in a different
form. According to his view, some change in the lungs, such as collapse or
retrocedent tubercle, leading to a diminution in size in one part, preceded
the establishment of emphysema. As the air-vesicles within the area of
disease or collapse did not expand during inspiration, an undue strain was
thrown upon those in the immediate neighbourhood by the incoming
air, and in consequence they became enlarged.
This opinion, as regards the general disease, has been completely dis-
placed by that to be next mentioned ; and as an explanation of the con-
ditions found around patches of collapse or of fibroid tubercle — compensa-
tory emphysema — it is believed that the distending force of inspiration,
although possibly not without effect, is subordinate to that of forced
expiration.
Expiratory hypothesis. — In 1845 Mendelssohn first advanced the opinion
EMPHYSEMA OF THE LUNGS 265
that emphysema is produced during a forced expiration. He believed
that the air is prevented from escaping from the upper lobes by the
compression of the lungs during forced expiration ; that consequently
the pressure within the lung is increased, and the air-vesicles undergo
dilatation. In 1857 Sir William Jenner stated the above-named hypothesis
in the following terms : " The lung during expiration is compressed
at different parts with different degrees of force. The parietes of the
thorax, in consequence of their anatomical constitution, yield to the same
force at different parts with various degrees of facility. The chosen seats
of emphysema are exactly those parts of the lung which are the least
compressed during expiration, and which are situated under those por-
tions of the thoracic parietes that give way the most readily before
pressure."
In a footnote to his paper on "Emphysema of the Lungs,'' in Rey-
nolds' System of Medicine, Sir "William Jenner stated that he was un-
acquainted with Mendelssohn's paper when he advanced this hypothesis in
1845 ; and that, so far as he was aware, the existence of that paper was
unknown in this coimtry until 1867, and rarely, if ever, referred to abroad
until that date.
Having regard to the above facts, to the singular completeness of
Jenner's papers, and to his demonstration of the exact sites of emphysema,
we may fairly regard him as having been the first to make known the
true mode of origin of the disease.
The increased pressure in the air-passages, which we have seen to be a
common antecedent of emphysema, may be induced in various ways.
Cough. — The almost invariable association of some degree of emphy-
sema with chronic bronchitis points to cough as the most frequent cause
of the disease. The chest having first been filled with air, the glottis is
closed, a violent expiratory effort is made during which the tension within
the air-passages is enormously increased, the glottis then relaxes, the air
passes rapidly through the narrow orifice, and a cough results. It is the
frequent repetition of this act which eventually induces a permanent
dilatation of the air-vesicles and interalveolar passages. The effect of
the compression of the lungs during a violent expiratory effort, such as
that above described, is to drive the air in all directions from the central
to the peripheral part of the lungs ; the result is the distension of those
parts which are least supported. As pointed out by Sir William Jenner,
these parts -are the apices, the anterior margin of the upper lobes, and
the margins of the bases of the lungs. These are the sites of the
primary lesions; but, in the course of the enlargement of the thorax
which they entail, the relative position of a given area of lung and the
chest wall^ gradually changes, fresh portions being brought into contact
with the intercostal spaces, the resisting power of which is less than
that of the ribs, and thus in course of time the change may become
general throughout the lungs.
Muscular effort. — It is probable that next to cough violent muscular
effort is the most common cause of emphysema. The mechanism is as
266 SYSTEM OF MEDICINE
follo-ws : — the lungs having been completely expanded by a deep inspira-
tion, the glottis is closed ; any severe and sustained muscular effort with
the thorax in this position necessarily subjects the lungs to strong com-
pression, the increase in pressure within the air -passages being most
eflfectual in distending the lung in those situations where the organ
meets with least support. Straining in constipation may have the same
effect.
Further reference will be made to causes of over -distension in
describing the etiological factors of the disease.
It will be convenient here to refer to those conditions of a temporary
nature which lead to over-distension of the air-vesicles. In such cases
when the cause is removed the effect may disappear ; but whether it does
so or not depends upon the duration of the exciting cause and the in-
tegrity of the elastic tissue of the lung.
The best example which can be given of this temporary over-disten-
sion of the lungs is the condition observed during a paroxysm of asthma.
At the height of the attack the lungs may be found distended with air to
a degree equal to that present in the most advanced cases of emphysema ;
but when the attack has passed off, the organs may return to their previous
size. It is rare, however, to meet with patients whose asthma is of long
standing who are not also the subjects of emphysema.
The mechanism by which this state of over-distension is produced
appears to be a matter of doubt ; the explanations vary with the hypotheses
concerning the cause of the asthmatic paroxysm. If the hypothesis of a
spasm either of the diaphragm or of the muscles of inspiration be held, there
is little difficulty in understanding why the chest is in a condition of
extreme inspiratory distension; if, on the other hand, we reject both
these views and accept that now generally received, namely, that the
asthmatic paroxysm is due to bronchial obstruction, the result either of a
spasm of the muscular fibres of the bronchi or of a fluxionary hypersemia
of the bronchial mucous membrane, the explanation of its mode of occur-
rence is not quite so obvious.
It is, as a rule, gradual in onset and also in decline, and is apparently
brought about in the following manner : — •
(i.) The bronchial obstruction induces increased inspiratory effort.
(ii.) The entering air passes the obstruction with difficulty, but
the gradually increasing prolongation and force of the expiratory act
shotvs that the air meets with still greater difficulty in escaping from the
lungs.
(iii.) Expiration, although prolonged, is not sufficiently so to produce
an equilibrium between the incoming and outgoing air ; a fractional addi-
tion is therefore made to the residual air by each completed act of respira-
tion, and in time the lungs become over-distended.
It may be objected that, as the force of expiration is greater than
that of inspiration, the obstruction should be more easily overcome by
the outgoing than by the incoming current of air ; but it would appear
that experience teaches us to rely upon forced inspiratory efforts to
EMPHYSEMA OF THE LUNGS 267
remedy a defective aeration of the blood, whereas the condition really
requires for its relief forced efforts limited to the period of expiration.
Another possible factor in the production of this state of extreme
distension is the compression of the smaller bronchi by the distended
alveoli, an effect necessarily more felt during expiration.
Other causes of temporary over-distension of the lungs are laryngeal
obstruction, from whatever cause arising, whooping-cough, acute bronchitis
in children, and severe muscular strain.
Causation. — Age. — It is a matter of common experience that the
disease may be met with at any age. Some of the most marked examples
are seen in young children. The atrophic form of the affection (see
Varieties of Emphysema, p. 269) is most often met with in old people.
Sex. — Men are naturally more subject to the disease than women, as
they are more exposed to the conditions which favour its development.
Occupation. — Any occupation inVolvlng severe muscular effort, especi-
ally if performed with the lungs distended and the glottis closed, tends
to produce emphysema. In all such efiforts the chest is forcibly com-
pressed by muscular contraction, and the act is equivalent to one of forced
expiration. The classical example of an occupation involving the latter
condition is that of a cornet-player. Smiths, hammermen, and porters
engaged in lifting heavy weights are aU liable to emphysema. Omnibus
and cab drivers, and all persons whose occupations involve exposure to
inclement weather, are prone to attacks of bronchitis, whence comes
emphysema. The inhalation of dust, a condition almost inseparable from
' many occupations, necessarily induces catarrh of the bronchi ; upon this
cough and emphysema follow.
Diseases such as whooping-cough and chronic bronchitis present the
conditions essential to the production of emphysema to the fullest extent.
The violent respiratory acts in many forms of dyspnoea may lead to
extreme over-distension of the lungs, which may be 'either temporary or
permanent. The same is true in cases of extensive collapse of the lungs
as regards those parts into which the air is free to enter. The mode of
production of emphysema in asthma and allied conditions has been con-
sidered above.
The onset of emphysema will naturally be favoured by any conditions,
such as chronic congestion from valvular disease and chronic bronchitis,
which tend to diminish the natural elasticity of the lungs. Advancing
age is a factor which operates in a similar manner.
Hereditary predisposition. — It has been suggested that there exists in
some individuals and families an hereditary tendency to the disease ; but
this view is rarely insisted upon at the present time. Various observers
have investigated this matter, the result being the supposed discovery of
the hereditary tendency in a proportion of cases varying from 1 2 per cent
(Lebert) to about 60 per cent (Fuller, Jackson) in adults, and 100 per
cent of cases in children (Jackson). It is probably true, as pointed out
by Sir William Jenner, that the tendency is not to the disease itself, but
to conditions which dispose to it.
268 SYSTEM OF MEDICINE
Although, however, we may not admit heredity in its most absolute
sense to be a cause of emphysema, it does not follow that what, in the
absence of precise knowledge, we call the " constitution " of the patient
has no influence in determining its occurrence. The tone of muscle and
its capacity for energy vary enormously in different persons, though
no structural diflFerences can be demonstrated ; and the same may be true
of the elastic tissues. That such is the ease is certainly possible, and
in my opinion probable ; if so, the occurrence of dilatation of the pul-
monary alveoli may well be brought about in certain persons by a degree
of increased pressure within the air - passages, such as accompanies
ordinary straining efforts, which we are not accustomed to regard as
adequate to the production of emphysema, and which, in persons of firmer
fibre, are not adequate.
All who have studied the subject of emphysema from a clinical stand-
point must have met with cases in which the ordinary proximate causes of
the disease seemed to be absent. In many of these the absence has,
it is true, been but apparent, for it , is difficult to realise how slightly
a chronic winter cough impresses itself upon the memory of some
patients ; hospital patients, indeed, rarely mention such an ailment unless
directly questioned about it. But due weight having been given to this
source of error, there undoubtedly remains a certain small proportion of
cases in which no adequate exciting cause can be discovered. This lack
of resisting power on the part of the elastic tissues of the lung may
certainly be acquired, it may possibly be inherited, and is probably a
common result of the degenerative processes incidental to advanced age.
A case recorded by Hugner proves clearly that after recovery from an
attack of pneumonia emphysema of the affected part may ensue upon the
resumption of an occupation, such as that of a comet-player, which
favours the occurrence of the disease, but which had been previously
followed without injury to the lungs.
Normal anatomy of a pulmonary lobule. — A lobule of the lung
may be regarded as a lung in miniature ; a clear idea of the structure of
a single lobule will therefore enable us without much effort to construct
the whole organ.
Each lobule, more or less cone-shaped, is surrounded by areolar tissue ;
at its apex the lobular bronchus, the blood-vessels, lymphatics, and nerves
unite to constitute it. The bronchus, after a short course within the
lobule, divides and subdivides, with at first but slight diminution in size,
forming passages which are termed the interalveolar or intervesicular
passages. The course of the bronchus is at first fairly straight, but as
the divisions increase in number and diminish in size the direction con-
stantly changes. As the alveolar passages approach the surface of the
lobule they cease to diminish in size. Each passage beyond the final
division ends in a blind extremity, which, if not dilated, often
appears to be so, from the fact, above stated, that the passages do not
diminish in diameter. In some cases, however, the ends of the alveolar
passages are really dilated, and from this appearance the name " infundi-
EMPHYSEMA OF THE LUNGS z6g
bula " has been applied to them ; but a distinctive name is scarcely neces-
sary. As the bronchus enters the lobule rounded orifices appear upon its
walls. These are the openings of the alveoli, which may be regarded as
the radicles of the bronchial tree. They are at first but few in number,
but gradually increase. As the air-channel passes onwards through the
lobule, and the interalveolar passages are formed, their walls become more
and more thickly studied with the orifices of the air-vesicles, until, by
the time the surface of the lobule is reached, the blind ends of the pass-
ages are found to consist entirely of the orifices of these small recesses.
From the foregoing description it will be seen that the air-vesicles of
the terminal passages open into a common space, adjacent vesicles being
separated by incomplete partitions ; and that all the air-cells of a single
lobule are, to a considerable extent, confluent one with another. Adjacent
interalveolar passages are separated by partitions formed at the site of
branching of the air-vessels.
The interalveolar passages and their terminations are chiefly composed
of unstriped muscular fibres, arranged circularly, and supported by a
delicate fibroid tissue mingled with elastic fibres. The walls of the air-
vessels consist of a delicate membrane crossed by a network of elastic
fibres.
The capillaries on the terminal passages are covered by epithelium
only on the surface looking towards the cavity ; those in the septa pro-
ject into the cavities on either side.
Morbid anatomy. — The primary lesion in emphysema consists in an
enlargement of the terminal interalveolar passages, which increase in size
at the expense of the alveoli opening into them. Sometimes, however,
the alveoli appear to be the first to undergo dilatation. In any case the
effect is, by pressure and stretching, to diminish the blood-supply to the
epithelial and vascular structures in their walls. The alveolar epithelium
undergoes fatty degeneration, the granules being aggregated round the
remains of the nuclei. The septa between adjacent alveoli are reduced
to small projections by a gradual process of wasting ; subsequently the
partitions between neighbouring alveolar passages are perforated, and
they become fused into rounded spaces, the size of which tends to increase
with the continued operation of the immediate cause of the disease. It is
obvious that this process must be accompanied by a great destruction of
the pulmonary capillaries, an important factor in determining some of
the effects of the disease. According to Eindfleisch, wide communications
are formed between the pulmonary artery and the pulmonary and
bronchial veins, thus relieving the tension of the former vessel, but allow-
ing the blood to pass through the lungs without undergoing proper
aeration.
Varieties of emphysema. — Certain varieties of the disease may be
recognised both clinically and pathologically; the morbid changes by
which they are characterised will now be considered.
Large-lunged emphysema (Chronic hypertrophic emphysema). — The objec-
tion to the term hypertrophous as applied to this condition is that its
270 SYSTEM OF MEDICINE
use connotes increased functional activity, whereas in emphysema the
opposite condition prevails. The name here adopted, which was first
suggested by Jenner, appears preferable, as it describes the condition
and involves no hypothesis.
When the thorax is opened the lungs not only fail to collapse, but
remain fully distended, and, when the smaller bronchi have been
obstructed from inflammation, may even bulge forward. The apices fill
the supraclavicular regions, and the enlarged anterior margins may be in
contact beneath the whole length of the sternum, the precordial area
being occupied by the distended auricular process of the left upper lobe.
The diaphragm is depressed owing to the permanently inflated condition
of the lungs. After removal, when the organs are held with the base
upwards, the distended and rounded edges of the lower lobes form the
sides of a deep cup.
The lungs in emphysema were likened by Laenneo to a piUow of
down, and the simile can scarcely be improved upon. They are soft and
non-crepitant ; when compressed a deep pit forms and remains. They
are pale gray in colour, and are marked by black pigment, scattered over
the surface in lines and spots, the lines in some cases mapping out the
lobules. On close inspection the superficial portions have the appearance
of a very fine froth, consisting of very minute air-bubbles covered by
the pleura. This is rendered more obvious by the use of a hand-lens.
In some cases large rounded air-containing bullae are present, usually
along the anterior margin of the upper lobes or around the bases, but
they may be absentwhen the disease is advanced and widely disseminated.
Some are attached to the lung by a narrow peduncle only, the auricular
process of the left upper lobe being a common site of this particular
lesion. They collapse when opened, and delicate fibrous bands, the
remains of alveolar septa and obliterated vessels, may then be found
crossing the interior.
These two forms, the " local " or " bullous " and the " general," are
too frequently associated to justify a separation in nomenclature ; but it is
important to bear them in mind, as vrill appear when we come to consider
the physical signs of the disease.
On section the lungs are bloodless and dry, except perhaps at the
bases, where oedema may be present. This, however, pertains more to
some complication, such as bronchitis or cardiac failure, and is no neces-
sary efiect of the disease.
If the section be made from the extreme posterior margin forwards,
the portion of the lung which occupies the hollow beside the spine wOl
often be found in an advanced condition of emphysema; large spaces
being present beneath the pleura, and extending for perhaps half an inch
or more into the lung.
The smaller bronchi are in some cases dilated to a slight degree, but
bronchiectasis is by no means frequently associated with emphysema.
Atheroma of the pulmonary artery is commonly present, and in
advanced cases patches may be found throughout the vessel, not even the
EMPHYSEMA OF THE LUNGS 271
smaller branches escaping : it is a result of the increased strain on the
walls of the vessel from the obstruction to the passage of the blood
through the lungs. There is very often a ' complete absence of pleural
adhesions, a condition rarely observed in adults unless they are subjects
of emphysema.
Small-lunged emphysema; Senile atrophic emphysema (syn., Senile
atrophy of the lungs). — The most striking clinical and pathological char-
acteristics of this condition of the lungs are indicated by its name. It
appears to be primarily an atrophic change, incidental to advanced age,
and shared by the lungs equally with the other organs of the body. Its
title to be considered either as a substantive disease of the lungs or as a
distinct variety of emphysema is doubtful. It never occurs apart from
a general condition of atrophy ; and the slight degree of emphysema which
accompanies it is probably induced by the cough of a bronchial catarrh,
from which the very aged are rarely quite free. It is, however, convenient
and in accordance with custom to describe it as a variety of emphysema.
The subjects of senile emphysema present a wasted, shrivelled, and
withered-up appearance : the thorax is rigid, the space within is small,
the lower ribs are almost in contact and very obliquely placed. On
opening the chest the uncovered area of the heart is not diminished,
it may even be enlarged j the lungs readily collapse, falling back towards
the spine ; they are smaller than normal, deeply pigmented, almost black
in colour ; light, dry, and easily compressible. On section they present
a coarsely reticulated structure. The vesicles are enlarged by a process
of fusion, the result of wasting of the septa ; and this change may in
places be so advanced as to involve adjacent lobules. Large bullae are
rare, but the margins are in some cases much dilated. The bronchi are
thin-walled, and have undergone dilatation ; the lining membrane is com-
monly inflamed, and the tubes contain puriform fluid. Collapse and
osdema are often present, and are generally most marked on the posterior
aspect of the lower lobes.
Local emphysema; Compensatory emphysema. — This form of the disease
is invariably secondary to some pulmonary lesion, most commonly to
tuberculosis which has undergone either complete or partial arrest. In
the presence of a contracting lesion within the lungs — for instance, a
cavity or an area of fibroid tuberculosis — either the surrounding tissue
becomes emphysematous or the pleuiu thickened ; the result being deter-
mined by the nature, site and extent of the lesion. In the case of a
lesion situated close to the surface, if the lung intervening between it
and the pleura be condensed, airless, and incapable of expansion, the
visceral and parietal layers of the pleura, partially united by fine fibrous
bands, tend to become separated. The space is at first filled with yellow
serous exudation, which ultimately undergoes transformation into a
thickened fibroid tissue almost cartilaginous in density. The apex of the
lung, in cases of very chronic pulmonary tuberculosis, when the upper
lobe is almost completely occupied by a contracted thick-walled cavity,
shows such a thickening of the pleura as is here described. If, on the
272 SYSTEM OF MEDICINE
other hand, the lung tissue around the lesion is not the seat of such
advanced changes, and still admits of the entrance of air, the surface vesicles
enlarge, coalesce, and form bullse, sometimes of considerable size. Such
a condition is commonly seen at the apex of the lung, and is a certain
guide to a contracted lesion within. The surface may be scarred and
puckered, and on section dense pigmented fibrous bands are seen sur-
rounding old fibrous, caseous, or calcareous lesions, and extending into
the neighbouring emphysematous tissue. The vessels and bronchi in
such an area are usually obliterated, but on its confines the latter may
be found dilated.
Another common site of local emphysema is the posterior and upper
part of the lower lobe. Here the change is secondary to a contracting
lesion, usually a cavity, at the apex of the lung ; and may occupy a
considerable area. In one such case observed by myself the posterior
aspect of the contracted upper lobe was completely covered by the upper
part of the lower lobe. No bullae are formed, but on section a coarsely-
reticulated structure is seen, replacing the normal tissue and reaching
downwards along the posterior aspect of the lobe.
In cases of fibroid transformation of tubercle the densely pigmented
contracting fibrous nodules are often foxind embedded in emphysematous
lung ; the whole presenting appearances which show unmistakably that
the fibrosis has preceded the emphysema.
Acute vesicular emphysema. — The definition of the disease given at
the head of this article does not include a lesion consisting merely in
an over-distension of healthy alveoli, such as is present in the above-
named condition. Atrophy of the alveolar walls is an essential part of
the morbid anatomy of emphysema, and in its absence we cannot recog-
nise acute vesicular emphysema as a true variety of the disease. It is
sometimes found after death from acute bronchitis, or from asphyxia,
which had been accompanied by violent inspiratory efforts ; or when,
from collapse or other cause, the air has been prevented from entering
portions of the lung, thus throwing an increased strain upon the alveoH
of other parts.
It may be demonstrated, however, by physical examination that a
similar condition is present in cases which are not fatal ; and also that
after a time the lungs return to their normal size, a proof of the absence
of structural damage.
The lung in such a condition of over-distension is large and pale,
and with a hand-lens the increase in size of the surface alveoli can be
readily seen.
Lesions associated with emphysema. — Lungs. — Although, in the
majority of cases, bronchitis and emphysema stand related to one another
as cause and effect, it is nevertheless true that when emphysema has
become established it increases the tendency to bronchitis.
The over-distended air-vesicles compress and obstruct the capillaries
and impede the circulation through the pulmonary and bronchial vessels.
The bronchial mucous membrane becomes congested, and the condition
EMPHYSEMA OF THE LUNGS 273
thus established greatly increases the liability to inflammatory attacks.
Rupture of dilated vesicles may lead to pneumothorax ; but if the pleura
overlying the site of rupture remains intact, interlobular emphysema
results. Death is rarely due to pneumothorax so caused, but one such
case has been observed by myself, and others are on record.
Bronchi. — As already described, the bronchi are often found obliterated
and forming thin fibrous bands in large emphysematous bullae ; they
are, however, occasionally, but not commonly, found dilated to a
moderate degree in less advanced cases of general emphysema, and more
often in localised emphysema. In the atrophic form the bronchial walls
are usually thin ; in other forms they may be somewhat thickened, as
may also be the walls of the vesicles and interalveolar passages.
Heart. — The obstruction to the flow of blood through the capillaries
of the limgs naturally increases the pressure within the pulmonary artery
and requires a more forcible contraction of the right ventricle. This
leads to hypertrophy of the ventricle, and thus for a time equilibrium
may be restored. But when, from any cause, the structural integrity of
the new muscular tissue is impaired, particularly if at the same time
greater stress is thrown upon the right ventricle, dilatation follows, the
tricuspid orifice enlarges, and the valve becomes incompetent.
The right auricle, probably already somewhat enlarged, now under-
goes stiU further dilatation, and the superior an(J inferior vense cavse are
similarly affected. Congestion of all the organs which are drained by
the systemic veins necessarily follows. The portal system may become
involved at a later period. This sequence of events is not uncommonly
initiated by an attack of bronchitis.
The dilatation and hypertrophy of the right ventricle, including the
conus arteriosus — ^for the latter is always involved — are usually found
on autopsy to be associated with similar but less advanced changes in the
left ventricle ; a result probably due, at least in part, to their intimate
association both in structure and functional activity.
Degenerative changes are often observed in the heart in emphysematous
subjects, and the impaired nutrition of the muscular walls may be due to
obstruction to the return of blood by the coronary veins.
As a result of the enlargement of the lung and the permanently
depressed state of the diaphragm, the position of the heart becomes
altered. It lies lower in the chest, and its axis is more nearly
horizontal. The front of the heart is formed entirely by the enlarged
right ventricle and auricle. The altered position and size of the organ
account for the pulsation commonly observed in the epigastrium in well-
marked cases of emphysema; but of these two factors the change of
position is the more important.
Secondary changes of a fibroid character are not infrequently found
in the tricuspid and mitral valves ; and, more rarely, in the aortic valve
also.
lAver. — The changes in the liver resulting from chronic venous con-
gestion are too well kiown to require complete description. The organ
VOL. V T
274 SYSTEM OF MEDICINE
is enlarged and the hepatic veins are dilated. The section presents the
"nutmeg" character, and there is some degree of induration; but
emphysema alone is as powerless as chronic mitral disease to produce a
true cirrhosis.
The kidneys may be enlarged and cyanotic, but in a considerable
proportion of cases they are granular from the presence of chronic
interstitial nephritis, a disease with which emphysema is not uncommonly
associated. The spleen is as a rule enlarged and hard, but its condition
varies.
Chronic venous congestion of the stomach may give rise to catarrh
and haemorrhage into the mucous membrane. The brain also shows
evidence of venous congestion.
As considerable differences exist in the symptoms and physical signs
which characterise the various forms of emphysema, it is necessary to
describe them under their respective headings.
Symptoms of large-lunged emphysema. — The symptoms strictly
referable to emphysema are very few, the condition, apart from its com-
plications, being one of which patients have little or no knowledge, and
one of which therefore they rarely complain.
Dyspncea is the most important symptom, but even this is seldom
mentioned until it has become somewhat urgent : it is in proportion to
the extent of the disease. At first slight, and only experienced on
exertion, especially on walking uphill, it may gradually increase, until in
the end not only exercise, but even movement becomes impossible.
It is always much increased during an intercurrent attack of bron-
chitis, and tends, as the disease progresses, to occur in paroxysms, a
condition to which the term " bronchial asthma " is usually applied. The
asthmatic element in such cases may either arise directly from the
emphysema — the more common order — or the emphysema may be a
consequence of asthma. The difficulty of breathing is increased by
anything which interferes with the descent of the diaphragm, such as
flatulent distension of the stomach or intestines, stooping, or sitting in a
low chair after a meal. Orthopncea follows as the disease progresses,
the patient sleeping either propped up with pillows or in a sitting position.
Cyanosis may be considerable, even whilst the patient is still capable
of movement — a combination rarely met with except in this disease.
Cough. — Sufferers from emphysema are rarely free from cough for
long intervals, although cough is, strictly speaking, due rather to the
condition of the bronchi than to the change in the lungs. It is loud,
harsh and wheezing, and, like the dyspnoea, may occur in paroxysms.
It is always more troublesome in the winter, and particularly so when
the weather is cold and damp, or when fog is present.
Expectoration. — Emphysema does not of itself give rise to secretion,
but it is by no means uncommon for patients to expectorate a small
quantity of niucus to which the descriptive word " pearly " is usually
applied. When bronchitis occurs, expectoration becomes profuse, and
passes through the various phases usual in this disease.
EMPHYSEMA OF THE LUNGS 275
Hmmoptysis, although an unusual complication of emphysema, may
occur, and may even prove fatal. It is generally small in amount.
Having regard to the frequent association of atheroma of the pulmonary
artery with emphysema, it is perhaps surprising that rupture does not
more often happen.
The appetite is often poor ; complaint may be made of flatulent dis-
tension of the stomach and intestines, and constipation is not uncommon.
The deficient aeration of the blood may give rise to drowsiness and
headache.
The arteries are badly filled owing to the distension of the venous
system, and consequently the pulse is small and weak. The blood-
pressure is low, but may be observed to rise during the act of coughing
(Jenner). In the later stages, when the muscular tissue of the heart
has undergone degenerative changes, its action often becomes irregular
and intermittent.
The veins of the neck are usually distended, and they may pulsate
and fill from below. Filling from below is a sign that the valves at the
orifice of the jugular veins are incompetent. Forcible pulsation usually
indicates that the tricuspid valve is incompetent, but a slight impulse
may be the result of the impact of the blood against the tricuspid
valve being transmitted through a distended right auricle to the over-
filled jugular vein, or it may possibly be due to the systole of the
auricle.
An impulse may also be produced in a distended jugular vein by the
systolic wave in the underlying carotid artery.
The physiognomy of emphysema is characteristic. In the earlier stages
of the disease the face is full, the lips are thick, and the mucous
surface is congested. At a later stage, when emaciation has occurred, the
appearance alters. The lines of the forehead are now deep, the brows
knit, the naso-labial folds distinct, the expression careworn. The face is
of a faintly bluish tint, the colour being well marked in the lips, which
are thickened; the eyes are prominent, and the conjunctives injected.
At a still later stage there may be well-marked cyanosis of the face.
The signs of venous congestion always become more obvious on exertion.
Clubbing of the fingers and toes is often well marked, especially
when emaciation has occurred.
The abdomen is usually somewhat distended ; the liver and spleen
are enlarged from congestion, and assume a lower position than
normal ; catarrh of the stomach and intestines is apt to cause dyspepsia
and flatulent distension. (Edema of the lower extremities is often
present in the latest stages of the disease, and dropsy of all the serous
cavities with anasarca may occur when there is pronounced failure of the
heart. All the symptoms above described become more marked during
inteucurrent attacks of bronchitis ; some, indeed, are present only at such
times.
Physical emmination ; inspection. — The chest tends to undergo en-
largement in all its diameters, but particularly in the antero-posterior,
276 SYSTEM OF MEDICINE
owing to exaggeration of the dorsal curve, and to the curvature of the
sternum in the opposite direction.
The angulus Ludovici, marking the junction of the manubrium with
the body of the sternum, is prominent, and the costal angle is much
widened. The vertical measurement is increased by the downward dis-
placement of the diaphragm, and the " oblique diameters " by the ribs
becoming more nearly horizontal and the interspaces wider. This form
may be modified by the presence of any of the deformities of the chest
due' to rickets or other causes, to which reference has already been
made ; but otherwise the general tendency of the chest is to assume
a rounded form — the so-called "barrel-shaped chest" of emphysema.
The rounded outline is often more marked in the upper part of the
chest, whilst in the lower the increase of the transverse diameter is more
obvious.
The clavicles are thrown forward, and the sterno-mastoids and other
muscles of the neck are tense, giving the neck a short and thick appear-
ance. The supraclavicular hollows may be deep ; but if the apices of the
lungs are markedly affected the normal depressions here may have
disappeared. The curvature of the spine causes the shoulders to be
round, and in extreme cases the shoulder-blades may assume almost an
horizontal position.
The upper intercostal spaces may present an even surface, but the
lower are often depressed. This becomes more marked on inspiration
owing to the non-expansion of the emphysematous lung. Bulging of the
spaces may be well marked when the patient coughs. The respiratory
movements are restricted, and the expiratory act is much prolonged not-
withstanding the forcible contraction of the abdominal muscles. The
gradual expansion of the chest during inspiration, which is characteristic
of health, tends to be replaced by a uniform upward hft, during which
the accessory muscles of inspiration stand out in strong relief. In some
cases, however, the infra-axillary regions are drawn inwards and the
sternum projected forwards, whilst at the same time the epigastric region,
instead of bulging during inspiration, may be visibly depressed. This
recession of the lower ribs during inspiration is often well marked, and may
accompany the deformity of the chest called the "transversely-constricted"
thorax, which is usually a relic of infantile rickets. The downward and axial
displacement of the heart, combined with the hypertrophy and dilatation
of the right ventricle, to which reference has already been made, are
jointly the causes of the epigastric impulse commonly observed in
emphysema. A horizontal sulcus is observed in some cases to extend
across the body from side to side about the level of the lower part of
the costal arch. A broad line of dilated venules is often seen in em-
physematous subjects tending obliquely upwards on either side along
the line of the lower costo- chondral junctions, and across the base of
the ensiform cartilage, and therefore corresponding roughly with . the
attachment of the diaphragm. It is rarely complete posteriorly,
Paipation. — The vocal fremitus is diminished
EMPHYSEMA OF THE LUNGS 277
The impulse in the precordial area is generally feeble owing to the
cushion of lung intervening betweeen the heart and the chest wall;
but the hypertrophied right ventricle, in the absence of much enlarge-
ment of the lung, may cause a heaving impulse in the lower sternal
region.
Percussion. — A hyper-resonant note will be found in regions such as
the precordial and hepatic, which are normally dull; or dulness may
still be present, but over a much diminished area ; whilst behind it
is by no means uncommon to find well-marked resonance as low as the
twelfth rib. Inspiration and expiration make but little change either in
the area of resonance or in the pitch of the note on percussion.
Auscultation. — The character of the respiratory murmur varies with
the form of the predominant lesion, whether this be of the bullous type
or general in its distribution. If " bullous," the breath-sound is weak
over the sternum and along the margins of the upper lobes, but harsh
beneath the outer half of the clavicle ; whilst in the " general " form the
breath-sound over the upper lobes is everywhere feeble. It is right to
state, however, that the opposite opinion is held by some authors. In
place of the normal vesicular murmur audible on inspiration the con-
tinuous low-pitched rumbling sound produced by the contraction of the
muscles is often very distinct.
When the disease is fully established the expiratory sound is almost
invariably prolonged, often very markedly so ; in fact, during an inter-
current bronchial catan'h its duration may be so prolonged as to be
nearly four times that of inspiration.
These changes in the respiratory sounds are usua,lly most obvious
over the upper part of the chest ; but when the posterior aspect of the
lower lobes is affected the breathing will be weak at the bases, and fine
crackling r&les may be present there also. These signs are important
both as evidence of advanced disease and of oedema of the affected parts
of the lung.
At the apex of the heart the sounds are feeble, the characters of
the first sound being determined by the relative preponderance of
hypertrophy or dilatation of the right ventricle. In the former case
it is low-pitched and prolonged, in the latter short and sharp, but
weak. The point of maximum intensity of the sounds at the base
is lower than normal, and, owing to the increased tension in the
pulmonary artery, the second sound is accentuated, and may be re-
duplicated.
A rough murmur is often audible in cases of emphysema about the
sternal end of the sixth left interspace and over the seventh rib, close to
the base of the ensiform cartilage. It is systolic in time, usually short,
sharp, localised, and superficial, and it often more nearly resembles a
rough reduplication of the first sound than a murmur. It may be due to
a " white patch " on the anterior surface of the right ventricle, a con-
dition often present in emphysema. The effect of change of position of
the body on this sound is variable. It may disappear or remain un-
278 SYSTEM OF MEDICINE
changed. The only importance of the sign arises from the fact that it
is very likely to be mistaken for the murmur of mitral regurgitation.
Symptoms of small-lunged emphysema. — In this form of the
disease the symptoms are much less pronounced. The most important
change in the lungs — the atrophy — is but a part of a general process of
wasting in which all the tissues of the body, including the blood, share
alike. The respiratory needs are therefore less, and they may be
adequately met by a smaller pulmonary area. The capacity for exertion
is limited because of the feebleness of muscular power ; and, in the absence
of effort, there may be little or no dyspnoea.
Another point of difference from the variety just considered is
that atrophic emphysema is rarely complicated by attacks of bronchial
asthma ; but intercurrent bronchitis may induce dyspnoea which, although
differing in its mode of onset, is hardly less in degree than that which
characterises the asthmatic paroxysm.
Physical examination; inspection. — The emaciated and withered
appearance of the subjects of this form of the disease has already been
mentioned. The evidences of venous obstruction, such as cyanosis and
clubbing of the fingers, are absent; as also are the effects which that
condition produces in the size, shape, and position of the heart. The
chest assumes the barrel shape as a result, not of a process of enlargement,
but of "shrinkage" in all its diameters, and especially in the lateral.
The gradual diminution in the size of the lungs is necessarily accom-
panied by a recession of the ribs, which assume a more oblique position.
The interspaces from the first to the fourth on the front of the chest are
often both wide and deep ; but the increased obliquity of the lower ribs
tends to approximate them, so that the interspaces may be obliterated,
■or adjacent ribs may even overlap each other.
Inspiration is shallow, the rigid thorax moves as a whole, the upper
interspaces recede, and descent of the diaphragm is restricted.
Percussion. — The note is hyper-resonant, but it tends to be clearer in
tone and more tympanitic in quality than in the large-lunged variety. The
area of precordial dulness is not diminished and may possibly be increased.
The former statement applies also to the hepatic dulness.
Auscultation. — The breath-sound is weak, but the expiratory sound is
not prolonged to nearly the same extent as in large-lunged emphysema.
Adventitious sounds are not necessarily present, but the coexistence of
chronic bronchitis is so common as to make their complete absence very
rare ; fine and medium bubbling r41es may be heard over the bases of
both lungs. Fine crackling ri,les may be audible over the same area if
<oedema is present.
Other pulmonary complications will give rise to the auscultatory signs
by which they are usually characterised, modified to some extent by the
presence of emphysema.
Symptoms of localised emphysema. — On reference to what has been
stated as to the mode of production and common sites of this variety
of emphysema, it will be seen that the symptoms must necessarily
EMPHYSEMA OF THE LUNGS 379
depend upon the condition to which it is secondary. It may, however,
be repeated that it is frequently a sequence of tuberculosis, and its pre-
sence at the apex of a lung should suggest the possibility of such a con-
nection.
An enlargement of one lung or of a portion of it, consequent on disease
and contraction of the opposite lung, is not necessarily due to emphy-
sema ; it may be a true hypertrophy. The test by which the two con-
ditions are distinguished is that of functional activity. If this is in-
creased, the enlargement must be regarded as hypertrophy ; if diminished,
as probably due to emphysema : , in the former case the breathing
is puerile, in the latter it is usually feeble with prolonged expiration.
Symptoms of aeute vesicular emphysema. — As already stated this
condition is only recognised as a form of the disease in deference to
tradition.
It originates during a state of extreme dyspnoea, the urgency of
which it doubtless increases ; but the result to the patient is probably
determined almost invariably by the nature of the exciting cause and not
by the effect produced upon the lungs. Cyanosis may very likely be
observed during the attack.
The chest will be in a condition of extreme inspiratory distension.
The nature of the breath-sounds and adventitious sounds will vary with
the exciting cause.
The diagnosis of the large-lunged form of emphysema rarely presents
much difficulty. It is suggested by a history in which cough and
dyspnoea are prominent features, or by the patient being engaged in
some occupation known to involve severe muscular effort ; it is confirmed
on examination by the alteration in the form of the chest, the hyper-
resonance on percussion, diminished movement and feeble respiratory
sounds — signs which are present on both sides of the chest.
Error has apparently arisen at times from pneumothorax being mis-
taken for this form of emphysema. In such cases the methodical ex-
amination of the chest has probably been neglected, and undue reliance
placed upon one step in the process, possibly on percussion. In pneumo-
thorax the enlargement of the affected side, the obliteration of the
interspaces, the absence of movement contrasting with the increased
movement of the healthy side— if it be healthy, the displacement of
the heart to the sound side, the more amphoric note on percussion, and
the absence of the breath-sounds, or their amphoric quality, are signs
which combine to form a picture that, in well-marked cases, should be
unmistakable.
It is possible, however, for a collection of air, confined by firm adhesions
to a very small part only of the pleural cavity, to give rise to signs
which may be mistaken for those of emphysema. Such a case, due to
the rupture of an emphysematous bulla near the base of the lung, came
under my own notice. It is sufficient to mention it as a possibility
to be borne in mind without discussing in detail the diagnosis of a con-
dition of such rare occurrence.
28o SYSTEM OF MEDICINE
Aneurysm of the transverse part of the arch of the aorta compressing
the trachea may be mistaken for emphysema with bronchitis. The
tracheal stridor and brassy cough, the dulness, or at any rate the
absence of increased resonance over the manubrium, and the loud tracheal
breathing over the same area usually suflnce to prevent error.
"Emphysema and bronchitis" is occasionally the diagnosis on ad-
mission to hospital of cases in which the primary disease is really stenosis
of the mitral orifice ; cardiac failure, pulmonary engorgement and oedema
have supervened, and the murmur has disappeared. After a few days of
rest and treatment considerable improvement as a rule takes place, the
murmur again becomes audible, and the true nature of the case is then
obvious.
True cardiac dyspnoea is distinguished from that accompanying em-
physema by its " panting " character ; but failure of the light heart often
follows upon . long-standing emphysema, and the dyspnoea is then the
resultant of the two conditions and partakes of the characters of both.
An examination of the sputum for tubercle bacilli should always be
made in cases of emphysema and bronchitis, particularly in such as are
accompanied by marked emaciation. In the fibroid form of pulmonary
tuberculosis, which is often associated with emphysema (not so-called
" iibroid phthisis "), bacilli may be absent and the true nature of the
disease may only be discovered on autopsy. The absence of pyrexia in
such cases is not a distinguishing symptom of much value ; fibroid tuber-
culosis being often unaccompanied by fever, at any rate for intervals of
considerable duration.
The diagnosis of the atrophic form of emphysema is but. rarely
attended with difficulty.
Prognosis. — True emphysema, that is, dilatation with atrophy, is a
permanent condition, with a decided tendency to advance. But whether
it increase, and if so, at what rate, depends chiefly upon the continuance
of the exciting cause, which, in the great majority of cases, is the cough
of catarrh or bronchitis. If the patient is able, by change of residence
or in other ways, to shield himself from adverse conditions of climate,
the disease may remain stationary. Under any circumstances its course
is chronic, and life only becomes endangered when complications arise.
The extent of the lesions will naturally influence the prognosis ; but
the efifect produced upon the heart and circulation is a far more important
factor in determining the probable duration of life. As dyspnoea is the
chief evidence of this efiect, its degree during rest and on exertion be-
comes one of the main elements in prognosis. The condition of the veins
of the neck as to over-distension, pulsation, and filling from below, is an
important guide to the state of the right side of the heart.
The existence of enlargement of the liver, oedema of the legs, ascites,
and albuminuria marks an advanced stage of cardiac failure.
The presence of renal complications, particularly chronic interstitial
nephritis, is of especial importance in prognosis.
Treatment. — Sufferers from emphysema rarely ask for advice on this
EMPHYSEMA OF THE LUNGS 281
ground alone, the disease being one of the existence of which the laity
may be said to be ignorant. As a rule, no complaint is made of the
accompanying dyspnoea ; the patient has become so habituated to it that
he has ceased to regard it. In the majority of cases the condition -is
discovered when an intercurrent attack of bronchitis leads to an examina-
tion of the chest. Atrophy of the alveolar walls, destruction of the capil-
laries, and wasting of the elastic tissues are changes which cannot be
repaired ; and a return to the normal state is only possible in the cases
of temporary over-distension which occur for the most part in young
subjects, as a result either of laryngeal obstruction, spasm, or whooping-
cough, or of bronchitis accompanying an acute disease, such as measles.
Much, however, may be done to stay the progress of the disease by
shielding the patient from further attacks of bronchitis, or by advising a
cessation of any occupation which necessarily involves a strain upon the
respiratory organs. Treatment may also be usefully directed towards
the relief of the secondary effects upon the heart and circulation.
Emphysema once established undoubtedly disposes to bronchitis ; it
is therefore of the first importance that all known causes of catarrhal
inflammation should be carefully avoided. Those whose means permit
will be well advised to spend the winter and spring in a warmer climate
than is to be found in this country at such times ; many sufferers, how-
ever, although they know this full well, are prone to delay their departure
unduly, and an early November fog finds them still here ; the result too
often is a severe attack of bronchitis and much increase in the emphy-
sema. Persons who are unable to leave home, if they hope to escape an
attack of bronchitis, must exercise the greatest care in avoiding cold
north and east winds, foggy and damp air, over-fatigue, or sitting in
draughty rooms, and anything likely to give rise to a chill. Notwith-
standing its unsightly appearance, a respirator, or woollen " comforter "
covering the mouth, by warming the incoming air is of real service in
warding off attacks of bronchial catarrh.
The conditions which give rise to increased pressure within the air-
passages have already been described ; it will be sufficient, therefore, to
state that it is absolutely necessary for the sufferer from emphysema to
avoid them if he wishes to escape an increase of his disease.
The effect upon the respiration is a useful test as to whether any
form of exercise is harmful either in kind or degree ; if it causes dyspnoea
it should be avoided. The bowels should not be allowed to become con-
fined, as, in addition to the gastro-intestinal derangements likely to ensue,
much harm may be done by straining efforts in defeecation.
In the article on " Aerotherapeutics " (vol. i. p. 315) a full description
is given of the various forms of apparatus used in the application of
condensed air to the body as a whole, and of condensed or rarefied air
to the respiratory surface in emphysema. Notwithstanding that much
has been done in recent years to render our knowledge of this branch
of treatment more exact it is still but little used in this country. This
is doubtless due to the fact that patients are rarely under treatment for
282 SYSTEM OF MEDICINE
emphysema apart from its complications ; and also to the small number
of compressed air baths available for use.
The condition of the lungs in emphysema indicates that expiration
into rarefied air should aiford relief. This proceeding causes a diminution
in the amount of residual air, and an increase in the volume of inspired air;
thus a partial retraction of the lungs and a rise in the position of the
diaphragm are brought about. These changes are accompanied by a
lessened circumference of the chest, and by an increase in the vital capacity
and of the force of inspiration and expiration. The apparatus of Walden-
burg, of which a description will be found in the article on " Aerothera-
peutics" {loc. cit), is most suited for this form of treatment. Expiration
into rarefied air produces a sense of extreme constriction within the chest
and certainly diminishes the amount of residual air. The "vital capacity"
of patients with emphysema under treatment by this method undoubtedly
increases ; but this result cannot be accepted as an absolute proof of its
value, as it also follows the use of the apparatus by those whose lungs
are structurally sound, practice enabling the individual to obtain a better
result.
The results obtained from expiration into rarefied air are, however,
much less satisfactory than those which attend the use of compressed air
applied to the body as a whole.
I have given a prolonged trial at the Brompton Hospital to the
use of the compressed air bath in the treatment of emphysema associ-
ated with bronchitis, and am able to support the favourable opinions
expressed by Dr. 0. Theodore Williams and others as to its great value.
Patients almost invariably state that they breathe more freely whilst
in the bath and after a considerable number of baths (from 20 to 30
or more) have been taken ; this feeling becomes continuous, and has
remained whilst the patients have been under treatment. The gi'eater
capacity for exertion which follows the use of compressed air baths in
emphysema has been tested by observation of the gradually increasing
facility with which patients thus treated have been able to mount a
flight of steps which leads from the basement, where the bath is situated,
to the " gallery " (wards) occupied by them. Patients who at first were
obliged to use the lift to return to their ward, or were only able to climb
the stairs with many halts to take breath, have been enabled gradually
to reduce the number of stoppages on the ascent ; and many have at
length been able to return from the basement to the uppermost floor
without stopping once.
In addition to the greater freedom of respiration and increased
capacity for exertion, the cough becomes less frequent and the quantity
of expectoration is reduced.
It is not quite clear how these favourable results are produced.
In a healthy person the efiect on the respiratory organs of submit-
ting the body as a whole to air gradually condensed to the extent of
three-sevenths or one-half an atmosphere is to cause diminished frequency
of respiration, enlargement of the lungs, increase of the vital capacity,
EMPHYSEMA OF THE LUNGS 283
and probably also an increase in the amount of oxygen absorbed. The
change is attributed to the greater density of the air, and consequently
to the increased amount of oxygen supplied to the lungs. The respira-
tory power and the elasticity of the lungs, both during and after the
bath, are increased ; the chest is enlarged in all its measurements, and the
diaphragm assumes a lower level. In the subjects of emphysema, how-
ever, the effect of the bath is to cause a reduction in the size of the
chest, as ascertained by measurement of the circumference ; and also in
the amount of distension of the lungs, as proved by the reappearance of
dulness in the precordial and hepatic regions. The diaphragm is raised
instead of being lowered, and epigastric pulsation may be replaced by an
impulse more nearly in the normal situation of the apex beat of the
heart.
It appears probable that the condensed air penetrates into parts of the
lungs which have been long unused in respiration, and in which air has
been, so to speak, imprisoned at a high pressure ; the escape of this air is
facilitated and contraction of the lung follows.
In some cases the improvement following the use of the bath is but
temporary, and in cases of emphysema accompanied by asthma I have
observed very severe attacks of dyspnoea to follow very shortly after a
bath. If this should occur after the second bath, it is generally better
to discontinue its use. Many cases of asthma are, however, greatly
benefited by this method of treatment.
For the details of this method the reader is referred to the article on
"Artificial Aerotherapeutics," vol. i. p. 310.
The treatment of an attack of bronchitis occurring in a patient the
subject of emphysema is not materially modified by the latter complica-
tion ; but the duration of the attack is sensibly prolonged, and the danger
to life is much greater, owing to the loss of power of expectoration which
results from the diminished elasticity of the lungs.
Spasmodic dyspnoea often accompanies an attack of bronchitis, and
requires the use of such remedies as stramonium, lobelia, belladonna,
grindelia, or iodide of potassium in large doses, in addition to the
ordinary drugs used in the treatment of bronchitis. The desirability of
employing morphia in such cases will depend chiefly on the relative pre-
ponderance of the spasmodic or the catarrhal factor. The nearer the
attack approaches in character to one of true asthma the greater is the
probability of relief from a subcutaneous injection of morphia ; whilst,
on the other hand, if the dyspnoea be chiefly due to the accompanying
bronchitis, the use of morphia may be attended with the greatest danger.
The history of previous attacks, the mode of onset, the presence of
pyrexia, the character of the adventitious sounds — for instance, the pre-
sence of fine or medium bubbling rales, indicative of an affection of the
smallest bronchi or of the alveoli — and particularly the condition of the
bases of the lungs, are some of the points to be considered in determining
such a question. In the treatment of the attacks of wheezing, so often
met with in emphysema, apart from any serious bronchial attack, a stimu-
284 SYSTEM OF MEDICINE
lating liniment containing turpentine and iodine rubbed into the chest is
often of much service. Iodide of potassium in doses of five, eight, or ten
grains three times daily, in combination with extract of stramonium and
carbonate of ammonia, generally affords relief. In the intervals of com-
parative freedom from such attacks, and often throughout the winter
months, the administration of cod-liver oil is hardly of less service than in
cases of pulmonary tuberculosis. It is of special benefit when nutrition
is failing, as is commonly the case in advanced stages of the disease,
and in the atrophous emphysema of the aged. Iron in combination with
spirits of chloroform is often taken by patients with emphysema with
much benefit.
Tiirpentine, terebene, and balsamic remedies are of service where ex-
pectoration is excessive ; this symptom is, however, due to the accompany-
ing bronchitis, and its treatment is described in the article on that
subject.
Cyanosis is an indication for venesection, and the necessity is urgent
when there is evidence of great over-distension of the right side of the
heart, with tricuspid regurgitation, pulsation in the jugular veins, and
oedema of the feet. Digitalis should be given as soon as the blood has
been drawn ; and its use may be necessary in cases which are not so
advanced as to require venesection.
When, as is not uncommonly the case, emphysema supervenes on
bronchitis of gouty origin, the existence of this factor in the case must
not be overlooked in the treatment. The same statement applies to the
coexistence of chronic interstitial nephritis. It must not be assumed at
once that the presence of a small quantity of albumin in the urine is due
merely to renal congestion ; search should be made for casts.
It is of great importance in cases of emphysema accompanied by
attacks of dyspncea, occurring at night, that the patient should not take
a heavy meal at seven or half -past and retire early to bed ; by so doing
he is very Hkely to induce an attack. Full time should be given for
digestion, and the lighter the evening meal the better; such patients
should dine in the middle of the day.
Few conditions apart from bronchial catarrh are so likely to induce
an attack of dyspnoea as flatulent distension of the stomach. This is
chiefly to be avoided by attention to diet ; and these patients are
nearly always well aware what food suits them and what does not.
A mixture containing bicarbonate of soda, tincture of nux vomica, com-
pound tincture of cardamoms or tincture of ginger, with a bitter infusion,
taken half an hour before meals, may prevent such an attack. A dose of
blue pill, taken twice a week at bedtime and followed in the morning by
a saline purge, is often beneficial in middle-aged subjects of the disease
who are well nourished and have a tendency to gout.
EMPHYSEMA OF THE LUNGS 285
Interlobular or Interstitial Emphysema
The escape of air into the connective tissue of the lung produces a
condition to which the above name is applied.
As stated in the previous section, it has nothing in common with
emphysema of the lungs but the name.
The air appears as rows of beads beneath the pleura and in the sub-
stance of the lung.
Wounds of the lung or ruptiu-e of the air-vesicles from over-strain
during violent cough are the most common causes of the affection.
I have specially observed it in connection with laryngeal diph-
theria, generally after tracheotomy had been performed; but it may
occur independently of that operation. The air, as pointed out by Dr.
Champneys, passes from the tracheotomy wound downwards into the
thorax behind the deep cervical fascia. From the mediastinum it may
spread along the connective tissue surrounding the bronchi and vessels,
and may appear on the surface of the lung as small beads of air beneath
the pleura.
Mediastinal and interlobular emphysema may occur in diphtheria when
tracheotomy has not been performed, probably from rupture of vesicles
upon the surface of the lung ; and pneumothorax, from perforation of the
pleura, may follow.
Pathology. — The following extracts from the post-mortem register of
the Middlesex Hospital (2) illustrate the changes met with in cases of
interstitial and mediastinal emphysema : —
Case 1. — Male, age Z\ years. Diphtheria ; tracheotomy. Extreme sub
cutaneous emphysema of the face, neck, and trunk ; collapse of both lungs ; media-
stinal and subpleural emphysema.
Case 2. — Female, eet. 5. Diphtheria; tracheotomy. Lungs fully dis-
tended ; no collapse ; air in anterior mediastinum ; membrane on fauces and in
larynx, trachea, and bronchi.
Case 3. — Female, set. 5. Diphtheria ; tracheotomy not performed. Em-
physema of root of neck ; mediastinal, interlobar, and interlobular emphy-
sema ; pneumothorax (R) ; pulmonary collapse.
Case 4. — Male, aet. 5. Diphtheria; tracheotomy. General emphysema of
subcutaneous cellular tissue of neck, trunk, and arms ; lungs almost completely
collapsed from double pneumothorax ; air in mediastina and around roots of
lungs ; membrane on tonsils and in larynx, trachea, and large bronchi.
Case 5. — Male, age 2 years. Diphtheria ; tracheotomy. Larynx completely
blocked with membrane, which extended throughout the trachea and main
bronchi ; lungs collapsed in patches ; emphysema of anterior mediastinum.
Case 6. — Male, age 1 1 years. Diphtheria ; tracheotomy. General em-
physema ; membrane in trachea and bronchi of left lung, latter collapsed ;
marked emphysema of anterior mediastinum.
Caae 7. — Female, age 4 years. Diphtheria ; tracheotomy. Interlobar em-
physema on right side ; air in anterior mediastinum ; membrane as far as
secondary divisions of bronchi ; numerous areas of pulmonary collapse.
286 SYSTEM OF MEDICINE
The preceding cases illustrate the lesions commonly found in associa-
tion with interlobular emphysema when that condition occurs in
diphtheria; the most important being general emphysema, pneumothorax,
and pulmonary collapse.
Symptoms. — In all the cases above described in which tracheotomy
was performed there would necessarily be urgent dyspnoea at the time
the trachea was opened. The dyspnoea would then be relieved, but the
occurrence of mediastinal and interstitial emphysema is accompanied by
an increase in the dyspnoea. If pneumothorax supervenes, the dyspnoea
becomes extreme.
Double pneumothorax is necessarily quickly followed by death.
The breath-sounds would almost certainly be weak or absent if the
connective tissue of the lung were infiltrated with air. Pneumothorax
would be characterised by its ordinary physical signs.
Interlobular emphysema is rarely recognised during life. It may be
suspected when subcutaneous emphysema is present, or when pneumo-
thorax occurs. The latter is a serious complication. It is probable that
the condition here described is often present but is unsuspected, and that
the air is absorbed when recovery takes place.
No definite treatment can be adopted for the condition.
J. K. FOWLEK.
REFERENCES
1. Ohampnbts. Med.-CMr. Trans, vol. Ixv. p. 75. — 2. Fowlbe, J. K. Fatho-
logical Report, Middlesex Hospital, 1882. — 3. Gaiednbb. Bronchitis, 1850, p. 62. —
Jennbr, Sir W. Med. -Ghir. Trans. yo\.:k\. — 4. Idem. Reynolds' System of Medicine,
vol. iii. — 5. Rainet. Med.-Ghir. Trans, vol. xxxi. — 6. Villbmin. Arch. gin.
1866, ii. 570.
J. K F.
ON ASTHMA AND HAY FEVER
Asthma is a paroxysmal dyspnoea which often manifests itself quite
suddenly and from a great variety of causes ; and which may subside
again with like rapidity. The respiration in the intervals may or may
not be normal.
It is usually divided into primary or idiopathic and secondary
or spasmodic asthma. The latter kind appears to originate from more or
less bronchial catarrh. In the management and treatment of the affection
it will be necessary to take this distinction fully into consideration ; but
seeing that spasmodic asthma can, and certainly does, occur independently
of local and chronic irritation, I shall first consider it in its simplest
form as the primary disease. I shall first describe the features of an
attack of asthma, and then discuss ia natural sequence its causation, its
pathologj', and the general management of the asthmatic patient.
ASTHMA AND SAY FEVER 287
Hay fever is often a spasmodic asthma in its purest form, so that the
two maladies will be considered in common.
Symptoms. — The asthmatic paroxysm may come on at any time. A
susceptible or morbidly paroxysmal subject — to be paroxysmal more or
less is a universal attribute of organic action — comes into contact with,
say, some animal or vegetable exhalation ; eats some indigestible article
of diet, or something that, while innocuous to the mass of mankind, is
known to be in some way prejudicial to particular individuals; or in
some other of many ways taxes his range of accommodation beyond the
margin of its power, and within a few minutes an attack will begin. The
beginning is said to be most frequent during the night, when the patient
has had his first sleep ; for instance, at two or three in the morning he
suddenly awakes with a stuffy feeling in his chest, and within a short time
he is in the throes of an attack of asthma. Thereupon he is compelled to
sit up in bed, perhaps to rush to the window ; the head is fixed, the
shoulders raised, the hands are often planted well down upon anything
firm upon each side to give purchase to the respiratory muscles, and so
the suflferer sits labouring at his breath. Sometimes he bends forward,
sometimes stands leaning upon some support; but the object in all cases
is the same, to give the respiratory muscles better or more fixed support
from which to act.
The pulse is usually but little affected, and the temperature is
normal.
In bad cases the face is of an ashy pallor, or it is gray and leaden, or
dusky from want of oxygenation of the blood ; the skin is covered with
perspiration, the eyes may look prominent, the nostrils may be diiated.
Few diseases produce appearances so distressing and so grave, and yet it
can fortunately be said that an attack of spasmodic asthma never kills.
Probably it supplies its own corrective in this, that after a certain time of
agony, or certainly of intense distress and anxiety to the patient, the
irritated centres become exhausted, the spasm is gradually relaxed, and
the patient sinks to sleep. In some cases the relief appears to be absolute ;
in the majority, however, it is only comparative, and more or less oppres-
sion is experienced for a day or two, sometimes for many days ; or the
malady may abide with the patient more or less continuously.
During an attack, although the patient is making violent efforts with
all the respiratory muscles, the actual movements of the chest wall are
little indeed. The chest may plunge, but there is no expansion of
the thoracic cavity. On the contrary, as the chest walls are pulled out-
wards all the more yielding parts are depressed and thus the intercostal
spaces become troughs. The epigastrium may be hollow or full ; the supra-
sternal and supraclavicular spaces are greatly exaggerated.
The actual condition of the chest during a paroxysm has been the
subject of some discussion. The generally accepted description, following
Salter, is that it is in a state of over-distension, the diaphragm being
depressed and the upper part of the abdomen being full (Hyde Salter
and Biermer). The movement is much restricted, and thus there is a very
288 SYSTEM OF MEDICINE
short, abortive, suddenly pulled-up inspiration, and an expiration perhaps
four or five times as long as it should be. The percussion of such a chest
gives a hyper-resonant note. But I am sure that I have seen, as stated
by Eiegel and others, another form of chest, where the lower parts, if not
retracted as some contend, were not unduly distended, and where dulness
rather than hyper-resonance was detected. And I have always supposed
that in these cases the obstruction in the smaller bronchia is so extreme
as to lead to a state of collapse. Wilson Fox oifered this explanation,
and the whole subject will be found discussed in his posthumously pub-
lished work, A Treatise on Diseases of the Lungs and Pleura.
The attack is, however, by no means always sudden in its onset,
perhaps not generally so. More or less wheeziness and constriction of the
chest may exist for a day or two beforehand ; there may be a short, rather
hollow cough, and, if the dyspncea be at all pronounced, much weariness
on exertion. Thus a mild or threatening attack may be recognised by the
onlooker in the disinclination to all movement generally shown by persons
thus affected.
If the chest of the asthmatic be auscultated during the paroxysm the
chief feature is an almost complete absence of respiratory murmur. The
chest, as I have said, plunges, but there is no corresponding inspiratory
wave ; there are sibilant rhonchi and muscular rumbles, and a variety of
odd noises, but no real ingress of air; and with the expiration there
may be, perhaps, a long, distant, soft sibilus, the sole evidence of
the respiratory ebb. The disease is often unequally distributed : one
side, or this or that portion of one lung is affected more than the other ;
the asthmatic storm flits about the lung, now here, now there, and
when the disease is thus unilateral or partial it is liable to repeat itself
thus ; so that we surmise that there is some local disease in the form of
bronchitis, emphysema, adherent pleura, and so on, which exercises a
permanently determining effect.
It is said that when an attack is over the patient is free from liability to a
recurrence for some time. But in all probability this depends upon the
past duration of the asthmatic habit. Asthma, like gout, although in its
earlier years markedly periodic in recurrence, tends, as the patient grows
older, to become erratic in its manifestations, both as regards the time of its
appearance and the form in which it comes. So that whereas in its earliest
appearances it comes and goes, maybe with some special regularity, later
in life it comes but it does not go, and the patient thenceforward is subject
to a more or less chronic bronchitis. And in all old cases, in which the
chest is damaged by the repetition of the paroxysms, emphysema is pro-
duced with its attendant chronic bronchitis.
As the attack ends, expectoration usually begins. In the earlier stages
of the paroxysm the bronchial tubes — to judge from the character of the
signs — are dry; the prevailing sounds in the chest being wheezing sibilus
and rhonchus. Under the intense oppression the patient longs to expec-
torate, but is not able to do so. But when subsidence approaches, small
gray pellets of mucus, of characteristic appearance, "like tapioca" (Salter),
ASTHMA AND HAY FEVER 289
" often filamentous in shape like boiled macaroni " (8), begin to appear
and gradually increase. In association with the appearance of crepitation
in the chest the sputum becomes more and more copious, thin and frothy,
till it may reach some considerable quantity. Blood seldom comes, but in
severe attacks it may, and, if so, generally in streaks.
The clinical history of spasmodic asthma is, however, by no means
completed by this description of a characteristic attack. There are
several other irregular states that to my mind are no less parts of the
disease. First of all there is hay fever, when brow ague, coryza, a
more or less general disagreeable stuffiness of the respiratory tract,
rendering nasal breathing a difficulty, and producing a more or less
chronic wheeziness and distress, last throughout the summer months.
At times there is some slight febrile reaction, but it is not often
great in degree ; there is rather the subjective feeling of lassitude
and heat than the objective evidence of actual pyrexia ; and perhaps,
on the whole, these rather indefinite symptoms are the more usual mofle
of its attack, although a definite attack of spasmodic asthma is by no
means uncommon.
Paroxysmal sneezing is another way in which the asthmatic respiratory
tract explodes. If we study asthma or the history of the asthmatic in
any comprehensive way, we cannot but be sure that, either as a substitute
or as part and parcel of the asthmatic attack, this sneezing must be taken
into account. It is often found in asthmatic subjects and in asthmatic
families, in which one member may have asthma and another exhausting
paroxysms of sneezing ; moreover, it often goes with asthma, the sneezing
gives the impetus of origin to the asthma, the irritation in the upper air-
passages gradually spreads down the bronchial tubes, and asthma more
or less severe results. In the history of asthma cases of this sort are to
be found in numbers ; but they need not be more particularly described,
for they are fully dealt with under an appropriate heading. I may
say this, however, that most of the cases of sneezing I have met with
have been in women, which is against the rule that prevails in asthma, in
which case men are in the proportion of two to one. There are authors
who attribute such cases largely to local disease in the nose, and beheve
that they are to be relieved, as also the asthma that accompanies them, by
local treatment of the nasal mucous membrane. One case may be quoted
that illustrates several of these points : a man, aged twenty-eight years,
who came of healthy, non-asthmatic stock, fell off a bicycle and smashed
his nose. Ever since that time, now twelve years ago, he has required
for his daily use six or seven pocket-handkerchiefs, and now he has
become asthmatic. His asthmatic attacks come on every month or six
weeks, and last from half an hour to a day and a half. He has had his
nose treated with decided benefit to his asthma, but he derives most
benefit from smoking medicated cigarettes. With reference to the nose
the experiments of Lazarus (7) are of much interest. This observer has
d.monstrated a certain relationship between the nasal mucous membrane
and the bronchial muscles, so that, by the application of weak electrical
vor,. V TT
290 SYSTEM OF MEDICINE
currents to the nasal mucous membrane, he was able to register a distinct
increase in the intra-bronchial pressure.
There is at least one other affection that I would include in the
clinical history of asthma, namely, the paroxysmal bronchitis of infants
and young children. It has always seemed to me that one of the most
interesting features in the study of medicine is the modification that
disease undergoes in the successive periods of life. It is not certain,
perhaps, that disease is so modified, but there is plenty of evidence
to point in that direction. For instance, when a man who in earlier
years had acute rheumatism is attacked in middle age with well-marked
gout, we may suppose that a common factor has been modified, so that
what did produce acute rheumatism at a later date produces gout. Now,
as regards asthma, I believe that something of this kind takes place.
Asthma, as I shall presently show, is largely a disease of childhood, but
it is not clearly present in the earliest years. Hyde Salter has seen two
cases in infants of fourteen and twenty-eight days, but such instances are
very rare. It frequently begins to appear at six, seven, or eight years of
age, and there are a fair number of suspicious cases at earlier periods
than this. In infancy, if asthma exists, as I believe it does, it shows
itself as a bronchitis, so far as the physical signs go ; but, if so, it is a
strange and interesting bronchitis, apart from the physical signs. It comes
on with remarkable suddenness ; it is mostly associated with fever ; it is
generally attributed to chill by the relatives : but there are reasons for
thinking that it owns a much greater variety of causes, such as over-
excitement, errors in diet, dentition, and so on. It clears up with
remarkable celerity and certainty ; it often leaves the child no worse
than it was before the attack. Such attacks as these occur in a particular
class of children, — children that give conspicuous evidence either of
coming of nervous stock, or of nervousness and excitability in themselves.
The whole history of these cases is explosive and nervous ; and it may
well be that, in the early history of the child's life, the ribs and other
parts of the respiratory apparatus are not sufiiciently developed to
produce asthma, as we expect to see it; so that the mode of the disease
is atelectatic or bronchitic. Asthma, in its ordinary manifestations,
requires certain conditions of respiratory power, which, in all probability,
the thoracic walls do not readily supply at that early period. Moreover,
there can be no doubt that in the seven stages of our existence — and this
answers to some extent the question I have already mooted — our various
viscera change places in their relative importance, not only in their
several bearings upon the well-being of the organism, but also in the
absolute degrees of their activities ; now one, now another, becoming a
centre of excitement and explosion, and thus of break-down in ill-balanced
organisations. In infant life the stomach tends to play the part of the
spoilt darling, and the lungs often have to pay the penalty for its caprices.
However well it may be, it would appear that often, as with many
another ill-bred person suddenly thrown into a position of trust and
responsibility, it is not equal to the occasion ; the household's teeth are
ASTHMA AND HAY FEVER 291
set on edge, and pulmonary catarrh or oedema or collapse is set up. It
seems to me that these sudden storms, which so expend themselves on
the lungs, or in the achievement of pyrexia, have much similarity to asthma
in their sudden mode of outburst ; they involve a similar area, and may
therefore not inappropriately be considered in the youngest children as
the representative of asthma. And having diverged from the immediate
subject to introduce that of the correlatives, substitutes, or derivatives of
asthma, I shall briefly indicate several other diseases that may in this
respect be considered with the gastro-pulmonary fever that I have just
mentioned. Some persons, for instance, have laid stress upon psoriasis
in this connection. I have myself known of a case where asthma and
psoriasis seemed to alternate in the same person, and I have also come
across this curiously suggestive alternation as regards eczema. The mother
of a family is the subject of spasmodic asthma. She has had four
children. In the first and third pregnancies she had no asthma, and in
each child bad eczema appeared, and death resulted in one from convul-
sions. In the second and fourth pregnancies the mother had bad asthma,
and the children hitherto have been healthy. I find from a collation of
my notes that no less than seven out of 125 cases of asthma were associ-
ated with severe eczema, and in two or three of these as the eczema went
the asthma came. Carl v. Noorden is perhaps the most recent author
who has drawn attention to the frequency with which asthma is associated
with eczema, but the connection has long been noted.
Again, I have elsewhere thrown out the suggestion that some of the
cases of paroxysmal sneezing, which, as I have said, are undoubtedly part
of the complete picture of asthma, may also be a part of the history of
Eaynaud's disease ; for they go with weak peripheral circulation, with
waxy fingers, with chilblains, and so on. All three are probably due to
allied causes ; and although in all the three the results are of different
order (in the case of the nose, turgidity; in that of the extremities,
cadaveric blanching or chilblains ; in the case of the lung, a supposed
spasm of the muscles of the smaller bronchi, leading to a temporary
collapse of the affected part of the lung), yet the clinical history iu all
of these is not unlike. In aJl there is the same tendency to suddenness
of onset, the same sort of rhythmical association between flux and its
opposite, the same curious vagaries of onset from causes that seem quite
inadequate.
Of other affections that surely belong to the same category is that
form of looseness of bowels which is so common in nervous subjects, and
in excitable children, where the mere ingestion of food seemi? sufficient
to provoke a stomach-ache and a profuse liquid evacuation from the
bowels. This is , perhaps the very commonest of the kind. Another is
urticaria, and it is not uninteresting to note that it is sometimes
associated with or replaces asthma, as a case of asthma produced by
contact vtdth cats will show. I have records of three such cases.
To complete the clinical picture, it must be said that although a
certain number of cases are inexplicable explosions, and all of them own
2g2
SYSTEM OF MEDICINE
sometliing of that character, yet many, perhaps most, have a local excit-
ing c:uise — a cause inefficient, it may be, to produce any such disagreeable
effects under healthy conditions of the nervous centres, but which under
diseased or ill - regulated conditions becomes an active source of
woriy and excitement. Such things are pneumonia, bronchial catarrh,
whoiiping-cough, and so on. Eighteen out of 125 are attributed to such
a cause.
Causation. — As to sex, it is usually stated that asthma occurs twice as
often in men as in women : 73 to 50 in my own cases. It might have
been anticipated that the less stable centres of the woman would be
the more likely to show a predominance, but it may well be that the
instability of womanhood works off in other ways. Salter considers that
tliis unexpected incidence of a nervous affection upon males may be an
argument in favour of the existence of some organic change in the lung.
Of age, Hyde Salter remarks that it is a commonly received opinion
that asthma is a disease of advanced life, but that it is not confined to
any one time of life ; so far, indeed, is it from being peculiarly a disease
of the old, that a larger number of cases take origin in the first ten years
of life than in any subsequent decade. This seems to me quite a correct
statement of the matter, for I find that, of cases in which the point is noted,
50 began in children of ten years and under, 31 in males, 19 in females:
it is interesting to note that the youngest case was in a little boy %\ years
old, whose father suffered from hay fever and asthma, and who was said
to have been quite cured by local treatment of his nose with the cautery.
In 23 cases the disease began between ten and twenty, 1 3 being males
and 10 females. In the period from twenty to thirty only 12 cases are
reported, 4 males and 8 females. In 36 cases, 24 men and 12 women,
the disease arose after the age of thirty. These figures indicate, too,
that the excessive incidence of the disease upon males is all along the
line, with the exception of the decade from twenty to thirty, in which
perhaps the numbers are not sufficient to base any conclusions upon.
Thus, in seventy- three cases out of 121 asthma began in subjects under
full age.
Hyde Salter's table of the age at which people have become asthmatic
is as under : —
During first year
Jrom
1 to 10 .
10 ,
20 .
20 ,
30 .
30 ,
40 .
40 ,
50 .
50 .
60 .
60 ,
70 .
70 ,
80 .
11 oases
60 „
)31p
30 „
12-8
39 ,,
17
44 ,,
19
21 ,,
9
12 ,,
5
■i „
1-7
1 ,.
0-4
225
Heredity. — Of 123 cases, 50 showed a well-marked neurotic inherit-
ance of one form or another; in 25 it was the direct transmission of
ASTHMA AND HAY FEVER 293
asthma or of hay fever. In 8 more one or other of the parents had
had rheumatic fever ; in other families there is a history of megrim ; in
others somnambulism and diabetes existed. And, indeed, in all this
group of diseases — in asthma, hay fever, and paroxysmal sneezing — the
number of the nervous phenomena that are to be found in the different
members of the family is conspicuous. Berkart, in some carefully
selected cases, found that in 16 per cent one or other parent suffered
from asthma.
Of other remoter causes one must certainly mention an idiosyncrasy
on the part of the subject — "individual constitution," as "Wilson Fox
calls it. What this is we know no more than why certain foods, which
for the majority of mankind are perfectly harmless, for a small minority
are active poisons. For my own part I am inclined to doubt whether
this constitution is ever wanting in the case of asthma, even though
diseased conditions be actually present that seem so immediately
provocative of an attack as naturally to be regarded as sufficient
causes.
Immediate causes. — Of the two groups of cases into which we divided
asthma at the outset, perhaps almost enough has been said incidentally
about idiopathic asthma. Given a certain morbid sensitiveness of
the nervous centres, anything seems capable of producing an attack.
It may be a nervous shock, over -fatigue of mind or body, too
monotonous a habit of living, too little exercise, too much food, indiscre-
tions of one kind or another in diet, changes of temperature, changes of
climate, a thunder-storm — changes in the weather seem to be particularly
prone to induce asthma, microbic organisms in the atmosphere, or
emanations of various kinds from animate (cat or horse asthma), inanimate
bodies (hay), and so on.
Of some of these emanations one would not wonder that dust, fog,
or pungent fumes of various kinds should now and again be responsible
for the production of the disease. But the peculiarity of asthma would
seem to be that it is evoked by irritants that under ordinary circum-
stances are no irritants at all (Salter). " One asthmatic is obliged to
expatriate himself in the hay season and take a sea-voyage ; another
cannot stay in a room in which a bottle of ipecacuan is opened ; a third
cannot stroke or nurse a cat ; another cannot go near a rabbit hutch ;
another is immediately rendered asthmatic by the neighbourhood of a
privet hedge ; another cannot sleep upon a pillow stuffed with feathers ;
another cannot use mustard in any shape, or bear it near her, so that
she dare not even apply a mustard plaster; and one young lady I
know who dare not pass a poulterer's shop."
I have myself knowledge of two cases of cat asthma. In one of
them the existence of cats is the bane of life, for before accepting an
invitation she is obliged first to ask, " Is there a cat ? " An attack of
urticaria and coryza followed by asthma has been noticed to come on
within ten minutes of having stroked a cat. At other times sitting in
a room in which there was a cat, without any actual contact with it,
294 SYSTEM OF MEDICINE
was sufficient to produce a bad attack, beginning within ten minutes of
entering the room.
Professor Cliflford AUbutt tells me of a little boy in whom horses
work similar effects. He cannot, therefore, ride in carriages or cabs ;
and it has been necessary to let him run home and get wet through,
rather than incur the greater evil of asthma, likely to be provoked by a
ride in a cab with his mother.
Such statements as these, Salter truly says, one would hardly
believe, were not their reality placed beyond doubt ; there is neither
invention, nor imagination, nor exaggeration about them.
Surgeon-Major Lethbridge Swayne, practising in Aurungabad, tells
me that asthma is quite common there in association with malaria ; and
that asthma often ushers in an attack of malarial fever, and has done so
in his own case several times.
Potain alludes also to the frequency with which amongst the
infections paludism plays the part of an exciting cause. The same
thing has been noticed with regard to that malarial disease, influenza.
Oases have, I believe, been recorded where influenza ushered itself in
by provoking a severe attack of asthma; I have seen such a case myself,
and shall record it later in this article. But it is seldom, perhaps, that
this is the case ; far oftener asthma comes on as a result of the post-
influenzal exhaustion of the nervous centres. I have notes of six cases
of the kind.
Of nervous shock, or strong emotion, I will only add that, as such
impressions are well known to bring on attacks, so they may also
remove attacks instantaneously and completely.
In all these cases examine the patient in an interval of freedom, and
there may be no evidence whatever of any disease. But of a large
class of asthmatics this cannot be said. In many an asthmatic, for
instance — 80 per cent of all cases, according to Dr. Theodore Williams —
there is evidence of permanent catarrh of the bronchial tubes (bronchitis).
A little fresh accession of cold, and on comes asthma. Hyde Salter
says much the same, namely, that 80 per cent of the cases of asthma in
the young date from whooping-cough, bronchitis, or measles. There
are other asthmatics who are gouty, and the gouty condition of blood
seems to provoke a catarrh, in this respect occupying an analogous
position to ague. The alterations of the ribs in old age lead to
pulmonary obstruction and emphysema, and so favour an asthmatic
paroxysm. The pulmonary congestions of chronic heart disease and
renal disease bring about the same end. Hyde Salter describes a peptic
asthma due to indiscretions in diet; but this seems to me to belong
more properly to the idiopathic group, the stomach being a common
point in the morbid circle from which the storm is set agoing. In
many even of these secondary cases, however, it is still supposed, as I
said at the outset, that some constitutional element or weakness allows
the local disease to start the train of peculiar symptoms.
There is, however, one group of cases to which I am not sure that
ASTHMA AND HAY FEVER 295
this applies. Every now and then an asthmatic appears to have
suffered, for the first time, in middle life, in whom there are no
obvious tendencies to neurotic ailments, and no evidence of existing
disease that might act as proximate cause. It is possible that a
percentage of these may belong to the group already mentioned, where
gout in the system or excessive vascular tension has been the cause ;
but I am not satisfied that these things explain all the cases of later
appearance. To judge from my own experience, they are prone to be
very severe, and to be but little amenable to treatment ; and I have
come to the conclusion that in certain cases there may be some rapid
onset of emphysema, some process of degeneration in the tissue of the
lung, such as was described some years ago by the late Dr. Greenhow.
Simple spasmodic asthma is very seldom seen in the wards of a
general hospital. It is of course found often enough in the degenerate,
in association with emphysema, chronic bronchitis, gout, and renal disease.
But in the primary pure form it occurs seldom indeed. There are
many reasons for this. Chief of them, perhaps, is that this disease
comes and goes; and for maladies of that kind the working-man cannot
afford to lie up. Indeed this applies to all classes of society. As
Berkart truly says, " Asthmatics are not disposed to consider themselves
as patients. Their suffering is forgotten as soon as it is over." But I
cannot help thinking that the affection is one that belongs more
peculiarly to the upper ranks of society. It may be, perhaps, that
the angular condition of the nervous centres, to which the disease may
be attributed, becomes rubbed down, so to speak, by the harder life
of the labouring classes ; just as such persons are less sensitive to
noise, less sensitive altogether to what one may call the smaller ills of
life.
BesuUs of asthma. — When a man has been the subject of asthma for
a long time, it is likely that he will present characteristic appearances
in his general physique and gait. He is usually very thin ; his back is
rounded, his shoulders are high, and he walks lethargically, with a well-
marked forward stoop. He sits, may it be said, turtle-like, with his
neck dropped into his chest. In long-standing cases the face is a little
dusky, the eye watery and perhaps congested; and there is often a
cough of peculiar timbre, moist and hollow, not easy to describe, but
evidently the product of feeble expiratory power. The asthmatic
speaks, too, as he coughs ; and for the same reason, that the tidal wave
of the chronic asthmatic is exceedingly shallow • for the spine is
rounded, the ribs stiffened and fixed, the chest elongated and depressed.
The morbid anatomy of asthma, saving perhaps one particular detail,
is comparatively small in amount and simple in kind. It is obvious
that all diseases, as they fall under the denomination of " functional,"
must proportionately be wanting more or less in those coarser changes
in structure that we look for in the study of morbid anatomy ; and so
it is here. The leading departures are most of them certainly con-
ditioned by, and secondary to asthma of long standing : they are the
296 SYSTEM OF MEDICINE
results of the impaired respiration, not the cause of the asthmatic
paroxysm. These are more or less chronic inflammation of the
bronchial tubes, shown by injection and thickening of the mucous
membrane, thickening of the muscular coat of the bronchial- tubes,
dilatation of the tubes, emphysema of the vesicular structure, more or
less thickening and atheroma of the branches of the pulmonary artery
in the lung, and hypertrophy and dilatation of the right side of the
heart. The changes in the skeleton that go with these have already
been mentioned ; these are the curved dorsal spine, the barrel-shaped
chest, the stiffened ribs, the generally wasted frame.
But we have still to consider in more detail the state of the bronchial
tubes, and the products that are shed from their mucous surface.
The most regular condition to be found in the asthmatic is more or
less mucus or muco-pus in the smaller tubes. This may be considered
perhaps to be a feature of the asthma itself, inasmuch as it is admitted
that in 80 per cent of the cases there is some organic change in the
lung.
Practically, all the controversies that have been waged over this
subject have centred in this : which is cause, and which is effect ?
Medicine, so eager to find a cause for everything, is unwilling to
accept anything as such that does not possess a definite basis of
structural change visible to the naked eye or to the microscope ; and
is willing to attribute the phenomena to any change that is demonstrable,
rather than incur the suspicion of going beyond the facts, of hasty
generalisation, or of appropriating prematurely the possessions of the
future.
From a very early time Leffevre, himself an asthmatic as recorded
by Berkart, had described the expectoration of a peculiar kind of sputum ;
but we may take up the matter at the later date when Curschmann re-
observed and redescribed peculiar elongated plugs or spiral bodies in the
expectoration of the asthmatic, to which he was inclined to attribute
considerable importance. To the formation of these bodies — " Cursch-
mann's spirals," as they have been called — spasmodic asthma has been
attributed. Their nature is yet in doubt, some considering them to be
inspissated epithelium, some fibrinous concretions from the smaller
bronchia ; I should myself suppose, although this view is combated by
Curschmann, that in their nature they are allied to the plugs that form
in the so-called plastic bronchitis ; and that like these — although their
formation is an acute process — they leave behind them some habitual
morbid condition of the bronchial tubes, and possibly also some proclivity
to the formation of such bodies in the individual attacked. There is no
doubt, moreover, that although more common in asthma, these bodies are
found in pneumonia and oedema of the lungs also ; and in certain
secretions from the conjunctiva (Gerlach). Altogether it seems im-
possible to consider their presence as satisfactorily explaining the onset
of a condition so peculiar as that of spasmodic asthma.
As little can be said of the Charcot-Leyden crystals present in the
ASTHMA AND HAY FEVER 297
sputum and interior of the spiral plugs, and likewise of the eosinophile
cells (Adolph Schmidt) in the blood and sputum of the asthmatic. I should
agree with Miiller and with Schmidt that the discovery of either of these
bodies ia the sputum does not definitely indicate the nature of the
disease from which the patient is suffering : if this be so, the contention
that they have any causal importance has little to support it.
Such, then, is the history of an attack of asthma ; such, and it is
but little, is the morbid anatomy that is associated with it. But these,
and certain physiological experiments, are almost the only data upon
which to frame a pathology of the disease.
Pathogeny. — A disease that is, or may be, so sudden as to be well-
nigh instantaneous in its onset — one produced under the influence of
strong emotion, one which, under such and other circumstances, may
subside as quickly as it came — can hardly be other than some functional
aberration of normal structures. The changes that seem most competent
to explain the phenomena of asthma are: (i.) A muscular spasm of the
smaller bronchia ; (ii.) Some rapid tumefaction of the mucous membrane
of the bronchia ; (iii.) A rapid production of collapse of parts of the
lungs. All these, as has already been said, are hypothetical causes
only, although each one of them can be defended by more or less
cogent arguments. The one most generally accepted of recent years, it
need hardly be said, is that the production of asthma is due to spasm
of the muscular coat of the smaller bronchia. The late Dr. Hyde
Salter, who was the chief and most able expositor of this view, makes
use of the following arguments in its favour : —
" In the first place, the sudden induction and remission of the asthmatic
paroxysm is consistent with this supposition ; in the second place, there
is abundant proof that the air in the lungs is locked up, and can neither
be got in nor out ; there is evidently plenty of air in the chest, percussion
is even over-resonant, yet the patient is as unable to drive air out as to
draw it in ; he can neither inspire nor expire ; he cannot discharge breath
enough to whistle, to blow out a candle, or to blow his nose. The
muscles of respiration tug and labour to fill and empty the chest, but
the chest walls remain almost immovable ; the inspiratory muscles
cannot raise them, the expiratory cannot depress them. On listening to
the chest we find corroborative evidence of the stagnation of the air.
The respiratory murmur is in a great degree lost. This absence of
respiratory sound, accompanied by violent respiratory effort, is one of the
most striking and suggestive of the facts of asthma. How can we explain
it except by supposing that there is some bar to the ingress and egress
of air ; and what can this bar be, unless it be spasm of the bronchial
tubes ? It cannot be inflammatory thickening of the mucous membrane
lining them ; for the sudden, almost instantaneous establishment and
remission of the dyspnoea is incompatible with this. It cannot be mucus
plugging the tubes, for the attack will often come and go without any
expectoration whatever. But we have still more positive and precise
evidence of the circumscribed narrowing of the air -tubes in the
298 SYSTEM OF MEDICINE
musical sounds that are present in asthmatic breathing. This symptom
has all the certainty and precision that characterise physical phenomena ;
and it shows that the air-tubes are the seat of constrictions which throw
the air passing through them into vibrations, and convert them into
musical instruments : since these musical sounds are multitudinous, the
points of constriction must be many ; since they are constantly varying
in locality and character, the constrictions of the tubes must be under-
going similar change. Lastly, the effects of remedies and their nature
tell the same tale, and point to muscular spasm as the immediate essential
condition. The most powerful remedies for asthma are what are called
cerebro- spinal depressants, such as "emetics, tobacco, etc., remedies
the direct effect of which is to relax muscular spasm" (13).
This view, originally affirmed by Reisseissen, who based it upon his
discovery of the presence of circular muscular fibres in the bronchial
tubes, has since then been proved on experimental observation by
numerous observers from C. J. B. Williams onwards, including Paul
Bert, Eiegel, Biermer, Lazarus, and others.
This spasm is held sufficient to explain a state of things round which
a good deal of controversy has centred, namely, the over-distension of
the chest that occurs in the asthmatic, associated with a dyspnoea that is
mainly an expiratory one. The obstruction in the tubes being incomplete,
it is said that the air, under the labour of forced inspiration, enters the
lungs, but that expiratory paralysis or obstruction prevents its getting
out again. It is objected, however, by Wintrich and others, that as the
expiratory force is greater than the Inspiratory this solution is not
satisfactory. The lungs under such circumstances should tend to
collapse. Wintrich, accordingly, believes the attack to depend upon
spasm of the diaphragm. But this explanation does not seem free from
difficulty ; for, as Wilson Fox says, the phenomena of " this condition are
widely different from those observed in spasmodic asthma."
No doubt if one is to accept as absolute that doctrine which teaches
that atelectasis is a necessary consequence of the collection of mucus in
tubes that narrow progressively from the trachea to the periphery,
because plugging of such tubes creates an inspiratory difficulty more
than an expiratory, the air being able to get out of such tubes under the
pressure of the expiratory force, but hardly to get in under the ordinary
inspiratory act, — there is a difficulty. The distended chest of asthma
contravenes the usual rule.
But the asthmatic state is a complex one, and it is to be explained
by no simple and universal law. In the first place, granting the exist-
ence in bronchitic states of conical tubes and adapted conical plugs, —
which, after all, is an imaginary description, — a spasmodic contraction of
the bronchial muscles is not the same thing as a plug of mucus in the
tube. In the one case the obstruction might, and probably would, to
some extent be on the side of expiration ; it could have no such effect
in the other, unless indeed the spasm were regular and rhythmical from
the periphery upwards towards the main tubes. A spasm of the tubes
ASTHMA AND HA Y FE VER 299
must tend to prevent air getting both in and out ; and the more in or
out according as the inspiratory or expiratory force is the greater.
But the expiratory force is said to be the greater, and so it may be for
ordinary respiration, but no one who has seen the forced action of the
ordinary and extraordinary muscles of respiration in the exceeding
labour of inspiratory efifort during an attack of asthma, can have any
doubt that the natural order is completely destroyed, or have any
difficulty in believing that the air is really sucked past the obstruction,
so that the lung becomes over-distended. Nor is it unimportant in this
regard to insist again that the obstruction flits about from one part of
the lung to another ; from one side to the other ; a temporary relaxation
of spasm which means a liability to compensatory over-distension of the
unlocked part.
Some authors, unable to get over the difficulties which this assump-
tion of spasm of the bronchia creates, have suggested a spasm of the
respiratory muscles ; others, again, a paralysis of the muscles of the
bronchial tubes. As regards the latter, admitting that under ordinary
circumstances the muscular coat of the bronchial tubes may be reckoned
as one of the forces of expiration, it is hard to think that its share can
be so great that its failure should constitute a departure from normal so
grave as asthma. More might possibly be said in favour of a spasm of
the muscles of respiration, for, if we run over the field of clinical
medicine, we are not unfamiliar with several curious vagaries of breath-
ing which are attributable to such a cause : Cheyne-Stokes respiration
is one of these ; the air-hunger of heart disease another ; the asthma of
uraemia another. All these, in common with spasmodic asthma, are
immediately conditioned by some convulsive or misapplied action of the
respiratory centre, and perhaps give some colour to the suggestion that
one of the factors in the production of spasmodic asthma may lie in
aberrant action of the muscles of the thoracic walls.
It must be admitted, however, in the present state of our knowledge,
or of our ignorance, that, although other explanations may seem to
some to be as good, the theory of muscular spasm is at any rate fairly
complete. It is a reasonable and satisfactory explanation of the facts,
and it does not appear that there is much that is convincing to be said
against it. Nevertheless, the hypothesis placed second in order is, I think,
almost equally good, that which assumes some rapid turgidity or erectility
of the bronchial mucous membrane. The capacity of such active con-
gestion, even in parts that are not naturally erectile, is well seen in
certain morbid phenomena — in some cases of Graves' disease, for example,
where from some sudden shock the eyes have as suddenly become pro-
minent ; that this is a purely vascular turgescence is shown by its com-
plete subsidence after death, and by the fact that the orbital or ocular
structures show no morbid change : now if we look to the respiratory
tract itself we all know only too well how near a common cold may
come to an attack of asthma. There is the initial irritation of the
nostrils, then the sneezing, then sore or dry throat, then some little
30O SYSTEM OF MEDICINE
tracheal worry, and finally a definite, albeit slight, bronchial stuflBness
and wheezing. Now in these cases the initial change is certainly
turgescence of the upper air-passages ; and so also is it in the cases of
paroxysmal sneezing, and in certain cases of local disease of the nasal
mucous membrane, of defiected septum, or of polypus.
It seems, therefore, a rational belief that what can be proved to exist
in the upper air-passages, namely, a definite erection or turgidity of the
nasal mucous membrane, may also take place lower down in the bronchial
mucous surface; and, so doing, accomplish much of what we call spasmodic
asthma. It may be thought, however, that swelling such as this is hardly
adequate to explain the sudden origin and subsidence of the paroxysm ;
yet it is quite competent to do so, for paroxysmal sneezing comes on
quite suddenly, and subsides again as readily if, from any cause whatever,
the attention be averted from the subjective discomfort. This hypothesis
also is not without a considerable body of influential support, dating too
from early times. Wilson Fox states that Bree, as early as 1807, held
some such opinion, considering that asthma was a convulsive attempt
to expel peccant material from the bronchial tubes. Traube considers
asthma as a very acute catarrh. Blackley contends that the asthma of
hay fever is the turgescence in the nose extending to the general bronchial
.mucous membrane. And Sir Andrew Clark considered the phenomena
of an attack to be explained by a vaso-motor neurosis, by which changes
analogous to those of urticaria upon the skin are produced.
To this it may be added, that Storck actually observed with the
laryngeal mirror that in certain instances of asthma the whole length of
the trachea and part of the right bronchus were deeply congested.
Berkart, however, will have nothing to do with a neurosis of any
kind. Although he admits the existence of a peculiar predisposition,
he will not allow that the history of the asthmatic attack, as
regards its sudden onset and sudden subsidence, is anything but vague
and untrustworthy report. He sums up his opinion thus : " The con-
clusion, therefore, seems irresistible, that what is commonly described as
bronchial asthma is an acute and progressive, nay almost erysipelatous,
form of inflammation, which extends from the pharynx upwards and
downwards, and is accompanied by a croupous exudation." But it is
impossible thus to discard so large a body of evidence, vague though
some of it admittedly be, as case after case of asthma supplies. And, if
not, then the surmise of an initial inflammatory process is much less
securely seated. Indeed, " an acute and progressive, almost erysipelatous
form of inflammation " may well be thought to land its advocate in even
greater difficulties, seeing that the disease is seldom associated with fever,
seldom with any pneumonia, and, as an attack, is never a cause of death.
I believe, on the contrary, that the explosive character of asthma is
absolutely certain. Let two cases suffice : — A gentleman was seized with
influenza, and it was ushered in by an attack of asthma. This condition
was supposed to have gone on to broncho-pneumonia, and this proved
intractable. At great inconvenience to himself, therefore, he obeyed the
ASTHMA AND HAY FEVER 301
order to take a long holiday ; and it was my good fortune to see him as
he passed through London, within two or three hours of his leaving home.
I was to find a particular focus of disease at an indicated spot. The
man told me, as so many asthmatics do tell us, that he felt his breath
relieved after he had been twenty minutes in the train ; and when I saw
him an hour or two later, no one could say that he was other than
absolutely healthy. The second case I owe to the editor of this work.
Dr. Allbutt was examining by auscultation the backs of the lungs of a
gentleman of neurotic habit, who was overworked and suffering from
pains which were suspected to be of the nature of angina pectoris. The
patient was sitting up in bed, and his face was under the observation of
his own medical attendant. After hearing a few inspirations of a
normal character, to Dr. Allbutt's surprise the inspiratory murmur
began to diminish on the left side, and in a few moments ceased. Per-
plexed by this strange event, percussion was quickly applied to the left
side of the chest, but with negative results. During this time the
family attendant, Mr. Bowman of Eipon, saw the patient striving for
breath ; and attention being drawn to his state, it became manifest that
he was in his first attack of asthma : respiration quickly became almost
inaudible over both lungs, and then, after a definite interval, sibilus
supervened. The attack followed the usual course, and the asthma
thereafter frequently recurred.
As regards the sudden occurrence of atelectasis pulmonum, alleged
as a cause of the disease, there is perhaps less to be said. Nevertheless,
it may be well to point out that, in infancy at any rate, there are cases,
and these by no means infrequent, where atelectasis occurs very
suddenly ; and there are cases where the auscultatory evidence makes
it probable that this condition flits about the lung in a manner almost
comparable to that of the migratory passage of the asthmatic paroxysm.
And for my own part, I believe it to be probable that acute collapse
of the lung occupies a much more important place in the production
of pulmonary affections than is supposed.
Diagrnosis. — It is not necessary to linger long upon this section of
the subject. It is true that many affections are called asthma that
are not so regarded in this article. The short breath and the dyspnoea
of chronic bronchitis, and the dyspnoea and orthopnoea of heart disease,
are often thus designated; in both of these the dyspnoea is rather a
subdued distress than the acute agony of spasmodic asthma ; so with
the air-hunger of some cases of renal disease, and of dilatation of the
heart. The inspiration is free in such cases, but panting ; it is not
a dyspnoea. And yet it must be added that sometimes, in the early
history of a granular kidney, the complaint of the patient may be chiefly
of asthma of a mild kind ; and without a general investigation of the
case, without the hard pulse, the thick first sound, and perhaps the
retinal changes, the real nature of the case might be overlooked. Of
other conditions more likely, perhaps, to give rise to mistake I incline
to place hysteria. I have certainly found myself occasionally in a
302 SYSTEM OF MEDICINE
difficulty between the one and the other, more particularly when it has
been necessary to depend upon the history of the attack as submitted
for an opinion, some time, it may be, after all the symptoms have passed
away.
I am reminded also by the editor, first of a restless disturbed
sleep, experienced by some persons, that is really a mild asthma,
although not recognised as such by them ; secondly, of that curious
faucial or laryngeal suffocative spasm, often in gouty people, that
awakens the subject of it in the middle of the night in terror lest
he should choke.
Mediastinal tumours and aneurysm of the aorta, by leading to
paroxysmal dyspnoea of a sort, are sometimes liable to be overlooked
in a hasty diagnosis of the more familiar disease. And there are
various obstructive maladies in the upper air -passages that may, in
like manner, cause difficulty at times. The safeguard against mistake
lies in the unfortunate fact that asthma is very common, and there-
fore in its usual features is very generally known ; and in respect
of other maladies, even should they be entirely paroxysmal which is
uncommon, each one has usually some peculiar feature of its own that
is sufficient to arrest the attention. Any one of these things may, of
course, exist in association with the special nervous proclivities of
asthma, and it might then become a matter of the greatest difficulty to
distinguish between the morbid occasions of the spasm. Nevertheless,
it may be doubted whether in practice this difficulty often arises.
Treatment. — We will first consider the principles and afterwards
the details, lest in the multiplicity of the latter, and in the urgency
and intractability of the disease, we lose our hold on the principles to
which details ought to be subordinate. As I have already said, to me
it seems impossible to doubt that asthma is one of those nervous actions
of which we see so many examples in our economy, and which have
been well called by Dr. Edward Liveing paroxysmal neuroses.
Epilepsy is one of these ; some forms of insanity are others ;
migraine is another ; asthma is another, and so on. Now all these
more or less obey this law, that the more they come the more they may.
Nervous actions, which in their essence and initiation are not abnormal,
by excess of energy, or of frequency, or of both, become abnormal ; and
ultimately a bad habit becomes fixed. Surely, both in epilepsy and
asthma there is much of habit in the intractability of the disease ; and
if control is to be gained over either, it must be by catching it in the
earlier days of its appearance, and by arresting it before it becomes
confirmed. We think that we can sometimes gain some control over the
convulsions of infancy ; we can perhaps keep them at bay sometimes,
and so stop the child from becoming epileptic. But what case is more
hopeless than that of the confirmed epileptic, even though he be
persistently stupefied with bromides ?
The case of asthma is a parallel one. - It has been contended that it
is a disease rather of childhood than of adult age ; and that to pay
ASTHMA AND HAY FEVER 3°3
attention to this fact, and to the suggestions that flow therefrom, offers
the best possible chance of stopping the attack, and of preventing the
fixation of the habit and the establishment of chronic asthma. The
chronic asthmatic is almost as hard to cope with as the chronic epileptic.
There are two methods of dealing with the asthmatic. On the one
hand, we may attempt to make the environment of the patient conform
to the conditions required by the individual ; or, on the other hand, to
harden the individual, to widen his range of accommodation, and so to
make him less susceptible. And in the matter of drugs somewhat
similar alternatives present themselves ; we may either give sedatives to
the over-sensitive nerve structures concerned, or give drugs, if such
there be, to raise the level of nervous action to that higher platform
that shall enable the perceptive centres to take less heed of their
unnatural worries.
But the asthmatic paroxysm is so distressing that, almost always,
the treatment of it usurps the first place ; and too often this urgency of
the situation upsets the perspective. If we are called to a patient in
the stress of a paroxysm of asthma, clearly, on all accounts, it must be
arrested as quickly as may be ; there is no time to be very careful and
consistent about ways and means. And the quickest way to relieve a
paroxysm of asthma is to make the patient inhale some fume or other,
as of nitre, nitrite of amyl, or chloroform ; or to give him an injection
of morphia or a dose of chloral ; indeed, as we all know very well, doctors
see paroxysms of this kind less often, because various patent powders
for creating fumes hold the field so largely that most people do without
us, and stick to their patent remedy.
Thus the treatment of asthma too often becomes a repeated sacrifice
to the paroxysm ; and the patient drags along, thankful for the small
mercy of temporary freedom from his troubles, and easy in mind if he
can carry in his pocket protection from those that are to come. But
this plan of campaign is ultimately a most disastrous one. It un-
questionably produces temporary ease ; but what happens afterwards is
this : the vapour, on reaching the mucous membrane, stupefies or
exhausts the nervous centres, and stops the spasm for a time. But at the
same time some of these remedies, by stimulating the mucous membrane
and provoking the flow of mucus, make the local erethism rather worse
than it was before. The more sedative kinds of inhalations do but
appease by offering bribes to vicious nervous influences. By and by
the nervous centres wake up again to find matters no better, rather the
contrary ; and then on comes the spasm again, and the whole process is
repeated ; and, with each repetition of the cycle, the nervous centres, as
their nature is, become more exhausted or more irritable, their sleep is
shorter, their spasm is more and more quickly repeated, and the poor
patient ultimately lands himself, with perhaps some lessening of the
severity of each paroxysm, in a more prolonged or persistent stuffiness
hardly less distressing to bear : all day long he appeals to his powder, and
becomes in fact the slave of an appetite that he has whetted and that he
304 SYSTEM OF MEDICINE
cannot now control. Thus ends the chronic asthmatic who betakes him-
self to vapours. But this is not all, for by common consent a repeated
application to some of these drugs, whether by making matters worse in
the lungs, or by worrying the cardiac ganglia or what not, tends to
dilatation of the heart, and is equivalent to a good many nails in the
coffin of the asthmatic. Moreover, this dread of the paroxysm itself
is carried into the preventive treatment of the disease, and the patient
is submitted to what may be called the glass-case treatment ; that is to
say, the temperament of the patient is ignored, or not considered as of
importance, and the disease is supposed to be brought on by chill. If
he be wealthy and adventurous, he fights his environment by running
away ; and thus he may, perhaps, get along pretty well. If the patient be
a child, it is probably kept indoors, except in the finest of summer weather ;
yet, nevertheless, the history too often is that "it has caught another
chill," but no one can say how. At first, perhaps,, the child had the
whole house to roam about in, but, as the " colds" recur, it is confined to
one room with a south aspect ; and yet things do not mend. So the doors
of the room are carefully screened, the windows perhaps pasted up, and
still the success being not all that can be desired, extra clothing may be
piled on. And ultimately the doctor finds somewhere hidden under
this heap of precautions a pale, moist, flabby, steamy thing, with big
eyes, thin cheeks, protruding ribs, and a more or less general bronchitis ;
a case of " successful " management, because no attack has occurred for
SDme weeks ! But is this to be called success ! This is to nurse the
powers into imbecility ; and the inevitable result is, that the first time
the patient puts his head outside the door a fresh cold is " caught," and
a fresh term of imprisonment is ordeied. I venture to say that if
asthma is to be prevented at all, it will never be kept at bay by hot-
house treatment such as this. Yet, unfortunately, it is easy to utter
destructive criticisms of this sort, but difficult to point to a better way.
I think there can be no doubt that the first requirement for the
asthmatic is to put him into a climate in which he can be much out in
the air. But there is the difficulty : we know so little about climate ;
and asthma is so individual a disease. No one can foresee in a
particular case whether this place or that will be suitable ; and, when
the issue is doubtful, experiments in moving invalids about are never
likely to be made with any great thoroughness. But for most
asthmatic persons there is generally for each his own place or places
where he is better or well. Thither he should be sent, at any
rate, for a time. This place may be at the sea ; or it may be inland ;
sometimes it is a dry place, sometimes a humid ; often even it is a large
town : " In the great majority of cases an urban air is the air that
cures ; and of a city air, that seems to be the best which is the most
urban — the densest and smokiest" (Salter) ; but wherever it be, the
patient should be out and about with very little restriction ; and an
attempt should be made by this means to render the morbid circuit less
prone to discharge. Of games and sports, all should be encouraged that
ASTHMA AND HAY FEVER 30S
are outdoor and healthful and invigorating. Some further remarks on
climate in the treatment of asthma will be found in the first volume of
this work (p. 293).
In diet it is necessary to be careful, but not too much so. It is very
easy to give a number of restrictions about food, and thus to make matters
worse ; yet asthma certainly often does seem to start from a meal that
has not been digested — one which may have been too large, of an
improper character, or taken at some irregular hour : the points to aim
at are good, plain, light food in moderate quantity and slowly ingested.
The asthmatic, particularly children, are often deprived of potatoes, of
starchy puddings, jam and sugar, and goodness knows what else, and on
the other hand are put on various meat juices and other good things
in the wrong place, so as to remove all rocks of offence from the path of
their pneumogastrics. But " if these things be done in the green tree,
what shall be done in the dry ? " What chance has such a child of
reaching old age ? Any food that is plain and wholesome and not
known to disagree may be allowed. It is a good thing to have the
chief meals early in the day, when digestion is vigorous ; therefore
breakfast and lunch — an early dinner — should be the main meals ;
anything taken later must be small in (quantity and of the most digest-
ible kind. All meals for the asthmatic should be small ones ; his
stomach should never be distended \md,e art. on Dietetics, vol. i. p. 398].
The bowels should be kept carefully regulated and sufficiently open by
taking some saline aperient, or other simple laxative. Every effort
should be made to keep the patient in as healthy and physically fit a con-
dition as possible. A tepid or cold bath should be taken in the early
morning, and the living room well ventilated.
These must be the general principles upon which to deal with the
asthmatic ; and the more unhesitatingly the younger the patient, and
the earlier in the course of the disease that he comes under treatment.
In considering the treatment by drugs, two divisions of the subject
naturally suggest themselves ; namely, those medicines that are useful
in preventing asthma, and those that are so when the actual attack is
threatening or in progress. Again, a distinction must be made
between the cases which seem to be pure nervous asthma, those which
have any degree of persistent bronchial catarrh, and those already
mentioned, which come on in later life, and may not irrationally
be attributed, on the one hand, to blood conditions that as a group may
for convenience be called gouty, and, on the other, to degenerative
changes in the tissues.
As a preventive remedy in the pure form of asthma, no drug is
in my opinion equal or nearly equal to arsenic. It should be taken for
three or four weeks, then omitted, and then resumed after an interval
of equal length ; and so on for three or four courses : and the drug
should from time to time be resorted to in periods when from any cause
the nervous centres begin to show signs of lowered tone. I have not
made much use of phosphorus, but it has been spoken well of, and it
VOL. V • X
3o6 SYSTEM OF MEDICINE
miglit also upon occasion be of value ; and so likewise with other good
nerve tonics, such as bromides or hydrobromic acid.
In cases where a persistent bronchial catarrh is at the bottom of the
trouble, there is obviously less to be expected from medicine, and a
suitable climate promises best; as a rule such cases do best in dry
and bracing air. A friend of mine thus circumstanced found himself
almost renewing his youth as he climbed the Malvern Hills. Others
again iind more relief in such places as Hastings, Ventnor, Bournemouth ;
some even in Torquay. Good results are claimed in the bronchial cases
for the sprays and waters of the sulphurous springs of Mont Dore, of
the Pyrenees, of Harrogate, and of the arsenical waters of La Bour-
boule. The two chief drugs from which much benefit is often derived
are strychnine in three to five-drop doses given steadily for some days,
and the iodides which often prove of great value. Perhaps the one
acts as a stimulant to the respiratory centre, the other as an expector-
ant. For the asthma that occurs in later life an eliminant treatment
is on the whole the best. It is in such cases that blue pill and colo-
cynth in moderate doses once or twice a week are useful, or saline
laxatives with careful attention to and restriction of diet. In these
cases, again, iodide of potassium,, perhaps by a depressing effect upon the
arterial pressure, will often help very considerably.
My friend Dr. Kingscote maintains that the asthmatic state is much
benefited by brine baths and systematic exercises, such as have been
elaborated at Nauheim, for the treatment of certain forms of disease of
the heart ; one can well understand that means of this kind, by stimulat-
ing the circulation and facilitating the flow of blood through the lungs,
may prove of much service.
To relieve an attack, or the semi-asthma that forebodes or lingers
after an attack, other means must be used. In the threatening of an
attack, or in the dyspncBa that lingers when the more acute symptoms
have subsided, many drugs have been tried, and at one time or another
succeeded. Of these I should put first a combination of iodide of
potassium with the etherial tincture of lobelia ; five, ten, or even fifteen
grains of the one, and ten or fifteen minims of the other, seem to bring
relief when other things may have failed. Some prefer stramonium
to the lobelia. The late Dr. Hyde Salter thought very highly of the
Datura stramonium and the D. tatula ; their best eff'ects are observed
when smoked like tobacco ; but they may also be given in a pill, extract,
or tincture. Sometimes a combination of iodide of potassium and
chloral hydrate has been efiectual. It is under such conditions as these
that the Euphorbia pilulifera and Grindelia robusta are most useful ;
the former may be given in a decoction, a wineglassful twice a day ; or
in tincture, ten to thirty minims, twice or three times a day, or as often
as may be requisite. The grindelia is in the form of a liquid extract,
and is given in similar doses to the tincture. This drug is also
recommended at the onset of an attack, in half-hourly doses, until
relief has been attained. I have known it to produce decided relief,
ASTHMA AND HAY FEVER 307
but I have not, upon the whole, been very successful either with this
drug or with euphorbia. In the thick of an attack the remedies most
in use are inhalations of various vapours ; and of these, perhaps the
commonest, and one of the most harmless, is blotting-paper soaked in
nitrate of potash, which will often relieve and sometimes very con-
spicuously.
There are many other powders made for the production of fumes ;
some are stimulating, and seem to zfiSi by provoking cough and the free
secretion of mucus ; others, and these I believe the less harmful, are of
a sedative nature. Some of them are made into cigarettes for smoking,
and most of them contain stramonium in some form.
Of inhalations available for more strictly medical uses, three may
be mentioned : nitrite of amyl, iodic ether spoken well of by Dr.
Thorowgood, and of course chloroform. In severe cases the last named
may be of the greatest possible value, although its effect is apt to be
but transitory, and the attack may resume its severity as the stupor of
the drug wears ofiF. Of all the other drugs that have been recom-
mended for the relief of the paroxysm, morphine probably stands first ;
a hypodermic injection of a sixth of a grain will often procure almost
immediate diminution of the violence of the dyspnoea, which gradually ends
in complete cessation of the spasm. Pilocarpine is also a valuable drug ; a
tenth to a quarter of a grain may be given hypodermically ; a free secretion
from the mouth and fauces is the result, and the spasm is thus relieved.
Sometimes the patient is sick, a thing by no means undesirable ; for an
emetic is one of the means advocated for arresting an attack, and no
doubt sometimes with marked success. A combination of bromide of
potassium and chloral is also a good sedative to give at the onset of a
paroxysm. Belladonna, hyoscyamus, and conium, though not of so
much value, are all of use in their way ; tobacco is also said, by virtue of
its powerful depressing action, to be a useful palliative drug. I have
heard it said of pilocarpine that the remedy is worse than the disease ;
and, considering the distressing nature of the malady, this is a serious
attack upon the benefit derived from it. If this be true as regards
pilocarpine, it must be still more apt for tobacco, which produces a
dreadful malaise, and is a difficult drug to control in those who are
unaccustomed to its use, in whom only it appears to have the effect
wished for.
Of stimulants, too, cofiee and alcohol may be mentioned. Strong
coffee is indeed a popular remedy that has often given relief, as also has
citrate of caffeine. As regards alcohol, I have no personal knowledge
of any special virtue, but Hyde Salter says of it, that while in many
cases it does not do much good, in some it has a most powerful efi'ect,
particularly when all other remedies have failed. It should be given
hot and strong. The compressed air treatment of asthma is described
in the first volume of this work (pp. 315, 316), to which the reader is
referred.
Hay fever, or hay asthma, is in the opinion of many a pure form of
308 SYSTEM OF MEDICINE
asthma, and with this opinion I myself coincide ; it is accordingly more or
less amenable, as are other forms of asthma, to treatment by drugs of the
same character. I refer more particularly to arsenic ; and I should main-
tain this even for nasal cases : it relieves the itching and smarting of the
eyes, the aching of the frontal sinuses, the itching of the nasal mucous mem-
brane and of the nose itself, the sneezing, the watery discharge, the occlu-
sion of the nostrils, the dryness and irritation of the lips and throat. But
Karl Binz and others have maintained that local remedies, used upon
germicide principles, give great relief in many of these cases ; and those
who have worked in the special department of diseases of the nose and
throat declare that, by paying special attention to the morbid erectility
of the mucous membrane over the spongy bones of the nose, this disease
may be much reduced. Binz advocated the irrigation of the nostrils
with a solution of quinine ; Sir Andrew Clark suggested some carbolic
pi'eparation ; and of late many have tried the application of solutions
of cocaine, more upon alleviative than upon curative principles, perhaps ;
unless alleviation be an earnest of cure.
No one can doubt that these various measures are all useful in their
proper place, nor can any one doubt that they have their dangers. For
instance, I saw but the other day a lady who for the discomfort arising
from the frequently recurring turgidity of the nostrils, which is
characteristic of hay fever, had betaken herself by medical advice or
without it to the use of cocaine locally. Accordingly, more or less, both
by day and night, she would pack her nostrils with a solution of cocaine,
of which one grain at each time was put into each nostril ; and there-
after, by means of hawking and spitting, and other contortions of her
pharyngeal muscles, the solution was spread all over the affected area,
and temporary ease was obtained. At least six grains a day were thus
disposed of, and sometimes more. The position to take with regard to
local treatment is this, as it seems to me : the local symptoms are not
the disease, and therefore, however necessary it may be at times to
relieve conditions that cause great distress by means of this kind, they
may do harm by inducing other morbid changes in the part, and con-
ditions that were but temporary may thus be rendered permanent. For
instance, a paroxysmal sneezing will stop immediately under the influence
of some diverting train of thought, just as asthma will stop under any
sudden and powerful mental stimulus. All must agree that if there be
any actual disease of the mucous membrane, whether due to the exist-
ence of polypus, of a deflected septum, or what not, it must be advisable to
get the mucous surface into as healthy a state as possible so as to remove
one obvious source of possible irritation. But for cases of asthma in
which there is no definite nasal worry, the question must at any rate be
considered an open one. If the neurotic origin of the disease be accepted,
as I think it must, no one can rest content with the treatment of a peri-
pheral symptom. Still, if it can be shown that a large measure of relief
is thus obtained, such an experience must of course be utilised upon the
principle that half a loaf is better than no bread. The difficulty of
ASTHMA AND HA Y FE VER 309
arriving at any sound conclusion as to the value of such treatment lies
in this, that the specialist and the physician see the cases at different
times : the one in the first flush of that post-operative quiescence that
we all so well recognise as a characteristic of nervous ailments ; the
other, when that quiescence has passed oS", and the old habit has resumed
its sway. I have known some patients to be apparently benefited, but
others who have n'ot received any adequate reward.
Prognosis. — I hold most strongly that asthma may be treated with
a large measure of success if it be taken in hand at the proper time, that
is in childhood ; and if it be possible to put the patient under suitable
conditions, — those conditions being, in brief, such as will allow of the
patient being turned into a good healthy animal. It is in -childhood, if
at any time, that the opportunity offers of educating the patient out of
a faulty habit into a better regulated state of his nervous centres. In
the case of the adult one cannot be so hopeful. One could not be so
hopeful of successfully combating convulsive attacks occurring late in life
as in those occurring in infancy ; and I fancy that the asthma that
begins in adult age is indicative of some deep ingrained nervous fault,
which is not readily to be controlled. Moreover, adults fall in less
readily with counsels of perfection, such as the radical cure of faulty
habits ; they are in distress, they insist upon a dose to set them right,
and if one man won't give it them, or does not hit upon the right thing,
they quickly resort to some one else, who manages things, as they think,
better. Still, even the adult asthmatic is sometimes a sensible person,
and many agree to desist from inhalations ; to take a drug, such as
arsenic, patiently ; or iodide, when an attack threatens ; or such other
drug as may seem best suited to the particular case : to act thus is in
most cases to procure considerable relief.
With regard, however, to that other group, when spasmodic asthma
occurs in middle age, and after ; when, as causes or provocatives, certain
changes in the tissues and organs, gouty and other, come into pro-
minence ; and when age with its paling vigour of function and its conscious
or unconscious indiscretions of living and other habits leads to the over-
charging of the blood with waste products, and to excess of arterial
blood-pressure, and thus to a true spasmodic asthma analogous to the
gouty vertigo and gouty convulsion occasionally seen in adult life : then
no doubt great relief, and even cure, may result from such drugs as blue
pill, iodide of potassium, and others, given with the purpose of reducing
the arterial pressure, or of eliminating waste products. More difficult
to speak hopefully of are the cases associated with and perhaps pro-
duced by a pre-existing bronchial catarrh. As Hyde Salter remarks,
we send such patients to the Riviera to relieve the bronchitis, and the
asthma is aggravated ; and thereby we see in a measure how essentially
independent the two conditions are ; and when, after travelling about,
they come to the land of promise so far as their asthma is concerned,
then perchance the climatic conditions are not suited to the bronchitic
affections. But even in such persons there is no doubt that, by dealing
3IO SYSTEM OF MEDICINE
with the bronchitis and by endeavouring to ameliorate it by means
of a suitable climate, the bronchial tubes will become more healthy, and
there may yet be scope for carrying out those principles of reinvigora-
tion of the nervous tone upon which I have dwelt ; and thus some of
the stress of the asthma may be relieved. Nevertheless, when the
best has been done, one cannot but regard the disease as serious,
and in too many cases baffling ; for even in cases where much good
seems to have been done, the disease reappears again, perhaps after
many years. In looking over notes of a number of cases, it comes
out clearly that in several where the disease existed from, say, the
age of three to ten years, it reappeared at forty or fifty. I have
already alluded to- the many points of similarity between asthma and
epilepsy ; and this is another feature of resemblance. We meet, too,
with many people who have lost the tendency, and who are still free ;
but many of these, although they say they have lost the asthma, are
still a little wheezy, and undoubtedly have some slight amount of
bronchial catarrh. So that on the whole there is a degree of un-
certainty about the fate of those who are asthmatic in early life. As
regards the actual duration of life, perhaps all that can be said is that
spasmodic asthma is compatible even with a long life. Of those who
become asthmatic in later years, excepting the group of cases due to high
arterial pressure already mentioned which may be a fairly large one,
most are likely to suffer severely ; and their disease is but too likely
to become more or less permanent.
James F. Goodhart.
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Blacklbt. Experimental Researches on the Causes of Catarrhus JEstwms (Hay
Fever). — i. Clark, Sir Andrew. American Journal of Medical Sciences, 1886,
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zum Asthma nervosum," Dent. Archiv f. klin. Med. Leipsic, 1883, p. 1. — 5a.
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J. F. G.
SYPHILITIC DISEASE OF THE LUNGS 311
SYPHILITIC DISEASE OF THE LUNGS
Our knowledge of the anatomical characters and clinical history of
syphilitic disease of the lungs is still very incomplete, notwithstanding
that much has been written on the subject. This is due in part to the
rarity of the affection, but chiefly to the difficulty until lately experienced
in distinguishing between the lesions of syphilis and of tuberculosis.
Up to the date of the discovery of the tubercle bacillus it was very
often impossible to determine with certainty during life whether a given
case of pulmonary disease were tuberculous or not; and after death appear-
ances which some considered to be distinctive of tubercle were said by others
not to possess this significance. Now, however, that we possess a test for
tuberculous lesions, it may reasonably be hoped that the whole subject of
syphilitic disease of the lungs will be placed upon a secure foundation.
That the disease is of rare occurrence is a fair inference from the fact
that the museums of the London hospitals and of the Eoyal CoUege of
Surgeons, all of which I have recently visited, contain only twelve speci-
mens which are believed to illustrate syphilitic lesions of the lungs ; and
of these, two may be excluded, as either not of that nature, or of a nature
so doubtful that in the present state of our knowledge they are inad-
missible as evidence. None of these specimens is from a case of congenital
syphUis.
Morbid anatomy. — The following pulmonary lesions have been
attributed to syphilis : (a) gumma ; (ft) white hepatisation (Virchow,
Weber), or "epithelioma of the lung" (Lorain, Eobin) ; (c) gray infiltra-
tion (Welch, Pancritius) ; (3) lobular pneumonia or broncho-pneumonia
(Fdrster, Welch) ; (e) fibroid induration ; (/) changes in the lymphatics
(Hermann Weber) ; (g) a destructive disease, the so-called " Syphilitic
Phthisis." It will be convenient to consider separately the lesions of the
hereditary and the acquired disease.
Hereditary syphilis. — The pulmonary changes in hereditary syphilis
may be either circumscribed or diffuse ; to the former the term "gumma"
is applied; the latter are classified under the head of "pneumonia." It
is, however, far more common to find the two changes associated than to
meet with either separately.
A. Gumma. — As this lesion is of comparatively rare occurrence in
congenital syphilis, and when present does not differ either in appearance
or in microscopical structure from that found in the acquired disease, a
more distinct picture of the morbid anatomy of the two afi'ections will be
obtained by describing it under the latter heading.
B. Pneumonia. — Two different lesions are included under this head-
ing— namely, "white pneumonia" and "interstitial pneumonia"; but of
these it must again be stated that they occur more often in combination
than apart.
312 SYSTEM OF MEDICINE
(a) White pneumonia (Virchow, Weber), Epiihelioma of the lung (Lorain,
Eobin). — This lesion, whicli in its true form is rare, is found only in the
lungs of still-born children, or of such as have survived their birth a very-
short time. Other unmistakable signs of congenital syphilis are usually
present, and in such cases gestation has seldom proceeded to the full term.
It is a diffuse change affecting a lobe either as a whole or in part ;
or one or both lungs may be completely consolidated.
In still-born children the affected part is bloodless and airless;
even if force be used, it may be impossible to inflate it ; but in infants
several days old the lung always contains some air.
The lung is much increased in size, and its surface may be marked by
the ribs. It is solid, dry, white, yellowish, or grayish white in colour ;
but sometimes presents a reddish marbled appearance. The section
differs from that of an ordinary pneumonic lung in that the granular
appearance characteristic of the latter is absent, the surface being smooth
and somewhat shining.
On microscopical examination in true cases the interstitial tissue is
not increased. The alveolar walls are thickened, and the small bronchi
and the alveoli are filled with masses of cells of which some are round
and others have more or less the character of epithelial cells : the cells
are for the most part undergoing fatty degeneration and are beginning
to break down. The alveoli are markedly enlarged. The colour of the
affected area is due partly to the above changes, but in part also to
diminished blood-supply the result of pressure upon the capillaries. The
lung tissue surrounding the consolidated part may show some degree of
emphysema. Ecchymoses may be present in the pleura, pericardium,
and thymus gland ; but these appearances are probably incidental to the
mode of death.
The bronchial glands are as a rule enlarged and on section dense,
from a new formation of fibrous tissue enclosing cells arranged in a con-
centric manner.
White pneumonia is a lesion of purely pathological interest, as, owing
to the filling of the alveoli with cells, the subjects of it, if not still-born,
are unable to maintain the respiratory function for any length of time,
and soon succumb.
(J) Interstitial pnewmonia. — This is the most common pulmonary
manifestation of hereditary syphilis ; but it occurs more frequently in
association with some of the changes described under " white pneiunonia "
than as a purely interstitial lesion. In its true form it is distinguished
by a small-celled infiltration of the interalveolar connective tissue, the
alveolar epithelium remaining unaffected. This change may be present
to a very varied extent. In some cases lungs thus affected appear normal
to the naked eye, the lesion being only discoverable on microscopic
examination.
In well-marked cases tbe lungs are large and hard and of a pale or
dark grayish red tint. The change may be present throughout the
organs, or a single lobe or portion of a lobe may be alone affected. To
SYPHILITIC DISEASE OF THE LUNGS 313
the naked eye the hing tissue presents a decidedly coarse appearance.
On microscopical examination a marked increase is seen in the inter-
alveolar and interlobular connective tissue, which forms broad meshes in-
cluding small spaces wherein the alveoli are either crowded together or
completely obliterated.
In some cases the interalveolar meshes appear to consist of a dense
capillary network, the vessels being dilated and tortuous. Around the
vessels and bronchi there is a marked increase of the connective tissue,
and the tunica intima of the small arteries is thickened. The alveolar
epithelium may show desquamative changes, and brown and yellow pig-
ment granules may be present.
Interstitial pneumonia is often found in association with congenital
syphilitic lesions in the skin, with interstitial hepatitis, and with changes in
the epiphyses ; but it is also found in cases in which gummata are present
in the lungs, liver and other organs. The change begins during foetal
life, and at birth may have affected the lungs extensively. In such cases
life is of short duration and death occurs from asphyxia, as is shown after
death by the frequent presence of ecchymoses in the pleura, pericardium
and thymus gland. When the change is less advanced at birth, such
children may die at a later period by a slow process of carbonic acid
poisoning, the first sign of which may be that a child previously fretful
and noisy becomes quiet.
In cases in which the other organs are healthy, or nearly so, life may
be prolonged for months or years ; such subjects are, however, specially
liable to acute disease of the respiratory organs, such as pleurisy, acute
bronchitis, and broncho-pneumonia.
From the above description it will be seen that the morbid processes
concerned in the production of the gummatous and diffuse changes found
in the lungs of syphilitic children chiefly affect the connective tissue and
small arteries. They are — (i.) A round-celled infiltration and proliferation
of the interlobular and interalveolar connective tissue, originating in the
cellular tissue around the bronchi, and leading to marked thickening of
the framework of the lung, (ii.) An isolated perivascular cell prolifera-
tion, which begins around the small arteries, and is accompanied by
changes in the tunica intima (Hochsinger). Both the periarteritic and
peribronchial granulations may occur as separate nodules or node-like
foci ; or they may be diffused over large portions of the lungs. A well-
marked desquamation of the alveolar and bronchial epithelium is almost
always present, but it is quite a secondary process.
In the account here given of the pulmonary changes found in hereditary
syphilis the descriptions of Heller, Spaundis, and Hochsinger have been
followed, and to these authors I desire to acknowledge my indebtedness.
Association of congenital syphilis and pulmonary tuberculosis. —
Syphilis, by lowering the resisting power of the individual, may dispose
to tuberculosis ; and it has recently been shown by Hochsinger that the
vims of syphilis and tuberculosis may be jointly transmitted from
parent to offspring.
314 SYSTEM OF MEDICINE
This observation is of much importance, and throws a new light upon
the nature of the pulmonary lesions found in infants the subjects of con-
genital syphilis. Hitherto it has often been assumed, on evidence which
is now proved to be insufficient, that such lesions are of syphilitic origin ;
whereas it is clear that they may be due to an associated tuberciilous
infection.
In three infants suffering from congenital syphilis, and presenting
symptoms of infiltration of the lungs, the pulmonary disease was found
after death to be due to tuberculosis and not to syphilis. Tubercle
bacilli were found in the lungs in all the cases.
The first case was observed in 1891 in a child not quite three weeks
old; the second in 1891 in a child twenty -four days old; the third
in 1893 in a child eleven weeks old.
Case I. — Anna B., set. nearly three weeks. The parents had been
married nine years. The father acquired syphilis shortly before marriage.
The mother died from pulmonary tuberculosis three months after the
birth of the child. The first and second children of the marriage were
still-born ; the third and fourth died during the first week ; the fifth and
sixth were living, ages four years and two years respectively. The case
of the seventh child is here described. From the time of birth she was
sickly and suffered from nasal obstruction, snufHes, and dyspnoea. Edles
were present in the chest. At the end of the second week a bullous
eruption appeared on the nates. The child presented all the ordinary
external signs of congenital syphilis, and was shown at the Vienna
Dermatological Society as a case of gummatous disease of the viscera.
On examination of the chest there was marked dulness on the left
side from the angle of the scapula downwards, vsrith bronchial breathing
over the dull area. The respiratory murmur was harsh over both lungs,
with rhonchi and coarse rales. The spleen was enormously enlarged,
extending as low as the anterior superior spine of the ilium; the liver could
be felt four fingers' breadth below the costal margin, it was hard and the
edge was rounded. The diagnosis was pulmonary and visceral syphilis.
Mercurial treatment was prescribed. The child died on the thirty-first
day after birth. On post-mortem examination the internal organs were
found extensively infiltrated with tubercle. Both lungs showed tubercles
varying in size from a miliary granulation to a walnut. A nodule' as
large as a hen's egg occupied the right middle lobe. The left lobe of the
liver was almost completely replaced by a caseous nodule; numerous
tubercles studded the right lobe. The spleen was enlarged to nearly
four times its normal size and contained similar deposits. Tubercles were
also present in the kidney, pericardium and peritoneum. The mesenteric
and bronchial glands were enormously enlarged, and in many places
caseous. Tubercle bacilli were present in all the lesions. None of the
lesions in the internal organs was of syphilitic origin.
Case II. — Victoria S., twenty-four days old. The mother had pre-
viously brought three children suffering from congenital syphilis to the
same clinic. She had previously stated that she had not had syphilis.
SYPHILITIC DISEASE OF THE LUNGS 315
Nothing was known of the father, and it is not certain that either parent
was tuberculous. The child had snuffles and presented all the char-
acteristic appearances of congenital syphUis. There was a confluent
papular syphilitic eruption on the nates and elsewhere. The percussion
note over the left lung was dull and the breathing bronchial, with con-
sonating rales. The spleen was slightly, and the liver markedly, enlarged.
The temperature was normal. Mercurial treatment was ordered.
The patient was shown at the Vienna Dermatological Society as a case
of syphilitic pemphigus and syphilitic pneumonia. The child died on the
thirty-eighth day.
On post-mortem examination the left lower lobe was solid from
grayish white infiltration. There was acute catarrh of the bronchi
of the left upper lobe and throughout the right lung, also of the larynx
and trachea. The mediastinal and bronchial glands were enlarged, but
not obviously caseous. The liver was large, reddish brown, somewhat
indurated and with rounded margin. On microscopical examination
of the lungs confluent peribronchial and perivascular tuberculosis was
found, with tubercle bacilli. In the liver recent interstitial inflammation
was present, with fatty degeneration of the liver - cells. No trace of
tuberculous lesions were found in any other organ than the lungs.
Case III. — Augusta Gr., eleven weeks old. The mother, set. 28,
was sufiering from pulmonary tuberculosis. She had had five illegiti-
mate children and denied having had syphilis. Nothing was known
of the father. The child presented the characteristic appearances of con-
genital syphilis, and had snuffles and a syphilitic rash on the buttocks.
The rash appeared during the third week. The childhad suffered from cough
since it was five weeks old. There was doubtful dulness over the right
lower lobe with bronchial breathing and abundant moist r^les. The liver
was very large and hard, with a rounded edge. The spleen extended four
fingers' breadth below the costal margin. The temperature was normal.
Mercurial inunction was ordered. The child died aged sixteen weeks.
Post-7nortem. — The right lower lobe was solid from a homogeneous,
grayish white infiltration. Grayish red and yellow tubercles were dis-
seminated throughout the upper lobe. The lower half of the left lower
lobe was collapsed. The bronchial glands were enlarged and caseation
was beginning. The liver was fatty and slightly granular. In the
portal fissure there was a caseous lymphatic gland the size of a hazel-nut.
The mesenteric glands were caseous. The spleen contained a large case-
ous nodule. Microscopic examination showed the characteristic signs of
" chronic tuberculous broncho-pneumonia, tuberculosis of the spleen and
mesenteric glands,' and syphilitic interstitial inflammation of the Hver with
well-developed inflammation of the vessels."
It is clear from the perusal of these cases that it will be necessary in
future, even when the evidence of syphilis in the foetus is undoubted,
to examine carefully for tubercle bacilli before a pulmonary lesion is
attributed to syphilis.
Acquired syphilis. — ^To present a trustworthy account of the morbid
3i6 SYSTEM OF MEDICINE
anatomy of acquired syphilis of the lungs is a far more difficult task than
that just attempted. In considering a matter of such uncertainty I have
preferred to rely upon evidence which is at hand and may be put to
the test, rather than upon that to be found in the records of a period
when, owing to the absence of any certain test for tuberculosis, the diffi-
culty of distinguishing between the pulmonary lesions of tubercle and
syphilis was almost insuperable.
A study of the specimens of pulmonary syphilis contained in the
London museums shows that the possibility of the changes being due to
tubercle was in nearly all cases carefully considered. These specimens
and the records connected with them probably constitute the most trust-
(Torthy evidence on which to base a description of the morbid anatomy
jf the acquired disease, and, as will be seen hereafter, they have been
hilly utilised.
Pathology and Morbid anatomy. — Bronchial catarrh may occur as a
manifestation of the secondary stage of syphilis, and possibly also of the
period of incubation (Walshe). The fact that bronchitis, occurring without
obvious cause in syphilitic subjects, may be greatly alleviated or cured by
the administration of mercury, is strongly in favour of this view. In the
late secondary and tertiary stages gummatous infiltration of the submucous
tissue of the trachea and bronchi is not infrequent, and may be followed
by the formation of fibrous tissue which, subsequently undergoing cicatrisa-
tion, produces stenosis, one of the most characteristic syphilitic lesions in
the main bronchi.
No definite statement can be made as to the most common period of
the occurrence of gumma in the lungs ; cases of which the real nature
could not be doubted have been recorded as early as two years and as
late as twenty years after infection.
The pulmonary lesions of acquired syphilis belong chiefly to the late
tertiary stage of that disease.
A. Gumma. — Gummata may occur either singly or in numbers, and
may vary in size from that of a hemp-seed or a hazel-nut to that of a
hen's egg, but the latter size is of rare occurrence. A gumma may be
found in any part of the lung, but more commonly within its substance
than upon the surface ; and more often about the root, near the large
vessels and bronchi, than elsewhere. The lower lobes are perhaps more
often affected than the upper.
A gumma is rarely seen in the very early stage, of which alone the
name is in any sense descriptive ; but it is said then to present a gelatinous
or glutinous appearance (1), thus resembling a similar growth in the liver.
At a later stage it is of a gray colour, tinged with various shades of a red,
white, or yellow, and presents on section a smooth and semi-transparent
appearance. At a still later period a gumma forms a well-defined nodule
of a yellowish colour, firm and dry. Inflammatory changes in the sur-
rounding lung may lead to the production of a well-marked fibrous capsule,
but this may be absent. The gumma may break down, and, its con-
tents having been discharged, an irregular cavity may result ; but this is,
SYPHILITIC DISEASE OF THE LUNGS 317
both absolutely and also in comparison witt the occurrence of a similar
change in caseous tuberculous masses, very rare.
The chief difference between a gumma of the skin, for example, and one
of the lung is that whilst the former tends towards necrosis the latter tends
to be transformed into a mass of scar tissue, the contraction of which
causes puckering of the surrounding lung and overlying pleura. By the
deposition of lime salts a gumma may become calcareous.
In histological structure a gumma of the lung does not differ essentially
from a similar growth elsewhere. In the early stage it is seen to consist
of a granulation tissue composed of small cells about -j-gVc in- in diameter,
arranged concentrically around the sheath of the small vessels, and in
some cases around the small bronchi. At a later stage the nodule becomes
opaque in the centre, and its cellular structure can no longer be recognised;
but fatty and albuminous granules are seen instead in the meshes of a
dense fibrous stroma. Finally it becomes converted into a mass of dense
cicatricial tissue. A gumma may form a centre from which a small-celled
growth may infiltrate the surrounding tissue, spreading chiefly along the
bronchioles.
The walls of the neighbouring alveoli are also infiltrated with small
cells ; and the alveolar spaces contain inflammatory products, due either
to epithelial proliferation or to the presence of cells of a character similar
to those constituting the nodular masses already described. Giant cells are
occasionally present, but are not so characteristic a feature of gumma as
of tubercle.
According to Dr. Councilman, the essential process in the production of
a gumma in the lung is a pneumonia with fibrinous exudation, accompanied
by fibrous change in the alveolar walls, the whole subsequently undergoing
caseation. The first step in the process is stated to be a hyaline degenera-
tion of the capillaries of the affected area; this is followed by atrophy of the
alveolar walls. The alveoli become distended with large pale epithelial cells
and fibrin ; the cells also undergo the hyaline degeneration, forming smooth
bodies staining with eosin, and varying in size from one-half the diameter
of a red blood corpuscle up to that of a large epithelial cell. The capil-
laries become converted into rigid tubes and their lumen is much narrowed.
Similar changes occur in the small veins and arteries. Immediately around
the bronchi and arteries there is a formation of connective tissue, and
here the alveolar walls show much thickening and contain many small
round cells.
The whole of the structures thus altered tend to undergo necrosis,
and when that change is complete a caseous-looking mass results.
The following descriptions of specimens in the Museum of Guy's
Hospital well illustrate the appearances presented by gummata in the
lungs. It will be observed that all the specimens here described were
removed from the lungs of adults.
No. 254. — A portion of the upper lobe of a lung showing on the cut
surface two masses, one of which was described in the recent state as
" consisting of a circumscribed nodule of a firm, yellowish, dry substance.
3i8 SYSTEM OF MEDICINE
corresponding in all particulars to that in the liyer (a gumma), except in
being somewhat less firm : the other is softening, breaking up, and in
process of forming a cavity. Histologically the nodules are seen to con-
sist of fibroid tissue with many areas of caseation and a few giant cells.
From the report of this case by Dr. Wilks the following additional
particulars have been derived : — The patient was a sailor, aged 29. No
history was obtained ; he was moribund from laryngeal obstruction when
admitted, and there was profuse expectoration of mucus and blood. There
was a scar in the groin, and phimosis from a contracting sore on the penis.
The whole mucous membrane of the larynx and trachea was deeply ulcer-
ated, and the walls thickened by an infiltration of fibrous tissue into the
submucous structure, producing great induration. The thyroid cartilage
was bare at one spot, the lymphatic glands in the neck were enlarged.
The liver contained a dozen hard, round, fibrous tumours — the largest
the size of a marble — ^yellowish white, tough, and of leathery consistence,
dry, and emitting no juice on pressure. In two or three the circumference
of the tumour consisted of a translucent structure ; and this was evidently
the more recent formation, the opaque and yellow parts being probably
tissue undergoing a degenerative change. At one spot a deep cicatricial
appearance was produced by the contraction of a group of these small
nodules.
Microscopically the nodules consisted of nucleated fibres and fibrous
tissue.
No. 255. — The lower lobe of a left lung from a man, aged 27,
who died from erysipelas of the larynx. The specimen shows at its
hinder part a large yellowish mass partially separated from the surrounding
tissue. Smaller nodules are seen in the adjacent lung. The pleura over
the gumma is much thickened. Histologically the nodule consists of fibrous
tissue which stains with difficulty. There were many gummata in the
liver. With the exception of the above lesions and some bronchitis the
lungs were healthy. There was a chancre on the penis and suppurating
buboes.
No. 256. — A portion of lung showing scattered through it several small
masses of irregular shape, yellowish in colour, and firm on section. These
masses are easily separable from the surrounding lung, which is healthy.
Histologically the nodules show a central area of caseous material sur-
rounded by a narrow zone of fibrous tissue in which are many small
round cells. The liver contained a single gumma, and was in a condition
of difiiise syphilitic hepatitis. There were several gummata in the testes.
From a man, aged 39, who had suffered from cough and dyspnoea
for six months. He was admitted for hepatic ascites and slight jaundice.
The following specimen from the same Museum illustrates the ap-
pearances presented by a gumma which has undergone fibrous trans-
formation : —
No. 253. — A section of a right lung. From a man, aged 36, admitted
for fracture of the cervical spine. At the upper part of the lower lobe is
a circumscribed patch of fibroid material with radiating processes extend-
SYPHILITIC DISEASE OF THE LUNGS 319
ing into the surrounding pulmonary tissue. The pleura over it is much
thickened. The interlobar septum is thickened, and from its upper
portion similar fine fibrous strands radiate into the upper lobe. Other
portions are very emphysematous (also fibroid and pigmented). No
tubercle was found anywhere. There was lardaceous disease of the liver,
spleen, and kidneys. Both testes were good specimens of syphilitic
orchitis.
The following description of a specimen in the Museum of St. George's
Hospital illustrates a combination of the caseous and fibrous stages of a
gumma (10) : —
" Section of a right lung near the root. In the posterior and upper
part of the lower lobe, close to the spine, there is an area showing marked
fibrosis ; situated within it is a caseous mass the size of a marble, some-
what loose. The overlying pleura is adherent and thickened ; bands of
thick grayish fibrous tissue pass inwards from the pleura, and joining with
each other form a meshwork." No tubercle in any organ ; surface of the
liver scarred from perihepatitis. Large caseous gumma near the portal
fissure, with smaller ones in its neighbourhood. Liver cirrhotic and
lardaceous. Grummata in both testes. From a male patient who con-
tracted syphilis in 1884, six years previous to his death. In 1886 he
suffered from syphilitic disease of the testes and sores on the right elbow.
Death was due to uraemia.
Lobular or Broncho-jmeumonia. — A careful review of the evidence on
which it is believed that inflammatory changes of the lobular or broncho-
pneumonic type occur as the direct result of syphilis impresses me with
the conviction that many of the cases described in the past as presenting
such lesions were really cases of tuberculosis.
In the following case (3), however, such a possibility may be excluded.
It will be observed that the pulmonary lesions were secondary to and
in continuity with the growth of large gummata in the liver and spleen.
The specimen is in St. George's Hospital Museum : —
Left lung. — The lower lobe is deeply congested and partially consoli-
dated ; the consolidation is in patches as in catarrhal pneumonia. Some of
these masses appeared purulent, others fatty or caseous. The size varied
from 3 mm. to | mm. ; each patch or nodule was surrounded by a deeply
congested zone. Right lung. — The lower lobe presented changes similar
to the above ; it was adherent to the diaphragm, through which a large
caseous gumma in the liver had extended into the lung. At the upper
margin of the caseous mass there was much fibrous induration and exudative
consolidation of the pulmonary tissue. For the microscopical changes,
which are given in great detail, the reader is referred to the original article.
There was a gummatous mass chiefly in the upper part of the right
lobe of the liver measuring 5J in. by 4^ in., and another occupying the
upper third of the spleen. That organ was greatly enlarged, weighing
2 lb. 6 oz. Both liver and spleen were firmly adherent to the diaphragm,
and the muscular tissue of the latter was in part destroyed by the
extension through it of the gumma in the liver. The specimen was
320 SYSTEM OF MEDICINE
taken from a man, aged 43, who contracted syphilis in 1861, t-wenty-five
years before his death. He had periostitis of the tibia in 1864, left
hemiplegia in 1871, and again in 1876.
Fibroid induration. — The following are the more important changes of
this nature which have been attributed to syphilis : (o) thickening extend-
ing from the hilum around the bronchi and vessels ; (6) isolated masses of
fibroid tissue in various parts of the lung ; (c) difiuse changes occupying
the whole or the greater part of one lung.
The marked tendency of gummatous lesions to spread along the vessels
and bronchi has already been referred to.
The following case (4) is an example of syphilitic fibrosis illustrating
the first variety of this lesion ; —
Woman aged 50. — Thrombosis of cerebral artery ; hemiplegia.
Pigmented excavated scars on left leg, due to old syphilitic ulceration.
Lungs. — -Emphysema. Eight lower lobe contained a deep depression
and a much-puckered cicatrix due to pigmented fibroid bands running into
the lung tissue. No caseous or calcareous nodules. No pleural adhesions.
Microscopical examination. — The fibroid tissue is arranged chiefly
around the vessels and bronchi with a more or less concentric disposition.
The coats of the vessels are much thickened. There is a small -celled
growth invading the alveolar walls, which are also much thickened. In
places the cells and nuclei are aggregated in heaps.
As an example of fibrosis in the form of scattered areas of induration,
the following case may be cited from the same source (4) : —
Woman aged 25. — Fracture of cervical spine. Pigmented and puckered
cicatrix and syphilitic ulcers on left leg. Calcified gumma in the liver.
Right lung. — Upper lobe healthy. Middle lobe presented in the
centre large irregular patches formed by radiating bands of fibroid tissue ;
also smaller scattered patches of the same nature : the bands whitish,
not pigmented. One patch contains a calcified nodule. No pleural ad-
hesions. Left lung. — Adhesions over lower lobe ; and whitish, puckered,
depressed fibroid patches with irregular thickening of the pleura. On
section extensive fibroid infiltration ; bands appear to run into the lungs
from the pleura. Some small rounded caseous patches are also present.
The following specimen from the Museum of Guy's Hospital (9) illus-
trates the appearances met with in " diffuse syphilitic fibrosis of the lungs."
The patient was a man, set. 54, who had suffered from winter cough for
some years.
No. 252. — A portion of a right lung in which there is a considerable
excess of fibroid material appearing on the cut surface as a delicate net^
work traversing the pulmonary tissue in all directions. The fibroid
change is less marked at the apex than at the base, in which latter
situation many of the air-vesicles are dilated ; over this area the pleura is
slightly thickened and is adherent. The dense fibroid tissue that per-
vades the lung shows, scattered through it, numerous collections of small
round cells not undergoing caseation. No giant cells are present. The
walls of the small arteries are thickened. One or two small cavities the
SYPHILITIC DISEASE OF THE LUNGS 321
size of peas, with soft caseous contents, were situated near the root of
the right lung, probably softening gummata ; no tubercle bacilli could be
found in them. The condition of the left lung resembled that of the
right. The liver was scarred ; the testes were fibroid. Death was due
to bronchitis.
Changes in the bronchial glands and lymphatics of the lung. — In a case
of syphilitic disease of the liver, lungs, dura mater, cranium and sternum,
recorded by Dr. Hermann Weber, the bronchial glands and lymphatics
of the lung presented the following appearances : — The bronchial glands
were much enlarged — some being of the size of a pigeon's egg, some only
that of a hazel-nut. From the grayish white section of the larger glands,
which were rather soft, a creamy fluid exuded, consisting of fat globules,
granular corpuscles, and an abundance of large cells in a condition of
fatty degeneration. The less enlarged glands were harder, their sections
offered a marbled appearance, large white patches, almost like bacon,
being interspersed with grayish red, very vascular tissue. No juice
exuded spontaneously or could be squeezed from the section. Large
nuclei and nucleated cells were the principal microscopical elements, with
a very small proportion of fibres thickly studded with nuclei. The
lymphatics leading from the lungs to the enlarged glands were dilated
and their ramifications on the surface and throughout the lungs were
distended with creamy fluid.
A similar appearance is described in the case of Drs. Delepine and
Sisley abeady quoted. " Immediately under the pleura there was
a network composed of ramified tracks. The appearance suggested
lymphatics distended with cells or some fatty products." The lymph-
atics of the subserous layer of the pleura were considerably enlarged
over areas corresponding to the yellow patches (? of syphilitic broncho-
pneumonia) within the lung.
Dr. Weber rejects the view that the bronchial glands were first
affected by the syphilitic virus, and that the engorgement of the pulmonary
lymphatics resulted from obstruction to the passage of the lymph.
A progressive destructive disease, the so-called " syphilitic phthisis."
It appears to me that the question of the existence of a syphilitic
lesion of the above form can only be settled by a careful study of cases
which fulfil the following conditions : —
(i.) The cases must be complete; that is, the symptoms observed
during life must be considered in connection with the lesions discovered
on post-mortem examination.
(ii.) The evidence of syphilitic infection must be undoubted.
(iii.) Repeated examinations of the sputum must have been made,
and tubercle bacilli invariably absent ; and the absence of tubercle from
the lungs (as the cause of the lesions) must be proved by post-mortem
examination.
(iv.) Syphilitic lesions about the nature of which there can be no
doubt must be found in other organs.
From such evidence alone can we hope to construct the clinical
VOL. V Y
322 SYSTEM OF MEDICINE
history and morbid anatomy of advanced syphilitic disease of the
lungs.
The following cases illustrate this variety of the disease : —
Case I. — Charles N., set. 38, bricklayer. In 1892 he suflfered from
cough, -with expectoration and pain on the left side of the chest. In 1893
he had night-sweats and dyspnoea. From January to May 1894 he
was an in-patient of the Brompton Hospital under the care of Dr.
Mitchell Bruce ; the diagnosis then recorded was " Syphilis (?), tracheal
stenosis, chronic bronchial catarrh, induration of the left upper lobe and
of the left base with pleural adhesions over that area. Cicatrisation of
the soft palate and adhesions of the right posterior pillar of the fauces
to the back of the pharynx." There were no bacilli in the sputum. He
continued fairly well until October 1894, when he expectorated a large
quantity of offensive purulent material for two consecutive days. Cough
was very severe at this period. His health subsequently improved, and
so remained until 20th February 1895; when in the course of a few
days he brought up about a quart of blood-stained sputum. Haemor-
rhage then ceased and dyspnoea diminished. On 5th March, cough and
dyspnoea increased and he became seriously ill, with constant headache
and slight delirium. CEdema of the feet subsequently supervened. On
15th March 1895, he was admitted to the Brompton Hospital under the
care of Dr. Percy Kidd. On admission he was reported to be fairly well
nourished. He stated that he had not lost weight, and, beyond an occa-
sional streak of blood in the sputum, there has been no haemoptysis.
There was marked stridor and severe cough. Eight lung resonant every-
where; breath-sounds much exaggerated, expiration prolonged. Loud
hoarse inspiratory and expiratory stridor all over the lung ; sibilant
rhonchi general. Left lung. — Expansion much diminished; resonance
much impaired front and back; breath-sounds weak; expiration pro-
longed ; fine crackling rales over the whole of lung ; vocal fremitus and
resonance diminished. Expectoration profuse and difficult to expel.
No tubercle bacilli found. Temperature, 99° F. It varied between that
point and 96° F. during the time the patient was in hospital. The
dyspnoea gradually increased, and death occurred on 10th April.
Necropsy. — Scars on tongue, glans penis, and scrotum ; and adhesions
of skin to left testis. Marked thickening of the right tibia. Larynx
normal. Trachea narrowed at the lower end. Recent ulceration from
cricoid downwards for two inches ; below this, down to point of bifurca-
tion, there was extensive scarring of the cartilaginous portion ; and also
at its line of junction with the posterior wall. The submucous tissue
was extremely thickened. Cartilages bare in several places. The main
bronchi were much scarred and showed extreme narrowing. The bron-
chus to the left upper lobe was impermeable to a probe. Eight lung. —
Old pleural adhesions over the upper lobe, recent pleurisy with effusion
at the base. Emphysema, with reticular fibrosis especially around
bronchioles. Deep in the upper lobe at the edge of one of the main
bronchi there was a large black fibroid mass, with fibroid radiation into
SYPHILITIC DISEASE OF THE LUNGS 323
the surrounding tissue ; elsewhere two small, hard, raised masses, one
with fibrous strands running up to it. Base solid from broncho-
pneumonia. No appearance of tubercle. Left lung. — Upper lobe
extremely contracted, containing no normal tissue. It consisted of
deeply pigmented blackish gray fibrous tissue surrounding the openings
of bronchial tubes, and bronchiectasis. At the centre there was a smooth-
walled cavity about the size of a small chestnut into which a bronchus
opened. No appearance of tubercle. Lower lobe. — Emphysematous,
with reticular fibrosis along the margin and at the base. Bronchi dilated,
but not to a marked degree. About the centre point of the outer margin
there was a small nodule, probably a gumma ; white and firm, and
surrounded by a pigmented fibrous capsule. The extreme base consisted
of indurated fibrous tissue extending from the pleura to a cavity, the
size of a marble, into which a small bronchus opened. From this cavity
fine fibrous bands radiated in all directions, producing extensive fibrosis
of the surrounding lung. Perihepatic and splenic adhesions. Liver
scarred and nutmeg. Spleen contained several calcareous masses sur-
rounded by a fibrous capsule. Testes fibrous.
Case II. — '&. D., set. 36 ; coachman. The family history is unim-
portant. At the age of 18 he had a sore on the penis, for which he was
treated for several months with medicine and a lotion. In 1890 he became
an out-patient under the care of the writer at the Brompton Hospital ; he
was suffering from cough and expectoration, which continued. There
was an enlarged gland in the inferior triangle of the neck on the right
side, dulness at the right apex, with feeble breath-sounds, and bronchial
breathing in the right supraspinous fossa. The liver was large, nodular,
and very tender. He took iodide of potassium in gradually increasing
doses and obtained some relief. He was subsequently an out-patient
at the Middlesex Hospital. In March 1893 he caught a severe cold,
but remained at work. In following April he noticed oedema of the
legs and scrotum. He was admitted into Middlesex Hospital, under
Dr. Cayley, on 13th May 1893. He was pale and emaciated, the legs
and scrotum were cedematous. He had troublesome cough, accompanied
by the expectoration of large quantities of extremely fcetid pus.
The breath was foetid.
Physical signs. — Expansion deficient on right side. Eelative dulness-
at right apex front and back, breath - sounds feeble over dull area.
Absolute dulness from level of fifth interspace in nipple line and in axilla
to base; behind from angle of scapula to base. Vocal fremitus and
resonance diminished, and breath-sounds scarcely audible over dull area.
Left side normal. No displacement of heart. Hepatic region prominent.
Liver dulness extended 3 inches below the costal arch in right mammary
line and almost to umbilicus in middle line. Liver somewhat soft and
elastic. Urine, sp. gr. 1004, neutral, contained albumin and fatty casts.
The expectoration consisted of frothy greenish pus, forming thick masses in
a watery fluid. It contained no tubercle bacilli.
17th May.— The chest was explored in the axillary and submammary
324 SYSTEM OF MEDICINE
region. No pus was found. 19th May. — ^Liver exposed by incision below-
costal arch, and a depressed cicatrix seen. The expectoration continued
copious, green, and foetid. Absolute dulness appeared over whole of right
side up to clavicle, with amphoric breathing and pectoriloquy below clavicle.
15th June.— Offensive pus was evacuated through a canula inserted in
third right interspace in mid-axillary line : a portion of the fourth rib
resected, lung incised, more pus evacuated, drainage-tube inserted. 19th
and 20th June. — Haemorrhage from wound. 21st June. — Death.
Necropsy. Abstract of notes : — Old syphilitic scar in trachea, six
rings above bifurcation, more recent scar at bifurcation, producing
stenosis of the main bronchi to the right upper and lower lobes. One
bronchial gland enlarged. Plexu^a over right lower lobe adherent and
much thickened. Bronchi much dilated beyond the site of stenosis. At
the base of the upper lobe were two large irregular cavities with sinuous
outlines communicating with large bronchi, lined by a distinct membrane,
and containing sloughy portions of lung tissue. The anterior cavity
had been opened by the incision. The section of the lung was smooth
and presented a finely speckled yellow appearance. No pus exuded from
the yellow spots on pressure. In the anterior part of the lower lobe
there was a large irregular cavity, the walls of which showed no sign of
any mucous membrane ; they were covered with yellowish gray sloughy
material. No tubercle present and no caseation. The lung puckered
in many places and fibrous almost throughout. Liver enlarged (76 oz.).
Large puckered cicatrix on the upper surface of the left lobe and many
similar cicatrices elsewhere. A cretaceous and caseous gumma on the
posterior aspect of the right lobe. Liver substance fatty and amyloid.
Kidneys large, pale, lardaceous, and fatty.
Case III. — -T. H., aet. 59; painter. Admitted into Middlesex Hospital
under Dr. Fowler, 4th February 1893. Father died aged 70; mother
aged 75. No history of tuberculosis in family. Accident to left knee
set. 19 years, followed by formation of an ulcer. Chancre on penis in
1858 (set. 25), secondary rash and sore throat subsequently. In 1864
ulcers on left leg and twice subsequently. In 1880 ulcer on right leg,
near external malleolus. Dry cough since 1887, worse in winter. Since
December 1892 severe paroxysmal cough with offensive muco-purulent
expectoration. Marked emaciation during this period.
A pale, gray-haired, emaciated man. Breath very foetid. Extensive
scars on left leg of old standing, more recent scars on right leg. Scar in
right lumbar region where incision was made for " abscess." Right lung. —
Hyper -resonant on percussion ; breath -sounds at apex bronchial, front
and back ; crackling rales in supraspinous fossa. Bronchophony and
pectoriloquy well marked in same area. Dulness over lower lobe to
angle of scapula, breath -sounds bronchial, with coarse crackling rales
over same area. Left lung. — Resonance impaired over clavicle
and in supraclavicular fossa, elsewhere hyper - resonance. Bronchial
breathing over upper lobe, front and back, with crackling rales. Breath-
sounds bronchial over upper part of lower lobe, with bubbling and coarse
SYPHILITIC DISEASE OF THE LUNGS 32S
crackling rales, the latter extending to the base. Urine, sp. gr. 1020;
no albumin. Expectoration copious, purulent, and offensive. Frequent
examinations made for tubercle bacilli, but none found. No elastic tissue
found. Temp. 98°, pulse 84, respirations 44. 21st February.*— Dulness
at both apices, and medium crackling rales. Temperature between
99° and 100° F. The respirations between 36 and 48. Severe cough,
and the breath and expectoration oiTensive. Died 23rd February.
Abstract of P.M. notes : — Scar on corona of penis with some
induration around. Calvarium thickened, dura mater adherent. Pleural
adhesions over both lungs. Eight lung. — Emphysema along anterior
margin and at base. Apex pigmented and consolidated from pneu-
monia and oedema. In lower part an oval cavity measuring ^\ inches
by 2 inches, in communication with main bronchus, and containing
greenish yellow, offensive, shreddy material. Below this for \\ inches
the lung gray in colour and almost solid, a few small cavities with
curdy contents. No tubercle found. The pleura covering the con-
solidated area much thickened. Left lung. — Upper lobe pigmented
and " nodular." A cavity, from bronchial dilatation, occupies the posterior
portion. The lower lobe emphysematous, and contained numerous en-
capsuled caseous masses about 2 mm. in diameter. Bronchial glands
pigmented, but not caseated. No ulceration in air-passages. No gummata
in Hver or spleen. Testes scarred and fibrous. Small white fibrous
nodule in right kidney.
The following cases are incomplete, and do not attain to the standard
of evidence laid down, inasmuch as the patients are believed to be still
living : —
Case IV. — Mary G., set. 33, married. Three children aUve, three
dead, — one still-born, one died a few hours after birth. Has had four
miscarriages. Admitted into the Brompton Hospital, 13th June 1894,
imder Dr. Fowler. No history of tuberculous disease in the family. Ten
years ago had some affection of the liver. Three years ago had an attack
of influenza followed by pleurisy (E) and congestion of the lungs. Eight
pleurisy recurred in August 1893. Has had a slight cough for three
years, worse since September 1893. Expectoration has been profuse, and
for the last two months foetid and of a bitter taste. In October 1893 it
was tinged with blood for three weeks. Dyspnoea worse since September
1893. Catamenia ceased since the birth of the last child on 30th
September 1893, at which time she caught a chill. In February 1893
patient noticed a swelling in the left loin, which at first gradually
increased in size and subsequently diminished. It is slightly movable
and is not tender. It is about equal in size to a small Tangerine orange,
is situated rather superficially, and over the erector spinse muscle ;
whether actually within the muscle cannot be determined. Emaciation,
cough, and weakness have been increasing lately, and night-sweats have
been continuous.
Physical signs. — Eight lung. — Marked flattening of the whole of the
right side, particularly in front. Measurement at right nipple level :
326 SYSTEM OF MEDICINE
rigtt 14 J inches, left 16 inches. Dulness over upper lobe, with distant
cavernous breathing and bronchophony front and back. Impaired reson-
ance over upper part of lower lobe posteriorly, where crackling rales are
audible; similar rales at the right base where percussion note is dull.
Left lung. — Harsh breathing general (? compensatory), no adventitious
sounds. Liver much enlarged and nodular on the surface ; margin ir-
regular, extends from the fourth space to below the umbilicus. Spleen
not enlarged. Urine free from albumin. Expectoration profuse and
foetid. No tubercle bacilli. From June to September the expectoration
sras usually foetid. Bacilli repeatedly sought for, but never found. The
cavity at the right apex extended. 5th September. — Eetraction more
marked at right apex. Cavity dry. Numerous crackling rales in axilla,
and all over base. General improvement. Liver appears more nodular.
October. — Large crackling rales over base and in axilla. Cavity at apex
dry. No bacilli to be found. Discharged 13th October. Intra-tracheal
injections of menthol appeared at first to have an effect in diminishing
and then removing the odour of the expectoration ; but subsequently the
foetor returned and appeared to be uninfluenced by their continued use.
The quantity of expectoration was small during the period over which
their administration extended ; but it had been steadily diminishing up
to the time when this treatment was commenced. The patient considered
that she derived benefit from the injections. The nature of the tumour
in the back was doubtful, it was believed to be a gumma in the super-
ficial part of the muscle. Inunction of mercurial ointment was made
daily into the back from 22nd September onwards.
Case V. — ^Edward C, set. 47 ; a waiter. Admitted into St. George's
Hospital, 13th April 1894, under Dr. Whipham.^ His father and mother
died of " consumption." Thirty years ago he had a hard chancre. He has
had syphilitic psoriasis of the palms. He has not had haemoptysis, night-
sweats, or emaciation. A fortnight before admission he was attacked
with severe pain on the right side of the chest and dyspnoea. On ad-
mission he was anaemic, and complained of cough and profuse expectora-
tion. The skin was of a brownish tint and presented numerous old
rupial scars. Eight lung. — Impaired resonance over upper lobe with
feeble breathing. Just below the second rib there is a small area of
increased dulness and cavernous breathing with whispering pectoriloquy.
There are rhonchi all over the right lung and to a smaller extent over
the left. The sputum is profuse and muco-purulent. No tubercle bacilli
were found on any occasion ; the examinations were made by several
observers. 15th April. — Ordered Potassii iodide gr. v., Liq. hydrarg.
perchlor. 3j- ter die. 28th April. — Expectoration and cough less.
Physical signs at right apex less marked. 2nd May. — Discharged to
Convalescent Home.
The following case illustrates the fact, first pointed out by Dr. Pear-
son Irvine, that stenosis of a main bronchus may give rise to destructive
^ The writer is indebted to Dr. Whipham for his kind permission to use the notes of
this case.
SYPHILITIC DISEASE OF THE LUNGS 327
changes in the lung. It will be observed that the case was one in which
a recent tuberculosis supervened on old syphilitic disease : —
Case VI. — Margaret S., set. 25. Admitted into the Brompton
Hospital, 25th June 1884, under Dr. Eeginald Thompson. Family
history good. G-ood health up to two years ago, when after marriage she
had " ulcerated legs." No sore throat or skin eruption. Cough, ex-
pectoration, pain in left side, dyspnoea, njght-sweats and emaciation have
been present for eight months. On admission the fingers were clubbed ;
there was a large circular ulcer on the back of the left thigh with some
scarring, and coppery staining about the knee and leg on the same side.
Cough more or less paroxysmal ; expectoration copious, nummular, and
purulent. No tubercle bacilli. Eight chest \f>\ inches, left 16^. Dul-
ness over left lung, absolute at base, where vocal fremitus is absent ;
elsewhere it is diminished. Bronchial breathing, pectoriloquy, and crepi-
tation over left upper lobe. Breath-sounds absent at base, some rhonchus
there. Slight crepitation at right base.
The ulcer on the thigh yielded to antisyphilitic treatment. The
physical signs remained much the same, except that the breath-sound at
the left apex became cavernous. There was well-marked pyrexia through-
out. The expectoration remained copious, at times it averaged a pint in
the twenty-four hours. Death occurred on 1st March 1885, and was
preceded by anasarca, ascites, and profuse diarrhoea.
Necropsy. — A few small scars in the subglottic portion of the larynx.
The lower half of the trachea marked by numerous stellate puckered
cicatrices, involving both membranous and cartilaginous portions, but
especially the latter. The origin of the left bronchus represented by a
small opening just admitting a probe ; the surrounding parts of the
tracheal wall extremely fibrous and puckered. Slight scarring in the
right bronchus about the origin of the upper lobar branch. Left lung
excavated from apex to base. Numerous trabeculated cavities in
the upper lobe intersected by tough pigmented bands : walls thin and
smooth. The cavities larger behind than in front, in the latter region
they were more numerous ; and the intervening fibroid induration was
more pronounced. Some bronchi appeared to expand uninterruptedly
into the smaller cavities. Numerous small cavities in the lower lobe
situated in indurated fibroid lung. The cavities contained extremely foetid
reddish fluid secretion, and in some places some soft putty-like material.
No tuberculous nodules in this lung. The contents of the pulmonary
cavities, including the liquid and caseous parts, were carefully examined
for tubercle bacilli, but none could be found. Eight lung crepitant, but
studded with large tuberculous groups which were most plentiful in the
middle lobe and lower part of the lower lobe. Lardaceous disease of
thyroid, mesenteric and mediastinal glands, also of the kidneys, liver
and spleen, and mucous membrane throughout the body.
The recent tuberculosis of the right lung was obviously quite uncon-
nected with the disease in the left, which was secondary to the bronchial
stenosis.
328 SYSTEM OF MEDICINE
This case proves very clearly that a progressive destructive disease of
the lung may result from syphilitic stenosis of a main bronchus ; but it
does not prove that this disintegration of the lung is due to the continued
action of the specific virus of the disease, as is the case in pulmonary
tuberculosis. The fact that lesions similar to those here described may
occur when the narrowing of the bronchus is due to pressure from with-
out, as by an aneurysm, shows that the bronchial obstruction is the
main factor in their production. Stenosis of the bronchus is followed by
retention of secretion in the tubes, and this by bronchiectasis. Decom-
position of the retained secretion induces inflammatory changes in the
surrounding lung, and finally the part so affected breaks down and
cavities are formed.
The cases here described prove that in individuals imdoubtedly
the subjects of syphilis, widely -spread destructive changes may be
found in the lungs ; and that such lesions may occur independently
of the presence of tubercle. Whether they are such as to entitle the
condition to be named " syphilitic phthisis " must be decided by those
who continue to use the word "phthisis," a term which many teachers
have ceased to employ.
If the name " phthisis " is given to a group of symptoms and morbid
changes, it can hardly be denied that a case (see Case I.) which is
marked by such symptoms as severe cough, dyspnoea, emaciation, fever,
night -sweats, profuse expectoration, and haemorrhage, and which, on
examination after death, is found to present signs of consolidation, fibrosis
and excavation of the lungs, belongs to this category. The task
before us, however, is to determine the nature of the pathological
lesions of pulmonary syphilis and of the symptoms which they produce ;
whether they are such as to warrant the use of a vague nomenclature
which it would be well to discard is a question of little importance.
It may be of service, however, to draw attention to the chief points of
difference between the pulmonary lesions of tuberculosis and syphilis.
I. Tubercle usually affects the apex of the lung, and subsequently
the apex of the lower lobe ; and tends to progress along a certain
route. The primary lesion of syphilis is often about the root and central
part of the lung ; the disease follows no definite line of march, and
gummata may be found in any position.
II. Both tubercles and gummata may undergo either necrosis and casea-
tion, or fibrous transformation ; but with caseous tubercle the tendency
towards softening and cavity formation is the rule, whereas a caseous
gumma very rarely breaks down.
III. The progressive destruction of the lung by a process of disin-
tegration leading to a gradual increase in the size of a cavity, a change
so commonly observed in tuberculous disease, is rarely if ever observed in
syphilis, except as a secondary result of stenosis of one of the main
bronchi.
lA' . In nearly all cases of advanced destruction of the lung occurring
in the subjects of syphilis, stenosis either of the trachea or of one of the
SYPHILITIC DISEASE OF THE LUNGS 329
main bronchi is present, whereas this lesion is very rare indeed in tuber-
culosis.
V. The cavities found in cases of pulmonary syphilis are usually
bronchiectatic, but not invariably so ; whereas in tuberculosis they are
commonly due to progressive destruction of the lung, but may be
bronchiectatic.
VI. The tendency to the formation of pulmonary aneurysms, -which
is so marked a feature in tuberculosis, is rarely observed in pulmonary
syphilis.
VII. Pulmonary lesions in tuberculosis are very common, whereas in
syphilis they are extremely rare.
The necessity for prolonged specific treatment is certainly more gener-
ally appreciated now than formerly ; and it is therefore probable that
rare as these lesions have been in the past, they will be still rarer in the
future. The conditions which favour their development are the neglect
of mercurial treatment shortly after infection, and anything which, by
lowering the general health, tends to diminish the resisting power of the
individual.
When our knowledge of the virus of syphilis is as complete as that
we even now possess of the bacillus tuberculosis, it may be possible to
state definitely whether the destructive pulmonary lesions found in ad-
vanced cases of the acquired disease are directly due to the continued
action of a specific micro-organism ; at present the problem remains un
unsolved.
Symptoms. — The only point worthy of mention in respect of syphi-
litic lesions of the bronchi is that the catarrhal signs which accompany
the secondary stage are, as a rule, general in their distribution ; whilst in
the tertiary stage they are more often localised, owing to the tendency at
that period to the formation of gummata in the main bronchi. Should
stenosis occur, there may at first be bronchial breathing limited in area,
and often most marked about the root of the lung posteriorly. As the
lumen of the tube diminishes, the breath-sounds, over the pulmonary area
which it supplies, become more and more feeble, and finally disappear
when air ceases to pass the obstruction. If bronchiectasis is forming be-
hind the site of stenosis there may be cough with profuse, purulent, and
foetid expectoration, accompanied by general signs such as emaciation and
moderate pyrexia.
In the cases described in this article it will be observed that cough was,
as a rule, the earliest and most prominent symptom. In the early stage
it may be due to irritation, the result of laryngeal, tracheal, or bronchial
lesions ; at a later period it is probably chiefly due to the changes within
the lung itself.
Dyspnoea comes next in point of frequency. It varies in severity with
the nature of the lesion : slight when this is limited, in cases of extensive
fibrosis or stenosis of one of the main bronchi it may be very severe.
The dyspnoea tends to become paroxysmal and to assume the characters
of bronchial asthma. Hmmojptysis has not been of frequent occurrence in
330 SYSTEM OF MEDICINE
cases observed by myself, but it may occur and may prove fatal. In
one case of syphilis of the bronchial glands, profuse and fatal haemorrhage
occurred from softening of the gland and its rupture into a main branch
of the pulmonary artery.
Expectoration may be profuse, purulent, and offensive. Fcetor of the
expectoration is common in cases of advanced pulmonary syphilis. The
sputum will be free from tubercle bacilli.
Pain may be present, but is not a very prominent feature of the
disease.
Emaciation is not, as a rule, nearly so extreme as in tuberculosis ; but
with advanced lesions in the lungs the difiference is not so remarkable as
to be of any value from a diagnostic point of view.
Night-sweats were present in several of the cases here described.
When extensive lesions are present, pyrexia may be considerable, and
of the hectic type commonly observed in tuberculous disease of the lungs ;
but in the early stages of the disease there may be a complete absence of
fever.
The general symptoms, as will be seen on reference to the cases
described, do not, in the presence of widely-spread lesions, differ markedly
from those of advanced tubercular disease of the lung.
Physical signs and Diagnosis. — The lesions of syphilis are rarely of
such a kind as to produce signs by which they can be distinguished
from others of an entirely different origin.
Consolidation and excavation will be recognised by their ordinary
signs, probably before their syphilitic origin is suspected ; and it appears
therefore unnecessary to describe them in detail, more particularly as in
the cases here recorded the results of the physical examination are given
in full.
The features of pulmonary syphilis are certainly not as yet so clear
that the disease can be recognised by any positive signs ; but by a process
of exclusion a diagnosis may generally be made.
The case will probably be regarded at first as one of pulmonary tuber-
culosis ; but repeated examination of the sputum and the failure to
discover tubercle bacilli will suggest another origin.
A careful inquiry, previously perhaps omitted, will now be made as
to syphilitic infection and as to the occurrence of any secondary or ter-
tiary manifestations of this disease. The absence of such a history in a
hospital patient will not exclude syphilis ; but it is rare in private prac-
tice for a patient to have had syphilis with tertiary symptoms and to be
ignorant of the fact.
Evidence of tertiary lesions in the larynx, liver, spleen, or testes is of
importance as showing that the viscera are affected.
Careful search should also be made for lesions of the calvarium, of
the dura mater, and of the sternum and ribs.
Speaking generally, the diagnosis of pulmonary syphilis from tuber-
culosis will depend far more upon the examination of the sputum than
on the results of physical examination.
SYPHILITIC DISEASE OF THE LUNGS 331
A careful examination of undoubted specimens of pulmonary syphilis
does not bear out the statement that the lesions are generally limited to
the middle part of the lung ; they are so often found elsewhere that their
more frequent occurrence in that part ceases to be a fact of much value in
diagnosis. It would be rash indeed to diagnose pulmonary syphilis because
of a lesion situated in and apparently limited to the middle of one lung,
without having previously demonstrated, by frequent examinations, the
absence of tubercle bacilli from the expectoration. Such points, however,
are not without importance, as being unusual in a case possibly hitherto
regarded as one of " phthisis " or " consumption," they may serve to arrest
attention.
Evidence of excavation and the expectoration of a foetid sputum,
which does not contain tubercle bacilli, should always suggest the
possibility of pulmonary syphilis. When the physical signs indicate
stenosis of the trachea, or of one of the main bronchi, and the presence
of a growth or an aneurysm can be excluded, it is very probable indeed
that syphilis is the main factor in the case.
Those who are content to diagnose " phthisis," and neglect the sys-
tematic examination of the sputum, will almost certainly overlook a case
of pulmonary syphilis if it should come in their way.
A striking example of this has recently come under my notice. A
military oflScer who had contracted syphilis some years back began to
suffer from symptoms of laryngitis ; and on examination of the chest well-
marked signs of disease were found at the apex of the right lung. The
laryngoscopic appearances did not suggest to several competent observers
that the lesion was due to syphilis, and the case was regarded as one of
" consumption of the throat and lungs." It occurred to a medical man
who saw the patient at a later period to examine the sputa for tubercle
bacilli, and, as none was found on repeated examination, doubt was
cast upon the diagnosis of " phthisis " ; mercury and large doses of iodide
of potassium were prescribed, and the patient rapidly improved ; but the
stenosis of the larynx remained.
Prognosis. — Extensive pulmonary lesions, particularly excavation
whether of bronehiectatic or disintegrative origin, and foetid expectora-
tion are certainly very grave complications of syphilis. If, moreover,
there is evidence also of gummatous hepatitis, albuminuria, and lardaceous
disease, recovery is scarcely possible, and life is not likely to be much
prolonged.
It is probable, however, that, with our present improved means of
diagnosis of tuberculosis of the lungs, syphilitic cases, which formerly
would have been considered tuberculous, may be recognised as syphilitic
at an earlier stage, and the patients under appropriate treatment may
recover. In an undoubted case of pulmonary sjrphilis, which came under
my own care at a late stage of the disease, the affection had been kept
in check for many years by repeated visits to Aix-la-Chapelle, and
by the active employment of antisyphilitic treatment. In any case seen
in an early stage, great improvement, if not complete cure, may reasonably
332 SYSTEM OF MEDICINE
be expected from the use of similar measures. There are, however,
limits to the action even of specific remedies ; and it is not to be expected
that lesions such as bronchial stenosis and dilatation, extensive fibrosis
and excavation, or gummata in a state of fibrosis vsdll disappear under the
administration of mercury or iodide of potassium.
Treatment. — If the disease in the bronchi or lungs is recognised
in an early stage, the patient should be advised to undergo a prolonged
course of treatment with mercury. Iodide of potassium in gradually in-
creasing doses is generally administered at the same time.
If, however, the disease is advanced, and the patient emaciated, it is
better first to try the effect of iodide of potassium alone ; giving at the
same time cod -liver oil and tonics. To maintain and improve the
strength and general nutrition of the patient are matters of as much im-
portance in the treatment of syphilitic as of tuberculous disease of the
lungs, and are to be secured by the same means.
The warm sulphur baths of Aix-la-Chapelle, in association with
mercurial inunction, enjoy a special reputation in the treatment of syphilis,
and are to be recommended to sufierers from pulmonary syphilis who are
able to go abroad for treatment.
When tuberculous disease of the lungs occurs in a syphilitic subject,
the treatment will be mainly such as is suited to cases of tuberculosis.
A mercurial course is rarely admissible, but iodine, in the form of the
syrup of the iodide of iron, may be given with advantage.
In cases accompanied by foetid expectoration, creasote vapour baths
and intra-tracheal injections of guaiacol should be tried.
Cases of syphilitic disease of the lung accompanied by bronchiectasis
have not, in the experience of the writer, been benefited by surgical
measures undertaken with a view to drain the cavities.
J. K. FOWLEK.
REFERENCES
1. Atlas d'anatomie patiwlogique, i. 7i6. — 2. Councilman. Johns HopTcins Hospital
Bulletin, ii. No. 11, 1891. — 3. Dbl^pine and Sislbt. The Specimens in St. George's
Hospital Museum, Path. Soc. Trans, xlii. 141. — 4. Gkbenfibld. Path. Sac. Trans.
xxviii. 248. — 5. Hellbe. "Die Lungenerkrankungen bei angeborener Syphilis,"
Deutsch. Archiv f. Tdin. Med. Bd. xlii. S. 159, 1888. — 6. Hoohsinger. Wiener
med. Blatt. Nos. 20, 21, 1894. — 7. Ievinb, Pbakson. Path. Soc. Trans, xxviii.-
XXX. — 8. KiDD, Perot. Path. Soc. Trans, xxxyii. 111. — 9. Pbekt, E. C. Report in
Path. Soc. Trans, xlii. 53. — 10. Rollbston, H. D. Path. Soc. Trans, xlii. 60. — 11.
Spatjndis. Ueber congenitale Limgensyphilis. Inaugural Dissertation. Freiburg,
1891. —12. Webbe, Hermann. Path. Soc. Trans, xvii. 152. — 13. Wbloh. De-
stritctive Lung Disease amxmgst Soldiers, Alexander Prize Essay 1872, p. 66. — 14.
WiLKS. Trans. Path. Soc. ix. 65.
J. K. F.
DISEASES OF THE PLETJEA
INTRAPLEURAL TENSION
In health the two layers of the pleura are in close contact, but they
are subject to a constant strain, which tends to separate them ; this is
called the intrapleural tension. It is for all practical purposes equal to
the elasticity of the lung, but opposite in direction ; and thus the elasticity
of the lung is positive and the intrapleural tension negative.
Whether in health there is any force existing between the layers of
the pleura — such as that of cohesion, as I suggested some years ago (1),
which neutralises the elasticity of the lung when fully expanded — is a
matter which is open to question. It is possible, and I think it probable ;
but the question need not be further considered here.
The forces, of which the intrapleural tension is the resultant, are, first,
the rigidity of the chest walls ; secondly and chiefly, the elasticity of the
lungs ; and, thirdly, the movements of respiration.
So far as the condition of the chest walls is concerned, where they are
fairly rigid, as in the adult, this factor may practically be disregarded ;
but not so in infants or little children, in whom the chest walls are soft
and yielding ; for then, under pathological conditions, part of the force
which would otherwise tend to separate the two layers of the pleura is
spent in drawing the chest walls in.
The condition of the chest walls and the elasticity of the lungs can-
not vary while observations on intrapleural tension are being made ; but
the third factor, namely, the movements of respiration, is one which is
constantly varying, and introducing variations in intrapleural tension
which have to be reckoned with. Thus during inspiration the lungs are
placed more on the stretch, and consequently the intrapleural tension is
greater ; during expiration the lungs are less on the stretch, and the
intrapleural tension is tlierefore smaller.
If the air in the tubes were stationary, as it is after death, the pres-
sure in the air-tubes would be that of the atmosphere ; but, during
respiration, the air, as it passes in and out through the air-tubes, meets
with some obstruction, which on inspiration amounts to about half a
millimetre of mercury, and on expiration from 2 to 3 millimetres. Thus
an oscillation in pressure is produced during the different phases of
respiration, which amounts to 2 or 3 millimetres of mercury; that is, IJ
to 2 inches of water. This is called the respiratory oscillation.
336 SYSTEM OF MEDICINE
If the movements of respiration were left out of account, the intra-
pleural tension would be equal to that of the atmosphere, minus the
elasticity of the lungs ; that is to say, it would always give a negative
reading on the manometer. It would then be equal to the elasticity of
the lungs with the sign changed, that is, - 6 to - 8 millimetres of
mercury.
During ordinary respiration the intrapleural tension is also negative
throughout ; for, if it is negative when the air is stationary, it will bo
more negative still on inspiration, the lung being more on the stretch ; and
during quiet expiration, even when from the normal elasticity of the lung
the 2 1 to 3 millimetres of mercury be deducted which represent the
obstruction in the tubes to which the air is subject on expiration, there
are still left 4 to 5 millimetres of negative pressure.
During violent expiration, of course, the pressure may rise consider-
ably, even to so much as 70 to 100 millimetres of mercury (3 to 4
inches) ; but it must be remembered that under normal conditions thid
pressure does not fall directly upon the pleura, ' but is immediately
supported by the chest walls. Under pathological conditions, on the
other hand, when the two layers of the pleura are not in contact, but are
separated by air or by fluid, pressure of any kind will make itself felt
directly by the contents.
There are two methods of determining the value of the intrapleural
tension. 1. In the one the elasticity of the lung is determined, and the
result, with the sign changed, is transferred to the pleura ; 2, in the other
the intrapleural tension is estimated directly by means of a trocar
introduced between the layers of the pleura.
In man both these methods of investigation are available after death,
but the latter only during Ufe, and this under pathological conditions.
In either case the reading is made upon a mercury- or water-mano-
meter. Water has been more commonly employed, because the oscilla-
tions are larger and are more easily read ; but the conversion is easily
made from the one to the other : thus 1 inch is equal to 25 millimetres,
and 1 millimetre of mercury is approximately equal to half an inch of
water or 12J millimetres of water.
Intrapleural tension is often spoken of as " intrapleural pressure,"
and thus confusion is introduced both in thought and in expression.
This confusion will be avoided if it be remembered that the values stated
are not actual pressures but readings on the manometer. For instance,
if the pressure in the pleura were equal to that of the atmosphere it
might be called 1, but as this would be indicated on the manometer by
the position of equilibrium which is marked zero, it is usually spoken of
as zero ; 1, 2, or 3 inches or millimetres would then represent 1, or 2, or 3
above or below the atmospheric pressirre, as the case might be.
The elasticity of the lung was estimated by Donders to be from 6 to 8
millimetres of mercury ; this, therefore, with the sign changed, would
represent the intrapleural tension.
An important series of observations of a similar kind was made by
INTRAPLEURAL TENSION 337-
Perls (2). After a tube connected with a manometer had been fixed into
the trachea, first one pleura and then the other was opened and the
pressures registered. The observations were made upon the dead body
of a man under a variety of different conditions, and the results are very
interesting.
Seeing how closely intrapleural tension is connected with the
elasticity of the lung this will be the natural place to consider various
pathological conditions under which the normal elasticity of the lung is
altered.
When one pleural cavity is laid freely open to the air there will
then be atmospheric pressure on both sides of the visceral pleura ; the
elasticity of the lungs will come into play, and the exposed lung will
collapse. But this is not all, for the alterations in pressure do not affect
the one lung only ; the mediastinum being not a fixed partition, but
a movable one, the elasticity of the opposite lung also comes into
play ; with the result that the mediastinum and the organs therein are
drawn over to the sound side. Thus it follows that the opening of one
pleura not only satisfies the elasticity of the one lung, but goes a long way
to satisfy the elasticity of the other. If, for example, the pressures be
reduced to figures, and we assume for the sake of illustration that in a
healthy man the total elastic contractility of the two lungs together
amounts to 50, the opening of one pleura may satisfy this elasticity to
the extent of 40, leaving only 10 for the unsatisfied elasticity of the
opposite lung.
Thus, in pneumothorax, which is the corresponding pathological
condition, if the lungs are healthy and their elasticity at its maximum,
the total respiratory capacity will be suddenly reduced by four-fifths. If,
however, the lungs be previously diseased or the pleura adherent, the
elasticity of the lungs will be either reduced or prevented from coming
into play ; and thus the change in respiratory capacity consequent on the
pneumothorax will not be so extreme. For these two reasons it is
evident why the sudden admission of air to the pleura should produce
more severe results in a healthy person than in one whose chest has been
previously diseased ; and a clinical paradox is explained.
Where the pleura is completely adherent the elasticity of the cor-
responding lung may be almost abolished ; but it is frequently retained,
though of course when retained it is unable to come into play. Under
these conditions the opposite lung often becomes greatly enlarged. This
has often been called "complementary emphysema," but in these cases
the elasticity of the enlarged lung is not diminished, as in ordinary
emphysema, but actually largely increased, so that the elasticity of that
one lung may be almost equal to the combined elasticity of two healthy
lungs. Thus it is made evident that this condition is not emphysema, but
hypertrophy, as there are also the best ©f clinical reasons for maintaining.
It should therefore be called, not complementary emphysema, but comple-
mentary hypertrophy.
VOL. V ' 7
'338 SYSTEM OF MEDICINE
There is good ground for believing that the contractility of the lung
is not simply elastic, but is due in some measure to the muscular fibre
with which it is so richly provided. If that be so, we may fairly speak
of " pulmonary tone " in the same way as we speak of " vascular tone " ;
and we may expect it to vary not only with local conditions of nutrition
in the lung, but also with defects of nutrition which are general.
Thus, in various local affections, of which pneumonia is the most
important. Perls found the elasticity of the lung greatly reduced ; as
well as in general diseases without any local affection of the lung, as
for example in typhoid fever, delirium tremens, erysipelas, phosphorus
poisoning, and after severe haemorrhage.
If, then, pulmonary tone be not simply elastic in origin, but in part
neuro-muscular, the loss of it may be met with under two different
clinical conditions : first, as the result of general causes — as an evidence,
for instance, of general neuro-muscular failure ; and, secondly, as a result
of local nutritive-disturbance.
As a neuro-paralytic phenomenon it might be placed in association
with the like condition in the abdomen (acute tympanites), which in the
same way may be due to general or local causes. For example, just
as in pneumonia, acute abdominal tympanites may suddenly manifest
itself — a phenomenon of fatal significance ; so with typhoid fever, or
any other specific fever, a similar condition may appear in the lung which
is likewise of fatal import.
The loss of pulmonary tone is indicated during life, just as it is after
death, by change in the percussion note ; the resonance becoming more
tympanitic and of that character which is generally known under the
name of " skodaic resonance." Without any local disease of the lung, I
have on several occasions seen this acute pulmonary tympanites set in ;
whatever the explanation of its occurrence, there is no doubt as to the
existence of the condition.
Where there is local disease in the lung, the other parts of the lungs,
as is well known, frequently yield a tympanitic percussion note. There
are several conditions under which this is met with ; the commonest
and easiest to explain is that which occurs with pleural effusion, when
the lung floating on the fluid yields this skodaic resonance. The
conditions and the percussion note are the same as are presented by the
lung removed from the body.
With complementary emphysema, where one part of a lung is diseased
and the other parts proportionately distended, similar hyper-resonance is
obtained. In this case the hyper-resonance is due to the over-distension
of some of the air-vesicles.
But besides these there is another condition which requires a
different explanation. Nothing is commoner in pneumonia than to
find the parts of the lung above or in front of the affected portion
yielding a highly tympanitic note; yet the pneumonic portions of
the lung are certainly not collapsed or smaller than they should be,
nor are they much larger : thus neither of the explanations just given
INTRAPLEURAL TENSION 339
is applicable ; the part of the lung where the hyper - resonance is
obtained is not collapsed on the one hand, nor over-distended on the
other. This condition, it appears to me, can only be explained on the
assumption of loss of lung-tone of neuro-paralytic origin and dependent
on nutritive disturbance. This view also obtains support from some of
Perls' observations, for among his cases are several instances of pneumonia
as well as some of embolism and gangrene ; and in all of them the elasticity
of the lung was very greatly reduced.
It is possible that the elasticity of the lung diminishes after death, but
there are no direct observations to prove this. We may assume at any rate
that for some hours after death the elasticity of the lungs is not materially
aifected.
In estimating the elasticity of the lung and the intrapleural tension
the condition of the abdominal muscles and of the diaphragm must not be
overlooked. "We have to reckon on the one hand, during life, with their
respiratory action, and on the other, after death, with rigor mortis ; but it
is not necessary here to do more than refer to these complicating factors.
THE PLEURAL CAVITY UNDER PATHOLOGICAL CONDITIONS
Under pathological conditions the two layers of the pleura may be
separated either by air or by fluid, and each of these presents its own
peculiarities and difficulties : thus, fluid has weight, but is practically
incompressible ; air is compressible, but its weight may be disregarded.
With fluid, therefore, the height of the column above the point of the
trocar will affect the manometer readings, while with air the position of
the trocar is immaterial. As in many respects the problem is simpler
in the case of air than of fluid, it will be well to begin with pneumo-
thorax.
Intrapleural tension in pneumothorax. — ^Air may gain access into
the pleura either from without through the chest walls, as by a wound, or
internally from the lung; and in both cases we have to consider, first,
the condition in which the air enters more freely on inspiration than it
finds issue on expiration, and, secondly, the condition in which there is no
abnormal obstruction either on inspiration or on expiration.
A. Where the air finds entrance through the chest walls.
(i.) By a punctured wound. — In this case, where the wound is a small
one and merely a puncture, though the lung be injured the air does not,
as a rule, find access to the pleura, but crosses the pleura and reaches the
subcutaneous tissue. The reason of this is very difficult to find, but of
the fact there is no doubt ; it need not, however, be considered here.
(ii.) Where the opening is a small one, so that the air finds easier
entrance than it finds exit. This condition will be the same as that in
which the air gains access to the pleura through the lung, and will be
better considered later.
(iii.) JVhere there is a large opening through the chest walls, at least as
large as the cross-section of the trachea. The air then enters and leaves
34° SYSTEM OF MEDICINE
the pleura without obstruction, that is to say, the pressure on both sides
of the visceral pleura is the same — ^namely, that of the atmosphere —
during all phases of respiration. Under these circumstances the elasticity
of the lungs comes simply into play, so that the lungs collapse.
It is no doubt true, as Bonders said, that in course of time under
these circumstances the lungs will become completely collapsed by virtue
of their own elasticity ; yet we have daily experience that this does not
usually occur, and when we consider the matter the reason is clear. It
is found in the fact which has already been stated ; namely, that the air
in the tubes is not subject simply to the atmospheric pressure during the
phases of respiration; on inspiration it is under a pressure somewhat
less than the atmosphere (by half a millimetre of mercury), and on
expiration under a pressure above that of the atmosphere (to the extent
of 1 J to 2 millimetres of mercury).
During expiration, therefore, the lungs will always be subject to the
distending force of IJ to 2 millimetres of mercury. There are no
observations to show how far the lung will be expanded under such a
pressure, but it cannot well be less than a half, and is probably more ; at
any rate we have daily demonstration of the fact that the lungs do not
collapse completely as the result of opening the side : on the contrary,
on opening the side for empyema it is a common experience to find the
lungs which have been completely collapsed by the effusion expand again
as soon as the pus is evacuated, so as to reach close to the chest walls
immediately after the operation. This may at first be the result of the
violent respiratory efforts or of the coughing which very frequently
follows the operation ; but this is not the only explanation, for it occurs
when there is no violent expiration or coughing, or persists when they
have passed off.
Two cases which I have recently recorded are of interest in this
respect, because the lung had been compressed by fluid for a long time —
eighteen months and five months respectively, one being a case of serous
effusion and the other of pyopneumothorax; in both, immediately after the
operation, the lungs were close to the chest walls, and within a week
had come into close contact with it everywhere except just round the
incision (3).
B. Where the air gains access to the pleura from the lung.
(i.) Theoretically it is possible that the opening through the lung
should be large enough for the air to pass freely in and out during
inspiration and expiration without obstruction ; yet this is a condition
which can hardly ever arise, and almost all the cases of pneumothorax
therefore come into the second category.
(ii.) That in which the opening through the lung is of such a kind
that though the air gains free entrance into the pleura during inspiration
it cannot find free issue from it during expiration. The result of this is
that during expiration the pressure rises and compresses the lung, which
gradually becomes more and more collapsed. Although it is true that
the mediastinum may be displaced to the maximum and the lungs
INTRAPLEURAL TENSION 341
be completely collapsed in cases where there is no expiratory compression,
still in the great majority of cases this rise of pressure during expiration
plays a very important part in the production of both these phenomena.
The division of pneumothorax into open, closed, and valvular, interest-
ing as it is in some respects, is of no practical importance from the present
point of view — that of intrapleural tension ; for in. a case of recent pneumo-
thorax as soon as the lungs are completely collapsed the hole becomes
closed, whether it be permanently sealed or not. During the early stages
pneumothorax is always ' more or less valvular ; in other words, the air
finds easier access during inspiration than it finds issue during expiration.
The intrapleural pressures during inspiration and expiration require,
in the case of pneumothorax, to be considered separately.
1. The inspiratory pressure. — When the lung has ruptured, air finds
access to the pleura during inspiration so long as the pressure in the pleura
is below that of the pressure in the air-tubes; that is, below the atmospheric
pressure : — although this has to be reduced, as already stated, by half a
millimetre of mercury, being the value of the obstruction which the air
meets with on its way into the lungs. The inspiratory pressure, therefore,
can never rise in pneumothorax above that of the atmosphere except under
one condition, namely, that in which there has been much dyspnoea ; for
as then the inspiratory efforts are considerable the air will consequently
continue to enter the pleura as long as the pressure at the end of each
inspiration is below that of the atmosphere and until it equals that of
the atmosphere, after which no more air can enter. It follows, therefore,
that if the patient survive and the dyspncea pass off, the inspiratory
pressure might be above that of the atmosphere to the extent of the
difference between the pressure on deep inspiration and the pressure
on ordinary inspiration. This is not very much, and in all probability
the excess of air, which represents the difference of pressure, is rapidly
absorbed.
In ordinary simple pneumothorax the inspiratory pressure is therefore
not, as a rule, above that of the atmosphere. If it be, some other factor
is required to account for it, and this almost without exception proves to
be the presence of fluid ; we may therefore conclude that whenever the
inspiratory pressure is much raised we shall probably find that fluid is
present as well as air.
2. The expiratory pressure. — The expiratory pressure in pneumo-
thorax is always positive. It is true that the mediastinum may be dis-
placed to its maximum in a case where the pressure in the pleura is zero.
Still the raised expiratory pressure tends to make the displacement ex-
treme or to produce it more rapidly ; while, as already stated, it is the
expiratory pressure which probably chiefly accounts for the complete
collapse of the lung.
3. The respiratory oscillation. — As this is the difference between the
pressure on inspiration and the pressure on expiration it will vary
according to the amount of dyspnoea or the violence of the respirations
at any given time.
342 SYSTEM OF MEDICINE
It might be thought, considering the violence of respiration in many
of these cases, that the respiratory oscillations would always be consider-
able. As a matter of fact this is not found to be so, and a little
consideration will show why this is the case; on the aflFected side the
chest is in a condition of maximum inspiratory expansion and cannot
alter from this on expiration ; while on the opposite side the lung is
prevented from expanding fully, by the amount of the reduction of its
volume on the displacement of the mediastinum and the organs connected
with it ; thus its elasticity also is reduced, being, as already stated, partly
satisfied. It is evident, therefore, that the total respiratory excursion of
the chest will be very considerably diminished and the respiratory oscillation
therefore small.
In a recently published paper (4) I have recorded a series of observations
upon the pressures in pneumothorax in eleven cases, some of which were
tapped several times ; so that there are records of twenty different
paracenteses.
The inspiratory presmre varied from zero to + 9, the several pressures
being 0, i, 1, 1|, 2i, 4, 4|, 5, 6^, 6^ 6|, 7, 8|, 8|, 9.
In two cases the inspiratory pressure was that of the atmosphere ;
that is, the reading of the manometer stood at zero. In both of these cases
fluid was present as well as air. From this it is evident that as soon as
the fluid formed the air must have been absorbed, since the opening into
the iung in both cases was closed.
In another case the inspiratory pressure, after having been in the two
first paracenteses positive, fell in the last two to zero ; and the change in
pressure was due to an opening of considerable size having formed into
the lung.
In all the other cases the inspiratory pressure was positive, and fluid
(sometimes pus, sometimes serum) was present as well as air ; thus the
statement already made is confirmed, namely, that when the inspiratory
pressure is much above that of the atmosphere the conclusion may be
drawn that fluid is present as well as air.
It is no matter of wonder that the inspiratory pressure rises when
fluid forms ; but it is surprising that the pressure is not much higher than
we find it. The highest pressure that I observed was nine inches of
water, but pressures as high and even higher have been met with in
serous eflFiisions. It follows, therefore, that when fluid forms in pneumo-
thorax a large amount of the air present must be absorbed as the fluid
forms.
We know, both as the result of experiments on animals and of opera-
tions upon man, as well as from observations of pneumothorax in man,
that air may be very rapidly absorbed from the pleura.
Even when fluid is present the pressure may not be above that of the
atmosphere, as we have already seen ; and . I think we may possibly
even go so far as to say that if the intrapleural pressure remains un-
usually high in pneumothorax it may be taken as an indication that
there is extensive disease both of the lung and the pleura ; so that the
INTRAPLEURAL TENSION 343
absorption of air which would ordinarily occur is prevented from taking
place.
The expiratory pressure also varied considerably from zero up to 13 J,
the actual figures being 0, 0, 1, IJ, 2 J, 2^, 4|, 5, 7, 8, 8|, 9, and 13 J.
The highest expiratory pressures are, as already stated, due to dyspnoea ;
that is, to violent expiratory efforts.
The respiratory oscillations in the same way showed great variations,
and fluctuated from zero up to 8. The largest were 8, 6f, 6|, 6, and 4.
In all these cases there was dyspnoea, and the large respiratory oscillation
was the result of the high expiratory pressure.
The lower respiratory oscillations were 0, J, \, 1, 1|, 1 j, and Z\.
Even where the inspiratory and expiratory pressures are high, the
respiratory oscillations may be small or absent ; thus in one instance
where the inspiratory pressure was + 9, the expiratory pressure was the
same, and the respiratory oscillation therefore 0. Per cordra even where
the inspiratory pressure is low, the respiratory oscillation may be con-
siderable if there be much dyspnoea ; for example, in a case in which the
inspiratory pressure was 0, the expiratory pressure was + 8, and the
respiratory oscillation therefore 8.
Where there is no dyspndfea the respiratory oscillations are apt to be
small, and may be completely absent.
These observations show that, in pneumothorax, whatever general
statements may be made, they have to be applied with caution in indi-
vidual cases, for it is impossible in any given case to forecast what the
actual pressures will prove to be ; and, finally, that although the results
obtained will have to be explained according to the peculiar circumstances
of each case, yet if this be done carefully, much information may be
obtained concerning the actual condition of the lung and pleura.
Intrapleural tension in serous effusion. — In health the pleural
cavity contains no fluid, and we often speak of it as dry ; yet this descrip-
tion is somewhat inaccurate, for there is in fact a constant circulation of
fluid into the pleura and out of it, the fluid being effused by the blood-
vessels and carried away by the lymphatics. The mechanism by which
this is performed has been described as "the lymphatic pump." It
consists of the lymphatic vessels with their stomata and valves, and is
worked by the respiratory movements. The course of the circulation in
the lung is from the pleural surface towards the root of the lung, as has
been determined by experiment ; and there is a similar circulation from
the pleural surface through the diaphragm and through the chest walls.
It is partly through the action of the lymphatic pump that the
negative pressure is maintained in the pleural cavity and the lungs kept
fully expanded.
There are two ways, therefore, in which fluid may accumulate in
the pleura : either it may be poured out into the pleura in larger
quantities than the pump can remove, that is, its amount may be
abnormal, or the amount of fluid not being above the normal, the pump
may be defective.
344 SYSTEM OF MEDICINE
In the case of pleural inflammation both these processes come into
play ; the amount of transudation is considerable, while the stomata and
smaller lymphatics are often plugged by deposits of fibrin. Thus in
inflammatory cases the fluid may accumulate with very great rapidity
and soon reach a large amount.
In the case of dropsy of the pleura consequent, let us suppose, on
heart disease, the explanation is probably also in great part mechanical.
Exudation under these conditions takes place from the blood-vessels into
the lymphatics of the lung, which become water-logged or choked ; thus
it is unable to carry oif the fluid from the pleural cavity, which 'conse-
quently accumulates in it. With dropsy, however, the accumulation of
fluid is much slower and the amount as a rule much less.
When fluid collects in the pleura it falls by its weight to the lowest
part ; and although the tension in the whole pleural cavity is diminished
in proportion to the amount of fluid present, still the effect upon the
different parts of the lung is different : thus the lowest parts suffer most
and become collapsed, while the upper parts of the lun(j remain dis-
tended ; yet the tension in the upper part of the pleural cavity is also
lower than it otherwise would be, as is shown by Calvert's observations.
The diminished tone in the lung or tetision in the pleura explains
the hyper-resonant note which is obtained in those parts of the lungs
which are floating upon the fluid.
In determining the intrapleural pressure in cases of fluid effusion
something will depend upon the seat of puncture. This Calvert has also
demonstrated; for if the mouth of the trocar be 1, 2, or 3 inches respec-
tively below the level of the fluid, there will be the pressui'e of a column
of fluid of this height to allow for. If, for example, the intrapleural
tension be equivalent to - 3 inches of water, and the amount of fluid
exuded into the pleura be sufficient to reduce this 3 inches negative
pressure to 2 inches negative pressure, it follows that if the mouth of
the trocar be 2 inches below the level of the fluid, a positive pressure of
2 inches will have to be added to the negative pressure in the rest of the
pleura, which will reduce the pressure-reading to zero ; or^ if the height
of the fluid be 3 inches instead of 2 inches, it would convert the pressure
at the point of puncture to a positive pressure of 1 inch. It is very
difficult to make due allowance for these variable conditions, so that the
pressure records in pleural effusions have not anything like the same
value as those in pneumothorax.
It might be supposed at first that with large effusions the pressure
would be high, with medium-sized effusions moderate, and with small
effusions low ; but actual observation shows that this is by no means the
case, for whatever be the biilk of the effusions the pressures may be high,
moderate, zero, or even below zero. Thus, among my own observations,
where the effusion was large and a considerable quantity of AxdA was drawn
off, the pressures were - 1, 2|, 4, 6, 8, 11|, and 18 ; where the effusion
was moderate - 1, 0, 4, 5, 8| ; and where it was small, 0, ^, 1\, 3, 5, 11.
The pressures, therefore, vary in a curiously irregular way, and it is
INTRAPLEURAL TENSION 345
difficult to see what the explanation can be. It is natural to attempt to
refer these variations to the different stages of the inflammation. Thus in
the early ingravescent stage, when the effusion is rapidly forming, the
pressures might be high, and low in the later stages when the fluid is
being absorbed. There is some evidence in favotu' of this view, but the
matter is by no means as simple as it would seem.
Bespiratory oscillations. — For the reasons- given when speaking of
pneumothorax the respiratory oscillation with serous effusion is likely to
be small ; as a matter of fact it is so, and not infrequently it is entirely
absent.
Now, as the action of the lymphatic pump depends upon the respira-
tory movements, and as these are indicated by the respiratory oscillations,
it is evident that in these cases the mechanism for the removal of the fluid
is at a standstill.
It is interesting to observe in some cases, though the respiratory
oscillation is absent when the puncture is first made, that after fluid has .
been withdrawn the respiratory oscillation begins to return, and at the
end of the operation may be fairly considerable. This is important, as it
explains what is often observed at the bedside, namely, that the removal
of a small quantity of an effusion may lead to the rapid spontaneous
disappearance of the rest. What it reaUy means is, that the lymphatic
pump has been set to work again. .
The intrapleural pressure in serous effusions is the resultant of three
forces : — 1. The respiratory movements. The effect of these has
been already sufficiently considered. 2. The force of inflammatory
exudation. We do not know much of the pressures under which the
exudation of inflammatory fluid takes place in the pleura ; but if we
may compare it with the knee-joint, which is more accessible to observa-
tion, we may be quite sure that it occurs under very considerable
pressure when we remember how tense the synovial sac becomes during
the early stages of inflammatory effusion. 3. The action of the lymphatic
pump is opposed to the first. We may presume that it is practically
equivalent to the elasticity of the lung, and therefore equal to 6 or 8
millimetres of mercury, when the lung is fully distended; but it is a
rapidly diminishing force as the lung becomes compressed, the stomata
closed, and the lymphatics collapsed ; and when the chest is full of fluid
it vanishes, for, as the respiratory oscillations show, the lymphatic pump
comes to a stop.
In the early stage of acute inflammation we may conclude that the
pressure may be very high when the effusion is a large one, or when
the 'effusion, if a small one, is encapsulated, that is, localised and not
general.
When the acute stage of the inflammation has passed and exudation
ceases, if the fluid begins to be slowly removed the pressure will fall ;
and • it is obvious, since the fluid is ultimately removed completely, and
the lungs come out into contact with the chest walls again, that in
course of time the pressure will even become negative. I do not see
346 SYSTEM OF MEDICINE
any way in which this can be brought about except through the inter-
vention of the lymphatic pump.
Intrapleural tension in empyema. — This is a much simpler prob-
lem than in the case of serous effusions. The pressures here are in
accord with what we know of suppuration elsewhere ; for the formation
of pus goes on under considerable pressure. It is only in the very
chronic so-called " cold " abscesses that the tension is low ; but even then
the pressure is probably above that of the atmosphere.
Thus among my own observations the pressure was considerably
raised in all cases, the lowest being + 3. The highest was +16, and
this was found with a very large effusion ; but, as I have said, small effu-
sions may have a very high pressure if they be loculated or encapsulated.
An interesting example of this was observed among the cases of serous
effusion ; for in one in which the pleura had been tapped twice, and the
pressure found on each occasion to be not raised, on the third paracen-
tesis the pressure was + 3 ; the effusion, however, was no longer serous, but
had become purulent: in other words, the general serous effusion had
been followed by a small localised empyema ; this was incised and then
recovery became complete.
The respiratory oscillation in empyema is always small and fre-
quently entirely absent.
From what has been said it is evident that the problem of intra-
pleural tension, especially under pathological conditions, is a very com-
plicated and difficult one, and requires much further investigation.
Samuel West.
KEFERENGES
1. Calvert. St. BaHhol. Sosp. Rep. 1892, p. 131.— 2. Other references :— vide
Researches of Loomis Laboratory, New York, 1890, and American Lancet, 1890, No. 11,
406. — 3. Garoand. Pneumodynamics. — 4. Pebls. Deutsch. Arch. f. Tcli/n. Med.
1869, vi. 1. — 5. West, S. Bradshawe Lecture 1887, reported in Brit. Med. Jour. — 6.
Idem. Med. Soc. Trans, for 1898, and Clin. Soe. Trans. 1898. — 7. Idem. Med.-Chir.
Trans, vol. Ixxxi.
s. w.
PLEURISY
The name Pleurisy {rj irXevpiTK voo-os, morbus lateralis, side-sore of
early English) formerly denoted that acute disease which is characteirised
by fever and severe pain in the side ; and the meaning of the word was
wholly clinical. After the time of Morgagni, when the influence of
morbid anatomy became predominant, the name acquired that anatomical
signification which it has since retained ; and for the last century or
more, pleurisy has been defined to mean inflammation of the pleural
membrane.
PLEURISY
347
I. etiology. — 1 . Age and Sex. — Pleurisy occurs at all ages : I
have evacuated pleural empyema in infants aged one month, three months,
and five months; and I^have drawn off three pints of serum from the
chest of a woman eighty-seven years old. The annexed table, drawn
up from the records of St. Bartholomew's Hospital for ten years (1884-
1893), shows the number of patients treated for pleurisy, and in whom
pleurisy was the main and foremost disease : it does not include the
cases in which pleurisy was secondary to some other disease no less
serious. The figures show : that pleurisy is much more frequent in
males than in females ; that pleurisy with effusion of coagulable
lymph or of serum (dilute liquor sanguinis) is most common in patients
between twenty and forty years old ; and that pleural empyema is
most common in patients less than ten years old.
Effusion.
Males.
Feinales.
CO
1
5 yrs.
and
under.
10 y.
15 y.
20 y.
SOy.
40 y.
50 y.
60 y.
Over
60.
1
Not \
purulent J
Purulent
466
155
186
61
48
48
25
53
59
32
50
15
54
22
179
48
149
17
85
23
35
6
15
0
651
216
Totals
620
247
96
78
91
65
76
227
166
108
41
15
867
2. Specific Poisons. — Pleurisy is due to irritation of the pleural
membrane by certain morbific microbes or poisons. It is difficult not
to believe that this proposition is universally true ; and true, even in
the case of pleurisy following upon an injury to the side, or upon
■exposure of the chest to cold, (i.) A heavy blow upon the chest, not
leading to more than bruising of the parts, and not bringing about any
solution of continuity, will sometimes be followed by constant pain,
and at length by serous effusion into the pleural cavity : in such a case
it is reasonable to suppose that the injury affords an opportunity for
infection, (ii.) Again, pleurisy, like pneumonia, will sometimes follow
so speedily upon great exposure of the whole body, or of the chest in
particular, to cold, that it is carrying scepticism to excess to doubt that
the exposure has something to do with causing the subsequent disease :
in this case, also, the cold may be supposed to bring about such an
altered nutrition of the parts as favours invasion by specific microbes.
But in by far the greater number of cases pleurisy is spontaneous,
and arises apart from the operation of any obvious antecedent cause.
Microbiology has thrown great light upon this spontaneous or idiopathic
pleurisy.'- The microbes which will account for most pleurisies are
three, — ^tubercle bacillus, streptococcus, and pneumococcus.
^ The following details concerning bacteriology are taken from an article by Dr. Netter
in the 4th vol. of the Traitl de mMecine, edited by Charcot, Bouchard, and Brissaud.
348 SYSTEM OF MEDICINE
(i.) Tubercle bacillus. — (a) Even before the discovery of the bacillus
of Koch, it was suspected that many cases of pleurisy with serous
effusion were due to tuberculosis of the pleura. But now it cannot be
doubted that tubercle is the commonest cause of pleurisy with serous
effusion, an opinion supported by the following facts : — Many of the
patients have inherited a tendency to tuberculous disease. Some of them
have suffered from manifest tuberculous disease before the pleurisy began.
Many of those who die are found by examination post-mortem to be tuber-
culous. Many of those who recover from the effusion suffer afterwards
from tuberculous disease, and especially from pulmonary consumption.
On the other hand, it is admitted that, even in cases which are un-
doubtedly tuberculous, bacilli are seldom found in the effusion, and cultiva-
tion of the fluid gives no result. Inoculation of the pleural serum into the
peritoneal cavity of guinea-pigs is more successful ; many of the animals
are infected thereby, {ji) Purulent effusion is less often dependent
upon tubercle. Empyema in a tuberculous subject is sometimes due, not
to the tubercle, but to streptococci or pneumococci : the distinction
depends upon microbiological examination.
(ii.) Pyogenetic streptococcus is the microbe most commonly found
in the pleural empyema of the adult. The morbific germ reaches the
pleura : — (a) Through the lung, in pneumonia, dilated bronchi, gangrene,
pyeemic abscess, tubercle, cancer ; (/3) through mediastinal organs, in
pericarditis, disease of oesophagus, abscess spreading from neck or throat ;
(y) through walls of chest, in penetrating wounds, abscesses, lymphangitis,
disease of breast, and especially cancer ; (8) from caries of vertebrae,
which is sometimes quite latent ; (e) through peritoneum, in peritonitis,
subphrenic abscess, suppuration of liver or spleen ; (f) through the blood,
in general diseases, scarlet fever, diphtheria, erysipelas. (7;) Adjoining
local disease sometimes seems to act as a mere irritant of the pleura,
and so to render it susceptible to purulent infection by the blood :
aneurysm of the aorta is an instance of this kind, the aneurysm itself
being possibly quite latent.
(iii.) Pneumococcus is the microbe most commonly found in the
empyema of childhood. In most of the cases it cannot be proved that
pneumonia preceded or accompanied the empyema, and this is especially
true with respect to children. In other words, primary pneumococcous
pleurisy is a common disease. When secondary to pneumonia there is
usually an interval of some days' duration between the defervescence of
the pneumonia and the occurrence of the symptoms and physical signs
of pleural effusion ; but sometimes there is no interval, the empyema
begins before the pneumonia has ended ; on the other hand, the
interval is sometimes much longer, several weeks or months. The
pleuritic effusion which is subsequent to pneumonia is not always
purulent, but is sometimes serous : in this serous effusion pneumococci are
found. Moreover, serous effusion, which is not secondary to pneumonia,
is due in a few cases to pneumococci.
(iv.) There are some other causes of pleurisy, but the specific manner
PLEURISY 349
in which they operate has not been discovered : such are superficial
haemorrhagic infarctus of the lung, nephritis, rheumatism, and gonorrhoea!
rheumatism.
II. Symptoms, that is to say, mgna, assidentia, are the signs which
are not pathognomonic or characteristic of the disease. Yet inasmuch
as these are the signs which the patient recognises, and which are,
therefore, the signs first recognised, they may be aptly discussed in the
first place.
1. Onset of the disease. — (i.) Latent. — The occurrence of one or more
of these symptoms marks the onset of the disease in most cases. But
in other cases the onset is not perceived : the disease at first is latent ;
and it is most likely to be latent when it is secondary to other serious
disease, the symptoms indicative of the onset of pleurisy being masked
by pre-existing symptoms dependent upon the primary disease.
(ii.) Manifest. — When the onset of the disease is not latent, the
indicative or invasion symptoms either (a) occur suddenly and decisively,
clearly marking the time at which the state of health passes into the
state of sickness ; or (/3) they occur gradually, so that it is not easy to
say precisely when the disease began. Whether they occur suddenly
or gradually, these symptoms, denoting the onset of the disease, are no
other than more or fewer of the symptoms which attend the confirmed
disease, and which will be described in the next place. The commonest
invasion symptoms are fever (with shivering or not), pain in the side,
vomiting, cough, quickness and shortness of breathing; in children
sometimes convulsions.
2. Fever. — Fever is not a constant symptom ; being slight and
temporary in pleurisy, with small innocuous exudation ; being present
in most, and yet not in all cases of larger effusion ; being absent
sometimes even in empyema.
(i.) In acute pleurisy the temperature seldom rises above 103°.
In pleurisy, as compared with pneumonia, the fever is not so high,
shivering at the onset is less common, and the duration of the fever is
indefinite.
(ii.) In chronic pleurisy no distinction can be drawn between serous
and purulent effusion by means of the characters of the fever, (a)
What is called serous effusion is not serous in the strict meaning of that
word, but is really a dilute lymph or liquor sanguinis ^ not free from
leucocytes. In pleurisy with serous effusion the temperature is often
(but not always) persistently raised ; and the fever not less or less
constant than that of a purulent effusion. When fever is present it
lasts until the effusion is wholly absorbed ; indeed, in cases of febrile
serous effusion defervescence is the best evidence that the effusion has
been absorbed, for physical examination is often of no avail in
determining this point. The type of fever tends to be quotidian
remittent. {^) In pleural empyema, when the pus is pent up or
^ A fact first recognised by B. G. Babington in 1830 : see Med.-Chir. Trans, vol. x-ri
p. 303.
350 SYSTEM OF MEDICINE
offensive, the temperature will be raised almost for certain. Evacuation
of the pus will be followed by defervescence, temporary or permanent.
In fistulous empyema the temperature is usually almost or quite natural ;
and a rise of temperature means that pus is pent up somewhere. The
type of temperature tends to be that of septic fever, namely, quotidian
remittent with evening exacerbation. Colliquative symptoms (heavy
sweats, and especially diarrhoea) sometimes attend the fever. Lastly,
in some cases of small empyema, even when undrained, the temperature
remains normal.
Local temperature. — That the affected side is sometimes hotter than
the other was known to ancient Greek physicians, who employed an
ingenious means of discovering the fact (see Hippocrates, De Morbis, iii.
chapter 16).
3. Fain. — Severe pain in the side was the main and constant sign
of the disease called pleurisy in the ancient sense of the word ; but the
pain of pleurisy, in the modern sense, may be severe, or may be not
severe, or there may be no pain at all. The pain is usually felt in the
side of the chest ; sometimes about the nipple, or above the clavicle, or
in the hypochondrium ; sometimes about the navel, or even in the iliac
fossa and lower belly, on the same side as the disease. The skin over
the affected side is often very tender. Marked spinal tenderness, in
some part of the vertebral groove in the dorsal region, is common.
The nature of the pain is a matter for debate ; probably there are
different causes of the pain. Intercostal or diaphragmatic cramp has
been suggested as an explanation of the stitch in the side. The pain
felt at a distance (namely in the abdomen) is probably conducted along
an intercostal nerve.
4. Dyspnoea. — Dyspnoea, manifested by frequent or laboured
breathing, is common. Patients kept in bed are apt to become ac-
customed to the want of breath, and so their dyspnoea may diminish
or even disappear ; although the quantity of pleural effusion (if present)
remain unchanged. Dyspnoea is in some cases greatly due to associated
disease, for instance, to chronic pneumonia on the same side as the
pleurisy. The dyspnoea of pleurisy without liquid effusion is chiefly
shortness of breath ; that is to say, inability to breathe freely and deeply
because of the pain caused thereby.
5. Cough and Expectoration. — Cough is usually present ; but in rare
cases there may be no cough, even in pleurisy going on to effusion.
Concerning the sputa. — The terms dry and humoral pleurisy, in
the old sense of these words, relate to the absence or presence of ex-
pectoration. For sometimes there is no expectoration, and therefore
no exspuition. But commonly there is expectoration, although the
humours coughed up are not always spat out. (i.) The sputa sometimes
consist of mucus nearly pure, judging from their colour and transparency :
when the mucus is thin and watery, like gum water, it is called pituitous.
(ii.) More often the sputa are mucopurulent, (iii.) More or less blood in
the sputum is not uncommon at the onset of the disease, (iv.) When
PLEURISY 351
an empyema has burst into a bronchus the sputa are almost pure pus.
(v.) It is a very uncommon event for a serous effusion to burst through
the lung, and so to be expectorated. Yet this seems to have happened
in a case narrated by Dr. Vincent Harris in St. Barthol. Hosp. Reports,
vol. xxiii. p. 34. Less uncommon is the muco-serous (or albumin-
ous) expectoration, which sometimes occurs during or soon after
paracentesis thoracis, and which will be described in connection with
that operation (p. 376). (vi.) Fcstid expectoration depends upon one of
two conditions : either a fcetid empyema has burst through the lung —
by far the more common case ; or a fcetid empyema, which has cer-
tainly not burst into the lung, communicates an offensive smell to the
secretions of the air-passages in the, neighbourhood, just as abscesses
near to the alimentary canal often acquire, for this reason, a disgusting
smell.
6. Vomiting and Diarrhosa. — Vomiting is common at the onset,
especially in children.
Diarrhoea is common in pleurisy with effusion, serous or purulent.
Diarrhoea sometimes occurs from the very onset of purulent pleurisy :
should vomiting, pain referred to the belly, and tenderness of the belly
concur with diarrhoea, peritonitis will be closely simulated at first sight.
This diarrhoea tends to be very obstinate, and in many cases cannot
be stopped until the empyema is cured. Diarrhoea and marasmus may
be the main symptoms of a small empyema. Should the patient die,
post-mortem nothing amiss with the intestines will be discovered by the
naked eye : it is a septic diarrhoea.
7. Septic infection of whole body. — (i.) Symptoms which are called
typhoid or putrid, and which are indicative of septic infection of the
whole body, are apt to accompany foetid empyema. The tongue is
dry and brown, the secretions become offensive to smell, the eyes
are yellowish, the face is dusky, the pulse soft and weak, conscious-
ness blunted, and muscular debility, or prostration, great, (ii.) Like
symptoms sometimes occur from the very onset of em.pyema which is
not foetid. In a state of good health sudden shivering occurs, headache,
cough, in some cases much pain in the side ; in others no pain at all.
The fever is high, the temperature often reaching 104° or more;
respiration frequent ; sputa not rusty. Consciousness becomes affected ;
in some cases so much that even as early as on the second day the
patient is deeply comatose ; but the degree of coma is apt to vary, so
that the patient, after deep unconsciousness, may become fairly sensible.
More or less delirium occurs in some cases, but in others none at all.
Morbilliform mottling of the skin (not much like the rash of typhus) ;
temporary redness, swelling, and tenderness of one or several joints;
enlargement of the spleen and diarrhoea may occur in some patients. The
urine may- be albuminous or not. The physical signs of effusion are
sometimes late to appear, and are apt to be mistaken for those of
pneumonia. The patient will die within ten or twelve days ; and whether
paracentesis be employed or not seems to make small difference. The pus
352 SYSTEM OF MEDICINE
has been found to contain pneumococci (21) ; but pneumococcous pleurisy
is seldom attended by these grave signs of universal poisoning.
8. Latent pleurisy. — Pleurisy is sometimes latent, in the sense that
the symptoms of the disease are slight, nay almost absent ; and this
even in the case of large effusion. But it is only in the neglect of physical
examination that pleurisy, unless its extent be very small indeed, can
ever be really latent.
III. Signs. — Signs which are pathognomonic, signs by which pleurisy
can, with certainty, be distinguished from other diseases, are of two
kinds ; namely, physical signs and the result of puncture. These
signs do more than this ; they enable us to distinguish two kinds of
pleurisy, which it is important should be distinguished ; namely, pleurisy
with exudation of coagulable lymph only, and pleurisy with liquid
effusion. Moreover, puncture enables us to distinguish the different
kinds of liquid effused.
A. Pleurisy with no liquid effusion. — 1. This condition often exists
unattended by physical signs of disease, or at most attended by signs
which are not distinctive ; such as some degree of retraction of the chest,
some loss of clear tone on percussion, some weakness of breathing
sound.
2. The only sign which is quite distinctive is friction sound. But
it is very far from being a constant attendant upon pleurisy, even when
the effusion is nothing more than coagulable lymph. Indeed it might
be said, and probably with truth, that even under these conditions
friction sound is more frequently absent than present. Friction sound
is to be recognised by its peculiar friction quality, giving the notion
either of rubbing to any degree between lightest grazing and harshest
scraping, or of creaking like that of leather. Friction is usually a very
local sound, heard over a small part of one side only ; and that part is
mostly where the rib movements are freest, namely, the lower part of
the chest, below the nipple or armpit, or about the angle of the
shoulder-blade.
B. Pleurisy mth liquid effusion. — 1. Before the effusion becomes
abundant enough to gravitate, a friction sound is sometimes (but
seldom) heard. Still more uncommon are signs which attend the
onset of pleurisy with effusion in rare cases, and which closely resemble
those of bronchitis. The distinction between the two diseases is
to be found in the fact that bronchitis very seldom affects one side
only, and that pleurisy with effusion very seldom affects both sides.
The signs referred to are these : — The affected side moves less freely
than the other ; the percussion note is raised in pitch and muffled over
the greater part or the whole of the side ; the sense of resistance to
percussion is increased ; the breathing sound is weak and attended by
widely-spread rale, which is quite indistinguishable from the rale of
bronchitis. This rale has been called friction-rale, thereby to indicate
the belief that the sound is produced in the pleural sac. But it seems
more probable that the rale really is a bronchial and mucous rale
PLEURISY 353
produced in the air-tubes, and that the catarrhal or bronchitic state of
the lung is due to its relaxation or deficient expansion consequent upon
the pleural effusion, small though it be. •■
2. Much more frequently, however, the earliest signs of pleurisy
with effusion are those which indicate that the effusion is already
abundant enough to have sunk to the lowest place. What constitutes
the lowest place depends upon the attitude assumed by the patient
while effusion is going on. At first, when the quantity is small, the
lung is simply relaxed by virtue of its own elasticity, and swims upon
the effusion ; but as the liquid accumulates, it compresses the lung and
renders it more or less empty of air.
(i.) The great sign of liquid effusion is a coextensive dulness to
percussion. This dulness is not wholly due to the effusion, but is
partly dependent upon associated collapse of lung ; that is to say, a
layer of liquid an inch or more thick would transmit percussion
resonance of the lung were the lung resonant. Dulness begins at the
lowest part of the chest behind, the note being natural elsewhere.
When the effusion has risen higher than the angle of the scapula, the
lung will have relaxed to such an extent as to give a clear tracheal ^
note above the nipple of the same side in front — a sign not always
present even in cases watched day by day from the onset. Whether,
by further increase in the quantity of the fluid, the whole back become
dull before the front is so at all, or whether the upper level of the
fluid be comparatively horizontal, depends upon the attitude assumed
by the patient while the efiusion is going on. Hence, when the effusion
is small the dulness may be wholly posterior, and sharply defined in
front by the posterior axillary line, the lateral region remaining reso-
nant. On the other hand, the upper limit of a dulness which occupies
the lower rather than the hinder part of the chest often rises higher
in the axillary region than in the back. Even when absolute dulness
is confined to the base, there is usually some impairment of resonance
all over the back on that side. The dulness over the effusion may be
far from absolute. The anterior clear resonance, when present, is
sometimes of cracked-pot quality. The effusion, even when partial,
does not shift its position easily or at all with changes in the position
of the body.
(ii.) In proportion to the amount of effusion the side is enlarged,
diaphragm depressed, and mediastinum displaced, (a) The side, com-
pared with the other, will possess these characters : shape, on horizontal
section, rounder ; antero-posterior diameter longer ; length from above
downwards diminished ; shoulder raised ; spine curved towards the
unaffected side. The antero-posterior enlargement becomes very obvious
when the physician stands behind the patient so as to look obliquely
over the shoulders and the front of the chest. Circumferential measure-
' What the Germans call " tympanitisoh.'' For the exact meaning of the technical
terms used in these pages with reference to percussion and auscultation, I must refer the
reader to my hook on those sulijects.
VOT,. V 2 A
354 SYSTEM OF MEDICINE
ments of the two sides are often made for the sake of comparison, but
be it remembered that, by the passage of the elliptical form into the
circular, considerable increase in the sectional area of the chest may occur,
whilst the length of the periphery remains the same. Moreover, the
displacement of the mediastinum thrusts the heart into the unaffected
side. Add this consideration, too, that the walls of the healthy side
must follow the antero-posterior projection of the diseased side ; and
then it will be plain why, as a matter of fact, the perimeter of the
affected side often measures very little more, nay, sometimes even less,
than that of the side which is not diseased. The cyrtometer, by
indicating shape as well as circumference, affords us the true means of
recording the amount of unilateral enlargement. (^) Displacement of
the mediastinum is indicated by displacement of the heart. Effusion
into the right pleura may displace the heart so as to cause its impulse
to be felt in the left axillary line, and in any interspace from the second
to the sixth. Effusion into the left pleura may displace the heart so as
to cause its impulse to be felt anywhere between its natural position
and the right nipple line, and in any interspace from the fourth to the
seventh, or in the epigastrium. When the impulse is felt to the right
of the natural position, it is often some part of the heart, other than
the apex, which strikes against the chest ; and this part is usually the right
conus arteriosus. When the heart is displaced to the right, there is, in
most cases, no considerable change in the relative position of base and
apex ; that is to say, the heart does not swing to the right upon its base
as a fixed point. Yet such a change in the attitude of the heart does
sometimes occur, and the very ventricular apex may beat in the right
nipple line. The displacement of the heart is often more or less than
might be expected ; for instance, it may remain unmoved by an effusion
of not less than a quart of serum into one pleura. Percussion of the
sternal region above the heart sometimes affords evidence of displace-
ment of the mediastinum : the upper part of the sternum naturally
yields a clear resonance ; under the pressure of a copious liquid effusion
into either pleura, the mediastinum bulges so much towards the un-
affected side as to afford absolute dulness to percussion in the sternal
region, and even somewhat beyond it. (y) Displacement of the dia-
phragm downwards is determined by ascertaining the position of the
liver, spleen, and stomach. When the quantity of fluid in the left
pleura is very great, the left half of the diaphragm may possibly be
depressed to such a degree that not only can the lower margin of the
spleen be felt, but even its upper margin, in fact its whole outline. At
the same time, the thrusting of the mediastinum and heart into the
right side of the thorax may depress the right wing also of the dia-
phragm to an almost equal degree ; a point ascertained by examination
of the liver.
(iii.) Vocal thrill is diminished where dulness to percussion exists,
and is wholly abolished in great distension of the side.
(iv.) The respiratory sound is at first weakly vesicular, and sometimes
PLEURISY 3SS
remains so throughout the disease. But often the breathing soon
becomes bronchial, sometimes even before the dulness becomes absolute.
With progressive increase of effusion the bronchial breathing tends to
become less and less loud, until, at last, it is wholly suppressed. But
sometimes, although the quantity of fluid be very great, loud bronchial
breathing is heard all over the affected side : the fact being that the
loudness depends, not inversely upon the quantity of liquor effused, but
directly upon the openness of the air-tubes; for liquid is a good conductor
of sound.
(v.) Vocal resonance is weak or bronchial in much the same manner
as the breathing sound. When the effusion is partial, with clear
resonance in front, the bronchophony is sometimes segophonic about the
angle of the scapula, ^gophony is a sign of little or no value. In
the first place, well-marked segophony is seldom heard ; next, it is some-
times heard over simple consolidation of the lung, such as is left by
absorption of pleural effusion ; and, lastly, segophony certainly does not
always attend thin layers of liquid in the pleural sac.
(vi.) By percussing the chest in front with two coins, and auscultating
behind as for the bell sound, a pleural effusion will sometimes be found
to transmit a clear metallic sound (penny sound, dgne de sou) quite
unlike that heard through healthy or solid lung.
(vii.) A small protrusion, in the lateral region, distended during
expiration, receding during inspiration, and due to perforation of the
pleura and intercostal space, may be met with even in moderate serous
effusion.
(viii.) A systolic murmur, having the characters of a pulmonary
obstructive murmur, sometimes concurs with pleural effusion ; dis-
appearance of the effusion being attended by disappearance of the
murmur.
C. Prnidwe. — Puncture of the chest, by means of a fine tubular
needle adapted to a small exhausting syringe, is the most decisive means
of determining the presence of pleural effusion. Moreover, puncture
ascertains the quality of the effusion. The bare suspicion of a pleural
effusion, however small it may seem to be, is a sufficient reason for
exploring the chest by puncture, inasmuch as we know that to pierce
the lung with a clean, fine needle is harmless.
Puncture is made where the signs of effusion are most marked ; due
regard being paid to the anatomy of the parts within, so as to beware
of wounding the heart, diaphragm, or great vessels. But, if possible,
let the puncture be made somewhere between the angle of the scapula
and the edge of the pectoralis major, and not much below the nipple level.
As matter of fact, the puncture is most usually made somewhere about
the angle of the scapula.
Puncture may lead us into error, (i.) In small, old empyemata the
enclosing walls are sometimes very thick, and it asks some faith in our
power of diagnosis to let us push the needle boldly through them so as
to reach the pus. (ii.) Pus is sometimes so thick that it will not pass
356 SYSTEM OF MEDICINE
through a fine needle : in this case a small quantity (less than a drop
perhaps) will probably have entered the needle, and can be blown out
and examined ; if there be pus, a larger needle must be used next time,
(iii.) Pus can sometimes be drawn from a bronchial tube, or from a
suppurating cavity within the lung, such as produced by tubercle,
destructive pneumonia, or actinomycosis, (iv.) The needle may draw off
pus from the pericardium or a subphrenic abscess, after perforating the
lung or the diaphragm.
D. Different hinds of liquid effusion. — It is by means of puncture that
the kind of effusion is discovered.
1. Serous effusion. — It has been already remarked that what is called
a serous effusion^ consists of diluted liquor sanguinis. The specific
gravity is usually from 1018 to 1024; but in proportion as the effusion
approximates to the nature of hydrothorax the specific gravity falls,
and it may be so low as 1006. Reaction, alkaline. Colour, yellowish
from serum-lutein. Proteids present : fibrinogen, serum-globulin, and
serum-albumin. A small quantity of sugar is often found. The liquid
is seldom or never quite clear and transparent. Opalescence, when
slight, is due to a few leucocytes, particles of fibrin, albuminous particles,
minute oil globules, cholesterin. When the turbidity is great the
effusion is called opaline or chylous, a condition which will be described
further on (see p. 357). The fibrin present coagulates soon after the
effusion is drawn off. The quantity of fibrin differs much in different
cases ; it may amount to no more than a few filaments floating in the
serum, or it may be so abundant as to coagulate into a firm jelly.
2. Purulent effusion. — Pleural empyema is probably such from the
first in most cases. Yet a serous effusion may possibly become purulent,
a change which is either spontaneous or the result of operation.
Spontaneously the change takes place slowly, a serous effusion becoming
gradually purulent in the course of about three weeks. When the
change is due to operation upon a serous effusion (that is to say, to
infection of the effusion by septic matters), suppuration occurs more
quickly, in a few days instead of weeks.
Pus is sometimes remarkably glutinous, so that, as it escapes during
paracentesis, it stands in a heap when drawn into an aspiration bottle.
Pus sometimes contains much gas in solution, so that it effervesces
in an aspiration bottle. Such pus is not necessarily offensive.
Pus is sometimes very foetid, and the cause is not always the same,
(i.) The cause is sometimes obscure, the pus is foetid from the first ; I
have known such a case to end in recovery after a single paracentesis,
without draining, (ii.) The cause is sometimes manifest ; the pus becomes
offensive through contamination with putrefactive microbes in such
manner as the following : — gangrene of lung, perforation of lung,
perforation from without (for example, an operation), perforation of
diaphragm by hepatic or subphrenic abscess, mere contiguity of an
offensive abdominal abscess without actual perforation. Foetid empyema
' Serum seu lympha coagulatilis, De Haen, Ratio Med. IV. cap. Iii. p. 74.
PLEURISY 357
Is sometimes associated witli — (i.) sloughing of pleural false membranes,
and even of the pleura itself (an offensive slough lying loose in the
empyematous cavity may be the cause of the foetor) ; (ii.) necrosis of
one or more ribs.
3. Blood mingled with effusion. — Not hsemothorax, which signifies
extravasation of pure blood into the pleural sac. The effusion, which
is bloody, is either serous or purulent, and the proportion of blood
differs much in different cases.
The conditions under which an effusion becomes bloody are these : —
(i.) Simple uncomplicated pleurisy, the haemorrhage being probably due
to rupture of embryonic vessels in the false membranes ; the hydrothorax
of heart disease ; the pleurisy of scarlatinal renal dropsy, (ii.) Acute
tuberculosis of the pleura, (iii.) Cancer, sarcoma, lymphadenoma of the
pleura, (iv.) Hsemorrhagic diathesis. The patient is sometimes markedly
aneemic from the loss of blood, sallow, cachectic. The prognosis
depends upon the cause, the fact of a bloody effusion in itself makes no
difference. Cancer of the pleura is by no means the most frequent
cause of bloody effusion, and the effusion in cancer is sometimes clear
yellow serum.
4. Opaline serous effusion. — The effusion is opaline, milky, in
consequence of abundant molecular matter suspended in it ; a few
leucocytes are often present, and sometimes a few red discs : these latter
may be numerous enough to give a reddish colour to the effusion.
Specific gravity the same as that of ordinary pleural serum. The con-
ditions of opaline effusion are these : —
(i.) Sometimes the opacity is really chylous ; for instance, if the
thoracic duct be torn across, so that chyle is effused into the right
pleura : in this case the molecules are all fatty, and rise to the top of
the effusion, like cream. Obstruction to the duct may possibly have the
same effect.
(ii.) But in most cases there is no reason for suspecting any lesion of
the chylous system. The particles are often by no means all fatty,
indeed very few may be fatty ; they seem to be some ill-known form
of proteid. Whence they come is quite uncertain ; disintegration of
pus globules has been supposed to be the source. Cholesterin crystals
may be present, usually very few, but now and then they are very
abundant, so that the opacity is chiefly due to them. No deduction
can be drawn, as to the nature of the pleurisy, from the fact of the
effusion being opaline.
E. Loculated empyema, or pleural abscess ; the purulent effusion not
occupying the whole of the pleural cavity, and being enclosed by ad-
hesions, the rest of the pleural sac being natural or obliterated by
adhesion.
1. The commonest seat of a circumscribed effusion is in the lateral
or posterior part of the lower half of the chest on one side. In this
case the diagnosis is easy enough by physical examination and puncture.
2. Loculated empyema sometimes lies between the base of the lung
3S8 SYSTEM OF MEDICINE
and the diaphragm ; mostly on one side only, but occasionally on both
sides, without communicating. The diagnosis depends upon the situa-
tion of the pain felt, namely, at the attachment of the diaphragm around
the lower margin of the thorax, upon immobility of the diaphragm and
liypochondrium on the ajBfected side ; upon increased resistance of the
hypochondrium to pressure ; upon the signs of more or less extensive
solidification of the base of the lung on the same side, in consequence
of collapse of the lung and associated congestion (a small empyema will
sometimes cause very extensive collapse, p. 368), indicated by loss of
percussion tone (now and then the tone is clear and tubular, the lung
being relaxed only), and weakened breath-sounds. The breathing is apt
to be painful and difficult. Diaphragmatic empyema is often associated
with subphrenic or hepatic abscess, and is often quite latent, found on
post-mortem examination only. When a loculated empyema of this
kind contains gas, diagnosis is often difficult (see page 370, Subphrenic
abscess).
3. Abscess between the lobes of a lung is less common. The pus is
very often discharged through the lung and expectorated, as early, it
may be, as three or four weeks from the onset of the pleuritic symptoms.
As a rule, it is only when the patient has begun to spit pus that the
disease can even be suspected ; physical signs, if any, are inadequate to
the diagnosis.
4. Empyema at the apex only of the pleural cavity is an uncommon
event, but one which sometimes occurs. Diagnosis is rendered all the
more diflHcult on account of the reluctance with which we make a
puncture in this dangerous region.
F. Pulsating Empyema. — That is to say, empyema which pulsates
rhythmically with the heart.
The empyema is commonly very large, occupies and fills the left
pleural cavity, (i.) The effusion usually points in one or two places,
which alone pulsate. This bulging occurs in the normal heart region
or in the lowest interspaces. In rare cases the protrusion has been
seen in the loin below the ribs. The bulging is never larger than an
orange. (ii.) Less commonly, the eflFusion nowhere points or bulges
through the chest wall. However, in these cases also, the pulsation is
usually limited to the normal heart region (to the left of the sternum),
or to the lowest three or four intercostal spaces. But sometimes the
pulsations are seen and felt over almost the whole of the left side.
Whether the empyema bulge or not, the heart is much displaced to
the right. Pericarditis may concur, but usually the heart remains
healthy. Auscultation of the pulsating part may detect conducted
heart-sounds. Palpation detects no thrill and no expansion like that
of an aneurysm.
Paracentesis very much helps the diagnosis. By removing part of
the liquid the pulsation ceases ; but the heart, being fixed by external
pericardial adhesions, does not return to its normal position. The
puncture needs not be made at .the spot which pulsates.
PLEURISY 359
The eifusion is mostly chronic, and the lung wholly collapsed.
Pneumothorax often concurs ; in this case, pulsation is conveyed by the
liquid only. The effusion is purulent in the great majority of cases,
but now and then a serous effusion has been known to pulsate.
Very seldom the empyema does not fill the whole pleural cavity, but
is loculated and enclosed in adhesions. This kind of pulsating empyema
always bulges ; it may be to the right of the sternum, but still in close
neighbourhood to the heart.
The diagnosis is from intrathoracic aneurysm, and from the very
uncommon condition of a pulsating cancerous tumour. Aortic aneurysm
and pulsating empyema may coexist.
Pulsating empyema is, in most cases, incurable.
IV. Course and Termination. — 1. Adhesions. — "When pleurisy
terminates favourably, it is by the formation of more or less extensive
adhesions between the opposed pleural surfaces, the pleural cavity being
proportionally obliterated. The patient has recovered, and it is assumed,
for this reason, that adhesion has occurred. Yet the recovery from
pleurisy without effusion, and even from pleurisy with effusion and
empyema, is often complete so far as physical signs are concerned ; and
the most careful examination fails to find contraction of the chest or
any other signs of past disease. If adhesion be attended by physical
signs, they are those which indicate unilateral contraction of the thorax
and imperfect expansion of the lung. The more marked these signs,
the more dense and tight may the adhesions be assumed to be.
2. Serous effusion. — (i.) Absorption. Serous effusion tends to be
spontaneously absorbed ; a large effusion may thus disappear in a week
or two.
The temperature, if it have been raised, usually remains raised until
absorption is complete.
The physical signs which indicate the progress of absorption are
these : — The diaphragm and mediastinum go back to their natural
position ; to follow the retreating heart, liver, and spleen is the best
means of marking the process so long as the quantity of effusion remains
great. The distension of the affected side becomes less, and accurately
to register this fact is an important service rendered by the cyrtometer.
When the effusion has so far diminished that the lung again comes into
contact with the chest wall, percussion usually enables us to follow the
falling level of liquid. And, at the same time, auscultation will some-
times inform us when and where actual contact of the opposed surfaces
of the pleura has occurred, friction sound being heard.
The manner in which the effusion is absorbed is not constant, but
usually the liquid disappears in something like the following order : —
From the vertebral groove near the root of the lung ; from the supra-
mammary region ; from the rest of the vertebral groove and infra-
scapular region ; from the inframammary region ; and, lastly, from the
lower lateral region, concerning which it is important to remember that the
lowest part of the pleural cavity, in the erect position of the body, is in
36o SYSTEM OF MEDICINE
the axillary line. Thus, the upper surface of the liquid, when it reaches
as high as two inches above the nipple level, is horizontal ; when lower
than this, the dulness forms irregular parabolic curves, which become
smaller and smaller, and last of all disappear in the lowest parts of the
thorax. But we must be prepared to meet with exceptions to these
rules, and to find the residue of liquid in almost any part of the chest.
Moreover, a large pleural effusion is sometimes absorbed, not from
above downwards, according to the rule, but equally all over the side
at once, friction or pleuritic rale becoming audible all over the side at
once.
Disappearance of effused liquid at any spot is sometimes attended,
for a day or two, by friction sound, indicative of restored contact between
the pleural surfaces, redux friction as it is usually called.
Dulness, practically absolute, and due to unexpanded lung, often
remains for a long time after all the effusion has been absorbed. For
this reason it is often impossible to say, from physical signs alone, when
th^ effusion has been absorbed. The physician must judge from all the
signs and symptoms taken together, and especially from permanent
defervescence, if the patient have been febrile. More or less dulness
often remains for the rest of life.
The latest physical sign, dependent upon absorption, is retraction of
the affected side. Cup-like sinking of the lower part of the sternum
occasionally ensues. In some cases these deformities tend to disappear
gradually, in others they are permanent.
A systolic murmur, having the characters of a pulmonary obstructive
murmur, sometimes concurs with pleural effusion ; disappearance of the
effusion being attended by disappearance of the murmur. A permanent
murmur of the same kind is sometimes heard when one side of the
chest is left contracted.
(ii.) Permanence. — If the whole lung be very much reduced in size
and quite inexpansible, a serous effusion will probably be permanent and
endure to the end of the patient's life. It is possible that, under these
circumstances, the chest walls may contract, and the mediastinum and
diaphragm be displaced to such a degree as to allow of absorption of
the liquid and obliteration of the pleural cavity; but these events seldom
happen in the case of serous effusion. The conditions of lung which
lead to its complete inexpansibility are two : carnification (see p. 368),
associated with tight, unyielding thickening of the pulmonary pleura ;
and contracting cancer, which may reduce the whole lung to a mass not
larger than the pancreas.
3. Empyema. — (i.) External rupture. — An empyema, left to itself, will
usually perforate the thoracic wall in course of time. The opening
mostly occurs in front ; a common situation is the fifth interspace in
the nipple line. But an empyema may point almost anywhere, from
just below the collar-bone to the loin or even the buttock. The first
effect of a pointing empyema in some cases is to produce what looks
like a mere subcutaneous abscess ; in fact an abscess of this kind over
PLEURISY 361
the ribs is often due to the perforation of a pleural empyema, even if
there be no signs of pleural effusion.
The course of an empyema (unless it be very small) which has been
allowed to discharge spontaneously through the chest wall, and which is
left to itself, is very tedious. If the opening close, it takes a long time
in doing so, but often it never closes. In either case the patient runs
the risk of a ruined state of health, complicated by lardaceous changes
in the viscera.
(ii.) Eupture through lung. — In this case a small hole, which allows
of direct communication between the empyema and a bronchial tube, is
made through the lung by ulceration ; or else, more seldom, the pus
filters through a small portion of lung which is spongy and penetrated
by many minute passages.
Empyema, which perforates the lung, is usually loculated, and often
so small and deeply seated that it cannot be detected by physical
examination. Such loculated empyemata often occur between the lobes
of a lung, or between the lung and diaphragm, or in the mediastinum
close to the root of the lung.
The expectorated pus is sometimes foetid, sometimes not. It is
sometimes foetid at first, and afterwards spontaneously ceases to be
foetid. In some cases the opened cavity contains air, in others not.
The microbe present is usually pneumococcus.
Eecovery often occurs, and in no great space of time, even when the
patient is left to the unassisted powers of nature, as is very often the
case, it being impossible to open a deeply-seated abscess by simple
paracentesis. Death may be very unexpected, the patient being choked
by the sudden discharge of a large quantity of pus into the air-passages.
Or death may be the termination of a long period of purulent expectora-
tion and gradual exhaustion of the patient's strength.
(iii.) Rupture into other parts. — Empyema will sometimes perforate
the pericardium, and in the case of pneumo-empyema the pericardial
sac may contain air as well as pus. The peritoneum may be perforated.
The empyema may discharge through the oesophagus. It is probable
that the cases narrated by older physicians, cases in which empyema has
been accompanied by a discharge of pus from the intestines or with the
urine, were really cases of empyema complicated with subphrenic
abscess.
(iv.) Incurable empyema. — Empyema is sometimes permanent and
incurable because associated with certain local conditions which prevent
recovery. The lung may be quite inexpansible, either carnified or
tightly bound by thickened pleura. Tubercle may have invaded the
lung extensively. When empyema follows upon pneumonia the
pulmonary inflammation sometimes is never resolved, the lung remains
hepatised, and if the patient live long enough the hepatisation will tend
to pass into cirrhosis. The corresponding branch of the pulmonary artery
may be closed by a thrombus. And, lastly, extensive necrosis or erosion
of the ribs may ensue, in which case the pus is not necessarily offensive.
362 SYSTEM OF MEDICINE
(v.) Great deformity. — More or less contraction of the affected side
is an almost necessary result of a healed empyema which has occupied
the whole or the greater part of the pleural cavity. When the lung is
totally unexpanded the contraction will be great, the spine much curved,
the mediastinum, heart, other lung, and diaphragm displaced towards
the affected side. In course of time the heart will become dilated,
especially the right chambers, and this is one way in which the patient
may die at last from the consequences of his empyema, even although
it may have closed long ago.
V. Associated diseases. — Pleurisy is often accompanied with other
diseases which impede or prevent recovery.
1. The pleura of the other side sometimes becomes inflamed, and the
patient suffers from double pleurisy. Eecovery, and quick recovery, is
not uncommon ; and even although the case be one of double empyema,
appropriate treatment will usually cure the patient.
2. Collapse of the lung on the other side may occur in an infant and
be necessarily fatal.
3. Gray indwration (fibrous change, cirrhosis) will sometimes ensue
upon collapse of the lung. But collapse may last for many years with-
out being followed by fibrous change, a fact proved by examination post-
mortem.
4. Gangrene of a portion of the lung may occur when foetid pus
penetrates it from an empyema — a serious complication.
5. Pneumothorax is often associated with pleural effusion, and in one
of two ways. Either the pneumothorax and effusion occur simultane-
ously, in consequence of rupture of the lung, in which case the effusion
is usually purulent, but may be serous ; or the pneumothorax is
secondary to the pleural effusion : an empyema has opened up a bronchus
by ulceration, or has discharged through the thoracic wall, or, what is
more common, a pleural effusion (serous or purulent) has been removed
by paracentesis, and air has passed out of the lung into the pleural
cavity, not through puncture of the lung, but through rupture of it by
atmospheric pressure from within.
6. Tubercle of the lung associated with pleurisy has been already
referred to. Also the fact that many cases of pleurisy are due to
tubercle of the pleura, the source of infection being, in some cases, the
bronchial glands, which lie at the root of the lung covered in places by
nothing but pleura. Tuberculous pleurisy is attended by exudation of
organisable lymph, or serum, or pus, or by hsemorrhagic effusion. But
pleural liquid effusion is sometimes concurrent with progressive
pulmonary consumption, a complication which cannot be detected by
physical examination until the effusion has been absorbed. Examination
of the sputa for bacilli affords the only means by which pulmonary
disease can be discovered during the presence of pleural effusion.
When, as is sometimes the case, the phthisis is on the side opposite to
that of the effusion, diagnosis is less difficult. More distant organs
sometimes suffer from tubercle during the course of pleurisy, and thus
PLEURISY 363
the patient's death may be hastened : the meninges of the brain are
especially apt to be so affected in the young. Lastly, this seems to be a
convenient place to say that a considerable proportion of persons who
have recovered from pleurisy become tuberculous afterwards, and die
within ten or twelve years from pulmonary consumption, or some less
common form of tuberculosis.
7. Pericarditis often coexists whether the pleurisy affect the left side
or the right. Sometimes, but seldom, perforation of the pericardium
has taken place. In any case pericarditis is apt to go on to large effusion
of serum or of pus. The pericardial effusion is usually not detected
during life, the physical signs of that condition being hidden by those
of the pleurisy. This is unfortunate, because the complication is very
serious, and the patients generally die. Pneumopericardium as a result
of pneumo-empyema has already been mentioned.
8. Peritonitis may concur. It is sometimes acute, purulent, and
speedily fatal. Or it is chronic, and in this case is often tuberculous,
ascites or universal adhesion being the result : the patient may recover
even after his pleural effusion has been complicated by ascites. The
certain diagnosis of acute and of chronic peritonitis is often impossible
during life. When ascites is present, the legs are sometimes anasarcous ;
this condition also may end in recovery.
9. Dilatation of the heart sometimes follows pleurisy, especially when
both pleurse are obliterated by old adhesions, and when the lungs are
imperfectly expanded. Under these conditions universal dropsy may
ensue.
10. Dropsy, that is to say, anasarca and ascites, sometimes occurs
even in acute pleurisy with effusion on one side only, there being no
evidence of nephritis or of disease of the heart, and the patient recover-
ing completely in about three months. In such cases the dropsy must
be due to stagnation of blood in the right side of the heart.
11. Nephritis, indicated by the appearance of blood and tube-casts
in the urine, sometimes occurs suddenly in the course of empyema under
treatment by drainage. The nephritis will probably last four or six
weeks and end in recovery. The cause is probably a morbid poison
produced by the empyema. That pleurisy and pleural effusion are
frequent complications of chronic nephritis may just be mentioned in
this place.
12. Abscess of the hrain is a consequence (not very uncommon) of
empyema. The abscess is usually single, and occupies either the
occipital or temporo-sphenoidal lobe : in a few rare cases many abscesses
have been found. The abscess sometimes bursts into the lateral
ventricle; and in this way even the subarachnoid space of the spinal
cord may become filled with pus. This cerebral abscess is probably
metastatic, and due to the transportation of a microbic embolus from
the thoracic disease ; but any other signs of pysemia are seldom observed
either before or after death : why the white matter of the brain
alone should be selected for embolism is unknown. The onset of
364 SYSTEM OF MEDICINE
cerebral abscess is very insidious ; for a long time the only symptom is
headache of varying severity, sometimes little, sometimes much : so far
as any distinctive symptoms go, the disease is latent. Towards the end,
a few days or a week before death, much more decisive signs of disease
are superadded to the headache ; namely, vomiting, optic neuritis,
general convulsions, coma. Or, as sometimes happens, the patient dies
very unexpectedly, without the occurrence of any grave warning
symptoms.
13. Hemiplegia due to softening of the brain is another possible
consequence of empyema. No doubt the softening is sometimes caused
by embolism of the middle cerebral artery ; the embolus being derived
from a thrombus which has formed in the heart or pulmonary veins
during the stagnation of the circulation which is a necessary result of
compression of the lung and displacement of the heart. Sometimes
hemiplegia occurs during or soon after paracentesis, a thrombus or a
portion thereof being dislodged during the commotion of parts which
must follow upon removal of much liquid. In rare cases this hemiplegia
is temporary, and the patient recovers in a few hours or days. But the
softening of the brain which causes hemiplegia is not always to be
explained by embolism ; it may be that no arterial lesions of any kind
are to be found after death ; and a local metastatic encephalitis, not
going on to suppuration, seems to afford the most probable explanation
(6a). Other symptoms may depend upon the softening, according to its
locality ; namely, aphasia and associated defects ; amaurosis, with a
natural condition of the retina. Or the softening may involve both sides
of the brain, with the consequences of general paralysis and dementia.
14. Lardaceous disease is a consequence which nowadays is seldom
met with. In this case the empyema is usually chronic and fistulous ;
but even a small empyema which has never been discharged may be
attended by this form of degeneration.
1 5. Clubbing of the finger - ends attracted much attention from the
ancient physicians. The symptom may be well marked at the end of a
fortnight from the beginning of an empyema. Clubbing will sometimes
disappear gradually when empyema has been cured.
Samuel Gee.
Morbid anatomy. — The pleural affection does not necessarily vary
with its exciting cause. Pleurisy, whether primary or secondary, may
present the same appearances both to the naked eye and to the micro-
scope. As in all serous inflammation, several factors are present :
hypersemia, proliferation, and desquamation of the endothelium, pro-
liferation of the sub-endothelial connective tissue cells, exudation of
fluid, and escape of leucocytes from the blood-vessels into the cavity,
the formation and deposition of lymph on the surface, and finally
the organisation of the lymph into fibrous membrane or adhesions. The
difference in different cases consists principally in the amount of fluid
and in the proportion of fibrin and leucocytes which it contains ; but on
PLEURISY 365
the one hand the same exciting cause may produce in one case a "dry"
pleurisy, in another a serous, and in a third a purulent effusion ; and on
the other hand these various forms may pass imperceptibly from one
into another. The driest pleurisy is attended with some fluid exuda-
tion, and the clearest pleural effusion contains some fibrin and some
leucocytes. These are, therefore, but stages in one process.
At the onset of pleurisy the surface of the membrane can just be
seen to have lost its polish ; and if the inflammation be more advanced,
the fingers also can feel a slight roughness. This is due both to endo-
thelial proliferation and to fibrinous deposit. If the disease go no
farther, these products may disappear, and the membrane show no sign
of the attack. But probably, in all cases which reach beyond the very
slightest degree, both the parietal and visceral surfaces become affected,
follow the plastic tendency of all serous membranes, and eventually form
adhesions with one another. The extent to which this takes place varies
from the production of a few fibrous threads to general adhesion of the
whole apposed surfaces.
If the inflammation be more intense, there is exudation of fluid con-
taining some fibrinous shreds. It varies from a few drachms up to an
amount sufficient to distend the chest and displace the viscera. The
amount of fibrin in it also varies greatly ; though produced wherever
the pleura is inflamed the fluid tends to collect at the lowest part.
Occasionally this tendency is counteracted by adhesions, so that a
fluid collection is limited to some other part of the chest than the base.
Where it lies it takes the place of the lung, which, thus relieved from
the suction of the chest wall, collapses beneath the fluid. When the
exudation is large enough to exert positive pressure in the thorax, the
lung is forcibly compressed also. While the fluid is effused, la vers of
lymph may at the same time be formed upon the pleura, and the mem-
brane thus formed may so swathe the lung that inspiration has not force
enough to expand it as the fluid is removed.
An originally serous effusion may become purulent ; but the great
rnajority of purulent effusions are probably purulent from the first. The
fluid in these cases varies greatly. It is sometimes liquid and laudable
with very little fibrin ; in others, and especially in chronic cases, the
fibrin may form large curdy masses ; in others, again, and especially in
those of a septic nature, the fluid is much thinner than pus. The
purulent or puriform effusion is usually inodorous ; but it may become
putrid when, by a wound of the chest or through the lung, access has
been given to the open air ; or when, as occasionally happens, the pleura
communicates with an abdominal abscess or with the alimentary tract.
Lastly, the effusion may be bloody or may be almost pure blood.
Pathogeny. — The exciting causes of pleurisy are manifold. Those
cases which are secondary to heart disease are, so far as we know,
mechanical in origin. Pleurisy occurring in the course of nephritis may
be of the same nature (2). But evidence is accumulating that under other
conditions pleurisy is directly due to microbes. Purulent effusions were
366 SYSTEM OF MEDICINE
the first to be studied from this point of view. Ehrlich found micrococci
in three cases of puerperal septicaemia with empyema. Eosenbach, Hoffa,
and Weichselbaum also verified their presence in all the cases of
empyema, eleven in number, which they examined. Kracht confirmed
this in ten cases. Frankel examined twelve cases ; in three cases of
primary pleurisy he found the streptococcus pyogenes ; in three the diplo-
coccus pneumoniae ; in four which were of tuberculous origin he discovered
the tubercle bacillus in one alone, the others giving negative results ; and
in two cases secondary to other abscesses he again found the strepto-
coccus. Meanwhile the influence of tubercle bacilli in the causation of
pleural effusions, whether serous or purulent, on which great stress had
been laid by Landouzy from the clinical point of view, had been studied
by Kelsch and Vaillard, Gombault and Chauffard, and Gilbert and Lion.
They were not very successful. Kelsch and Vaillard, inoculating in
animals, could only reproduce tubercle from two out of four empyemas,
and from one out of ten serous efiusions. Gombault and Chauffard
failed nine times and succeeded eight times. Gilbert and Lion failed
altogether in twenty cases. Levy examined fifty-four cases, of which
thirty -seven were serous, seventeen purulent efi'usions; six were
secondary to typhoid fever, of which three contained staphylococcus
pyogenes, and three were negative ; nineteen were secondary to
pneumonia, broncho-pneumonia, or influenza, of which three were nega-
tive ; fourteen revealed diplococcus pneumoniae, and two contained the
staphylococcus ; in one of these also the diplococcus was found. In
fourteen tuberculous cases Levy failed to find the tubercle bacillus. In
one case secondary to rheumatism, and in seven secondary to heart
disease, nephritis, and cancer, the result was negative ; but in one
haemorrhagic effusion secondary to infarct of the lung and in six other
mixed cases the staphylococcus was present. Eenvers and Prince
Ludwig Ferdinand confirmed these results. Pansini in fifteen serous
effusions had five negative results, but found tubercle bacilli six times,
diplococcus thrice, and streptococcus or diplococcus once ; in eight
empyemas he found tubercle bacilli thrice ; and in all but one of the rest
the strepto-, staphylo-, or diplococcus. In one sanguineous effusion
he found the tubercle bacillus. Netter (13) examined 109 cases of
empyema : the diplococcus was present twenty-nine times alone, thrice
with streptococcus ; streptococcus was found alone in forty-eight cases,
and staphylococci in two cases. Of fifteen cases of foetid effusion sapro-
phytic organisms were found in all, and of twelve tuberculous cases the
tubercle bacillus was present in six. He points out the much greater
benignity of the diplococcus, and explains by this fact the more frequent
recovery of children; for of twenty-eight cases in children the diplococcus
was present alone or with the other two cocci in fifteen — a rate of 53
per cent, which is exactly that of the streptococcus in adults. In
a second paper (14) he stated that he had been able to produce tubercle
by inoculating guinea-pigs with the serous effusion drawn off by a Pravaz
syringe in seven out of twelve cases which could be diagnosed clinic-
PLEURISY 367
ally as tuberculous, and in eight out of twenty cases of " idiopathic "
pleurisy. Koplik gives confirmatory evidence of cases in children.
Sacaze found tubercle bacilli at the beginning of a serous effusion,
but failed to produce it later ; which result throws some light on the
difficulty always encountered in showing its presence, even when clinical
evidence of a tuberculous process is strong. Hanot discovered the
bacillus in a hsemorrhagic effusion (7) (21).
Both serous and purulent effusions, when primary, are therefore due
to the three micrococci mentioned, and to the tubercle bacillus ; and
this so frequently, that as observers become more skilled this rule will
probably be found universal. More than one of the above authors
venture to state that where micrococci are not present the case will
almost always prove to be tuberculous. Hsemorrhagic effusions when
not due to cancer or to some rarer cause are also probably tuberculous.
The pathology of rheumatic pleurisy is as yet unknown ; and the
same may be said of the pleurisy which French authors (1) describe as
occurring in the secondary stage of syphilis.
W. P. Hereingham.
VI. Diagnosis. — ^Pleurisy is simulated by certain other diseases in
respect either of symptoms or of physical signs.
1. The pain of pleurodynia is, by itself, indistinguishable from that
of pleurisy. Diagnosis becomes possible when there are other signs or
symptoms of pleurisy ; for pleurodynia is mere pain, and pleurisy is
sometimes indicated by pain alone.
2. The rale (not friction sound) which in rare cases attends the
onset of pleurisy closely resembles the rale of bronchitis (see p. 352).
The difference lies mainly in this, that the rale of pleurisy tends to be
heard over one side only of the chest, and the rale of bronchitis over
both sides. Pleuritic rale is soon superseded by other signs of pleurisy.
3. Acute collapse of extensive portions of lung is a condition which is
very apt to occur in young children as a result of obstruction to a
bronchial tube.- The case of obstruction by an inhaled foreign body
need not be considered here, for the whole course and symptoms of this
accident are not at all like those of pleurisy with effusion. But bronchial
catarrh, and even slight bronchial catarrh, will sometimes cause exten-
sive collapse in a young child, or in a very feeble patient who is not a
young child. Bronchitis setting in suddenly, with fever, cough, tight-
ness of the chest, vomiting, and followed in a day or two by the signs
of collapse at the lower part of one lung (namely, dulness to percussion
and weak breathing), counterfeits pleurisy with effusion very closely.
Diagnosis may be impossible at first. Usually the catarrhal infarct
soon clears up ; if it be deemed necessary a puncture may be made.
4. Chronic collapse of lung and Cirrhosis are two conditions which
closely resemble each other in the living subject, and which often can-
not be distinguished excepting upon the post-mortem table. Nor is it
of any practical importance that they should be distinguished ; the
368 SYSTEM OF MEDICINE
useful term carnification (invented by Laennec) may be taken to include
them both. Tbe physical signs of carnification of the lower lobe of a
lung and those of a small pleural effusion are the same, excepting that
the chest may be distended on one side, and the heart be displaced away
from the disease in some cases of local pleural effusion. But now and
then the chest is contracted and the heart not displaced even in a pleural
effusion. The symptoms afford no help to diagnosis, and the right
understanding of a case may be rendered all the more difficult by the
fact that carnification is not only a constant result of pleural effusion,
but often persists long after the effusion has disappeared (see p. 360).
The chief means of distinguishing between the two conditions is
puncture. Yet, under these circumstances, puncture sometimes fails to
detect pleural effusion, and chiefly for this reason, that carnification is
often much more extensive than the effusion which causes it. For
instance, a small pleural effusion, lying upon the diaphragm or in the
posterior mediastinum, will sometimes be attended by collapse of the
whole lower lobe of a lung ; and this carnified lung being the only
portion of disease which is in contact with the chest walls, the physical
signs will be wholly dependent upon the carnification, and if puncture
be made it cannot hit the effusion unless the needle go right through
the lung. Wherefore it may be impossible to say whether there be an
effusion or a mere carnification. Sometimes the expectoration of a small
empyema occurs so as to clear up our doubts.
5. Titberculous phthisis of a lower lobe resembles a small pleural
effusion in many respects which it seems hardly necessary to enumerate;
puncture and microscopic examination of the sputa are the most trust-
worthy means of distinction. But there is an especial form of pleurisy
which, for a time, is indistinguishable from pulmonary tuberculosis. In
this case the pleurisy involves the whole of one side, which is retracted,
it may be considerably, and moves much less freely than in health. The
percussion note is raised in pitch and muffled over the greater part or
the whole of the side ; the sense of resistance is increased ; when the
disease affects the left side the superficial area of cardiac dulness is
extended. The respiration generally is weak, and attended by friction
sound at some part, or by widespread rale indistinguishable from the
mucous rale of catarrh or phthisis (see p. 352). At places the breath-
sound may be bronchial, in all degrees of intensity, up to perfect
cavernous resonance. Add to these signs hectic fever with diarrhoea
and vomiting, and it is easy to understand why pleurisy of this kind is
apt to be mistaken for phthisis more or less advanced. The pleurisy
terminates in one of two ways. Either the physical signs of disease
gradually disappear, excepting perhaps that a slight unilateral retrac-
tion of the chest, or a cup-like depression of the sternum, is left behind,
the patient recovering at the same time his former state of health ; or
signs of a small effusion slowly appear at the base, and, when the chest
is punctured, a little pus is withdrawn and the case comes into the
category of empyemi. Whenever the signs of a case of supposed
PLEURISY 369
phthisis are in some respects peculiar ; whenever they indicate advanced
and extensive disease, but limited to one side of the chest; whenever
cavernous signs are heard in unusual places ; — it is well to weigh the
possibility of simple pleurisy, and not to rest confidently in the
diagnosis of phthisis until tubercle bacilli have been found in the
sputa.
6. Acute pnewmonia is seldom mistaken for pleural effusion unless
the tubes of the pneumonic lung be so plugged with mucus that conduc-
tion of the breath-sounds is obstructed. It much more often happens
that a small pleural effusion is mistaken for pneumonia. The physical
signs of the two diseases may be the same, and even puncture is not
always decisive ; should an empyema be confined to the apex of a pleural
cavity, so infrequent an occurrence, compared with the frequency of
apex pneumonia, will render diagnosis unusually difficult (see p. 358).
The symptoms of the two diseases may be the same, especially in the
pleurisy which is due to pneumococcus (see p. 352) ; not seldom in this
case the patient dies before certain diagnosis becomes possible : a
physician well read in the book of nature knows that he cannot always
distinguish between pleurisy and pneumonia.
Chronic pneumonia — that is to say, hepatisation slow to resolve — will
resemble in many respects pleural effusion supervening upon pneu-
monia.
7. Malignant twnour of the lung closely resembles pleural effusion
in respect of the physical signs. A tumour does not often cause
. enlargement of the affected side, or displace any organs^ yet now and
then a quickly growing tumour will produce these effects. When dul-
ness begins not at the bottom of the chest ; when there is a great extent
of absolute dulness in front and none behind ; when, in the midst of a
great extent of dulness, we detect one or more small insulated patches
of resonance (perhaps quite clear or even cracked-pot), we may debate
the existence of solid tumour. The crucial test is puncture.
A large serous effusion (see p. 362) is sometimes the necessary result
of contracting cancer of the lung. The nature of the case may be
suspected if cancer can be discovered elsewhere, and especially if large
hard glands can be felt above the collar-bone or in the armpit. '
8. A large hydatid cyst will yield most of the signs of pleural effu-
sion ; namely, unilateral distension of the chest, displacement of the
diaphragm and mediastinum, dulness to percussion, and weak or absent
breathing sound. An exploratory puncture is the most decisive means
of diagnosis ; the fluid of hydatid being free from albumin and more
watery than that of pleural effusion, to say nothing of the possible dis-
covery of echinococcus hooks. But if the hydatid have suppurated, the
nature of the disease is sometimes not suspected until a fre6 opening has
been made, such as to permit the escape of hydatid membrane. (For
full discussion of Thoracic Hydatid, vide vol. ii. p. 1137.)
9. Actinomycosis of the base of the lung simulates pleurisy with
effusion, and is, indeed, sometimes attended therewith. The diagnosis
VOL. V 2 b
370 SYSTEM OF MEDICINE
cannot be made until the fungus is discovered in the sputum, or until
the growth perforates the wall of the chest i^tnde vol. ii. p. 81).
10. Subphrenic abscess is much more common on the right side than
on the left, for reasons which become clear when the antecedents of the
abscess are considered. It is often, if not always, associated with
pleurisy on the same side, and usually with empyema, due to perfora-
tion of the diaphragm or not. Hence empyema on the right side
in a person who has probably suffered from tropical hepatitis, from
simple or cancerous ulcer of the stomach, or from other causes of sub-
phrenic abscess, should always lead us to reflect upon the possible
coexistence of this disease. The pus of subphrenic abscess and of the
empyema is foetid. The abscess, even if there be no empyema, may
burst into the lung, and lead to expectoration of most offensive pus.
Whether there be an associated thoracic empyema or not makes little
difference so far as the physical signs of a subphrenic abscess are con-
cerned ; for the empyema is local, enclosed in adhesions, and not nearly
filling the pleural cavity. The signs are both abdominal and thoracic,
sometimes more the one, sometimes the other. The abdominal signs
are : (a) fulness and tightness in the hypochondrium ; (b) the liver
depressed, sometimes, but by no means always ; moreover the liver is
sometimes much depressed in uncomplicated thoracic empyema. The
thoracic signs are : (a) dulness to percussion and signs of pleural
effusion at the base, whether there be a pleural effusion or not ; in the
latter case the diaphragm is much pushed upwards, and the lung pro-
portionally collapsed : (^) the heart's apex beat is sometimes displaced
even in subphrenic abscess without empyema, but more often is not
displaced. Puncture, made as for pleural effusion, will probably reveal
the presence of pus, but will not tell us whether the pus is
above the diaphragm or below it. Uncomplicated subphrenic abscess
may be mistaken for simple thoracic empyema, even after the abscess
has been emptied of pus by aspiration ; the needle having gone right
through the diaphragm, which has been pushed much upwards, as high
it may be as the third rib. Even resection of a portion of a rib, and
exploration of the pus cavity by the finger, do not always enable us to
say at first whether we have opened a cavity above or below the diaphragm ;
or, in the former case, whether the diaphragm be perforated or not.
Subphrenic abscess often contains gas derived from perforation of
the alimentary canal or from decomposition. In this case the disease is
apt to escape discovery by physical examination, because there is no
dulness to percussion. Sometimes the percussion note is clearer than
natural ; and sometimes the clear note is more extensive also, so that
the liver dulness disappears. The resonance may possess amphoric
quality. Auscultation usually detects one or more signs of a large
cavity containing air ; namely, amphoric hum (attending the sounds of
breathing, speaking, and of the heart), metallic tinkle, bell sound, and
succussion splash. If the diaphragm be perforated, the empyema will
be a pyopneumothorax.
PLEURISY 371
11. It is sometimes hard to decide whether /riciiow sound, heard over
the heart region be plev/ral or pericardial. Pleural friction may be
produced by movement of the heart alone ; as pericardial friction may
be under the influence of breathing movements.
12. Large effusion into the left pleura may cause bulging of the
chest in the heart region, such as to raise the question of concurrent
pericardial effusion; for the two diseases are often associated (see p. 369).
The diagnosis depends mainly upon the result of emptying the left pleura
by paracentesis, whereby alone can the signs of pericardial effusion
become manifest. When a rib has been resected in the treatment of
empyema, the finger passed into the pleural cavity may possibly be able
to feel a bulging pericardial sac.
13. When pericardial effusion is attended by extensive collapse of
lung, and the chest is punctured with a view to determine the cause of
the dulness, the needle may go right through the lung and discharge
liquid from the pericardium ; and, until examination post-mortem, the
physician may rest in the unshaken belief that the liquid came from the
pleura.
14. The manner in which pulsating empyema counterfeits aneurysm
has been already referred to (p. 358).
15. An abscess in the thoracic walls may be the only evidence of a small
empyema (see p. 360) which has penetrated an intercostal space. Even
when the abscess has been opened it is not always easy to say whether
it communicates with the pleural cavity or not. It is possible that
pleurisy may be the cause of abscess in the thoracic walls without
actual perforation of the pleura. But more commonly parietal abscess
(as distinguished from pointing empyema) is due to such causes as
injury, pyaemia, periostitis of a rib, or necrosis of the same ; and this
" peripleuritis " may perhaps sometimes set up pleurisy. Lastly, in
all cases of superficial abscess the question of actinomycosis must be
pondered.
VII. Prognosis. — It seems to be unnecessary to reiterate many pro-
gnostics, which will be found in their appropriate places in the foregoing
and following pages. But one fact of great importance demands special
attention, namely, the occurrence of unexpected and speedy death in
cases of pleural effusion. The conditions of this unexpected death are
not always the same.
(i.) The sudden rupture of an empyema (and it may be quite a small
empyema) into the lung is sometimes sufficient to suffocate the patient
in a few minutes.
(ii.) Much more often the death occurs apart from any discharge of
the efiusion. The effusion is usually large, filling up the whole or greater
part of the pleural cavity. The effusion is usually serous. Whether it
be on the right side or on the left makes no difference. Suddenly, and
often after a little exertion, the patient is seized with dyspnoea or faint-
ness, or both. The lipothymial symptoms soon predominate ; the skin
becomes cold and clammy or sweating, the face and lips assume the wan,
372 SYSTEM OF MEDICINE
dusky, livid colour of a dying person, the pulse is small and irregular ;
death ensues within half an hour or an hour. The explanation of the
speedy death is mostly found post-mortem in thrombosis, of the right
side of the heart, consequent upon stagnation of the circulation through
it, dependent upon the collapsed state of the lung. This heart thrombus
has one of two results : either the thrombus is propagated into the
pulmonary artery, and thence into that branch of it which supplies the
unaffected lung; or an embolus, derived from the heart thrombus, is
driven into the pulmonary artery, or a large branch of it. But throm-
bosis meet to explain the death is not always found ; sometimes a
latent pericardial effusion is present ; but sometimes nothing sufficient
can be found, and in cases of this kind hypothetical explanations have
been offered, such as twisting of the large vessels at the root of the
heart, bending of the inferior vena cava at an acute angle, compression
of one auricle of the heart, degenerative changes in the muscular tissue
of the heart.
(iii.) Frothy serous expectoration sometimes suffocates the patient
during or soon after paracentesis of the chest (see p. 376) ; or, in very
rare cases, may even supervene upon large effusions apart from
paracentesis.
VIII. Treatment. — ^A. In the treatment of pleurisy with no liquid
effusion, the main indication special to the disease is to relieve pain.
The most effectual means of doing so are two : subcutaneous injection of
morphia at the seat of pain, or the application of a few leeches. In
many cases much less decisive means are sufficient : warmth by hot-
water fomentations or linseed-meal poultices ; a mustard poultice, or a
turpentine fomentation.
B. The treatment of pleurisy with effusion relates almost wholly to
removal of the effusion.
When the effusion is believed to be recent, not large, and not
purulent, it is best to defer operation for a week or two, so as to see
whether the liquid can be removed spontaneously without operation. It
is probable that absorption may be assisted by sundry means : iodide of
potassium in moderate doses should be given ; the affected side of the
chest should be painted with tincture of iodine two or three times a day ;
blisters, the size of the palm of the hand, or less according to the size of
the patient, may be employed, one blister at a time, and the sore
allowed to heal as soon as possible. In the case of children blisters
should not be used.
But the question of paracentesis is always foremost in the mind, and
may be discussed under four heads : when, where, and how the operation
should be performed, and, lastly, certain dangers which sometimes attend
the operation. The age of the patient is never taken into consideration.
I have treated successfully by paracentesis patients three months old
and eighty-seven years old.
I. When should paracentesis he performed ? — The answer to this question
depends upon the quality of the effusion.
PLEURISY 373
1. Pus must be removed as soon as possible. If it be bloody, or if
the pleura contain air as well as pus, the same rule holds good. Free
evacuation of pus may be expected to bring the patient's temperature
down nearly or quite to the normal ; if this be not the result, we may
assume that there is some retention of pus. Any subsequent rise of
temperature, after a fall to the normal, will most likely be due to im-
perfect drainage. But perfect drainage cannot always be attained,
especially when a small quantity of pus is secreted in an inaccessible
cavity shut off from the rest ; in cases of this kind time usually sur-
mounts the difBculty, the retaining lymph breaking down under per-
sistent drainage.
2. Serum should be removed by paracentesis in all cases which
present an effusion so great as to fill the pleura, or which are attended
by any distress of breathing, or which show no signs of being absorbed
after a week or ten days of the other treatment already described.
II. JVTiere should paracentesis be performed ? — 1. When the effusion is
small the puncture must be made where the effusion is believed to be.
2. When the eflrasion is great, so that the pleural cavity is full or
almost full, the best place for puncture is in the middle line of the
axillary region, about the horizontal level of the nipple or a little below
it, where the intercostal spaces are wide and the muscular integuments
thin. Another part of the chest which is often chosen for puncture is a
spot just below the angle of the scapula, but the lung is sometimes
adherent to the chest wall here, and will therefore be pierced by
paracentesis ; in this case pneumothorax is apt to ensue, and, what is
a result far worse, but less frequent, sloughing of the perforated lung.
Probably no part of the chest can be chosen as being entirely free from
the risk that paracentesis may perforate collapsed and adherent lung,
but the risk is less at the spot first recommended for the place of puncture
than at any other situation.
III. Sow should paracentesis be performed ? — 1. Serous effusion should
be removed by means of a trocar and canula. Whether suction be
employed or not is, in most cases, a matter of no great consequence. If
suction be not employed, a canula connected with a long india-rubber
tube should be used, the free end of the tube being kept under liquid,
so that no air can enter the chest. On the whole, suction is to be pre-
ferred, for in this way small obstacles due to fragments of lymph
floating in the serum can be overcome. It is best to make no more
vacuum than is necessary to maintain a gentle flow of liquid. As much
liquid is to be drawn off as possible without causing any serious
discomfort to the patient. Suction is to be stopped if the flowing fluid
become bloody, if the patient feel much pain in his chest, or if he
begin to cough much; in which last case, there is the risk of serous
expectoration (p. 376).
The pain of puncture is diminished if the skin be previously frozen
by ice, or by an ether or chlorethyl spray.
It happens sometimes, but not often, that the most powerful suction
374 SYSTEM OF MEDICINE
can extract no more than a small quantity of the effusion. The usual
cause of this difficulty is found in a fragment of lymph which blocks the
canula or obstructs its orifice. But sometimes, even when the effusion
is free from floating lymph, it is impossible to evacuate the chest. Cases
of this latter kind, which are uncommon, are probably to be explained
by a lung rendered inexpansible by thickened pleura or by obstructed
air-tubes. Nothing more can be done than to draw off as much serum
as possible, and to repeat the paracentesis in a day or two.
Very often a single paracentesis cures the patient, the little liquid
left being soon absorbed. But sometimes the effusion returns, and the
rule of practice is to repeat the operation as often as seems necessary.
In rare cases an abundant effusion will continue for an indefinite time,
but even then the only treatment is paracentesis repeated as often as
necessary. Drainage by a permanent opening is out of the question,
and would be certain to convert the serous effusion into empyema, to
the great danger of the patient's life.
There is no reason for fear lest paracentesis alone and without
drainage should convert serous effusion into pus, provided that all the
instruments used be surgically clean.
2. Empyema is to be treated by incision and drainage.
(i.) When the quantity of pus is not very large it is best to make a
permanent opening and drain at once. In some cases thorough and
speedy drainage cannot be obtained unless a large opening is made by
excising a portion of one of the ribs ; and, therefore, to avoid all doubt
upon this point it is good practice to resect a rib in all cases.
(ii.) When the empyema fills the pleural cavity it is safer to remove
as much of the pus as possible by paracentesis at first, and to make the
incision a day or two afterwards. The sudden discharge of a very large
quantity of pus from the chest causes a great shock to some patients,
and previous paracentesis lessens the shock. Paracentesis, and some-
times even a single paracentesis, can cure empyema. I have known a
single paracentesis cure a stinking empyema of considerable size. And
I have known paracentesis, which removed more than five pints of pus
from the pleura, to be followed within a week or two by effusion of clear
serum to the same amount in the same pleura. But cases of this sort
are very uncommon, and incision and drainage are the proper treatment
of empyema.
In order, then, that the drainage may be thorough it is best to remove
a small portion of one of the ribs. Incision is made right down upon the
rib, the periosteum is separated all round by an elevator, and the rib is
divided in two places by cutting forceps, so that about an inch can be
removed. It is not good practice to swill the empyematous cavity out ;
nothing is gained by removing false membranes in this way ; a foetid
empyema is soon deodorised by thorough drainage and careful antiseptic
dressing, and even if not, washing out does not help. Moreover, in-
jections are dangerous if there be an ulcerous opening through which
they can enter the lung ; the shock which immediately ensues upon
PLEURISY 375
such an entrance puts life in jeopardy. Even if there be no such
ulcer, injections are dangerous. I have known a patient die very
suddenly during injection, when but a very small quantity of a weak
carbolic acid solution had been injected ; no chloroform was given, and
nothing could be found post-mortem to explain the death. But sudden
syncope coming on in this way is not always fatal. The cause of the
syncope is not understood ; a case has been recorded in which the
right chambers of the heart were found post-mortem to be distended with
gas. The syncope is sometimes followed by convulsions and coma ; in
this case death usually ensues within twenty -four hours. If the
temperature rise much above 105° recovery is very unlikely. Yet
recovery even after convulsions may occur ; temporary palsy of a limb
or of one side of the body has been noted upon cessation of the con-
vulsions. In other cases the sudden syncope has been attended by
palsy without convulsions, by spastic rigidity of a limb or of the jaw,
or by aphasia ; these symptoms commonly pass away in an hoqr or less.
Convulsions and paralyses of this kind are probably epileptoid in
nature, and quite different from the paralyses which will be spoken of
hereafter, and which are due to embolism.
If there be any probability of the coexistence of pulmonary tubercle
the line of treatment is not so clear. To release the lung from compres-
sion may accelerate the infective and destructive changes going on
therein ; to say nothing of the debilitating effect of a free purulent dis-
charge, which there is but small chance of stopping. Under these cir-
cumstances it is best to resort to paracentesis several times at least, the
result being watched before proceeding to drainage.
In dealing with small deeply-seated empyema, such as that which so
often leads to foetid expectoration, it is sometimes necessary to remove
portions of two or three ribs, so that adhesions can be broken down and
the cavity opened by the finger. To cut through the lung in such cases
many cost the patient his life.
For a day or two after opening the chest the discharge will probably
continue to be abundant. It will then, in most cases, gradually lessen
until it ceases altogether in a few weeks, three or more. In proportion
as the discharge becomes scantier the drainage-tube must be shortened,
so as to allow the sinus to heal from the bottom.
The temperature ought to fall almost or quite to the normal after
the pus has been discharged. Should the temperature remain raised,
there must be either retention of pus or some other concomitant disease.
When, after the fever has ceased, the temperature rises again there is
probably retention of pus, and should the temperature not fall again in
a few days the sinus should be probed, and a longer piece of tube be
inserted if necessary. But the temperature will often rise for a few
days without obvious retention of pus, and will fall again without
obvious increase in the amount of discharge.
When the sinus shows no tendency to close it is best to wait two
or three months before undertaking any further operation. But when
376 SYSTEM OF MEDICINE
the discharge continues for a longer time (and these remarks apply also
to cases of neglected empyema which has been allowed to open spon-
taneously), and it seems necessary that something else should be done
(especially when the discharge remains abundant and the health of the
patient suffers), a more extensive operation must be performed. Longer
portions (two or three inches) of three, four, or more ribs in the neigh-
bourhood of the sinus must be resected, so as to allow the chest walls
to fall in and meet the lung. The cases in which the discharge is not
finally arrested by this operation are very few.
IV. Dangers of paracentesis. — 1. Serous (or albuminous) expectoration.
Paracentesis, by suction, of a pleural effusion is sometimes followed by
expectoration of blood-serum. If a patient begin to cough much during
the operation it must be stopped at once, and the patient be carefully
watched. It is very probable that a small amount of serous expectora-
tion under these circumstances is not uncommon ; it is only when the
secretion^ is abundant that the condition is dangerous and apt to end in
speedy death. Serous expectoration mostly ensues during or directly
after the operation, but sometimes an hour or two will elapse before
the secretion becomes dangerously abundant ; the latter cases are less
serious. When abundant serous expectoration follows rapidly upon
paracentesis the patient may die suffocated within half an hour. The
stuff expectorated is frothy, viscid, transparent, neutral, or alkaline,
yellow or yellowish green, with a specific gravity of about 1020, and
rendered almost solid by heat and a drop or two of acetic acid.
Chemically the sputum consists of serum-albumin and a little mucin.
On standing there falls a scanty deposit of pus and blood corpuscles.
Post-mortem the lung is oedematous, and usually fully expanded. Con-
comitant disease, such as disease of the heart, mediastinal tumour, or
hsemoptoic infarcts, favours the occurrence of serous expectoration.
2. Pneumothorax sometimes follows withdrawal of a pleural effusion.
The cause is not always the same, (i.) In some cases the lung has been
injured by the operation, an accident especially apt to occur when
collapsed lung, undiscoverable by physical examination, is adherent to
the chest wall, so that the trocar goes through the lung, (ii.) Sometimes
the air comes from a spontaneous rupture of the lung ; softened tubercle
may give way ; in empyema there is sometimes a small ulcerous breach
in the surface of the lung existing before the operation, or merely
collapsed lung may burst in some small spot in the process of expansion
during paracentesis by suction, (iii.) The pus of empyema sometimes
contains so much gas dissolved in it that in some cases this is a very
probable cause of pneumothorax.
3. Haemorrhage from the pleuritic membranes is sometimes the
result of paracentesis. If the blood flow at all freely, the operation
must be stopped, and it is seldom that any bad consequence follows.
But death has been due to this cause, the pleural cavity being found
post-mortem to contain a large quantity of blood.
4. Fatal haemoptysis has ensued upon evacuation of empyema in
PLEUKISY 377
pulmonary phthisis, which has gone on to the formation of cavity con-
taining a small aneurysm.
5. Embolism of distant arteries, by coagula dislodged from the
pulmonary veins, may be the result of paracentesis. The most common
result is hemiplegia (see p. 364), which is usually incomplete. Embolism
of both iliac arteries has been known to occur.
6. Sudden death has followed soon after paracentesis in rare cases,
even when the pleura has not been washed out (see p. 376). In one case
of this kind the right side of the heart was found to be iilled by a clot,
formed in all probability during life. In other cases no satisfactory
explanation of the death has been forthcoming ; all operations involve
the possibility of the patient dying suddenly.
The treatment of foetid expectoration from a small deeply-seated
empyema, which cannot be laid open by an operation, is the same as
that of a similar condition in phthisis.
Subsequent deformity. — Not much can be done to expand the
collapsed lung, and to counteract the deformity of the thorax and spine
which is apt to follow upon chronic pleurisy. Exercises for the arms
should be prescribed, especially such as tend to open the chest in front ;
for instance, drawing the body up by the arms clinging to a horizontal
bar, skipping backwards, the use of a chest-expander behind the back,
or of dumb-bells and appropriate drilling.
Samuel Gee.
references
1. Brousse. Ann. de dermat. et de syphil., Paris, 1894, vol. v. p. 965, who gives
references to all previous papers. — 2. Dickinson. Med.-Ohir. Trans, vol. Ixxv. p. 317.
— 3. Ehrlioh. GhariU-Amnalen, 1880, vol. vii. p. 202. — 4. Fbankbl. Charit4-
Annalen, 1888, vol. xiii. p. 147. — 5. Gilbert and Lion. Annates de I'Institut
Pasteur, 1888, vol. ii. p. 662. — 6. Gombault and Chauffard. Bulletin de la soc.
mid. des h6p. de Par. 1884, vol. i. p. 309. — 6a. Handford. Clin. Soc. Trans, vol.
xxii. p. 19. — 7. Hanot. Bull, de la soc. mid. des Mp. de Par. 1893, vol. x. p. 732.
— 8. HoFFA. Fortschritte der Medicin, 1886, vol. iv. p. 76. — 9. Kelsoh and
Vaillard. Archives de physiol. norm, et path. 1886, vol. ii. p. 162. — 10. KoPLlK.
Amsr. Jour, of Med. Science, 1891, cii. p. 40. — 11. Kkacht. Quoted by Levy. — 12.
Levy. Arch. f. exp. Pathol, u. Pharmak. vol. xxvii. p. 369. — 13. Nbtter. Bull,
de la soc. mM. des h6p. de Par. 1890, vol. vii. p. 441. — 14. Ibid. 1891, vol. viii. p.
176. — 15. Pansini. Centralhlatt f. allg. Path. 1893, Jan. 15. — 16. Prince Ludwiq
Ferdinand. D. Arch. f. klin. Med. vol. 1. p. 1. — 17. Renvers. Chariti-Annalen,
1889, vol. xiv. p. 188. — 18. RosENBACH. Mikro-organismen bei der Wundinfections-
kranhheiten. — 19. Sacazb. Rev. demM., Paris, 1893, xiii. p. 313. — 20. Wbiohselbaum.
Medizinischer Jahrbilcher der Gesellschaft der Aerzte, 1886, p. 550. — 21. Other papers
are Goldscheider, Zeitschrift f. klin. Med. 1892, vol. xxi. p. 363 ; Pruddbn, N. Y.
Medical Journal, 1893, vol. Ivii. p. 696; Washbourne, Med.-Chir. Trans. 1894, vol.
Ixxvii. p. 179. — 22. Flbxnee. Joii^. of Exiper. Med. vol. i. p. 559.
S. G.
W. P. H.
378 SYSTEM OF MEDICINE
PNEUMOTHORAX
Hydrcypnemnothorax ; PyopnmmotJwrax
Definition. — By pneumothorax is meant the presence of air in the
pleural sac. Generally speaking, the air or gas is accompanied by serous
fluid or pus ; hence the synonyms hydro- or pyo-pneumothorax to denote
one or other of these composite conditions.
Etiology. — Although causes leading to the production of pneumo-
thorax are fairly numerous, most of them, as detailed by various
observers, are of remarkably infrequent occurrence ; indeed the disease
itself may be said to be rather uncommon.
The oft-quoted statistics of Saussier (12) give the relative frequency of
the causes in 131 cases as follows ; —
Phthisis .
Empyema
Gangrene of lung .
Emphysema of lung
Apoplexy of lung .
81
29
7
5
3
Fistula between pleura, liver,
and intestine . . .2
Abscess of lung . . .1
Cancer of lung .... 1
Hsemothorax .... 1
Hydatids ... 1
Even this considerable list is by no means complete, and several
additions have to be made — most of them, however, of rare occurrence.
For example, pneumothorax may be brought about by external injiu-y —
such as a perforating wound of the wall of the chest, by the wound-
ing of the visceral pleura by a fractured rib, or even by heavy blows
or falls, apart from wound or fracture. Indeed, cases of pneumothorax
occur from time to time of which no cause is discoverable (6).
Internal injury also must be credited with the production of some
cases of the disease, as when a bougie, in its passage through a
cancerous oesophageal stricture, has perforated the diseased wall of the
tube and entered the pleiu-al sac. Ulceration of a bronchial . tube,
.however produced, is another possible cause ; perforation of the diaphragm,
brought about by suppuration resulting from a perforated gastric ulcer,
another ; and finally, cases occur in persons, otherwise apparently in
robust health, as a result of strain, that is, of strenuous muscular effort with
the glottis closed. All these varieties of causes group themselves in
two divisions : the one containing those in which the perforation causing
pneumothorax results from injury or disease directly affecting the lungs
themselves, or the bronchia (and this is the more important) ; and the
other containing those in which the causes of perforation are external to
the pleura. An additional variety is attributed by some authors to the
gaseous decomposition of liquids, such as pus, pathologically present in
the pleura : this, if it ever occur at all, is infinitely rare ; there is
good reason to doubt whether it does occur.
PNEUMOTHORAX 379
All observers are agreed that pulmonary tuberculosis, producing per-
foration by ulceration of the visceral pleura, is by far the most frequent
cause of pneumothorax ; and most of them place the proportion of such
cases at about 90 per cent of the whole. The relative frequency of the
disease in cases of phthisis is variously stated by different authorities as
being from 3 to 14 per cent (4). My own experience would suggest the
smaller number as being nearer the general average. It was found
present twice only in 60 post-mortem examinations made on cases of
phthisis at the Middlesex Hospital in the years 1877, 1878, and 1879.
It should be added that men are more apt to be attacked by pneumo-
thorax than women ; and it is a disease especially of the earlier periods
of adult life. This latter is to be expected from its connection with
pulmonary tuberculosis.
Patholog'y and Morbid anatomy. — The mode in which air gains
access to the pleura in such cases as those of external injury, or the
bursting of an empyema, are so obvious as to require no explanation.
With regard to the tuberculous cases, which, as we have seen, form an
enormous majority of the whole, it is in the acute forms that pneumo-
thorax is most apt to occur. Those in which the disease of the lung
progresses slowly are comparatively little likely to perforate, owing to
the formation of protecting adhesions between the visceral and parietal
layers of the pleura. In the former class of cases tuberculous masses
become softened, and break down close under the surface of the lung;
necrosis of the overlying portion of the pleura takes place ; and some
effort, or an attack of coughing, is sufficient to determine a rupture, or it
may occur without any apparent exciting cause.
In connection with this portion of the subject it is interesting to
note how the conservative processes of nature tend to the prevention of
pneumothorax. In the more slowly progressive cases of pulmonary
tuberculosis perforation of the pleura is anticipated by the formation of
inflammatory adhesions — such inflammation being apparently set up by
the commencing necrosis of the pleural tissue. Were it not for this,
pneumothorax, instead of being a somewhat uncommon event, would be
a very frequent if not an invariable incident in the course of caseous
tubercle in the lungs.
In a few instances the perforation seems to take place by the extension
towards the surface of a cavity itself, or by a sinus proceeding from the
cavity. With very rare exceptions the disease is unilateral ; and the left
pleura is much more frequently the seat of the lesion than the right.
Usually there is only one perforation, which may be found at almost any
part of the lung. The common site, however, is the lower part of the upper
lobe, or the upper part of the lower lobe ; and the reason for this is that
the higher parts of the lung are usually the seat of pleural adhesions,
which, as we have seen, prevent perforation.
The size of the perforation varies much ; in great degree according
to the length of time the patient survives. It may be large enough to
admit the tip of the finger, or so small as to be discerned with difficulty ;
38o SYSTEM OF MEDICINE
indeed, it is often not discovered at all, being overlaid with lymph which
has become organised in the repair of the mischief. The opening may
be direct or valvular; and these conditions have an important bearing on
treatment and prognosis, as well as on the amount of "suffering to which the
occurrence of the lesion gives rise. "When the perforation takes place,
the elastic traction of the affected lung is neutralised, and the heart and
mediastinum are displaced towards the sound side. If the opening be
direct and free, air passes out of the pleural sac as well as into it, and
there may be no intrapleural pressure ; if, on the other hand, the opening
be valvular, air enters the pleura during inspiration, and as the respiratory
movement is reversed, the valve closes so that no air can escape : the con-
sequence is that the pleura gradually becomes as full of air as bulging of
the chest, shrinking of the lung on the affected side, depression of the
diaphragm, and displacement of the mediastinum will permit. {Vide
article " Intrapleural Tension," p. 335). The quantity of gas present
depends on various circumstances — chiefly on the presence of serum or
pus in the pleura, and the condition of the lungs themselves, especially
of that which is perforated. Adhesions and consolidation tend to mini-
mise the quantity, while the opposite conditions favour the largest
possible accumulation.
The gas itself, as regards its chemical composition, very much re-
sembles expired air; it consists of nitrogen with oxygen and carbonic
acid, together with sulphuretted hydrogen in cases where a foetid liquid
is also present in the pleural cavity. The proportion of oxygen and
carbonic acid may vary from time to time ; but this matter, however
interesting, is of no practical importance.
When a rupture of the pleura is due to one of the simpler causes —
such as injury or the gi'ving way of an emphysematous vesicle, the
opening is soon closed, the air becomes absorbed, and the previous state
is completely restored. But it is different with the tuberculous per-
foration : here, owing to the leakage of septic liquid from the pulmonary
cavity into the pleura, acute inflammation of the pleural membrane is set
up, which may be both intense and widespread. Following this comes
more or less rapid effusion, which is most likely to be purulent.
On post-mortem examination the escape of pent-up air, when the. cut
is made through the chest wall for removal of the sternum and rib
cartilages, may bear witness to the intrapleural pressure which sometimes
exists. The mediastinum and heart are displaced towards the sound
side ; and shrinking of the affected lung, much or little according to
its condition as regards intrinsic disease or "adhesions, vrill be observed.
"Where the pneumothorax has lasted for some time the pleural surfaces
are covered with quantities of lymph (the result of the pleurisy), which,
as before mentioned, may render the discovery of the perforation difficult
or even impossible. In ordinary cases the lung may be adherent in
part to the chest wall at the apex, and may be the seat of cavities
and of nodules of caseous tubercle. The opposite lung may show a
similar state ; or, if the perforation have occurred early in the history
PNEUMOTHORAX 381
of the tuberculous condition, it may be perfectly sound. The pleura
contains serous fluid or pus, the quality of the liquid as well as its
quantity depending to some extent upon the time which has elapsed
since the occurrence of the perforation. Exceptions to this rule, how-
ever, may be found in cases which have proved rapidly fatal, as there
may not have been time for an obvious effusion to take place.
Symptoms. — In the ordinary case the patient, perhaps during a fit of
coughing, is attacked by agonising pain in the chest, a feeling as of
something having given way, and perhaps of fluid trickling down inside
his chest, together with great difficulty of breathing. Any of these
symptoms, however, may be wanting ; in some cases all of them may be
comparatively inconspicuous. Nor will this appear strange when we
consider that the accident, as it may be called, of pneumothorax often
occurs in patients already acutely ill, with rapidly caseating or softening
tubercle, probably confined to bed, and sufiering from, respiratory dis-
comfort and thoracic pain. Pulse and respiration rate are both increased,
the latter more so than the former ; the patient is cyanosed, the expression
anxious, the alee nasi working, the heart palpitating, the extremities cold,
the voice weak, the temperature lowered, and the body bathed in cold
sweat — in fact, as regards his general condition the patient is in a state
of collapse. Dyspnoea, which is perhaps the most characteristic of the
symptoms, is often extreme and distressing, the patient feeling as if he
were about to be suffocated. It is most marked when the perfora-
tion through the pleura is valvukr, because the condition producing
dyspnoea is aggravated with every inspiration ; and it may readily
happen, especially if the function of the opposite lung be impaired by
disease, that the case may speedily have a fatal issue. The decubitus
of the patient varies a good deal in different cases. There may be
orthopnoea, or he may lie half propped up on the back, or on either side.
In a case recently observed the position chosen was semi-prone towards
the sound side, with the head low.
Physical signs are often more definite than the symptoms. The
following points are to be noted : —
Inspection. — The shoulder of the affected side is elevated, the inter-
costal spaces partially or wholly obliterated, the side distended, and the
movements of respiration diminished or altogether absent. The respiratory
movements of the sound side are correspondingly exaggerated. The
heart's maximum impulse may be seen displaced towards the sound side ;
although, owing to the rapid and disturbed respiratory movements together
with the weakness of the heart's action, it may be difficult to make out.
Palpation. — This means may enable the last-named point to be more
distinctly perceived ; and by it we can also appreciate the diminution or
abolition of respiratory movements : tactile fremitus is also abolished.
Displacement downwards of the liver or spleen may be observed according
to the side afiected ; and the displacement may be very considerable in
amount if the pleural cavity contain much air or liquid, or both. This
change has an important bearing upon treatment, since downward dis-
382 SYSTEM OF MEDICINE
placement of the diaphragm forms such a large pocket for the accumula-
tion of pus that its amount is very apt to be underestimated ; thus steps
for its prompt removal may not be taken.
Percussion. — The presence of air in the pleura gives rise to a marked
change in the percussion resonance ; the note is over-resonant, and may
generally be described as tympanitic. When the tension of the walls,
however, becomes very great, there is a change in the note, so that it is
shorter and of higher pitch, and hence of a less tympanitic quality. The
" cracked pot " sound might be expected in cases where the perforation
between the lung and pleural cavity is open and free ; and some writers
state that it is present occasionally, although rarely. The characteristic
note may not be made out over the whole of the alGfected side ;
adhesions fixing a portion of lung to the thoracic wall may prevent it,
and this condition is of course most frequently observed at the apex of
the lung. Or the presence of an accumulation of liquid — purulent or
otherwise — at the base of the pleural cavity will cause a dulness in the
percussion note over the area so occupied. In the latter case the dulness
and tympanitic resonance may be made to alter their relative positions
by changes in the position of the patient's chest.
The normal area of cardiac dulness is abolished in cases of left-sided
pneumothorax; and in any case, owing to great displacement of the
mediastinum, the tympanitic note often encroaches considerably on the
sound side.
Lastly, there is what is known as. the bell sound, the "bruit d'airain''
of Trousseau, an interesting phenomenon which may be said to belong
partly to the domain of percussion and partly to that of auscultation. It
is recognised when some part of the side which is distended with air is
auscultated, while a coin placed on another part is struck with another
coin or some similar hard substance, such as a key. The sound conveyed
to the ear of the listener is of a ringing metallic quality often closely
resembling the tinkling of a small bell.
Auscultation. — When the opening is valvular, and the pleura has become
as full of air as possible, no breath-sound may be audible, except perhaps
along the spine where the compressed lung lies ; but when the opening is
patent, breathing of an amphoric quality is well heard, as a rule, both
with inspiration and expiration.
It was formerly thought that there must be a passage of air through
the perforation in order that breath-sounds may be heard, but this opinion
is no longer held. If air enter and leave the lung at all, as it may do in
parts where adhesions have prevented complete collapse, breath-sounds
of the quality referred to, although distant and feebly conducted to the
ear of the observer, may often be heard, even through the pneumothorax.
The amphoric breath-sound, when present, is most likely to be easily
detected just over the site of perforation. Voice and cough sounds have
a metallic ring in cases where the opening into the pleural cavity is free ;
and, in connection with the cough especially, the phenomenon known by
the name of " metallic tinkling " is often well heard. It is not due, as
PNEUMOTHORAX 383
was thought by Laennec, to drops of fluid falling in the air-filled cavity ;
but it may be produced by various adventitious sounds having their
origin in the lung.^
Finally, there is the succussion sound, often associated with the name
of Hippocrates, because it was first described by him. To elicit it, the
patient, preferably sitting up, is sharply jolted or shaken, while the
observer has his ear applied to the chest ; or, if not acutely ill, he may
be made to shake himself so as to bring out the sound. It is caused by
the splashing of the liquid effusion in the cavity containing also air, just
as it would be produced in a cask having similar contents ; and it is of
the metallic ringing quality which characterises all the adventitious sounds
of pneumothorax. The patient himself may be conscious of the presence
of fluid in his chest, while under examination he may both hear and feel
the splashing of the fluid.
Diagnosis. — As many of the phenomena accompanying the majority
of cases of pneumothorax are of a definite and striking character, the
diagnosis, generally speaking, is not a matter of much difficulty. The
essential points are : over-resonance ; absence or great enfeeblement of
breath-sounds (these, if present at all, being of amphoric quality) ; displace-
ment of the heart, and the bell sound. These are perhaps more than
enough for diagnosis ; and they are necessarily strengthened if we have
a history of sudden attack of pain in the chest with dyspnoea. The only
class of cases at all likely to give rise to doubt are those in which the
pneumothorax is partial, and limited by old adhesions between the pleural
layers.
From emphysema, which in some points may seem to resemble
pneumothorax, the distinction is easily made by the fact that emphysema
is bilateral, and that in it there is no lateral displacement of the heart
and no bell sound ; also, that the resonance of emphysematous lung is
not so tympanitic as is the rule in pneumothorax. It must be admitted,
however, that rare instances occur in which the distinction is a fair point
for discussion. I can recall two such cases : the diagnosis of emphysema,
however, was duly made in both cases.
From a large pulmonary vomica pneumothorax is distinguished by
the absence of the bell sound, a duller quality of resonance, even where
the conditions of the cavity are most favourable for confusion of diagnosis,
and the absence of displacement of the heart ; or, at any rate, if the
heart be displaced, it is towards the affected side, and is due to contrac-
^ In a case seen by me about fifteen years ago In a healthy, athletic young man of some
twenty years of age, the air escaped into the pleural cavity with a succession of tinkles or clicks.
These were audible in all parts of the large room, and continued until the family medical
attendant arrived, probably two hours, so thai he also heard them plainly. Before my
arrival they had ceased. I suggested that the sounds were due to a rupture of a tiny
bubble at each issue of air. Their frequency varied, they came much faster at first and
grew rarer. Inspiration, at any rate at ilrst, increased the number and loudness of the
tinkles. The rupture was brought about by an attempt to bend the body backwards so as,
if possible, to touch the ground with the hands without removing the toes from a line. The
patient, whose pneumothorax on our examination was considerable, soon got well and
has remained well. — Ed.
384 SYSTEM OF MEDICINE
tion of the lung. The side of chest affected would also be rather retracted
than distended. Metallic tinkling and amphoric breath-sounds may, of
course, both be obtained in cases of cavity ; and, indeed, even the succus-
sion sound, if the cavity be large and contain a quantity of liquid.
From pyopneumothorax subphrenicus — the name given by Leyden (10)
to a condition in which an abscess cavity receiving air through a fistulous
perforation from an air-containing viscus (most commonly perforating
ulcer of the stomach) is found below the diaphragm, the principal guide
to diagnosis is to be found in the history of the case.
Lastly, resonance and breath -sounds somewhat resembling those of
pneumothorax are occasionally found at the apex of the lung in cases of
pleural effusion ; and sometimes over part of a lung consolidated by
pneumonia. The site of the physical signs here, and a careful estimation
of the condition generally, will probably prevent any mistake in such cases.
A few other rare conditions, such as hernia of a part of the stomach,
or colon, through the diaphragm, have simulated pneumothorax : such an
accident is usually the result of injury, and it can generally be distin-
guished without much trouble.
Should there be any difficulty in deciding on the causation of a case
of pneumothorax, the withdrawal of a few drops of fluid from the pleural
cavity, if such be present, and its examination for tubercle bacilli may be of
material help. This was done in a case recently under my own care, and
it furnished positive results. Careful attention to the physical signs and
symptoms of the case will probably enable the physician to arrive at the
correct conclusion as to the nature of the perforation in the l^ing, which
is important from the point of view of treatment.
Prognosis. — The prospects in a case of pneumothorax depend chiefly
on its cause. In the simple and traumatic class of cases the opening soon
becomes sealed by inflammatory exudation and the air is absorbed. In
all the other varieties prognosis must be guided practically by the under-
lying disease. The tuberculous cases, which, as we have seen, form a large
majority, end for the most part unfavourably, and that at no distant date.
The shock and intensity of the early symptoms may even cut life short in
a few hours. At the same time, much depends upon the condition of the
opposite lung, as well as upon the presence of adhesions limiting the
extent of the pneumothorax in that which has become perforated.
Although it may seem paradoxical to say so, patients who, before the
occurrence of the pneumothorax, had been in comparatively sound con-
dition are, so far as pneumothorax is concerned, in greater danger than
those whose affected lung has been much crippled by disease ; and this is
chiefly due to the fact that in the latter case the system has gradually
adapted itself so far to its changed conditions as to tolerate an amount
of interference with normal function which would excite much greater
disturbance if it fell upon the patient with all its force suddenly. The
same thing is seen in cases of ordinary pleuritic effusion. If this occiu-
very slowly, the physical signs may indicate that one side is practically
full of fluid, and no respiratory distress, apart from exertion, may bo
PNEUMOTHORAX S^S
complained of ; while a second case in which half the quantity of fluid is
present may be characterised by great dyspnoea if the accumulation have
been rapid.
Both clinical and pathological experience go to show that even in
tuberculous cases of pneumothorax rare cures have taken place; but in the
great majority the outlook is a very dismal and discouraging one.
Treatment. — In most cases this can only be palliative and symptom-
atic. So far as drugs are concerned, opiates and stimulants comprise
practically all the medicines likely to be useful. Morphine, either by the
mouth or subcutaneously, is perhaps the best of the former class ; alcohol
in some form of the latter, but its effects may be helped by ether and
ammonia. The opiate acts beneficially by relieving pain, checking the
cough, and diminishing the discomfort of the patient generally, especially
that resulting from the dyspnoea ; and the stimulants are called for both
to counteract the collapse first occurring, and to help the heart to carry
on its work in which it is handicapped both by the alteration in its posi-
tion and the obstruction of the circulation through the compressed lung
tissue. Some external applications are useful. Dry cupping may be
recommended if the dyspnoea and cyanosis be great; and where pain,
resulting from the accompanying pleurisy, is much complained of, the
application of two or three leeches and hot fomentations are likely to
give relief. Subsequently strapping the side may be thought of.
Sooner or later the question of paracentesis will, in- most cases, have
to be considered. If there be evidence that the pressure within the thorax
is considerable, we have practically no choice ; especially if, owing to the
valvular character of the perforation, this pressure be increasing. A fine
trocar should be used, but no aspiration. The danger, of course, is that
the diminution of the intra-thoracic pressure may encourage the reopening
of the perforation which may have been closed by lymph, a condition
on which our hopes for a cure of the pneumothorax depend ; but it is
better to run this risk than to allow the patient to die from asphyxia and
exhaustion. If the opening should not have closed, the passage of the
trocar will at least do no harm, and it will enable the presence or absence
of intra-pleural pressure to be demonstrated. After puncture, strapping of
the affected side, in order so far to prevent the recurrence of distension,
may be employed in some cases with advantage. The only danger which
attends puncture is that subcutaneous emphysema, partial or general, may
spread from the seat of it ; but this rarely happens, and all risk may be
practically abolished by keeping up a little pressure on the wound after
the puncturing instrument has been withdrawn.
In any case when there is evidence that the pleural cavity is partly
occupied with liquid, it is wise to explore from time to time to ascertain
the nature of the liquid. If serous, the general condition of the patient
will be no worse than if air alone were present ; probably indeed better,
as the pressure exerted on the lung may tend to check the progress of
disease in it, and will promote the effectual sealing up of the perforation.
If the liquid be foetid pus, nothing but harm can come from letting it
VOL. V 2 c
386 SYSTEM OF MEDICINE
remain in the pleura, and it ought to be freely evacuated at once. But
there is an intermediate class of cases in which the fluid is purulent, not
foetid ; and it is more difficult to decide what should be done here, and
when. In such a case, if the pneumothorax have resulted from the rup-
ture of an empyema into the lung, the chest should be freely opened and
drained ; and the same would hold good if the empyema had ruptured
through the chest wall, the opening which nature makes not being, as a
rule, sufficient for free drainage. And even in the case of pyopneumo-
thorax of tuberculous origin, a consideration of general principles dictates
the free evacuation of the pus, the case being thus converted into an
empyema with some chance of the perforation in the lung being closed,
followed by slight re-expansion of lung and obliteration of the pleural
cavity. It is true that tuberculous patients in whom this is done rarely
recover ; this, however, is not because of the removal of the pus, but of
the progress of the disease which produced it. On general grounds it is
something of an opprobrium to allow a patient to die with a large
quantity of pus in his chest.
.The diet shotild be light and nutritious, and the bowels must not be
allowed to become constipated. The treatment does not differ otherwise
from that of phthisis pure and simple.
The question of prophylaxis is a more difficult one, and has reference,
of course, almost solely to tuberculous cases. In them, as has been pointed
out by Dr. Henry Thompson (14), there may be a warning of coming
danger. His view is that a hint of impending perforation may be found
in a persistent and prolonged decubitus on one side, on account of pain
and cough when lying on the other side is attempted ; and that such a
condition suggests the presence of cavities underneath a part of the pleura
unprotected by adhesions ; for with adhesions there would be no such
severe and continuous pain. Under such circumstances strapping of the
side is more than ever advisable ; medicines should be administered to
keep down the cough, which in these cases is apt to be frequent and
exhausting, as well as superfluous : this form of cough, says the author,
" is imminently dangerous from the strain it puts upon the damaged lungs,
and upon their frail investing membranes." Every physician must have
seen cases which correspond exactly to his description.
David W. Finlay.
REFERENCES
1. Catlet, W. " Pneumothorax occurring during the course of Typhoid Fever,"
Trans. Glin. Soe. Lotid. 1884, vol. xvii. p. 52. — 2. Coats, Joseph. LectvA-es to
Practitioners on the Fathohgy of Fhthisis Pulmonalis, 1888, p. 226. — 3. Eighhobst, H.
(Quoting Biaoh's list of 918 cases of pneumothorax occurring during a period of thirty-
eight years in the three great hospitals of Vienna) JTandbiich der speciellen Path, und
Therap. 1885, vol. i. p. 522. — 4. Fox, Wilson. Diseases of the Lungs and Pleura,
1891, p. 1104.— 5. Gairdnbr, W. T. "Relation of Pleurisy to Phthisis Pulmonalis
and to Pneumothorax," International Clinics, Philadelphia, 1891, vol. i. p. 62. — 6.
GooDHART, J. F. " Case of Pneumothorax first on the right side and a Year later on
the left side, without any discoverable Cause," Trans. Clin. Soc, Lond. 1896, vol.
PNEUMOTHORAX 387
xxix. p. 109. — 7. Hale White, W. "Two cases of Pyopneumothorax in the Course
of Typhoid Fever, both due to Straining at Stool," Trans. Clin. Soc. Land. 1896, voL
xxix. p. 105. — 8. Hall, F. db H. "Cases of Pneumothorax in Persons apparently
healthy," Trans. Clin. Soc. Land. 1887, vol. xx. p. 153. — 9. Johnson, Geo.
" Sudden Perforatiye Pneumothorax with rapid and complete Recovery," Trans. Clin.
Soc. Land. 1882, vol. xv. p. 159. — 10. Letden. Zeitsch. f. hlin. Med. Berlin, 1879,
1. 320. — 11. Powell, Douglas. Diseases of the Lungs and Pleurae, 3rd edit. 1886,
p. 130. — 12. Satjssiee. Becherches sv/r le pneumothorax et les maladies qui le pro-
duisent, etc. Paris, 1841. — 13. Stokes, W. A Treatise on the Diagnosis and Treat-
ment of Diseases of the Chest, New Sydenham Soc. 1882, p. 559. — 14. Thompson,
Henky. Clinical Lectures and Commentaries, 1880, p. 51. — 15. Walshb, "W. H. A
Practical Treatise on Diseases of the Lungs, 4th edit. 1871, p. 299. — 16. West, S.
"Complete Recovery from Pneumothorax without Effusion of Fluid," Trams. Clin. Soc.
Lond. 1884, vol. xvii. p. 56. — 17. Idem. "A Contribution to the Pathology of
Pneumothorax," ia»ce«, 1884, vol. i. p. 791. — 18. Idem. "Cases of Pneumothorax,"
Trans. Clin. Soc. Lond. 1886, vol. xix. p. 227. — 19. Idem. "Prognosis of Pneumo-
thorax," Lancet, 1897, vol. i. p. 1264.
D. W. F.
N.B. — Dr. Frederick T. Roberta's article on " Diseases of the Mediastinum
and Thymus Gland " has been carried forward to the end of the Diseases of the
Chest, in the sixth volume, where fuller justice can be done to the subject.
DISEASES OF THE CIECULATOEY SYSTEM
GENERAL FEATURES OF THE
BLOOD
METHODS OF CLINICAL EXAMINA-
TION OF THE BLOOD
CARDIAC PHYSICS
CHLOROSIS
PERNICIOUS ANEMIA
SPLENIC ANJEMIA
HEMOPHILIA
HEMORRHAGES IN NEW - BORN
CHILDREN
PURPURA
SCURVY
INFANTILE SCURVY
HEMOGLOBINURIA
LEUCOCYTHEMIA
DROPSY
HEART DISEASES-
CONGENITAL MALFORMATION OF
HEART
DISEASES OF THE PERICARDIUM
DISORDERS OP FUNCTION, IN-
CLUDING STRAIN
INJURIES BY ELECTRIC CUR-
RENTS OF HIGH PRESSURE
DISEASES OF THE ENDOCARDIUM
DISEASES OF THE MYOCARDIUM
CHRONIC VALVULAR DISEASES-
DISEASE OF THE AORTIC AREA
OF HEART
DISEASES OF THE MITRAL
VALVE
To te completed in Volume VI.
GENERAL FEATUEES OF THE BLOOD
In the following pages I propose to treat in a very general way of such
of the salient features of the blood as are likely to be referred to, or
ought to be attended to in discussions on the nature and treatment of
disease. A very large number of these features will in succession be
necessarily discussed in detail by my brother contributors in connection
with various diseases, and I must content myself with a very rapid
survey of the whole field.
I begin with a remark which, though exceedingly commonplace,
ought always to be distinctly borne in mind. Blood (and when we use
the general phrase blood, we mean blood as it is discharged from the
heart, not blood taken from any particular blood-vessel) is within very
narrow limits uniform in composition and character under very varying
circumstances ; but that uniformity is the result of the delicate balancing
of the many changes which the blood undergoes in nearly all the several
parts of the body. As it flows through the capillaries of each of the
tissues the blood puts on special characters, so that the blood of one
vein differs, and may differ widely from the blood of another vein ; but
the changes thus brought about are of such a nature, and are so adjusted
by a variety of influences, that the mingled blood of all the veins as it
issues from the heart is under normal circumstances the same. Any
marked alteration in the features of the blood flowing from the left side
of the heart means something wrong in the tissue changes or some dis-
turbance of compensatory influences.
Another general preliminary consideration deserves attention. The
corpuscles are the only independent intrinsic constituents of the blood,
the only idiohaemic elements. While the constituents of the plasma are
continually passing through the capillary wall to and from the tissues, the
corpuscles as a rule remain within the blood-stream. The red corpuscles,
born in corners of the stream, in the red marrow or elsewhere, never
leave it save under the most exceptional circumstances ; the white cor-
puscles may at times wander out of it, but do not leave it to any great
extent, at least save under special influences ;. whereas all the constituents
of the plasma are continually coming and going. And while the circum-
stances determining the entrance and exit of the latter, whether these be
activities of the tissues, or the physical conditions of the circulation, are
392 SYSTEM OF MEDICINE
very largely under the dominion of the nervous system, the behaviour of
the former cannot be directly influenced by it ; it is only in an indirect
way that any nervous event can affect a corpuscle of the blood.
In connection with this aspect of the blood it ought to be remem-
bered that the changes which are continually being effected in the
blood have, so to speak, two objects in view. The purpose or function of
the blood is undoubtedly to nourish the tissues, to carry to a tissue its
appropriate food, and to sweep away from it its waste matters ; and the
primary object of the changes going on is to fit the blood for this pur-
pose in respect to all the tissues. But it thus nourishes the tissues by
means of the mechanism of the circulation ; blood is driven in a certain way
round and round the body. That it may be properly so driven certain
physical qualities of the blood are necessary. For instance, the proper
circulation of the blood is dependent on the blood possessing a certain
viscosity ; an increase or decrease of that viscosity means an interference
with the due stream ; and so with other qualities of the blood. These
physical qualities are maintained by the action of the tissues ; and this part
of the work of the tissues is no less important than that part by which each
tissue fits the blood for the nourishment of its brother tissues. Further,
while it is true that in the act of nourishing a tissue the essential factors
are the transit from the blood to the tissue of certain substances, and the
transit from the tissue to the blood of certain other substances, it is no
less true that the transit in each direction is dependent not only on the
presence of those particular substances in the blood and in the tissue, but
also on the presence of other substances which indirectly determine the
transit. Thus to take as an illustration an extreme case : — granted that
in any case the essential fact of the nourishment of a tissue is the transit
from the blood to the tissue of sugar, that transit will not be the same if
the sugar is offered in simple aqueous solution, as if it be presented as
part of the compound plasma of blood. Most probably, in the internal
struggle for existence, the economical result has come about that the
substances which are actually employed for the nourishment of the tissues
are, to a large extent, also used for maintaining these other qualities of
the blood. But it is also probable that such an economy is not complete.
Indeed it may be regarded as an open question whether the meaning of
the large proportion of serum-albumin in the plasma is not to be sought
for in the presence of this body in such quantity being necessary for the
adequate flow of blood through the blood-channels, and for the proper
transit of proteids other than itself and of other substances from the
blood to the tissues, rather than in the nutritive value of the substance
itself.
Again, we have evidence that the blood protects the tissues against
the action of bacteria and like organisms. In this aspect it governs the
nutrition of the tissue in a way different from either of the above.
In any case, in discussing the harm which may accrue as the result
of any change introduced into the blood, we ought to bear in mind that
the harm may be wrought in one or other of the ways to which we are
GENERAL FEATURES OF THE BLOOD 393
calling attention. Likening the blood to a medicament, we may say that
it may fail not only through error in the quantity or quality of the
active drug, but also through the vehicle or medium being unsuitable.
Bearing these considerations in mind, we may inquire what are the
several changes which may take place in the blood. And we may first
turn to the changes of blood as a whole.
Volume, or quantity of llood.- — The space supplied by the combined
vascular channels contains a quantity of blood, which under ordinary cir-
cumstances is in man calculated to be equal in weight to about one-
thirteenth of the whole body. This mode of stating the quantity pre-
supposes a certain normal composition and specific gravity, as indeed does
also the method of determining it ; since the quantity remaining in the
body after all that can be shed has been shed, is calculated upon the
amount of hsemoglobin retained in the body.
We have in fact no accurate observations on the volume of blood
irrespective of its composition. Probably the mere volume is of no great
moment. As a mere store of material it contains probably a surplus of
everj'thing, and a little less or a little more of the whole surplus cannot
produce any great effect. Of more importance is the volume in relation
to the total capacity of the blood-channels. But this capacity is variable,
and by vaso-motor action can be so adapted to the quantity present, at
least within certain limits, that the rate of flow and the pressure on the
capillary walls remains, within limits, the same with varying quantities
of blood. Hence, also, within limits, neither the addition nor the with-
drawal of blood produces any marked change in the blood -supply to
the several tissues. Neither plethora, in the old senBe, nor its opposite,
has any physiological significance. At the same time it must not be
forgotten that an excess of blood may lead to an accumulation in the
venous channels on the other side of the capillaries, and while not directly
affecting the supply to the tissues, may produce physiological efiects.
Reaction. — Since blood is the great agent of the chemical changes of
the body, the chemical reaction of the blood as a whole assumes great
importance. The chemical changes wrought by means of the blood must
be influenced by the blood being alkaline, neutral, or acid ; and by the
amount of its alkalinity or acidity. Normal blood is alkaline, the
alkalinity in man being equivalent to that of from 320 to 390 mgms. of
sodium carbonate for every 100 grms. of blood. This normal condition
is like the other normal conditions of the body, an equilibrium established
between contending processes and hence complex in origin. The reaction
actually tested is that of the plasma, but this is governed by processes
taking place in the red corpuscles ; for these bodies, by virtue of changes
taking place in them, can give up to or take from the plasma substances
whereby the alkalinity of the latter is increased or diminished. It is
apparently through the action of the red corpuscles that the alkalinity
of the plasma (or serum) decreases after blood is shed, and that an
increase of carbonic anhydride in the blood actually increases instead of
diminishing the alkalinity.
394 SYSTEM OF MEDICINE
This complexity is illustrated by the experience that the alkalinity,
while it may be diminished by the continued administration of acids,
cannot be correspondingly increased by the continued administration of
alkalies ; that it is not influenced by the secretion of gastric juice, and that
the diminution of alkalinity by violent exercise is less than that by
moderate exercise, being moreover largely dependent on the proportion
of proteid matter in the food taken at the same time. The alkalinity of the
blood is part and parcel of the alkalinity of the tissues in general ; it is
not the consequence of the alkalies in the food being in excess of the acids,
but comes about because the general metabolism of the body results in
an alkaline reaction. The white corpuscles appear to have no share in
the matter, but the red corpuscles, as we have just said, do seem to play
a part.
Specific gravity. — Since the corpuscles are heavier than the plasma,
the specific gravity of the whole blood may be affected by a mere change
in the number of red corpuscles. It may, of course, also be afiected by
a change in the density of the plasma and corpuscles (for a change in the
one would bring about a change in the other) without any change in the
number of corpuscles. Or a change in the number of coipuscles and a
change in the density of the plasma might occur at the same time,
the change in the two factors being in the same or contrary direc-
tion. As a rule, perhaps, a low specific gravity is accompanied by a
scantiness of haemoglobin due, most frequently, to a diminution in
the number of red corpuscles, but sometimes to the corpuscles con-
taining less haemoglobin.
In health the determination, by various methods, of the specific
gravity of the blood has given results varying from 1050 to 1060, the
more common result being about 1056. Though the blood in diiferent
veins may differ in specific gravity, the venous blood is not materially or
uniformly denser than arterial blood. The blood of the pregnant female
is of low, that of the foetus or new-born animal of high specific gravity.
In certain diseases, especially in anaemia, and particularly in pernicious
ansemia, the specific gravity may be very low 5 cholera and diabetes are
the only diseases in which it is known to rise beyond the limit
observable in health. It is worthy of notice that any obstruction to
the flow along the vessels at once distinctly increases the specific
gravity. Haemorrhage lowers it, but the normal or nearly the normal is
very quickly regained. Dilution of the plasma by the injection of innocu-
ous dilute fluids, normal saline fluid for instance, similarly lowers it ; but
the effect also soon passes off, and though by repeated injections a low
specific gravity may be maintained for some time, yet a rise to the
normal or nearly to the normal speedily follows the last injection. The
return to the normal after dilution may be explained by the escape of
water from the interior of the vessels, and this appears to take place
chiefly in the splanchnic area. The interpretation of the effects of
hismorrhage is not so clear. We may suppose that the lost volume of
blood is in the first instance replaced by plasma only. Though we know
GENERAL FEATURES OF THE BLOOD 39S
that hsemorrhage stimulates the production of new red corpuscles, it is
difficult to believe that these can make their appearance in sufficient
numbers to account for the regained density, seeing that this may occur
within less than half an hour. It looks as if the system got rid of the
water of the extra plasma, and regained its density by acquiring a smaller
volume.
Whatever view we take of the nature of the process of transudation
of Ijrmph, a lowered specific gravity due to a diluted plasma must,
by the changes in the osmotic powers, influence that process, and so the
nutrition of the tissues. Hence the effect of a low specific gravity thus
caused will be different from a low specific gravity due merely to a
scantiness of red corpuscles ; the latter will also have effects, but of a
different kind. In attempting, therefore, to explain any feature of
disease by reference to a low specific gravity, it becomes important to
ascertain the exact way in which the specific gravity is lowered. Further,
a change in the osmotic powers of the plasma directly affects the cor-
puscles ; in this way actual destruction of the red corpuscles (haemolysis)
maf be brought about. Again, when the specific gravity of the blood is
raised by a relative increase of red corpuscles, the resulting increase of
friction, both internal friction of corpuscle with corpuscle, and friction of
the corpuscles against the vascular wall, affects the physics of the circula-
tion ; such a blood is driven along with greater difficulty.
We may now turn to the particular changes of the blood either going
on continuously or taking place from time to time. These fall into two
categories : the changes effected by the several tissues on the blood as it
is passing through the capillaries, and the events which occur in the
blood-stream itself.
1. The changes effected hy the tissues. — These may be subdivided into
three main groups : those effected by the advehent tissues which, through
the alimentary canal,^ bring material to the blood, by the excretory tissues
which remove material from the blood, and by the metabolic tissues which
change the blood as it passes through them.
To deal in detail with the normal changes so effected would be to
traverse a great part of physiology, and to deal with the abnormal ones
would be trespassing on the fields of others ; with regard to the
advehent tissues it may, however, be worth while to point out some of
the more striking ways in which something wrong in their action may,
by modifying the blood, work mischief in the animal economy.
Assuming that proteids are chiefly converted into peptone and albu-
mose, but to some extent into leucin and other deproteonised bodies, that
the peptone and albumose, in the act of absorption, are converted in one
or other of the natural proteids of the plasma, and that all the digested
proteids are carried to the liver, there to undergo a secondary digestion
before they are thrown on the blood-stream, the following are some of
the errors of digestion to be borne in mind as possible causes of disease,
apart from mere excess or deficiency of normal action. The proteids
' We may in this relation neglect tie entrance of oxygen through the lungs.
396 _ SYSTEM OF MEDICINE
TD.SLJ be absorbed in some form other than as peptone or albumose. The
conversion of the peptone or albumose into the natural proteid of the
plasma may fail or may take the wrong direction. The elements of the
proteid converted into leucin and other substances may be in excess
or may be deficient. Some one or other of the digested proteids
may pass into the lymph -stream instead of into the portal blood, and
be thrown into the general blood-stream in an unprepared condition ;
the importance of this diversion is shown by the fact that when in the
dog the portal blood, instead of being allowed to pass through the liver,
is carried, artificially, into the inferior vena cava, proteid food has
poisonous effects.
Our knowledge concerning the digestion of fats is at present very
imperfect and uncertain. But assuming that all the fats pass into the
lymph-stream and not into the portal blood, and are carried in the lymph-
stream in the main as neutral fats (having been synthesised again by the
epithelium, even if, in the very act of absorption, they have been split up
into fatty acids), but partly as soaps, and that both are subjected to some
unknown influences during the passage along the lymphatic tract, we ^ay
assume that the blood will not be the same if the fats should find their
way into the portal blood, or if the proportion of neutral fats to soaps
should be changed, or if the lymphatic tract should fail to exert its normal
influence on the fats during their passage along it.
Assuming that carbohydrates are converted into maltose, and that
this is chiefly absorbed as dextrose into the portal blood, but partly
undergoes a further change, by fermentation, into lactic or even into butyric
acid, the following are some of the errors to be borne in mind. The
conversion of maltose into dextrose may fail or come short, or some sugar
other than dextrose may be formed. The sugar formed, of whatever
nature, may pass, not into the portal blood, but into the lymphatics, and
be thrown on the general blood-stream without having passed the gaunt-
let of the liver ; and this seems a possibility especially well worthy of
notice. The proportion of carbohydrate converted into lactic or other
acid may be in excess, or deficient ; and abnormal acids may be formed
and pass into the blood.
With regard to the excretory tissues, I will content myself with the
remark that these fall into two classes in respect to the influence which
they exert on the blood. On the one hand — as in the case of the kidney
and urea — the act of secretion may be the simple one of picking up from
the blood a substance already existing in it ; variations in the activity of
the excretory organ in such a case have no other effect than that of
removing more or less of the substance from the blood. On the other
hand, the act of secretion may be more complex and include metabolic
activity ; the substance excreted is formed in the excreting organ pre-
vious to its ejection ; as, for instance, in the secretion (which, so far as the
blood is concerned, is excretion) of pepsin or the bile acids. In such a
case, in the act of secretion the antecedent metabolism may go wrong
and the blood in consequence be affected.
GENERAL FEATURES OF THE BLOOD 397
To deal with the changes in the blood effected by the metabolic
tissues would lead me through a great part of physiology and into dis-
cussions concerning the nature of many diseases. I must confine myself
to one or two general reflections.
Certain tissues have what may be called an outward function, by
which they affect parts other than themselves, such as a muscle in moving
a limb, a secreting gland in pouring forth its secretion, and so on. In
such cases the metabolism is the means of carrying out the function, and
may be considered as brought about for that purpose. This is conspicu-
ously the case in a muscle. Undoubtedly the muscle in contracting
pours into the blood, either directly or indirectly through the lymph-
stream, what we speak of as waste products. These waste products, like
other waste products, may be capable of utilisation, but they are pro-
duced, not for that secondary purpose, but because they necessarily result
from the act of contraction. Other tissues, of which the suprarenal
capsule may be taken as an example, have no such outward function. They
undoubtedly produce changes in the blood,' but these changes serve no
purpose in the organ itself. They are brought about for the sake of the
blood itself ; the blood so changed serves useful ends in the economy.
Other tissues, again, afford a combination of these features. And, indeed,
perhaps the distinction just made is after all not a valid one. Each of
the tissues becomes adapted to thrive on the blood as affected by the
other tissues. Hence, even admitting that the metabolism of muscle was
in the first instance directed merely to give rise to contraction, and so to
movement, the products of the metabolism being also in the first instance
carried to other tissues merely to be prepared for excretion and excreted,
it might easily arise that some turn in the muscular metabolism con-
sistent with the efficacy of the muscle as an engine of movement was of
advantage to one or other of these secondary tissues. If so, this would
in the course of development become fixed and exaggerated. Hence we
may be wrong in supposing that muscular metabolism is shaped solely and
exclusively for the good of muscular contraction. And, indeed, we have
hints that it is not. The hygienic effects of muscular exercise are mani-
fold and far-reaching; it brings about changes in the circulation and
respiration which have indirect effects on the other tissues quite apart
from what is going on in the muscles themselves. Still it is difiicult to
resist the suspicion that the good effects are in part due to the actual
metabolism of the muscle itself; whether it be that substances in the
blood arising in other tissues are drawn into the complex vortex of that
metabolism and made use of in an anabolic way, or whether some of the
stages of the muscular katabolism, and we may well believe that these
are many, cast off into the blood from the muscle subserve useful ends
in other tissues. If there be any truth in this suggestion we may look to
further study of the blood to explain, on the one hand, how disorders of
the muscular system may arise from events in other tissues, and, on the
other, how this or that tissue having no other connection with the
muscles than through the blood, may suffer when, as in certain nervous
398 SYSTEM OF MEDICINE
affections, so large a proportion of the muscular system is out of order
that the few which are sound cannot effect what is needed.
There is, of course, one metabolic feature which stands apart from all
others in being common to all the tissues : in every tissue oxidation is
always taking place, ox3'gen being supplied by the blood, and in every
tissue carbonic anhydride is a conspicuous product of the chemical
changes. This is true even of the liver, whose main blood-supply has
already been used for oxidation purposes and become venous. The
salient features of this respiration of the tissues, as it has been called, are
two. In the first place, since carbonic anhydride is only one of the
several products of the oxidative metabolism, and that metabolism com-
plex in character, the carbonic anhydride not arising from the direct
oxidation of carbon, but as the last step in a chain of events, no direct
proportion obtains at any moment between the oxygen absorbed and the
carbonic anhydride given out ; the latter may be given out in quantity
by a tissue which at the time is taking in no oxygen, and may not
have taken in any for some time previously. In the second place, while
the physical conditions of the lungs are such that arterial blood has
always the same proportion of gases, and these sufficient to cover all the
respiratory needs of all the tissues under ordinary circumstances, these
needs are very variable, the several tissues differing from each other, and
the same tissue having different needs at different times. Hence the
respiratory activity of any tissue, the amount of oxygen it takes in, and
the amount of carbonic acid it gives out, are determined by the tissue
itself, not by the character of the blood. The margin of the respiratory
value of arterial blood is so wide that it is only under extreme circum-
stances, those approaching asphyxia and such as cannot long be main-
tained, that the character of the blood at all affects the respiratory
activity of the tissues.
2. The changes taking place in the blood-stream. — "We may now turn to
the changes which we may speak of as changes taking place in the blood-
stre.im itself. In attempting to deal with these, however, we come
upon an important preliminary consideration. In what has gone
before we have had to do with the particular changes in the blood
brought about by particular tissues, that is to say, by the action of
the elements of the tissues lying on the other side of the wall of
the vascular channel, and exerting their influences across that wall.
That the tissue produces the change may be ascertained by various
experiments or observations directed to this or that tissue, such as by
removal of the thyroid and the like. But the blood may and indeed does
undergo changes which we cannot, as yet at least, attribute to the action
of any particular tissue. For instance, the introduction of a disease or
toxic agent under certain conditions leads to such changes in the blood
that the serum acquires in relation to the toxic agent properties
spoken of as antitoxic ; these properties may have a different origin
in different cases, but in some cases at least are probably due to the
'veneration in the blood of an antitoxic substance, an antitoxin. It
GENERAL FEATURES OF THE BLOOD 399
may be, of course, that the antitoxin is produced by the activity of
some particular tissue ; future researches may show this. But there
are at least two other possibilities. The whole lining of the vascular
channel constitutes a tissue whose influence cannot be ignored; and
the corpuscles, both red and white, constitute a floating tissue of
whose influence on the plasma there can be no doubt. The former
may be attributed mainly to the epithelioid layer ; and in the absence
of any knowledge that the activities of the cells constituting this
layer differ in different parts of the system, — that they are different,
for instance, in the veins from what they are in the arteries, or in the
large vessels from what they are in the minute vessels — we may assume
that the influence is chiefly exerted in the minute vessels, where the same
bulk of blood is exposed to a larger area of lining. We may probably
also assume that this influence is in the active metabolic tissues more or
less overridden by that of the tissue itself, and that it is most prominent
in a passive tissue like the connective tissue. Such an influence cannot
at present be appraised ; it seems, however, obvious in the phenomena of
the clotting of blood, and ought not to be ignored. . In the production of
antitoxins, and in respect to other changes in the blood-stream, we have
to bear in mind possible actions on the one hand of the epithelioid lining,
and on the other hand of the corpuscles.
We may consider first the corpuscles. These, and hence the events which
they bring about, are, unlike the tissue with which we have been dealing,
free from the direct influence of the nervous system. By way, as it were,
of compensation, they are exquisitely sensitive to changes in the physical
and chemical condition of the plasma ; and the consideration of their
functions largely resolves itself into a study of the manner in which they
react toward such changes.
T]ie red, corpuscles. — The main function of these is, of course, to carry
oxygen from the lungs to the tissues. In the lungs the haemoglobin
becomes saturated or nearly saturated with oxygen ; this is given up to
the several tissues according to their wants, the exact amount given up
at each transit differing in different tissues and in the same tissue at
different times ; while the amount of oxygen in arterial blood is fairly
constant, that of venous blood is very variable. By adequately
increasing the partial pressure of the oxygen in inspired air, not only is
the hsemoglobin completely saturated, but an additional quantity of
oxygen of high respiratory value is carried by the plasma. Under
ordinary conditions, however, all the oxygen used by the body is thus
carried by the hsemoglobin. Hence the quantity of hsemoglobin in the
blood determines the respiratory capacity,, but, as we have just seen, not
the respiratory activity ; this is dependent on the extra-vascular elements
of the tissues. This quantity is mainly dependent on the number of red
corpuscles, but not wholly so. A specimen of blood having the same
number of red corpuscles may contain less hsemoglobin than another
specimen, the difference depending not so much on the size of the
corpuscles, though these may vary somewhat, as on the amount oi
400 SYSTEM OF MEDICINE
haemoglobin carried by the same bulk of stroma. It has been iirged that
different kinds of hsemoglobin exist, one kind carrying per unit of weight
more or less oxygen than another ; but this is doubtful.
Though the haemoglobin does not carry carbonic anhydride in the
same distinct way that it carries oxygen, there are reasons for thinking
that the former is not, as was once supposed, carried exclusively by the
plasma ; the haemoglobin has some share in the matter, but the exact
way in which it acts has not as yet been made clear.
The red corpuscle, however, must not be considered as simply a
respiratory agent carrying oxygen and influencing the carriage of carbonic
anhydride. It consists of a stroma as well as of haemoglobin; and though
that stroma has lost its nucleus, and with it the power of reproduction
and other vital prerogatives, it is still alive, and is still capable of influen-
cing the plasma. The existence of such an influence, which though it may
be physical, osmotic, in its nature must depend on the condition of the
stroma, is shown by the fact that the entrance and exit of oxygen are
accompanied by the transit from the plasma to the stroma, or vice versa, of
various salts, notably sodium chloride. The action of each corpuscle
in this direction is of course insignificant; but the combined action of
the multitude of corpuscles must not be neglected ; and in tracing
out the effects of diminished numbers, or other abnormal conditions
of the corpuscles, regard must be had to this and other possible
actions of the stroma as well as to the respiratory activity of the haemo-
globin.
Even under circumstances which are compatible with health, the
number of red corpuscles in a given bulk of plasma may vary consider-
ably. This in a great number of cases is due, not to a change in the
number of corpuscles themselves, but to variations in the plasma. Never-
theless it may at times be due to the corpuscles being more or less
abundant ; for the mean population of red corpuscles at any one time is
undoubtedly a balance between the number of old corpuscles which have
disappeared and the number of new corpuscles which have appeared.
Though we have no means of directly determining the average duration
of life of a red corpuscle, it must be short, since the whole quantity of
bilirubin secreted in the bile is supplied by the haemoglobin of red
corpuscles, and the production of this must entail a large daily destruc-
tion ; and though the origin of the main urinary and other pigments is
at present obscure, we ought probably to conclude that an additional
destruction of red corpuscles takes place in order to provide an additional
quantity of haemoglobin for these. To meet this daily destruction a large
daily birth must also be going on. We have evidence that in the adult this
birth takes place in the abundant venous sinuses of the red marrow of
bone, out of special nucleated corpuscles (erythroblasts) lodged there ; but
that it may also occur in the spleen or even elsewhere, at any rate under
certain circumstances. Some observers, however, still maintain that the
precursor of the red corpuscle is a minute spindle-shaped body, the
haematoblast, not unlike a blood-platelet which, living in the blood-stream,
GENERAL FEATURES OF THE BLOOD 401
is developed into a red corpuscle by becoming enlarged, rounded and
coloured.
It is worthy of notice that the loss of blood seems to be a most potent
stimulus for the activity of this process of the production of new corpuscles,
whatever be its exact nature and seat. This we may interpret as signify-
ing that the erythroblasts in the red marrow (we are here adopting the
most generally received opinion) are so influenced by the changes in the
plasma contingent upon a paucity of red corpuscles — so feel these changes,
we may say — as to be stirred up to reproductive activity. We cannot at
present explain this more fully ; it seems to be one of the many instances
of that response of living matter, as a manifestation of " irritability," to
chemical changes in its surroundings which is denoted by the phrase
" chemiotaxis."
Probably the circumstances which determine the maintenance of the
balance between destruction and birth act in this chemiotactic manner ;
but the details of such an action and the causes of its failure in disease
are at present obscure. The technique of the determination of the number
of red corpuscles and the quantity of haemoglobin will be expounded else-
where (pp. 430 and 440), and the sources of fallacy pointed out. But
we may here remark that the observations which seem to show that
dwelling in a high altitude increases the number of corpuscles, and so the
available stock of haemoglobin, and thus provides a respiratory compensation
for the rarefied air, do not seem to have been adequately checked in view
of possible fallacies. Otherwise we might conclude that the pressure of
oxygen in the plasma, as determined by the quantities of oxygen held in
the red corpuscles, is an important chemiotactic stimulus for the repro-
ductive energy spoken of above.
The details of the manner in which the destruction of red corpuscles takes
place are at present obscure. There is no satisfactory evidence that the dis-
integration of red corpuscles which may be directly observed in the spleen
pulp is the chief source of bilirubin ; indeed, it seems probable that this
does not at all serve as such a source, the destruction being there carried
on beyond the pigment stages. Some observers maintain that the free
haemoglobin required for the bilirubin is obtained by a breaking up of the
red corpuscles in the liver itself under the direct influence of the hepatic
cells. But a number of facts, such as the presence of free granules in the
plasma, render it extremely probable that the disintegration takes place in
the blood-stream, and that the haemoglobin and other products are strained
off by the liver and other organs. We say other products, because the
stroma as well as the haemoglobin has to be got rid of ; in what way
this is effected and what becomes of the stroma is not at present known.
The white corpuscles. — These, though far less numerous than the red
corpuscles, yet by reason of their individual activity may be regarded as
exercising a more potent and a more varied influence on the general nature
of the plasma, and so on the events of the body as a whole. So many
facts of the life-history of the white corpuscles, such as the relation of the
haemic white corpuscles, or those of the blood proper, to the ccelomic
VOL. V 2d
402 SYSTEM OF MEDICINE
corpuscles, or those of the lymph spaces, the circumstances attending their
birth and destruction, their entrance into and exit from the blood-stream,
and hence their paucity or abundance either in the general blood-stream
or in particular vascular regions, have to be treated in such detail else-
where that we may confine ourselves here to very general considerations.
Further, without discussing the relations of the various kinds of white
corpuscles to each other, — whether for instance they are, so to speak,
distinct species, or genetic phases of one or more forms only, assuming
provisionally a distinction between the hyaline forms and the granular
forms, and recognising the significance of the further division of the latter
into basophil and oxyphil, — that is to say, into those which have affinities
for basic and those which have affinities for acid dyes, and therefore
presumably for bases and acids generally — as indicative of important
differences in the metabolic processes in each, but neglecting the distinction
between finely and coarsely granular as of secondary importance, — we may
turn to the following considerations : —
Both kinds of corpuscles, being alive, are engaged in metabolic activi-
ties, and hence both take up from the plasma as food and give up to it
as waste substances in solutions; indeed, we have direct experimental
evidence of this. In this way they must be constantly exerting influ-
ences over the plasma. Besides this, those which are actively amoeboid
may be assumed to be occupied, as occasion demands, in taking up from
the plasma particles not in solution. Again, the granular corpuscle,
which seems to be the seat of special metabolic activity, such as may
fairly be called secretive, may be assumed to discharge, also as occasion
demands, special substances bodily into the plasma. We have direct
experimental evidence of both these acts in the case of corpuscles placed
in artificial conditions, for instance, in a " hanging drop," and subjected
to an artificial stimulus, such as the presence of a micro-organism ; and
we may fairly assume that a similar behaviour obtains in the blood-
stream under appropriate circumstances.
The same experimental observations show us, as indeed we might
a 'priori conclude, that in the exercise of their functions these corpuscles
are exquisitely sensitive to changes in their surroundings — that is, in
the plasma — especially perhaps to changes of a chemical kind ; so that
what is called chemiotaxis plays a most important part in their life-
history. By virtue of this kind of irritability they react towards changes
in the plasma too minute to be ascertained by any means of physical or
chemical analysis at present in our power.
Thus the white corpuscles must be considered as exerting on the
plasma during their life influences the exact nature and extent of which
the circumstances of the moment determine ; and scanty as the white
corpuscles are, these influences must be of great moment to the body,
and an excess or deficiency of the white corpuscles as a whole, or of any
particular kind, must affect in an important manner the qualities of the
plasma, and so the welfare of the body. Relying on the experimental
evidence, we may conclude that the especially amoeboid hyaline corpuscles
GENERAL FEATURES OF THE BLOOD 403
have as their work the duty of clearing the plasma of the free particles
which appear in it; it must be confessed, however, that we have not
adequate evidence of their performing what might be expected to be a
prominent task, namely, that of clearing the plasma of the globules and
spherules of fat poured into it by the lymphatics, and indeed the labours
in the amoeboid way of either these hyaline or other corpuscles are of less
moment than that of discharging into the plasma (whether the act be
considered a secretion or not) various substances destined to produce
certain effects. This seems to be especially the task of the granular
corpuscles ; and, as we have seen, the work of the basophil corpuscles
is probably different from that of the oxyphil, though we are perhaps
not in a position at present to define the difference. In some cases the
substances discharged into the plasma are, we have reason to think, of
the nature of ferments ; and thus we may see, in a general way, how a
change in the plasma so subtle as to escape ordinary physical and
chemical analysis may, by acting on these exquisitely sensitive organisms,
give rise to the appearance in the plasma of an agent whose effects on
the plasma, and so on the body, are out of all proportion to its weight
or its bulk. The clotting of blood may be taken as an instance of this
activity of the white corpuscles. Put briefly, the clotting of shed blood
in vitro is due to the conversion by the agency of the body known as
fibrin ferment of the substance fibrinogen present in solution in the
plasma into fibrin insoluble in the plasma. The conversion is not a simple
and direct one ; another body or other bodies than fibrin being formed
out of the fibrinogen at the same time, and the weight of fibrin formed
being less than that of the fibrinogen used up. The change, moreover, is
not effected at one step, a precursor of fibrin, but unlike it soluble in the
plasma, being formed between it and fibrinogen. The change is further
dependent on circumstances other than the mere presence of fibrinogen
and ferment in a liquid medium at a suitable temperature. Thus the
presence of a calcium salt is equally essential ; in its absence clotting
does not take place. And the presence of other substances may on the
one hand hinder, and on the other hand hasten the completion of the
act. As regards the nature and origin of the ferment, many observers
have come to the conclusion that it is of the nature of the bodies called
nucleo-proteids ; and there is considerable evidence that the ferment
which is absent from the blood at the moment it leaves the blood-vessels
is furnished upon shedding by the white corpuscles, or by some, that is a
certain kind of them, through a discharge from their bodies, which may
take on the form of an explosive disintegration.
It has just been said that blood at the moment of being shed appears
to contain no fibrin ferment. But the absence of clotting from blood
within the lung vessels under normal circumstances cannot be due merely
to the absence of fibrin ferment, since very considerable quantities of
active ferment can be injected into the circulation without necessarily
causing clotting. If we assume (and the assumption, though probable, is
still an assumption, though the evidence that circulating blood contains
404 SYSTEM OF MEDICINE
fibrinogen is strong) that clotting within the blood-vessels is, like that in
vitro, a conversion of fibrinogen by the action of fibrin ferment, we may-
infer from this that the blood contains, or may contain, substances or
agencies antagonistic to the action of the fibrin ferment or fibrinogen.
That such substances or agencies may be generated in the blood-stream is
shown by the action of peptone, or rather albumose. If this substance be
added to shed blood, it does not prevent clotting ; injected into the circu-
lation it does do so, not only in blood while still within the blood-vessels,
but after it has been shed. We may conclude that the albumose, while
circulating in the blood-stream, provokes some of the tissues so to add to
or so to alter the blood as to give rise to a something antagonistic to
clotting. It has been suggested that this efiect is produced while the
blood passes through the liver, it being asserted that the antagonistic
action of the albumose is not manifested if the blood be prevented from
passing through that organ. Even if we regard this particular view as
not distinctly proved, the albumose effects illustrate the infiuence of what
we may generally call " the tissues " on the process of clotting. Con-
versely, the presence in the blood-stream of a substance which seems to
be a nucleo-albumose brings about extensive intra- vascular clotting, though
the addition of it to shed blood has no such effect. The complexity of
the reaction is illustrated by the fact that if the same substance be
injected slowly, so that a small proportion is brought to bear on the blood
at any one time, its action is reversed ; it is antagonistic to clotting, and
produces immunity towards its own clotting influences.
Our knowledge will not at present allow us to difierentiate the several
" tissues " in respect to this influence over clotting ; but accumulated
evidence shows that in this respect the epithelioid lining of the blood-
vessels themselves plays an important part : when the inner coat, of
which the epithelioid lining may be regarded as the active element, is
diseased or in an abnormal condition, intra-vascular clotting takes place at
the spot. The mere fact that the clotting is so limited to the spot, and
does not become general, indicates of itself that the process by which the
clotting is brought about is a complex one. An essential factor in the
matter seems to be an aggregation of white corpuscles ; and the experi-
ence that a like aggregation takes place, not only over a diseased or
injured inner coat, but also over an inert body, such as a needle or thread
inserted into the blood, may be taken as indicating that the corpuscles are
gathered together by chemiotactic influence. By a chemical touch they
recognise the difference between the normal epithelioid cell and an altered
one, or an element of the connective tissue underlying the epithelioid
lining, or some quite strange body. And we may perhaps also conclude
that the same chemiotactic stimulus which brings them together excites
them to an unwonted metabolic activity, whereby clotting comes about.
But beyond this difficulties arise. The fact that the clotting is limited
to the immediate neighbourhood of the exciting cause shows that the
general blood-stream is not affected. We may take these phenomena as
indicating that in the general blood-stream the influences antagonistic to
GENERAL FEATURES OF THE BLOOD 40S
clotting are prepotent, and that the action of each corpuscle is thus
limited to its immediate neighbourhood. What that action exactly is we
do not at present clearly know, and we need not discuss it here. It is
sufficient for our present purposes that it illustrates the theme in hand —
the possible influences which the white corpuscles may exert under the
direction of their chemiotactic sensitiveness. It follows that these must
not be left out of coimt in inquiries and discussions concerning the modifi-
cations produced in the blood-stream by various agencies ; as, for instance,
in the important problem how a toxin generates its antitoxin. That in
the instance of clotting the eifect is total and limited is probably a
special feature having a teleological explanation ; in the more ordinary
cases, where the general welfare of the body has to be cared for, we might
expect that the influences exerted by the corpuscles would be general
too. And though in the same instance of clotting the corpuscles them-
selves do all the work, not calling in at aU the aid of what we call the
tissues, this does not preclude the view that in other actions the corpuscles
may effect their purpose indirectly through some influences of the tissue
excited by their action ; whether it be the tissue lining the blood-vessels
generally or the extra-vascular elements of one or another organ of the
body.
The peculiar bodies known as blood-platelets are regarded by some
as a third structural element of the blood ; but it_ is still difiicult to
make any definite statements about these. On the whole, the evidence
goes to show that they must be considered as existing in normal blood,
but this in respect to our present theme is of secondary importance, since
undoubtedly in abnormal circumstances they are present in large numbers.
We are not, however, at the present moment in a position to state
authoritatively what is their real nature ; whether they are destructive
formed elements, minute nucleusless corpuscles of a special kind, and
therefore agents, or whether they are deposits, precipitations of a special
kind, so far analogous to granules, and therefore products. In the
absence of exact knowledge, it would not be profitable to attempt to
inquire what may possibly be the exact nature or limits of the influences
which they may exert.
Besides the changes which may be brought about by each corpuscle,
white or red, in an area of plasma immediately surrounding itself,
we must take into account changes induced by substances more
generally diffused in the plasma, and which, since they are at least
usually present in the plasma, we may speak of as proper to the
plasma, and that quite irrespective of the causes which lead to their
presence ; whether, for instance, they are products of the activity of the
tissues, having not more than a transitory stay in the blood, or whether
they belong to the blood itself. For instance, the evidence is clear that
the blood normally contains an amylolytic ferment, though the quantity
or at least the energy of it seems to vary widely in different animals ;
and there is like evidence that a peptic and even a tryptic ferment are
also present. Our knowledge of the more easily studied amylolytic
4o6 SYSTEM OF MEDICINE
ferment is greater than that of the others ; but even in regard to this we
are not as yet sure whether it is a body sui generis, or whether it is
merely the result of a back flow from the amylolytic pancreas and salivary
glands, merely passing through the blood on its way to be got rid of.
The undoubted fact that sugar (dextrose) rapidly disappears even in shed
blood has led some to speak of the existence in the blood of a sugar-
destroying body or ferment, and the absence from or the excess of such
a body in the blood has been appealed to in explanation of diabetic
phenomena. The existence of such a body cannot at present be con-
sidered as definitely proved ; but there can be little doubt that the plasma
does contain a number of bodies, some of which may be of the nature
of ferments, others mere chemical substances acting in a simple and more
direct manner; and that variations in one direction or another of the
quantity of such a body present in the plasma may exert a great influence
on the economy, and, indeed, produce morbid symptoms. Bactericidal
substances in the plasma afibrd an illustration of the newly discovered
constituents we are now discussing.
Thus, when we have to consider the effects of introducing the blood
of one animal into the blood-vessels of another, we have to take into
account not only the general properties which may be regarded as common
within Kmits to all animals, but special properties differing in different
animals ; and these may in large part depend on the presence, relative or
absolute, of the bodies just spoken of. One practical value of the
transfusion of blood seems to be to supply adequate oxygen by means
of the haemoglobin. The mere bulk of blood, as we have urged above,
is, owing to the adaptive action of the vessels, of secondary importance
from a mechanical point of view, unless the loss be very great ; and after
even great loss of blood, that which is left is probably sufficient to meet
the more slowly developed needs of nutrition other than those of
oxygen. Against this view may be urged the clinical experience that
the injection of simple saline solution is beneficial. If this be so in cases
where the loss is not too great to be compensated by vaso-constriction,
the increase of the bulk by the saline must work beneficially in some
other way than by restoring the mechanical conditions of the circulation.
Such supply of oxygen by means of the transfused blood is of course
temporary only; the foreign corpuscles soon cease to be recognised
in the blood-stream ; they disappear, but during their stay they have
met the demands of the tissues for oxygen, until such time as an adequate
supply of native corpuscles has been obtained by new formation. There
are no reasons for thinking that the red corpuscles of one animal, provided
that difference of size does not bring mechanical difficulties to the circula-
tion, may not serve as oxygen-carriers to the tissues of another animal.
Nor are there reasons for thinking that the substances which serve as the
general basis of nutrition for the tissues of one animal — dextrose for
instance, and proteids, or whatever they be — will not serve in like manner
for the tissues of another animal. Difi'erences, relative or absolute, in the
salt of the plasma may render the blood of one animal unfit for another ;
GENERAL FEATURES OF THE BLOOD 407
but probably the chief cause of the blood of one animal, for instance of
a toad, being unfitted for and acting as a poison towards the tissues of
another animal, for instance of a frog, is to be sought in the presence in
the plasma of one or more of the bodies referred to above.
While the blood, then, is traversing any part of its circuit, making its
way through the capillaries of the tissue, we may recognise on the one hand
the changes which are being brought about by the tissue itself, and on the
other hand those which are being wrought in the blood itself ; either by
means of the corpuscles, or by other bodies, by organisms or chemical
substances, including ferments present in the plasma. To these we ought
to add, perhaps, the influences exerted by the epithelioid lining of the
blood-vessels, influences which probably are insignificant and overridden
in the capillaries, but make themselves felt in the larger vessels, and
may be diiferent in different parts of the vascular system — in the veins,
for instance, and in the arteries, and in different veins.
The changes eff'ected by the tissues and those carried out by the
blood itself are ndt, however, independent the one of the other ; they
react upon each other in many ways, and in all inquiries this should be
clearly borne in mind. Thus, granted that the white corpuscles have as
their rdle the influence which they exert on the plasma surrounding each,
the very number of these corpuscles, either in the general blood-stream or
in special parts of it, is influenced by changes in the body, in the tissues,
or in the blood itself ; and a mere change in number, even if each corpuscle
maintained the same action as before, would modify the events of the
body. The number of corpuscles present in the blood -stream may be
altered, a hypoleucocytosis or a hyperleucocytosis may be brought about by
certain treatments, and whether the alteration of the population be due
to actual destruction or new growth, or to mere temporary withdrawal or
flushing, the mere fact that the population is not the same must influence
the p vents of the body ; or again, supposing the population to remain
the same, the action of this or that tissue may so influence the corpuscles,
or a certain kind of them, as largely to modify their actions.
On the other hand, as we said above in speaking of the white
corpuscles, the action of the corpuscle is not limited to its immediate
neighbourhood. It, for instance, may discharge a substance or sub-
stances into the plasma, either by way of secretion, or in a more extreme
case by actual disruption ; and this or they may provoke this or that
tissue to an altered action, and so indirectly produce a marked change
in the blood.
Such efiects may be especially perhaps looked for as belonging to the
white corpuscles ; but the theme on which we are dwelling may be
illustrated by the red corpuscles. The blood of an asphyxiated animal is
poisonous ; that is to say, when introduced into the blood-vessels of
an animal it produces effects which must be attributed, jiot to a mere
deflciency of oxygen, but to the presence of unwonted substances in the
plasma. During asphyxiation the lack of adequate oxygen so modifies
the metabolism of the tissues, probably the muscular tissues in particular,
408 SYSTEM OF MEDICINE
that the plasma receives from those tissues abnormal products which
act as poisons. This is an extreme case, the very violence of which
puts a clue in our hands; but we may safely conclude that milder
circumstances produce effects which, though less in degree, are on the
same lines. We may infer that a deficiency in red corpuscles, or in
haemoglobin, or indeed possibly some change in the nature of the
haemoglobin, though not pronounced enough to produce direct res-
piratory troubles, may so influence the metabolism of the tissues that
the blood becomes abnormal in other respects than its mere shortcoming
as a carrier of oxygen, and so produce results in the body having
apparently no connection with the oxygen-supply.
Examples like the above might easily be multiplied ; but enough has
been said to illustrate the important view of how manifold are the
agencies, actual or latent, which work upon the blood. The apparent
sameness which is the blood's salient feature is but the resultant of a
multitude of actions, which in health are successfully co-ordinated to each
other, but which in disease cease to fit. In attempting to track out the
genesis of a malady the interweaving of these many threads of the
blood's life must always be borne in mind.
M. Foster.
THE CLINICAL EXAMINATION OF THE BLOOD
Although hardly appreciated at their true importance, routine examina-
tions of the blood are capable of afibrding valuable assistance iij the
diagnosis, prognosis, and treatment of certain pathological conditions.
In a certain number of diseases, among which may be mentioned leukaemia,
pernicious anaemia and chlorosis, the diagnosis may be rapidly and
accurately arrived at by examination of the blood alone ; while, conversely,
should the appearances now known to be characteristic of one or other of
these diseases not be found, they can as certainly be excluded. Many
other diseased conditions there are also in which, although we may not be
able to evolve a diagnosis from examination of the blood alone, yet we
can often obtain evidence of much value when considered in relation to
the results of other diagnostic methods.
Such examinations also throw light on the progress of disease, and
furnish a means of judging the results of treatment more accurately than
would otherwise be possible.
Within the last few years much attention has been devoted to the
simplification of the various methods employed in the examination of the
blood ; and concurrently, by the introduction of more perfect instruments,
a notable advance has been made in the accuracy and precision of our
THE CLINICAL EXAMINATION OF THE BLOOD 409
results. Of no less importance is it that at the present time we can carry
out all the necessary details of an investigation without the expenditure
of more than a few drops of blood.
While, therefore, in order to justify its title, the present article will
deal only with the technique of such methods as require for their perform-
ance a minimal quantity of blood, the clinical observer may rest assured
that, with due care, the ease and rapidity with which the various examina-
tions can be carried out need involve no sacrifice of accuracy.
In systematic investigation of the blood the necessary procedure will
consist of several distinct processes, as follows : —
I. Microscopic examination of — (a) the fresh blood ; (5) dried and
stained blood-films.
II. Estimation of the specific gravity of the blood.
III. Estimation of the colouring matter.
IV. Enumeration of the corpuscles (red and white).
V. Estimation of the alkalinity.
VI. Determination of the coagulation time.
VII. Spectroscopic examination.
VIII. Bacteriological examination by means of stained specimens and
of cultivations.
As a general rule, however, it will hardly be found necessary to carry
out this scheme in its entirety ; although experience alone can decide to
which points in any given case it is desirable that special attention should
be directed.
I. Microscopic examination of the blood. — To obtain blood
for examination. — The skin of the part selected, which may be
either the finger-tip or the lobe of the ear, is first washed with soap
and water, and then dried carefully with a clean cloth. Ordinarily
it is not necessary to employ antiseptic solutions. The skin is punctured
with a quick stab either of a lancet provided with a means of regulating
the extent of protrusion of the blade, which has been specially devised
for the purpose, or a bayonet-pointed surgical needle of triangular section,
which is perhaps more likely to be at hand. An ordinary sewing-needle
should be employed only in default of anything better, as, however sharp
it may be, it is more painful to the patient in its passage through
the skin, especially if it be pressed slowly in instead of being plunged
with one quick motion to the required depth. To avoid possibility of
ill effect the instrument should be sterilised in the flame of a spirit-lamp.
This precaution is indispensable when a bacteriological examination of the
blood is to be made. On no account must any pressure be employed to
expedite the flow of blood ; nor before pricking should a tape or string
be wound round the end of the finger. Professor Sherrington and myself
have shown that under such circumstances as these temporary stasis of
the blood-flow through the capillaries, with the addition of the lymph
derived from the surrounding tissues, are sufiicient to bring about so rapid
and profound an alteration in the composition of the blood — affecting as
410 SYSTEM OF MEDICINE
it does the number of the corpuscles, the haemoglobin power, and the
specific gravity — as to render any conclusion based on examination of
the blood thus obtained quite valueless under such circumstances. It is
true that without compression of the part it is not infrequently a matter of
difBculty, especially in patients suffering from certain kinds of anaemia, to
obtain more than a drop or two of blood ; although this difficulty may
sometimes be overcome by making the puncture a little deeper. It is in
such cases especially that Cabot strongly recommends puncture of the
lobe of the ear, as in cases of pernicious ansemia, in which attempts to
get blood from the finger had failed, he found no difficulty in getting it
from the ear. He is, moreover, of opinion that the ear is decidedly less
sensitive than the finger ; and that there is an advantage, particularly in
the case of children, in a process which the .patient cannot watch. Again,
in a sleeping patient the ear is usually more accessible than the finger.
A word of caution is necessary lest the patient be the subject of
haemophilia, in which case haemorrhage, even from the tiniest wound, is
apt to be profuse and difficult to stop. Hence it is always a wise precau-
tion to make inquiry concerning former bleedings. If, on puncturing the
skin, the blood-flow is fairly free, it is as well to reject the first few drops,
wiping them off with a clean cloth as they exude, so that any extraneous
bodies about the seat of puncture may be washed away. All blood
examinations should be made at about the same hour, in order that the
results obtained may be comparable one with another ; and the time of
examination and the hours of the meals should be recorded. This is
specially desirable when enumeration of the leucocytes is in question, as
allowance can then be made for digestion. But, if possible, examinations
should be carried out before the first meal of the day is taken, for thus
only can any approach to scientific accuracy be obtained.
Histologrieal examination of the blood. — It will generally be advis-
able to examine the blood both in the fresh state and also by the staining
of dried cover-glass films, which have previously been fixed in one way or
another.
Examination of fresh llood. — -The first point is to ensure the most
perfect cleanliness of all slides and cover - glasses. Each observer
prefers his own particular method, the exact details of which may be
immaterial so long as thorough cleansing is secured. The use of soap
and water may be sufficient for this purpose ; but it is usually desirable
either to boil the glasses in a strong solution of sodium carbonate, or to
wash them in a mixture of potassium chromate and sulphuric acid. In
either case they must receive a final wash in alcohol. To obtain a
specimen of blood, a cover-glass, properly cleansed in one way or another,
is held in a pair of forceps or edgewise between the thumb and first
finger, and its under surface brought down into contact with a drop of
blood as it oozes from the puncture. The cover-glass is then, as rapidly
as possible, laid on a glass slide, when the weight of the cover-glass causes
the blood to spread out under it in a film of fairly even depth. If the
subsequent examination is likely to take some time, it is well to prevent
THE CLINICAL EXAMINATION OF THE BLOOD 411
evaporation by painting round the edge of the cover-glass with vaseline
or castor oil. If, moreover, the slide and cover-glass be slightly warmed
before use, or if some form of warm stage be employed, alteration in the
appearance of the blood will take place less rapidly than would otherwise
be the case. The specimen is now to be examined under the microscope,
first with a comparatively low power, and afterwards, if thought desirable,
with a ^ oil immersion lens. Microscopical examination of a specimen
of fresh blood discloses the size and shape of the red corpuscles and the
fashion of rouleaux formation. Thus also the relative proportions of
erythrocytes to leucocytes, and the number of blood-platelets present, can
be roughly estimated, and, by the appearance of fibrin filaments, the rate
of coagulation. In such a preparation the filaria sanguinis hominis, and
likewise the malarial parasite, may be studied in the living state.
Examination of fixed blood.- — For study of the finer structure of the
blood corpuscles, and more particularly of the leucocytes, it is necessary
to stain the blood-film which has previously been dried and fixed. In
order to obtain satisfactory results special attention must be directed to
the preparation of the blood-films, so as to obtain a perfectly thin and
even layer of blood, the process being carried out as rapidly as possible
so as to prevent the occurrence of histological changes.
Preparation of the films. — After thorough cleansing of the cover-
glasses, the under surface of one of these is brought into contact with the
drop of blood as it emerges from the puncture. A minimal quantity of
blood having thus been taken up, the cover-glass is gently dropped upon
another ; after which, with the aid of fingers, or, better still, of forceps,
the two cover-glasses are again separated by a lateral sliding motion of
one on the other. In this way a thin and, if the process have been skil-
fully carried out, an even layer of blood is left on one surface of each
cover-glass. These must now be left exposed to the air until the blood-
films are thoroughly dry. For this purpose it is convenient to place them,
face upwards, on a slip of paper, and to cover them with a watch-glass, or
with one-half of a Petri dish, so as to prevent deposition of dust on the
film surface during the process of drying.
Fixation of the films. — Before staining the blood-films they must be
" fixed " in one way or another ; otherwise the staining solutions are apt
to dissolve out the haemoglobin from the red corpuscles, or even to wash
the thin layer of blood from the surface of the cover-glass. The method
of fixation advocated by Ehrlich is a long and tedious one, involving the
heating of the films for an hour or more on a brass plate to one end of
which a Bunsen flame is applied. The point at which the cover-glasses
should be placed on the plate is estimated by noting within what distance
drops of water, let fall on its surface from a pipette, rapidly evaporate
instead of assuming the spheroidal state. Or, on the other hand, the
cover-glasses may be placed in a hot-air oven, the temperature of which
is maintained at about 120° C. for a similar length of time.
Equally good results, however, are to be obtained, according to Hardy
and Kanthack, by the far simpler and more rapid method of passing the
412 SYSTEM OF MEDICINE
cover-glasses three or four times through the upper portion of a Bunsen
flame, as is now ordinarily done in the manipulation of cover-glass speci-
mens in bacteriological work. Other observers, again, fix blood-films by
methods other than heating. Mkeforofi', for instance, whose method is
recommended by Sherrington, advises the immersion of the specimens in
a mixture of equal parts of absolute alcohol and ether for periods of
from five to twenty minutes. For special purposes, such, for instance,
as the demonstration of karyomitosis, fixing solutions containing bichloride
of mercury, picric acid, or other reagents may be employed.
To stain the blood-films. — For the method usually employed in the
investigation of the histology of the various formed elements in the blood
we are indebted to Ehrlich and his pupils. He not only demonstrated,
in the first place, that the protoplasm of certain leucocytes contains
discrete granules, but he further determined the existence of a definite
relationship between the chemical constitution and the staining capacity of
these cells. Thus his method and his classification of the blood-cells are
based on a scheme of the micro-chemical reactions of their granules.
According to Ehrlich, the various stains employed in histological work
may be divided into two main groups : (a) acid stains ; (J) basic stains, —
admixtures of these in certain proportions furnishing what he has called
neutral stains. The stains included in the first class are classified under
the term "acid," for the reason that although chemically they are
neutral salts yet the staining principle is the acid radicle ; in other
words, the stain reacts tinctorially as a free acid.
Thus ammonium picrate is an acid dye because the picric acid is
obviously the staining element, the ammonium base being inert in this
respect. Of the other " acid " dyes the most useful for histological
purposes are eosin, aurantia, induline, and orange Gr. ; of these the first
three stain well in concentrated glycerine solutions, while the last is
generally employed dissolved in water.
Again, the " basic " stains are so called for the reason that in their
case it is the base and not the acid on which the action as a dye depends.
Of the basic stains one of the best known perhaps is fuchsine, which
chemically is hydrochlorate of rosaniline. Here the rosaniline is the
staining principle and not the hydrochloric acid. Another most useful
basic stain is methylene blue, of which the alkaline preparation devised
by Lofiler is of special value. Other basic stains in frequent use are
methyl- violet, methyl-green, and safranin. Both " acid " and " basic "
stains are employed in histological work on the blood for the reason that
certain of the cell granules react to acid stains only, and are therefore called
"oxyphil granules"; while others, which are more readily tinged with
basic dyes, are described as " basophil." The term neutrophil is now very
generally abandoned, as Hardy and Kanthack and other observers have
shown that the so-called " neutral " mixtures of Ehrlich react tinctorially
as acid dyes, and that the fine granules contained in the cell substance of
what he has described as a " neutrophil " leucocyte are really oxyphil in
their aflinities. Ehrlich's original staining method has been found some-
THE CLINICAL EXAMINATION OF THE BLOOD 413
what cumbersome and inconvenient in use, mainly on account of the
length of time consumed in carrying out the various details of it.
Fortunately, however, standard oxyphil and basophil reactions may be
obtained by the simple and rapid modification of Ehrlich's method intro-
duced by Hardy and Kanthack. They proceed as follows : — Thin films
of blood or lymph dried in the air and afterwards passed three times
through a Bunsen flame are floated on a solution of 0'5 grm. eosin in
100 cub. cent, of 70 per cent alcohol for half a minute or less (acid stain).
Excess of eosin is removed by washing in distilled water. The film is
then dried by gentle pressure between sheets of blotting-paper, again
passed three or four times through the flame, and counterstained in
Lofiler's methylene blue solution (basic stain). After being again washed
and dried, the films may be mounted in Canada balsam.
A description of the histological appearances brought out by the
employment of this method and the system of classification based upon it
will be found under the heading "Leucocytes."
Stain reactions of the blood in diabetes. — ^Bremer devised a modifi-
cation of Ehrlich's method as an aid in the diagnosis of diabetes. He
found that the red corpuscles of diabetic blood could not be stained with
eosin as in normal blood ; although, nevertheless, they reacted to the various
so-called acid dyes. He therefore employed a special eosin-methylene
blue stain, by the use of which the red corpuscles of normal blood are
stained violet, of diabetic blood a greenish colour.
Lupine, however, has shown that this reaction is not absolutely
characteristic of diabetes, since he has obtained it also with leuksemic
blood. Bremer, partly for this reason and partly because his original
eosin-methylene blue stain was difiicult to prepare, has, more recently,
altered and simplified £he method considerably. The blood-film, after
drying in the air, is exposed to a temperature of about 135° C. for from
six to ten minutes ; accuracy at this stage of the procedure is of special
importance, as unless the temperature exceed 129° C. the test becomes
untrustworthy. The slides, together with control slides made from normal
blood, are next stained for about a couple of minutes in a 1 per cent
watery solution of Congo red, or in Biebrich scarlet, or with the ordinary
Ehrlich-Biondi stain. The specimens are then rapidly washed and dried.
With Congo red diabetic blood is usually not stained at all, while
non-diabetic blood is coloured red ; with Biebrieh's scarlet an opposite
effect is obtained, the diabetic corpuscles are stained, the normal ones
are not.
Whether these different reactions are due to the presence of sugar in
the blood, to an alteration in alkalinity, or to some other cause, is as yet
undetermined.
The Fed corpuscles or erythrocytes. — Under normal circumstances
the red corpuscles have the form of biconcave discs of a fairly uniform
diameter of about ■^^5*'^ °f ^'i xrit^. When seen under the microscope
in a single layer they are of a yellowish red colour and are non-nucleated.
In a film of moderate thickness, shortly after removal of the blood, the
414 SYSTEM OF MEDICINE
corpuscles exhibit the physical peculiarity of running into small aggrega-
tions or rouleaux, so called from the supposed resemblance to a heap of
coins.
In many forms of disease, particularly in wasting diseases, and in
pernicious anaemia more especially, not only are the form and consistence
of the red corpuscles liable to considerable alteration, but a marked
diminution in their numbers is usually obvious on examination.
The number of red corpuscles normally present in the blood has been
estimated by Vierordt at 5,000,000 to the cubic millimetre in man, and
about 10 per cent less in woman. In the condition known as oligo-
cythcemia, however, the number of corpuscles in the blood may become
greatly decreased, sinking as low as one million per cubic millimetre ; or,
in severe cases of pernicious anaemia, even to half a million and under. The
number of corpuscles is also diminished in leukaemia, and to a less degree
usually in chlorosis and such cachexies as phthisis and the various forms
of malignant disease. The number falls also, temporarily, after severe
haemorrhages, whether due to traumatism or to disease, as, for instance,
after the intestinal bleeding of enteric fever. Should oligocythaemia be
present in high degree, this will usually be apparent in the abnormally
pale colour of the blood, and the obviously lessened number of corpuscles
in fresh microscopic preparations. When the diminution in the number
of corpuscles is less, the employment of more accurate methods will be
necessary ; and in any case trustworthy information as to the actual con-
dition present can only be obtained by enumeration of the corpuscles by
means of special instruments devised for this purpose. Under certain
circumstances the size of the corpuscles may undergo considerable change,
the diameter sometimes becoming increased to as much as double the
normal length (from 7'5 /x, to 10 /* or even 15 /a). ' This condition, named
macrocythcemia, is apt to occur to a certain extent in any case of severe
anaemia, but more especially in that form known as " pernicious." It
must be carefully distinguished from the swelling of the red corpuscles
which is prone to occur in hydraemic blood.
By microaythcemia, on the other hand, is understood a diminution in
the diameter of the red corpuscles. These smaller bodies, or microcytes
as they are called, are often globular in form, and of a more intense
colour than normal. They are commonly present in pernicious anaemia,
and occur in most other forms of anaemia, especially when severe ; also in
certain toxic conditions and infectious diseases, and after extensive burns
and large haemorrhages. At present, however, but little is known of
their significance, and consequently no information of importance in
diagnosis is to be derived from their discovery. Some observers are of
opinion that they occur as the result of degeneration of the normal red
corpuscles. Gram and Graber, indeed, go so far as to regard these
microcytes as the result of changes in the blood after death.
Occasionally the red corpuscles undergo marked variations in shape,
becoming pyriform, spindle-shaped, reniform, cup-like, or knobbed. A
certain proportion of them, however, retain their normal form. This con-
THE CLINICAL EXAMINATION OF THE BLOOD 415
dition, named poikilocytosis — which is believed to be due in some measure
to a lessened consistence in the stroma of the corpuscles — has been noticed
in leukaemia and in anaemic states, more particularly in pernicious anaemia.
Such remarkable variations in the shape of the corpuscles have indeed
been regarded by some authors as pathognomonic of the latter disease.
As is well known, orenation of the red corpuscles, giving rise to the so-
called mulberry and thorn-apple forms, may occur as the result of evaporation
in normal blood at a varying interval after its withdrawal from the circula-
tion ; but a little experience will prevent any likelihood of confusion with
the change under consideration. Nucleated red cmpusdes are found not
infrequently in the blood in pernicious anagmia, and in leukaemia of the
myelogenic kind, and again after extensive haemorrhages. They may vary
considerably in size, the presence of the larger variety (megaloblasts)
being considered to be of especially grave significance.
The white eorpuscles or leucocytes. — Leueoeytosis. — Comparatively
little was known of the differential characteristics and properties of the
white corpuscles of the blood, or leucocytes as they are now more
generally named, until the introduction by Ehrlich of special staining
methods, by means of which the various forms of leucocytes can readily
be distinguished one from another. The work of Hardy and Kanthack,
and also of Professor Sherrington, in this country has added largely to
oiu- knowledge of the subject ; and these observers, by simplifying the
methods originally devised by Ehrlich, have rendered them more readily
available for clinical research.
At the present day the name " leucocyte " has a somewhat wider
significance than that of a mere synonym for the different forms of the
white corpuscles which, under normal circumstances, can be demonstrated
in the blood. The name as now employed includes also wandering cells,
which may be found in the lymph-stream, in the serous cavities, and in
the intercellular interstices of the tissues. Consequently leucocytes may
be classified as — (a) tissue, and {fS) haemic.
The cells belonging to each of these classes are subdivided, again,
according to their reaction to certain staining reagents, thus ; —
MO h"\ I coarsely granular.
V / jV I finely granular.
(i) Basophil I TT^^ ^T'^"-
^ ' ^ ( finely granular.
(«) Hyaline {l-fj
The classification of leucocytes as tissue or haemic leucocytes re-
spectively, although convenient, is by no means definite. Dr. GruUand
states that when the blood is first formed in the embryo, for a time it
contains no leucocytes whatever, so that none of the leucocytes are
aborigines of the blood ; the coarsely granular basophil cell is found in
the tissues alone, while the finely granular oxyphil cell is rarely met
with elsewhere than in the blood : but, on the other hand, certain cells.
4i6 SYSTEM OF MEDICINE
which at one period of their life-history must be looked upon as tissue
leucocytes, may later be discharged into the blood-stream.
Of the hsemic leucocytes the f/nely grcmular oxyphil variety is by
far the most common normally, since it constitutes about 75 per cent
of all the leucocytes present in the blood. The cell has an average
diameter of 10 /x, and is vigorously amoeboid. Its name is derived
from the fact that the cell substance contains numbers of fine granules,
which refract light to a slightly greater degree than the ground
substance in which they lie. This cell can also be distinguished from
other leucocytes by the irregular and multipartite nucleus, which usually
appears to consist of a number of separate lobes linked together by fine
chromatin threads. After death the various nuclear segments take on a
more regular distribution in the cell -protoplasm, forming rosette -like
masses ; but, when living, the shape of the nucleus is constantly under-
going variation, for which reason it is generally described as "polymorphic.''
Opinions differ as to the cause of this diversity of shape of the
nucleus, but, as has been shown by Professor Sherrington and others,
it is most probably to be attributed to distortions produced by the extreme
amoeboid activity of the cell body. This cell is markedly phagocytic ;
but, as Professor Halliburton and Dr. Brodie have shown, it is readily
killed and broken up by contact with solutions of certain nucleo-albumins.
Vacuoles, probably containing fluid, are often to be seen in the protoplasm
of .the cell.
The finely granular oxyphil leucocyte corresponds to that named
" neutrophil " by Ehrlich and his pupils ; Hardy and Kanthack having
shown that the former name is the more correct, since the granules,
especially under certain conditions, obviously react to acid dyes. This
leucocyte appears capable of undergoing multiplication in the blood-
stream ; but it is somewhat doubtful whether such multiplication takes
place more commonly by karyomitosis, or by direct division of the cell.
The coarsely granular oxyphil cell difi"ers from the finely granular variety,
not only, as its name implies, in the larger size of the contained granules,
but also in the larger size of the cell itself ; the average diameter being
about 12 /i. When examined "on the warm stage it is found to be
amoeboid, but it contains no vacuoles, and is never phagocytic. The
horse -shoe -like or reniform nucleus is fairly regular in shape. The
granules contained in the cell substance are comparatively few in number
and of large size. This is specially noticeable in certain of the lower
animals. The granules are highly refractive, and have a marked affinity
for " acid " dyes, by means of which they can be readily stained. As they
colour deeply when treated with osmic acid, the granules might be regarded
as fatty -in nature, but they are not soluble in alcohol or ether.
The coarsely granular leucocyte has a fairly wide distribution in the
various fluids and tissues of the body ; but in the blood itself it does not
usually constitute more than about 2 per cent of all the leucocytes present.
It is, however, of special interest since, although it is not phagocytic, it
apparently has certain functions of a secretory nature. Thus Hardy and
THE CLINICAL EXAMINATION OF THE BLOOD 417
Kanthack have shown that the injection of a culture of anthrax into the
blood of an animal causes a rapid disappearance of the granules in the
cell protoplasm, and that such disappearance seems to be accompanied by
and related to the secretion of a substance possessed of germicidal pro-
perties. Another special point of interest is that the granules of the
coarsely granular leucocyte contain appreciable amounts of iron and
phosphorus. It is not improbable, therefore, that, although themselves
quite colourless, they are related to the hsemoglobin of the red corpuscles,
which latter they also resemble in their proteid nature, marked refraction,
and strong affinity for "acid" dyes. In this connection, also, it is of
interest to note that the coarsely granular cell is to be found in specially
large numbers in bone-marrow.
The basophil leucocyte, both of the finely granular and the coarsely
granular variety, requires but brief mention, as under normal conditions
the first form is rarely, the second never found in the blood. The finely
granular leucocyte is occasionally met with for an undetermined period
after the beginning of digestion, and apparently under certain pathological
conditions, for GriinTjaum has found it in excess in the blood of ursemic
patients. This cell is of small size, spherical, and in its cell protoplasm
contains numerous minute granules, which are deeply stained by methylene
blue. The nucleus is irregular in shape. A sub-variety of the coarsely
granular leucocyte — the " mast-zellen " of Ehrlich — in which the cell body
is filled with large granules, which are stained of an intense violet-purple
by methylene blue, has been found by Professor Sherrington in the blood
of patients dying in the reaction stage of Asiatic cholera ; and by myself
in some cases of leukaemia.
The small hyaline leucocyte, or lymphocyte as it is frequently called,
from the fact of its presence in large numbers in lymphoid tissue in all
parts of the body, is about the size of a red corpuscle of the blood. It
consists of a minimal quantity of protoplasm free from obvious granula-
tion, in which is embedded a large spherical nucleus readily stained by
methylene blue or other dyes.
The lymphocyte, numbers of which are continuously being shed into
the blood by the thoracic duct, is apparently an immature form of cell.
It is not amceboid. The number in the blood undergoes phasic variation,
reaching its highest point between two and three hours after digestion
has begun. The average number in the blood ranges between 10 and 20
per cent of all hsemic lymphocytes. This proportion, however, may be
greatly exceeded in the form of disease known as " lymphatic leukaemia,"
in which the lymphatic glands undergo enlargement.
The large hyaline leucocyte, or myelocyte as it is also named, possesses
a larger amount of protoplasm than the smaller variety. The nucleus is
usually spherical or reniform, and fairly regular in outline. As it possesses
a comparatively small amount of chromatin, it does not stain well with
aniline dyes. The cell has not been proved to be amoeboid, but never-
theless seems capable of acting as a phagocyte. In the blood it is less
numerous than the lymphocyte, forming usually less than 10 per cent of the
VOI-. V 2 E
4i8 SYSTEM OF 'MEDICINE
hsemic leucocytes. Increase in the number of lymphocytes is usually
accompanied by increase in the total number of myelocytes also ; this being-
specially noticeable in the leucocytosis which accompanies the anaemia of
pregnancy, and that which ensues on typhoid fever. In lymphatic
leukaemia, however, enormously as the number of lymphocytes in the blood
may be increased, no such increase in that of the myelocytes has been
observed. During life the cell protoplasm is apparently homogeneous,
but, when dead, staining by means of methylene blue shows it to be full
of exceedingly fine granules embedded in a matrix which does not take
up the stain.
Leucocytosis may be most simply defined as a condition in which the
number of leucocytes in the peripheral circulation is above the normal
standard.^ It is practically impossible, however, to lay down any exact
rule concerning the numbers of the white corpuscles or the excess
which should be held to constitute leucocytosis. In the same normal
individual variations occur at different times, and different individuals
exhibit considerable range in the numbers of leucocytes in a similar
volume of blood, according in some measure to the physical development
and habit of life of each of them. Taking these factors into consideration,
we shall not err to any great extent if we look upon the normal range in
the adult as extending between a minimum of 6000 and a maximum of
10,000 leucocytes in a cubic millimetre of blood. Any number of
leucocytes below the arbitrary limit of 6000 will constitute a hypo-
leucocytosis, or leucopenia as the condition is also named ; whUe an excess
above 10,000 would constitute leucocytosis. The ratio of white cor-
puscles to red is of itself of comparatively little importance, since conditions
which cause an increase, for instance, in the number of white corpuscles
may bring about concurrently an increase in the red.
It is, therefore, the absolute number of leucocytes in a cubic milli-
metre of blood which must be determined in each case. It is of no less
importance, however, to determine the relative numbers of each kind of
leucocyte present, as by such dififerential enumeration it becomes possible
to discriminate the particular form of leucocytosis with which we have to
deal in any given instance.
Leucocytosis may be either physiological or pathological. These two
kinds may be distinguished by the fact that in the former the increase
affects all varieties of leucocytes, with the exception of the coarsely
granular oxyphil cell; while in the latter it is, for the most part, the
finely granular oxyphil cell which is present in excessive numbers.
Physiological leueoeytosis has been found in newly-born infants, in
the later stages of pregnancy, more particularly in primiparse, and during
the process of digestion. Massage, as Dr. Weir Mitchell has shown, is
found in many instances to induce moderate leucocytosis, and so likewise
does the temporary application of cold in the form of bath.
Leiuxcytods in the new-bom is probably to be explained by inspissation
^ LeulcEemia, or leuoocythsmia, which would be included under this definition, is treated
of elsewhere. See Dr. Muir's article later in this volume.
THE CLINICAL EXAMINATION OF THE BLOOD 419
of the blood in conjunction with more or less continuous digestion
leucocytosis. Rieder and other observers have shown that hyaline cells,
particularly lymphocytes, are more abundant in the blood of the new-
born than are the other varieties of leucocytes^ There is also a definite
increase in the number of coarsely granular cells. The actual number of
white cells present is considerably greater than in the adult, ranging as
it does from 15,000 to 30,000 per cubic millimetre. The number rapidly
declines, however, during the first two years of life, until at the end of
such period the adult normal has probably been reached.
The leucocytosis of pregnancy has no clinical significance ; and, since it is
not present in the early stages, it is also valueless from the diagnostic point
of view. Again, it is by no means of invariable occurrence, especially in
multiparas ; while it is liable to occur also in cases of spurious pregnancy.
Digestion leucocytosis usually occurs in healthy persons, and comes on
at a somewhat variable period after ingestion of food ; beginning generally
about one hour after food, increasing in amount for the next two or three
hours, and afterwards gradually disappearing again in three or four hours
more. In a few instances the blood of persons apparently healthy shows
little or no digestion leucocytosis ; this, in some cases at any rate, seems
to be dependent upon chronic constipation, as Von Limbeck has shown.
The effect of proteid food is especially remarkable in bringing about
digestion leucocytosis ; a mixed dietary is followed by a less striking
result, while a vegetarian diet apparently exerts no appreciable influence.
The increase in the number of leucocytes following the ingestion of a
meal rich in proteids may amount to as much as 30 per cent, or even
slightly more. It should be remembered, however, that the actual
number present will depend on the standard normal to the particular
individual during the passive phase of his digestive functions. It is
always advisable, therefore, to make a control reckoning of the number
of leucocytes in the early morning before the patient has broken his fast.
Starvation in man, especially when of considerable duration, has been
found by Luciani and Von Limbeck to result in a notable diminution in
the total number of leucocytes. Prof. Sherrington, who has studied this
subject in the lower animals, finds that while this is so, yet at the same
time, contrary to what obtains during the opposite phase of digestion
leucocytosis, abstention from food leads to a decided increase in the
numbers of the coarsely granular cell.
Diseases, especially those of malignant nature, which lead to
difficulty either in ingestion or digestion of food — among which
may be mentioned carcinoma of oesophagus or stomach — tend eventually
to bring about not only disappearance of digestion leucocytosis, but an
actual leucopenia.
Pathologrieal leueoeytoses. — For descriptive purposes these may be
classified under the following heads : — (i.) Inflammatory leucocytosis ; (ii.)
Toxic leucocytosis ; (iii.) Leucocytosis of certain infectious diseases ; (iv.)
Leucocytosis of cachexia and malignant disease ; (v.) Post-hsemorrhagic
leucocytosis.
420 SYSTEM OF MEDICINE
(i.) Inflammatory leucocytosis, resulting from simple traumatism with-
out bacterial infection, has recently been the subject of careful investiga-
tion by Prof. Sherrington. In his observations he was able to distinguish
three definite stages of the process : — (a) A leucopenic phase, or hypo-
leucocytosis, during which the total number of hsemic leucocytes falls ;
{h) A stage of hyperleucocytosis ; (c) A second but inconstant stage of
leucopenia.
The preliminary stage of hypoleucocytosis affects all the different
kinds of leucocytes, but perhaps the finely granular variety more
especially. This diminution holds not only for a xmit volume of blood,
but also relatively for the number of chromocytes, and this in spite
of coincident apoplasmia or inspissation of the blood.
In the second stage, that of reaction, a hyperleucocytosis occurs in
which both the finely granular and hyaline leucocytes are concerned.
Although this is the case there is a continued fall in the numbers of the
coarsely granular variety. Finally, after a variable interval, the leuco-
cytosis passes away, and may be succeeded by a fall which, on occasion,
may again reduce the number of leucocytes below the normal average.
(ii.) Toxic lehbcocytosis. — Under this heading may be considered the results
of subcutaneous, intravenous or intraperitoneal injection of various toxic
substances, whether employed therapeutically or not. It has long been
known that extracts, protein or dead cultiu^es of bacteria, filtered yeast-
cultures, organic substances such as fibrin ferment, hemi-albumose,
peptones, nuclein, and leech extract, as also curare, tuberculin, pyocyanin,
uric acid, and urates, have the effect, on injection, of bringing about a
marked and rapid diminution in the number of the leucocytes. This stage
of hypoleucocytosis, leucopenia, or leucolysis, as it was named by Lowit in
accordance with the hypothesis advanced by him that leucocytes undergo
actual destruction, is in turn followed by a hyperleucocytosis of greater or
less degree, provided that the dose of toxic material received into the
system be not sufficient to cause death. That the preliminary leucopenia
is not due to a leucolysis has been proved by Goldscheider and Jacob,
who have demonstrated that the leucocytes vanish from the peripheral
circulation in consequence of their having become stored in the capillaries
of the lungs. This process probably occurs in the liver and spleen also.
During the second stage these leucocytes find their way once more into
the general circulation, together, as certain observers believe, with others
of more recent origin.
(iii.) Leucocytosis of certain infections. — In many of the acute infectious
disorders leucocytosis has been found, more particularly in small-pox,
scarlet fever, diphtheria, pneumonia, acute rheumatisfli, anthrax, erysipelas ;
and perhaps in measles. Leucocytosis has also been described in typhoid
fever ; but most observers are now of the opinion that it does not occur
in the absence of complications. Leucocytosis is not apparent in tuber-
culosis or in influenza. The same has been said of malaria, but Dr.
Billings has put on record a series of observations which tend to show
that definite stages of leucopenia and leucocytosis undoubtedly present
THE CLINICAL EXAMINATION OF THE BLOOD 421
themselves in the course of this disease ; although these variations, being
of slight extent, have been overlooked by other observers. In pneumonia,
on the other hand, the process is generally so well marked as to afford
most valuable aid in the diagnosis and prognosis of the disease.
The increase in the number of leucocytes is due to increase of the
finely granular oxjrphil variety; it begins with the rise of the temperature,
and, except in cases of extreme gravity, not only continues but increases
up to the crisis, at which stage a well-marked leucocytosis is a very
favourable sign. On the other hand, if leucocytosis be absent or ill
marked, the case will probably end in death. In scarlet fever and other
diseases, in the course of which leucocytosis is ordinarily demonstrable,
we can in like manner judge in great measure of the severity and the
probable termination of any given case by the extent of the leucocytosis.
This being so, it is obviously desirable that the blood should be more
generally examined in infectious disease than has hitherto been customary.
The importance of these observations is confirmed by the work of Everard,
Demoor, and Massart, who state, as the result of the inoculation of guinea-
pigs with varying doses of pathogenetic organisms, that while the primary
result is invariably a fall in the number of leucocytes in the blood, this in
turn is succeeded by a leucocytosis in those instances in which the
animal eventually recovers. They add that, in immunised animals, a
leucocytosis appears immediately, no stage of leucopenia being obvious.
Septic infections, whether due to streptococci or staphylococci, are
usually associated with a definite leucocytosis, the number of leucocytes
being often increased as much as fourfold. Such diseases as erysipelas,
cellulitis, and puerperal septicsemia come into this category, and also
suppurative inflammations or abscesses in any part of the body.
That the presence of collections of pus may be diagnosed from the
occurrence of leucocytosis is a fact of much clinical value. Thus Stengel
has found, as the result of examination of the blood in a number of cases
of appendicitis, that in those in which suppuration had supervened,- in
consequence of the presence of the staphylococcus albus, the number of
leucocytes varied from 15,000 to 40,000^ while in the non-suppurative
cases leucocytosis was extremely moderate or absent.
Von Limbeck has indeed asserted that leucocytosis only appears when
exudation into the tissues occurs, and that the extent of leucocytosis
which accompanies it is directly dependent on the degree of cellular rich-
ness of the exudate. Thus leucocytosis is a usual concomitant of inflam-
mations of serous membranes, whether of the peritoneum, pleura, or
meninges. The extent of leucocytosis, however, often bears no relation
to the amount of the exudation ; and in tuberculous inflammations of
serous membranes leucocytosis is invariably absent, unless in the case of
secondary septic infection.
(iv.) Leucocytosis of cachexia and malignant diseases. — During the course
of many cachectic diseases a leucocytosis of considerable extent is apt to
arise. Stengel finds that this is particularly the case in congenital
syphilis and rickets, the increase in the number of leucocytes being some-
422 SYSTEM OF MEDICINE
times so great as to simulate leukaemia. In such cases the diagnosis is
the more difficult as the increase in numbers mainly concerns the hyaline
leucocytes.
In the moribund a, "terminal" leucocytosis is frequently observed,
especially in the subjects of protracted chronic disease. This is merely
an exaggeration of the leucocytosis of cachexia. According to Cabot and
others, this condition is specially apt to supervene in fatal cases of
pernicious anaemia. The explanation of the condition is by no means
simple ; but it has been suggested that a terminal infection or a retarda-
tion of the circulation, with fall of blood -pressure, may bring about a
discharge of leucocytes into the circulation.
The leucocytosis of malignant disease is believed by some authors to be
due to the cachexia of the later stages. Others look upon the inflamma-
tion surroTinding the focus of disease as the immediate cause. Leuco-
cytosis is more pronounced in sarcoma than in carcinoma, and tends to be
more marked the less circumscribed the growth.
(v.) Post-Jicemorrhagic leucocytosis. — Loss of blood, especially if serious in
amount, is rapidly followed by a leucocytosis, the extent of which is more
or less dependent on that of the haemorrhage on which it ensues. It may
appear within an hour or so, and may persist for several days.
Observers differ somewhat as to the exact nature of the leucocytosis ;
some assert that the finely granular oxyphil (adult) cells are increased
both absolutely and relatively, others that the most noticeable feature is
an excess of the mononuclear hyaline corpuscles, and more particularly of
the lymphocytes. It is not improbable, however, that these apparently
divergent results may have relation to the cause of the haemorrhage,
whether traumatic or pathological, in each particular instance.
Concerning the actual causation of leucocytosis much difference of
opinion exists. The current hypothesis is that the process mainly depends
on what is named " chemotaxis." Thanks in large measure to the
researches of Schulz, Von Limbeck, and of Goldscheider and Jacob
abroad, together with those of Sherrington, and Hardy and Kanthack in
this country, much light has recently been shed on the processes concerned
in leucocytosis.
The mass of experimental evidence that has accumulated as the result
of the labours of various workers in this field all tends to support the
chemotactic hypothesis of leucocytosis, according to which leucocytosis
must be regarded as in the main a phenomenon dependent on a chemical
stimulus of a more or less intensive character, which is enabled to act on the
haemic leucocytes, and also on the blood-forming organs, through the
medium of the circulating blood.
As previously stated, the injection of bacteria, or their metabolic
products, whether toxins or proteins, or even simple traumatism, brings
about, in the first instance, a rapid disappearance of leucocytes from the
peripheral circulation.
This phase was thought by Jiowit to be due to an actual destruction
of corpuscles, to which process, therefore, he applied the name leucolysis.
THE CLINICAL- EXAMINATION OF THE BLOOD 423
This view is now no longer tenable since, as Schulz first indicated, the
more or less complete disappearance of leucocytes from the peripheral
•circulation is due to an altered distribution ; the leucopenia or hypo-
leucocytosis being coincident with a storage of leucocytes in the internal
organs. That such is the case has been definitely proved by Goldscheider
and Jacob, who found that the leucocjrtes accumulate chiefly in the
«apillaries of the lungs and liver.
This stage of hypoleucocytosis is due, as it appears, to a repellent
action on the circulating leucocytes, and is in turn followed by
a hyperleucocytosis or increase in the white corpuscles, provided that
the injury inflicted on the organism be not of so severe a character
as to render recovery improbable. This hyperleucocytosis may be due,
as Schulz has suggested, to a secondary change in the distribution of
the leucocytes, which, having been just previously packed away in the
capillaries of certain of the viscera, now once again find their way back
into the peripheral circulation, together with others which for the time
are carried along with them, the increase in numbers above the normal
being thus accounted for. The researches of Goldscheider and Jacob,
however, afford reason to believe that this explanation is insufficient to
account for the facts, and that at this stage the total number of leucocytes
in the blood may be positively increased, although the place of origin of
such additional supply may be difficult to determine.
Goldscheider and Jacob were able, indeed, to demonstrate that during
this stage of hyperleucocytosis not only is the number of leucocytes in the
capillary area of the pulmonary circulation equal to that of the leucopenic
phase, but may be actually greater than before. It would seem fairly
•certain, therefore, that under the influence of chemotactic attraction the
"blood-forming organs are excited to greater activity, the result of which
is seen in an abnormal output of cells which may happen to be stored at
the time in these areas, together with simultaneous multiplication of
leucocytes.
From experimental evidence we learn that the extent of the repellent
action exerted on the haemic leucocytes, as well as that of the subse-
quent leucocytosis, are determined, in large measure at any rate, by
the virulence and the amount of the particular material injected. Thus
the more potent the influence on the organism generally, the more pro-
nounced will be not only the preliminary leucopenia, but also the
secondary leucocytosis. It must be understood, however, that this state-
ment only holds good up to a certain point; for when the dose and
virulence of the noxious agent are sufficiently intense, and the consequent
depression is so profound that the system is unable to rally, leucocytosis
■does not occur. It is possible, therefore, in most cases, to judge from
the presence or absence of leucocytosis whether in any particular
instance recovery will or will not take place— a sign which, as I have
stated, has already been found of great assistance in the prognosis of
.•specific infections in man.
In certain instances leucocytosis arises without any preliminary
424 SYSTEM OF MEDICINE
leucopenic phase. This occurrence has been described by G-oldscheider
and Jacob as a result of the experimental injection of a glycerine extract
of spleen ; and the same has been noted in animals which are either
naturally or artificially immune.
II. Estimation of the specific gravity of the blood. — Until
recently records of the specific gravity of the blood in disease have
been very scanty, as it was necessary to remove a considerable quantity
of blood for the purpose ; moreover, the operation, involving as it usually
did the use of the specific gravity bottle, was by no means an easy one.
Moreover, by this method it was practically impossible, except with very
elaborate precautions, to take the specific gravity of uncoagulated blood ;
hence defibrinated blood was used on the assumption that its specific
gravity does not appreciably differ from that of the fluid circulating in
the living vessels.
The ingenious method devised by the late Professor Eoy, however,
affords a means of making rapid and accurate observations at the expense
of a single drop or even a fraction of a drop of blood.
Roy's method consists in observing whether a drop of the blood, rapidly
withdrawn from the circulation and placed in a solution of known specific
gravity, rises, sinks, or remains stationary in this solution.
Certain modifica,tions of detail have been suggested by Dr. Lloyd
Jones, and by myself, which have rendered it more easily applicable to
clinical requirements.
The requisite apparatus consists of —
1. A series of solutions of various specific gravity, ranging from 1025
to 1070, one member of the series corresponding to each unit of the third
place of decimals. For ordinary use, however, a much less number will
suffice, as the numbers at the ends of the scale are seldom if ever required.
In any case, however, for an extended series of observations, a consider-
able quantity of fluid corresponding to each degree employed should be
provided. Roy originally used water to which glycerine was added in
each case until the mixture was of the necessary specific gravity ; but such
solutions are apt to be untrustworthy, as the specific gravity is not constant,
particularly if, as is often the case, a mould develop on the surface of the
fluid. Fluids more suitable for the purpose may be made up from a stock
solution of equal parts of glycerine and distilled water saturated with
Barff's boro-glyceride and magnesium sulphate, with the addition of a small
quantity of corrosive sublimate. If the specific gravity is to be lowered,
this stock solution is diluted with water, and its density can be increased
to any needful extent by the addition of more glycerine and boro-
glyceride. Solutions thus made have a constant specific gravity. More-
over, blood does not clot very rapidly in them. The accuracy of the
graduation should be ensured in the first instance by testing the specific
gravity of the fluids with an accurate hydrometer, and by controlling
these results with the balance. Small quantities of these fluids should be
kept in a series of two-ounce bottles, the stoppers of which have been care-
THE CLINICAL EXAMINATION OF THE BLOOD 425
fully greased so as to prevent any change of density by evaporation. The
small bottles are best fitted into wooden stands for convenience of transit.
2. A number of glass pots about \\ inch deep and half an inch wide, of
which probably at least half a dozen will be required for one observation.
3. Fine capillary pipettes, formed by drawing out a piece of small
glass tubing ; the last quarter of an inch should be bent at right angles to
the stem. To the opposite and wider extremity a piece of india-rubber
tubing should be fixed, to which the mouth may be applied when the
contents of the pipette are to be expelled.
It is usually possible, with practice, to make a fairly accurate guess at
the specific gravity of the blood in each case, so that six or more of the small
pots may be filled from the small bottles (by means of a fairly large
pipette) with fluids of the densities likely to be required. Otherwise in a
first observation every alternate number may be omitted so as to have a
longer range at hand. A finger is then cleaned, and a fairly large drop of
blood obtained by puncture with the precautions already laid down (p. 409).
The drop is drawn by suction into one of the capillary pipettes, and, the
pipette being lowered at once beneath the surface of the fluid in one of
the small pots, some of the blood is gently blown into it. If the pipette
be held so that the end is horizontal, the drop of blood expelled, if of the
same density as the fluid contained in the pot, will have no tendency
either to rise or to fall ; if its specific gravity be higher than that of the
fluid it will tend to fall, if lower to rise. With a little care it is com-
paratively easy to find the fluid in which it remains stationary, or at
any rate to hit upon two adjoining numbers, in one of which it may
slowly rise, and in the other slowly fall. To obtain a reading correct to
a decimal part of a degree we shall carefully mix measured quantities of
the two numbers between which the specific gravity has previously been
found to lie, and in this manner readings to one-half or one-third of a
degree, or even to one-tenth of a degree, may be obtained. It is worthy
of note that the portion of the blood last expelled from the pipette is not
infrequently some 0'0005 above that of the portion first expelled. This
difference is due partly to capillary action in filling, and partly to friction
of the blood against the wall of .the pipette. If extreme accuracy be
desired, the difficulty can be overcome by using the corresponding portion
of each drop withdrawn.
In order to avoid any trace of admixture of two successive drops of
blood, and t» avoid the rapid clotting which goes on in the drop received
into a pipette in which blood has previously been received, a fresh pipette,
recently drawn in the blow-pipe flame, should be used for each observation.
It is also necessary to see that the pipettes are carefully dried, as during
their cooling moisture tends to condense in them.
Method of Hammersehlag. — This, which is essentially a modification
of that originally devised by Eoy, differs from the latter in that mixtures
of chloroform and benzol are employed instead of more or less dilute
glycerine solutions.
The supposed advantage of Hammerschlag's method is that a drop of
426 SYSTEM OF MEDICINE
blood -wlien introduced into such a mixture as that devised by him does
not tend to mix with it, but retains the appearance of a red bead.
Estimations are made in one of two ways : (a) A number of small
pots are prepared, containing a series of mixtures of chloroform and
benzol previously made up, and ranging in specific gravity from about
1035 to 1060. Into several of them in turn a drop of blood is intro-
duced, by means of a bent capillary tube, until that mixture is found in
which the drop of blood neither rises nor falls, {fi) Chloroform and
benzol are mixed in an ordinary urinometer glass in such proportions
that, when tested by means of a urinometer possessing a somewhat
extended scale of graduations, the specific gravity of the resulting mixture
is found to be about that of normal blood (1055-1069). A drop of blood
is then blown out into the mixture at a point beneath the surface by
means of a bent capillary tube. If the bead tend to sink, chloroform is
added drop by drop ; if, on the contrary, the bead tend to rise, benzol is
added in like manner. After every such addition the whole contents of
the urinometer glass should be thoroughly 'fetirred by means of a glass
rod in order to ensure the uniformity of the specific gravity of the whole
mixture. As soon as the drop of blood no longer shows any tendency
either to rise or fall, the specific gravity of the surrounding liquid is
obviously equal to that of the blood itself. AU that now remains to be
done is to take the specific gravity of the chloroform and benzol mixture
by means of the urinometer, and the result thus obtained furnishes the
required specific gravity of the specimen of blood.
Hayeraft's method. — Two mixtures of benzyl chloride (sp. gr. 1100)
and toluol (sp. gr. 0870'6) are made, the one (A) having a specific gravity
of 1070, and the other (B) having a specific gravity of 1020. With
a cubic centimetre pipette, graduated to xuTr*li •'■•'•i ^^'^ *'••'• °f -^ ^^
measured off into a glass tube, and the drop of blood to be tested is
then allowed also to flow into the tube. The drop of blood, having
a difierent surface tension, does not mix with the solution, but floats
on its siuface as a tiny red globule. The graduated pipette is now
filled with solution B, which is allowed to run slowly into the mixing
tube, the tube being shaken after each addition. As B flows in, the
specific gravity of the mixture falls, and after each addition and shaking
the red globule returns more and more slowly to the surface. At last it
tends neither to rise nor sink, and, the specific gravity of the mixture being
now that of the blood itself, this can readily be calculated or read off
from the table attached to the apparatus ^ sent out by the maker. Sup-
pose 0-5 c.c. of B to have been added, the total weight of the fluid
divided by its volume will give the specific gravity of the mixture : —
1 C.C. at sp. gr. 1070 ..... 1070
■5 „ „ 1020 510
1 -5)1510
1053
' Made by Mr. Fraser. Lothian Street, Edinburgh.
THE CLINICAL EXAMINATION OF THE BLOOD /^zy
As the mixtures of benzyl chloride and toluol expand with heat
they will vary in their specific gravity, so that, if exactitude be re-
quired, a correction for temperature must be made. The solutions
A and B are prepared at the temperature of 15'6° centigrade, or 60°
F., and if the temperature of the room be also 60° F. no correction
will be needed. If, however, the surrounding temperature be higher
than 60° F. the specific gravity of the fluids will be lowered, the
fall of specific gravity being, roughly, at the rate of one degree for every
2°F.
In his original paper Haycraft warns those who may employ his
method that it is well not to allow the fumes of benzyl chloride to get
into the eyes, as, the vapour being very irritating, somewhat painful
smarting may result.
Method of Schmaltz. — Mention must be made of this method because,
although somewhat tedious, it gives very accurate results, and a large
amount of work has been carried out by its means. As, however, it
involves the use of delicate chemical balances it is hardly likely to come
into general use in clinical work. The blood, of which the specific
gravity is to be determined, is carefully weighed in a small capillary tube
(pycnometer) of known weight. By subtraction the weight of the blood
is obtained, and if this be divided by the weight of an equal amount of
water the specific gravity of the blood is obtained.
Whatever the method, it is, of course, only the specific gravity of the
blood, as a whole, which is thus determined. To what particular factor or
factors, in each instance, alterations in the specific gravity of the blood
are to be attributed remains to some extent a matter of conjecture. It
is obvious that the alteration may be due to one or more of the following
causes : —
1. An increase or diminution in the number of corpuscles in a given
volume ; the specific gravity of individual corpuscles, and of the plasma
remaining unchanged.
2. An increase or diminution in the density of the plasma ) the specific
gravity and the number of corpuscles remaining unaltered.
3. A simultaneous increase or diminution in density both of cor-
puscles and plasma, with or without alteration in the number of corpuscles
in a given volume of blood.
Schmaltz, from observations with his capillary pycnometer, concludes
that, broadly speaking, the specific gravity of the blood varies directly as
the percentage of haemoglobin, but is largely independent of the number of
red corpuscles. Hayem states that the specific gravity depends on the cor-
puscular richness of the blood — the difference possibly being caused by the
passage of a certain amount of plasma into the lymph spaces. Dr. Lloyd
Jones expresses somewhat the same opinion. Certain experiments of
my own appear to show that, in the healthy animal at any rate, a
rise of density of the blood, produced artificially, is accompanied by a
•somewhat closely corresponding rise in the number of red corpuscles.
428
SYSTEM OF MEDICINE
These experiments further show that so long as the density remains un-
altered, even under abnormal circumstances, the number of the corpuscles
may also remain practically unaffected.
Again, in cases of paroxysmal hsemoglobinuria, when, during the
paroxysm, the red corpuscles are broken up and the dissolved haemoglobin
has escaped from the blood, the diminution in number of the corpuscles
is accompanied by a concurrent fall of the specific gravity of the blood ;
as the following observations show : —
Speciflo Gravity
No. ot
of the Blood.
Red Corpuscles
Before paroxysm
. 1-0523
3,910,000
After
. 1-0315
3,680,000
Before ,,
. 1-0675
-3,710,000
After „
. 1-0505
3,440,000
Before „
. 1-0516
3,270,000
After
. 1-0506
2,970,000
After
. 1-0470
2,760,000
I have also shown that the specific gravity of the plasma itself usually
falls concurrently with that of the total blood ; this being especially the case
after experimental injections into the blood-vessels, and in those cases in
which the specific gravity of the blood as a whole has been lowered by
hfemorrhage. It is also very noticeable in severe eases of pernicious
anaemia. At the same time there can be no doubt that in the lowering
of specific gravity which may occur under these various circumstances,
the substance of the coloured corpuscles has its share of the additional
amount of water, and that these corpuscles themselves also become of
less specific gravity than previously.
If we desire to observe the specific gravity of the blood serum or plasma
we may use Eoy's method, the blood having previously been centrifuged
in capillary tubes.
Professor Sherrington thus describes his method of obtaining the serum
or plasma from small quantities of blood : — " A drop of blood, as it exudes
from a prick in the skin, is taken by capillarity into a fine freshly-drawn
glass tube, like a vaccine tube but longer, and bent into a U -shape. The
capillary U-tube is then placed, with its bent end downwards, into a
' bucket ' on the centrifuge, or on a radial slot on a vulcanite disc ; the
two open ends will then be toward the centre of rotation, and in a few
minutes after the instrument is set in action a clear layer of serum or
plasma is obtained in each limb of the tube."
Sherrington and myself have examined the specific gravity of the
blood of a number of cases in well-marked ansemia ; more than a hundred
cases have been observed, with the results given in the appended table.
Observations on other diseases have not been by any means so many,
but the results are given for purposes of comparison. The observations
were taken for the most part at the same time of day, about 11
A.M., a point which Lloyd Jones has shown to be of importance. For
comparison certain results arrived at by Quincke and others, ■ work-
ing with the older methods, are also brought together in the table, as
THE CLINICAL EXAMINATION OF THE BLOOD
429
well as some of those obtained by Lloyd Jones, who worked with Roy's
method.
In the table the numbers on each side of a hyphen denote the maxi-
mum and minimum of the observations relating to the particular diseases ;
where one number only is given, this is the only one recorded.
Specific Gravity of the Blood in Various Diseases.
Disease.
Sherrington and
Copeman.
Lloyd Jones.
Quincke.
Becquerel and
Bodier.
Anaemia :
1041-1043
1032-1045
1035-2-1049-1
1045-8 (mean of
Chlorosis '
(severe cases)
(probably in-
cluded cases of
pernicious an-
aemia)
observations
on six chlorotic
girls)
Pernicious
1027-1034
1029-1040
ansemia
Leucocythsemia
1048-5-1051
(1 case in last
stage) = 1032
...
1044-3
(1036 - 1049-5
Robertson) range
of five oases
Gastric ulcer
1038 (very an-
8emic)-1060-6
Lymphadenoma
1062
Hsemoglobinuria
1047-1057
Cardiac
1033-1052
Compensated
1052-5 (mean of
(none congeni-
1054
series of 24 oases)
tal)
Uncompensated
1051-6
Congenital
1061-1072
1050-2 (mean of
series of 31
cases in third
stage)
Diabetes
1058-1061
1054-1061
1054-9-1059-6
Cirrhosis of liyer
1046-1052
1049 -6 (with hae-
, with ascites
mophilia)
Acute nephritis
1041-1057
1038-1060
Chronic nephritis
1054-5-1060
1034-5-1060
1047-3-1048-7
Uraemia
1052
...
1050-5
Tuberculosis (of
1048-5
kidney)
Tuberculous peri-
1057-1059
tonitis
Chorea
1050-1054
Chronic hip dis-
1042-1047
ease
Dysentery
1049-1052
Chronicplumbism
1031
Myxoedema
1058-1062
It is worth noting that it is not possible in some cases to form a correct
judgment of the probable specific gravity of the blood from the appear-
ance of the patient, as, under certain circumstances at present but ill
understood, the tint of the skin is not always indicative of the poorness
or richness of the circulating blood. Oppenheiiner, in the course of a
series of observations on the enumeration of the blood corpuscles -(vith
' Schmaltz, using his capillary pyonometer, found the blood in chlorosis possess a specific
gravity of 1030-1049 (29 cases). But he apparently includes cases of pernicious ansemia.
430 SYSTEM OF MEDICINE
the hsemocytometer, frequently came across such apparent discrepancies,
which he attributes to irregular circulation.
Shock. — In the condition known as " shock," which is apt to supervene,
to a greater or less degree, on serious injuries and on surgical operations —
more particularly when the contents of the abdominal cavity are in any
way interfered with — the specific gravity of the blood becomes raised,
sometimes to a marked extent, as was first demonstrated experimentally
by Sherrington and Copeman. This observation has since been abun-
dantly corroborated by the result of the investigations of Griinbaum and
others on the human subject. It is thus apparent that valuable infor-
mation as to the condition of a patient subsequent to severe accidents
or operations is obtainable by examination of the specific gravity of the
blood. A well-marked rise of specific gravity, under the conditions in-
dicated, is of distinctly unfavourable import. (See Art. "Shock and
Collapse," vol. iii. p. 320.)
III. Estimation of the colouring matter in the blood.^ — Various
methods have been elaborated from time to time for the estimation of
hsemoglobin, but the colorimetric method is the only one which is
sufficiently rapid for clinical purposes. Of the colorimetric instruments,
devised for these estimations, those best known are Gowers' and v.
Fleischl's. The latter apparatus is in general use on the Continent and
in America, while, not unnaturally perhaps, the former is better known
and more often employed in England. Although both these instruments
require brief description, yet it is probable that they will be abandoned
before long in favour of a more accurate hsemoglobinometer recently
introduced by Dr. Oliver. In the colorimetric method a more or less
diluted blood solution is compared with a colour standard which, in
Oliver's and v. Fleischl's instruments, consists of tinted glass, and in that
of Gowers of a glycerine-and-water solution of picric acid and picrocarmine
solidified with gelatine. In the first two cases a definitely diluted blood
is compared with standards of varying intensity, while in the third
the blood solution is gradually diluted until its tint corresponds with
that of the fixed standard. If any approach to accuracy in the results
is to be looked for in the use of any of these instruments, we must
provide —
(i.) A standard light.
(ii.) A reflecting surface of standard tint.
(iii.) A means of cutting off extraneous light.
(i.) The employment of a standard light is of special importance since
the results obtained will vary with the nature, and, to some extent, with
the intensity of the illumination. As it is practically impossible to ensure
in every series of observations made by different persons that the source
and intensity of the light employed shall be identical, it is desirable, in
recording the results of hsemometric observations, that a note of the nature
and position of the light employed should be appended. On this point
Dr. Oliver strongly insisted in his Croonian lectures for 1896, in which he
THE CLINICAL EXAMINATION OF THE BLOOD
431
demonstrated, by means of curves, the extraordinary divergence in colour-
value of progressive dilutions of blood when estimated, by means of Lovi-
bond's graded glass colour standards, in dayUght and by candle-light
respectively.
The colour-curves drawn up by him are made by entering the colour
units on the side of the diagram to form abscissae with the standard grada-
tions which appear at the foot. By daylight (Fig. 11) it will be observed
that the colour-curves of the blood are made up of varying proportions of
red, orange, and yellow. In the lower percentages (10, 20, 30, and 40)
red does not exist as a separate colour ; it is only present in combination
with yellow, as an orange made up of equivalent proportions of each. In
these lower gradations the place of red is taken by yellow.
UNITS OF
COLOR
4
....
^~
"■"
,^_
7
r
/
/
/
^
7
*■
■^
V
•i"
^
/
0^
^
I-'
/
^
^
/
^
/
^
^.
/
l^
T>[
■/
/
/
/
/
/■
/
■^
,
/
■~
is
If
X
»^'
Fia. 11. — Specific colour-curve of blood, daylight (Oliver).
Between gradations 40 and 50 yellow dies out, and then red appears-
and increases progressively until at the highest grade it is the dominant
colour. In these daylight gradations the curve of orange is the pre-
dominant one, though it begins to die out in the higher part of the scale.
By candle-light (Fig. 12) the colour-curves are quite different and are
less complicated.
Red is predominant throughout, except at the lowest grade, where it
is subordinate to orange. From this point upwards orange gradually
diminishes, and at 90 vanishes entirely; the highest grades are dis-
tinguished by pure red. The remarkable difference between the colour-
curves furnished by the two kinds of light is doubtless due to the
preponderance of yellow in the candle-flame.
Again, as Mr. Lovibond had previously observed in the matching of
some of the aniline dyes. Dr. Oliver finds that the solution of blood
possesses the quality of colour-purity, as distinct from colour-depth and
colour-composition, or brilliancy in a remarkable degree ; for it remains after
these others have been duly matched. In the hsemoglobinometer devised
432
SYSTEM OF MEDICINE
by Mm this difficulty is met by using one of the lower grades of the blue
glasses as a cover-glass to the blood-cell— an adjustment which does not
disturb the correct reading of the hsemoglobin.
(ii.) Whatever source of light be employed the rays should be reflected
from a " dead " surface of a pure white colour. In the instructions sent
out with Growers' hsemoglobinometer, it is suggested that the estimation
should be made by holding the tubes between a white cloud and the eye
of the observer ; or that light should be reflected from a sheet of white
paper held at an angle with the tubes. Sherrington, in measuring the
amount of hsemoglobin in the blood by the Gowers' instrument, employs
UNITS
"
~^
'
~
'
— 1
COLOR
9
y
/
/
8
/
/
7
/
/
6
/
y
5
/
^'
y
4
3
/
^1
y
3
A
y
2
'^
z'-
ly
1
y^
—
-
7<
•y
-^
——
-.
._
)hJ
^N
■X.
^
20 30 40 SO 60 7.0 SO 90 JQQ 110 120
Uh H/tnuu.
Fig. 12. — Specific colour-curve of blood, candle-light (Oliver).
the light of a Welsbach lamp reflected from a vertical sheet of white
paper not otherwise illuminated. To secure absolute uniformity of tint
in the reflecting surface Lovibond uses pure, freshly precipitated calcium
sulphate compressed into a slab. This material, which answers admirably,
has been adopted in the construction of Oliver's and v. Fleischl's hsemo-
globinometers.
(iii.) Increased accuracy in hsemometric observations may also be
obtained by examining the blood solution and the colour standard through
a tube of metal, or other material, of about ten inches in length and
blackened within. The exclusion of outside light is thus ensured as well
as the maintenance of a definite distance between the observing eye and
the objects to be compared.
Oliver's hsemoglobinometer. — This apparatus is an adaptation to
hsemometric work of the tintometer, an instrument invented some yjears ago
by Mr. Lovibond of Salisbury for the purpose of estimating with scientific
accuracy the true colour intensity of different substances, whether solid
or liquid, which are employed in various manufacturing processes. As in
THE CLINICAL EXAMINATION OF THE BLOOD 433
the original instrument, use is made of tinted glass standards, with which
the solution of blood, diluted to a definite degree, is compared by light
reflected from a surface of pure calcium sulphate — the examination being
made through a camera tube to exclude outside light.
With the tintometer which, before the introduction of Oliver's instru-
ment, had been employed by myseK for some years past in the estimation
of the colour intensity of the blood, three sets of definitely graded glasses
are provided ; one for each of the dominant colours, red, yellow, and blue.
The graduations in each set are of equivalent value, the test of which is
the production of a neutral tint when equivalent grades of the three
colours are mixed. On the other hand, any shade or degree of colour can
be matched by appropriate combinations of non-equivalent grades, and
the measurement thus made can be recorded numerically and so repro-
duced at will. By means of Lovibond's standards Oliver has determined
the colour value of progressive dilutions of normal blood by uniform
candle-light, and also by daylight. Corresponding to these values he pro-
vides a series of glass standards by comparison with which the percentage
colour-intensity of any sample of blood can be read off at once. Oliver has
done good service in so simplifying the use of the tintometer that, while
his modification is much more compact and so more readily applicable to
clinical work, all the essential points of the original instrument are
retained. In the haemoglobinometer, however, provision is made for
utilising a double instead of a single transmission of light through the
blood solution and the standard glasses. The originator of this method
asserts that greater accuracy of estimation is rendered possible when such
double transmission of light is utilised, especially if working with speci-
mens which, as in the case of blood obtained from cases of severe anaemia,
present a low colour intensity. On the other hand, when the colour more
nearly approaches normal it is possible to carry out an estimation with
half the quantity of blood that would otherwise be requisite.
The apparatus as sent out for use consists of — (i.) an automatic blood-
measuse; (ii.) a mixing pipette; (iii.) the blood-cell and cover-glass; (iv.)
sets of standard gradations ; (v.) riders ; (vi.) the camera tube ; (vii.)
standard candles ; (viii.) a bottle of antiseptic fluid, a lancet, needles, and
thread.
(i.) The automatic blood measure has a capacity of 5 c.mm., and fills
readily by capillary attraction. It is made of stout glass, and the end
presented to the blood is well polished, so that all traces of blood can be
removed from it by the finger. The bore is dried out before an observa-
tion by passing a needle through it threaded with darning cotton. The
handle is useful for stirring together the blood and water in the blood-cell.
(ii.) The mixing pipette is provided with a rubber nozzle which fits
over the polished end of the blood-measurer, and ensures the complete
rinsing out of the blood with the first few drops of water.
(iii.) The blood-cell is of more than sufiicient capacity to ensure the
complete liberation of the haemoglobin. When filled level with the rim
it yields a blood solution of rather less than 1 per cent. It is itself the
VOT,. Y 2 F
434
SYSTEM OF MEDICINE
measure of the amount of water to be added, and it is quite easy to fill it
accurately.
Fig. 13. — 01iver*8 haemoglobinonieter. a, Sets of standard colour grades ; 6, guarded lancet ;
c, automatic blood -measure ; d, mixing pipette; e, blood-celland cover-glass.
(iv.) The standard gradations are arranged as circular discs in two
slabs, six in each; and they represent divisions of 10 degrees of the
scale from 10 to 120 inclusive.
THE CLINICAL EXAMINATION OF THE BLOOD 43S
(v.) The riders 'are small squares of tinted glass provided for the
reading of the degrees between each standard gradation. In use the slip
of colourless glass is placed over the cover of the blood-cell, so as to
balance the effect of the layer of glass of the rider which is laid over the
standard. Two sets of riders have been arranged ; one suitable to ensure
the finer readings — for example, of 1 degree for physiological observation,
and the other, suflScient for ordinary clinical observation, to enable the
observer to determine differences of 2 degrees. For the reading of the
units nine riders are required, which are grouped into three slides. It
should be premised that the value of the riders is neither the same in
the two standards required for candle-light and daylight, nor in the
upper and lower halves of either standard. This want of uniformity
arises, as previously stated, from the differences of the specific colour-
curves in the two standards, and in the two portions of each. In the
transition grades — the lowermost of the upper half and the uppermost of
the lower half — this rule does not accurately apply ; but inasmuch as the
departure is constant in aU observations, and is moreover slight, it may
be disregarded for the sake of simplicity.
The daylight standard is less well adapted to the finer readings than
the candle-light one, because the value of each rider becomes equal to
2 degrees in the upper half of the scale and 4 degrees in the lower
half ; and when candle-light is used each rider has an equivalent value in
the six stronger grades of 1 degree and a double value in the six weaker
grades of 2 degrees. For ordinary readings one rider only is used,
namely, that which is equivalent to 5 degrees in each slab of the
standards. Therefore each set of six standard gradations, whether for
candle-light or daylight, has its own rider. When the blood solution is
deeper in colour than any particular standard gradation, but is over-
stepped by the rider, the mean between the two may be taken as the
reading j and the same rule will apply when the colour of the blood is
higher than the rider, but is not so high as that of the next standard
grade above. Hence this single rider may be made to provide readings
of 0-25 and 0-75.
(vi.) The camera tube. — A tube of simple construction is provided
which, being collapsible, will pack into a small compass with the other
parts of the apparatus.
(vii.) The standard candles are of such a size as to afford a suitable
and sufficiently uniform intensity of light. The position of the candle
should be such as to furnish a high light, the flame being three or four
inches above the cells. The observer will soon learn how to adjust the
distance to the best advantage, so as to match the colours with the
greatest certainty and accuracy. The actual distance does not affect the
reading ; but if the candle be placed too near, the glare becomes dis-
tractingly strong, especially when the lower grades, which require less
light than the higher, are under observation.
The bore of the blood-measurer is first dried with the needle and cotton,
and the polished point is presented to the drop of blood. The pipette must
436
SYSTEM OF MEDICINE
be quite filled, and if more than one application to the drop be needed, there
must be no break in the column of blood. Any blood adhering to either end
must be carefully wiped away with the finger. The rubber nozzle of the
mixing pipette, charged with water, is now adjusted over the polished
end of the pipette, arid the blood washed into the blood-cell by pressing
through the water drop by drop. The handle of the pipette is then used
as a stirrer, and further additions of water, if required, are made so to
Fig. 14. — Camera tube for use with Oliver's liaemoglobiuometer,
impinge upon it as to graduate the size of the drops required to fill the cell
accurately. It is easy to do this when the observer catches the reflection
of a window on the surface of the fluid. A final thorough mixing with
the handle will be required, and, to secure a level filling, another slight
addition of water may be necessary. The cover-glass is then adjusted,
when the presence of a small bubble signifies that the cell has not been
overfilled. Finally, the blood-cell is placed by the side of the standard
gradations, and the eye quickly recognises its approximate position on
the scale. If the blood solution be matched in depth of colour by one
of the standard grades the observation is at an end ; but if it be higher
THE CLINICAL EXAMINATION OF THE BLOOD
/^yi
than one gradation, but lower than that above it, the blood-cell is placed
opposite to the former and riders are added to complete the estimation.
It is advisable to take a standard time, say ten seconds, for looking down
the tube. If the eyes are strained with long working, it is well to look
for a moment on the inside of the lid of the instrument case, which is
lined with green morocco, complementary in colour to the blood and the
colour-standards. This change rapidly restores the acuteness of ob-
servation.
In the more elaborate form of tube employed by Dr. Oliver the eye-
piece is provided with a collar into which is let a piece of green glass.
He finds that the most delicate appreciation of difference between , the
Pig. 15. — Gowers' hsemoglobinoraeter.
A, Bottle witli pipette stopper for holding the diluting solution ; B, capillary pipette for measuring
the blood ; C, graduated tube for measuring the amount of bsemoglobin ; D, standard tint of
normal blood ; B, support lor D and C ; P, puncturing needle.
tints of the blood solution and of the standard is obtained by from time
to time intercepting the impression of the discs by the finger, while the
candle-flame is viewed for a few seconds through the green glass.
Gowers' hsemoglobmometer. — This instrument consists of two small
glass tubes of the same size. One contains a standard tint corresponding
to a dilution of 20 cubic mm. of blood in 2 cubic centimetres of water
(1 in 100); the standard is made of glycerine jelly tinted with carmine
and picrocarmine. The second tube is graduated, so that 100 degrees
are equal to 2 centimetres (100 times 20 cubic millimetres).
Twenty cubic millimetres of blood are measured by a capillary
pipette (similar to, but larger than that used for his hsemocytometer),
and after placing a few drops of distilled water in the second tube,
this quantity of the blood is ejected into the bottom of it. The
mixture is rapidly agitated by a rinsing action, and distilled water is then
added, drop by drop, from the pipette stopper of a bottle supplied for
438
SYSTEM OF MEDICINE
that purpose, until the tint of the dilution matches that of the standard.
The amount of added water indicates the amount of hsemoglobin present.
As average normal blood yields the tint of the standard at 100 degrees
of dilution, the number of degrees of dilution necessary to obtain the
same tint with a given specimen of blood is the percentage proportion of
the hsemoglobin contained in it. For instance, let 20 cubic millimetres
of blood from an anasmic patient give the standard tint at 30 degrees of
dilution, this specimen would contain only 30 per cent of the normal
quantity of hsemoglobin. By ascertaining the corpuscular richness of the
blood with the hsemocytometer we can compare the two. A fraction, of
which the numerator is the percentage of corpuscles, gives at once the
average value per corpuscle. Thus, if the blood containing 30 per cent
of hsemoglobin contain 60 per cent of corpuscles, the average value
of each corpuscle is %%, or one -half of the normal. Sir William
Growers suggests that in using the instrument the tint be estimated by
holding the tubes between the eye and a window, or by placing a piece of
white paper behind the tubes. Care must be taken that the tubes are
always held in the line of light, not below it, as in the latter case some
light is reflected from suspended corpuscles from which the hsemoglobin
has been dissolved. If all the light be transmitted directly through the
tubes the corpuscles do not interfere with the tint. During 6 or 8
degrees of dilution it is difficult to distinguish a difference between the
tint of the tubes ; it is necessary, therefore, to note the degree at which
the colour of the dilution ceases to be deeper than the standard, and also
that at which it is distinctly paler. The degree midway between these
two will represent the hsemoglobin percentage. The instrument is
accurate within 2 or 3 per cent.
In order to obtain the greatest amount of accuracy in determinations
of the hsemoglobin power of specimens of blood by
means of Gowers' instrument, it is desirable not only to
compare the tint of the contents of the two tubes by the
aid of a standard artificial light reflected from a white
surface, but also to cut off extraneous light as much as
possible. With the old form of this instrument the
writer finds that this may be effectually done by fixing
an upright metal screen to the base in which the tubes
are supported. This screen should have two narrow
perpendicular slits corresponding to the central portion
I ii LSI — 1 of the tubes ; and it is well to have a movable slide of
I V^jfsiji \ metal, working in the slits, which can be brought down
r level with the uppermost point at which the diluted
' °'^ " — blood stands in the graduated tube.
In the newer form recently brought out by Messrs.
Hawksley an attem'pt is made to produce a similar effect
by flattening the tubes, so that their contents present a more uniform
tint from edge to edge, and by fixing the tubes in their support parallel
to one another, but diagonally across the stand instead of side by side.
Fig. 1^. — Gowers'
hsemoglobinometer ;
improved form.
THE CLINICAL EXAMINATION OF THE BLOOD 439
By looking at them in the proper position their adjoining edges appear
to overlap, and as no white hght is visible between the two tubes their
respective tints can be more accurately compared.
V. Fleisehl's hsemoglobinometer.^This instrument consists of a
small metal stage, somewhat like that of a microscope, having on its
upper surface a metal cylinder 1^ centimetres in length, which is open
above and closed beneath by a glass plate, and is divided by a vertical
metal partition into two equal parts. Beneath the stage a movable
Fia. 17.— Von Fleisehl's hsemometer.
metal frame supports a long and narrow wedge-shaped slab of coloured
glass, the colour ranging froni deep red purple at the thickest end to
clear glass at the opposite end.
The frame supporting the glass wedge moves on a rack and pinion
attachment in a horizontal direction, so that every portion of the wedge
can be brought in succession beneath the base of one of the cells formed
by the divided metal tube. This portion of the cylinder is intended to
be filled with water, the other half with diluted blood. By means of a
reflector, the face of which is formed of a Ittyer of pure calcium sulphate,
light is directed upwards through the two cells. The source of light
44° SYSTEM OF MEDICINE
should always be a standard one, such as a Welsbach burner of known
illuminating power — artificial light being, for several reasons, much better
than daylight.
Capillary pipettes, for measuring the requisite amount of blood, are
supplied with the instrument, their capacity being such that, when
healthy blood is used, the colour of their contents on dilution to the
requisite extent corresponds to that of the portion of the red glass wedge
opposite the 100 graduation.
One of the pipettes, held by means of a short and flattened wire
handle, is first completely filled with blood by capillarity, the pipette
being afterwards carefully wiped to remove any blood from its sides or
ends. Without loss of time the blood is transferred, by means of a to-
and-fro motion, to one of the compartments of the divided metal cylinder,
into which a few drops of water should previously have been poured.
The expulsion of the blood from the pipette may be aided by pressing
through it a drop or two of water by means of a glass tube provided with
an indiarubber nozzle. Both compartments are now to be completely
filled with water, that containing blood also being carefully stirred by
means of the pipette handle, to ensure thorough mixture of the contents.
Care must be taken that the fluid in one cell does not overflow into that
in the adjoining cell, and that the metal cylinder is so placed in position
on the stage that the base of the cell containing water is situated exactly
over the coloured wedge of glass, while the light thrown upwards from
the reflector reaches the eye through both compartments in equal amount.
By means of the rack and pinion adjustment the wedge of glass is now
moved backwards or forwards until the colours in both compartments of
the cylinder correspond. The frame carrying the glass wedge is graduated
along one side, and the number denoting the percentage of haemoglobin
in the specimen of blood under examination is read ofi' directly through a
small opening in the upper surface of the stage. It is by no means easy,
however, to match the colour of the blood solution accurately, for reasons
that have already been stated ; and this is particularly the case when
the amount of hsemoglobin in the blood is small. The graduation of
the instrument is also somewhat inaccurate, percentages of -80 or 90
only being usually shown in examination of blood which is apparently
normal. Cabot recommends the observer to look at the "divided
cylinder" from one side, so that the image of the two cells shall fall on
the lateral instead of on the upper and lower portions of the retina ; under
which circumstances, he says, a more correct judgment is possible. He
further advises that the source of light should be placed at such a dis-
tance from the instrument as to reduce the intensity to a point barely
sufiicient for the estimation. Comparison of the colour value of the
blood solution with that of the glass wedge will also be easier if both be
observed through a tube or roll of paper blackened on the inside.
IV. Enumeration of the blood coepuscles. — This method consists
in the dilution of the blood to a considerable but known extent, and the
THE CLINICAL EXAMINATION OF THE BLOOD
441
subsequent counting, under the microscope, of the number of the corpuscles
in a small and measured amount of such diluted blood. A comparatively
simple calculation, mil then enable us to estimate the number present in
any given bulk of the blood originally taken for our purpose. In both
of the modes, which will be described in detail, the corpuscles in the
small sample of diluted blood are reckoned by means of a series of
micrometer squares ruled over a certain area of the glass floor of the
chamber or cell.
In Gowers' hsemocytometer, the instrument which up to the present
has been in most general use in England, measured quantities of blood
and of the appropriate diluting solution are drawn up in a couple of
pipettes of known capacity, the mixture being afterwards efiected by
blowing out the contents of each of the pipettes into a small glass pot in
which they are thoroughly stirred. In the Thoma-Zeiss instrument one
pipette serves not only for the measurement both of blood and diluting
solution, but also for ensuring the subsequent admixture of one with the
other. The exact composition of the fluid employed for dilution of the
blood is to some extent a matter of indifierence, provided that it be of
such a nature as not to act injuriously on the corpuscles, and of such
specific gravity that the corpuscles readily sink in it. A normal saline
solution (NaCl 0"7 per cent in distilled water) serves the purpose; or a
solution of sulphate of soda having a specific gravity of 1025, as suggested
by Gowers, may be employed. Other useful solutions are the fol-
lowing : —
Hcuyem's Fluid.
Mercuric bichloride
Sodium chloride .
Sodium sulphate
Distilled water .
0-25 gram.
0-5 „
2-5 grams.
100-0 C.C.
Thoma's Flmd.
Acetic acid
Distilled water
0-3-0-5 C.C.
100 C.C.
Eecommended by Thoma as useful in the determination of the number
of leucocytes, the red corpuscles being dissolved by the acetic acid.
Toisson's Fluid.
Methyl violet
Sodium chloride .
Sodium sulphate
Glycerine
Distilled water .
0-025 gram.
1-0
8-0 grams.
.30-0 CO.
160-0 C.C.
The addition of the methyl violet or other aniline dye facilitates the
counting of the white corpuscles by staining them, and so rendering them
more conspicuous.
442
SYSTEM OF MEDICINE
Sherritigton's FlvM.
Ehrlicti's purified metliyleiie blue . 0-1 grm.
Soilium cUoride . . . 1"2 „
Neutral potassium oxalate . . 1'2 „
Distilled water .... 300-0 c.c.
In this solution both chromocytes and leucocytes may be studied for
an almost indefinite length of time without losing their characteristic
appearances, especially if the examination be carried out on the warm
stage.
Fig. 18.— Gowers' hieiriot^ytometer.
A, Pipette for measuring the diluting solution ; B, capillary tube for measuring the blood ; 0, cell
with divisions on the floor, mounted on a slide, to which springs are fixed to secure the cover-glass ;
I), vessel in which the solution is made ; E, spud for mixing the blood and solution ; F, guarded
spear-pointed needle.
Gowers' hEemoeytometeF. — This instrument, a modification by Sir
W. E. Gowers of that originally devised by MM. Hayem and Nachet,
consists of (a) a small pipette, which, when filled to the mark on its stem,
holds exactly 995 cubic millimetres — this pipette is furnished with an
indiarubbertube and mouthpiece to facilitate filling and emptying ; (6)
a capillary tube marked to contain exactly 5 cubic millimetres ; also
filled with an indiarubber tube and mouthpiece; (c) a small glass jar
in which the dilution is made ; (d) a glass stirrer for mixing the blood
and solution in the glass jar ; (e) a brass stage plate, carrying a glass
slip on which is a cell one-fifth of a millimetre deep. The floor of this
cell is divided by ruled lines into one-tenth millimetre squares. Upon
THE CLINICAL EXAMINATION OF THE BLOOD 443
the top of the cell when in use rests a cover-glass, which is kept in its
place by the pressure of two springs fixed to uprights at each end of the
stage plate.
The instrument is employed as follows : — 995 cubic millimetres of
the solution are first placed in the mixing jar, after which 5 cubic
millimetres of blood are drawn into the capillary tube from a puncture in
the finger, and then blown into the solution. The two fluids are well
mixed by rotating the stirrer between the thumb and the finger, and a
small drop of this diluted blood is placed in the centre of the cell. The
cover-glass is now gently lowered upon the cell and secured by the
two springs, after which the plate is placed upon the stage of the
microscope. The lens is then focussed for the squares. In a few
minutes the corpuscles will have sunk to the bottom of the cell, and are
seen at rest on the squares. The number is then counted, and the cubic
area of diluted blood over each square is of such amount that this multi-
plied by 10,000 gives the number in a cubic millimetre of blood. Taking
5,000,000 corpuscles as the average per cubic millimetre for healthy
blood, the average number in two squares of the cell is 100. Con-
sequently the number of corpuscles present in two squares (ascertained by
counting a larger number, such as 10 or 20, and taking the mean) ex-
presses the percentage proportion of the corpuscles in the specimen of
blood under observation to that of health ; or, made into a two-place
decimal, the proportion which the corpuscular richness of the specimen
bears to that of normal blood taken as unity. In making such examina-
tion a suificiently large drop of blood must be obtained by puncture with
the point of the lancet without the employment of much pressure, for if
the finger be much pressed or squeezed or ligatured, the relative amount
of serum and corpuscles contained in the sample of blood abstracted is
liable to be afiected, and thus to afford inaccurate and consequently
valueless results. It is somewhat difficult to draw the exact quantity of
blood into the capillary tube, because in removing the blood from its
point a little is easily drawn out of the tube ; it is therefore better to
draw rather more than the required quantity into the tube, then to
remove the blood from the point with a soft cloth, and keep the cloth in
contact with the point while the extra blood is blown out. A little of
the diluting fluid should be drawn into the tube after the blood is
ejected to ensure the removal of all the corpuscles. The smaller end of
the stirrer may be used to remove the drop of diluted blood from the
mixer to the cell. This drop must be deposited in the middle of the cell
over the ruled squares, and care must be taken not to rub the stirrer on
the engraved portion of the floor. The lines which form the divisions of
the micrometer cell may be made more distinct in the following manner :
— With a sharp penknife scrape a little of the lead of an ordinary soft
lead pencil so that it falls into the middle of the micrometer cell, then,
with a clean dry finger-tip, or a knot tied in a small piece of chamois
leather, rub the powdered lead well over the cell ; it may then be wiped
in the ordinary way, and any of the lead which remains in the corners of
444
SYSTEM OF MEDICINE
the cell easily dusted away with a camel-hair brush. Powdered carmine
may be employed in a similar fashion.
The cover-glass should be held in a horizontal position as it is being
lowered on to the cell. When this has been done, the drop of solution
should appear as a disk as nearly as possible in the middle of the cell,
and care must be taken that the fluid does not run to the sides of the
chamber. The two springs are to be carefully placed opposite
each other by lifting them on the cover-glass, and not by
"sliding" them.
Gowers advises that the corpuscles should be counted in
or near to the centre of the drop, and says that by raising the
objective out of focus the white cells may readily be dis-
tinguished by their greater refractive power. A light which
should not be too intense, and the position of which is so
arranged that the rays when reflected upwards pass diagonally
across the squares, will give the best illumination for both
sets of lines. The whole process from beginning to end need
not occupy more than a quarter of an hour.
The blood should not be drawn until the diluting solution
has been placed in the mixing jar and the capillary tube is
ready for use. The blood should be expelled immediately, as
otherwise it may coagulate. Immediately after use, the pipette
aTid capillary tube should have clean water drawn up into
them ; this may be followed by alcohol and ether if rapid
drying be necessary. If either be obstructed, a horse hair
or a piece of fine brass wire will probably clear it ; or it may
be cleared by placing it in nitric acid, all trace of which must
afterwards be removed with water. In standardising the
pipettes, the residual fluid, that which unavoidably adheres to
the inner walls of the tubes, has been allowed for, so that
the quantity ejected is exactly that indicated by the division
upon each tube.
The cell must be cleansed after each observation by means
of a small camel-hair brush and some clean water, after which
it is dried carefully with a soft cloth. The cell must never
be iised a second time whilst damp, or the globule of fluid
will at once disperse over its surface, and the corpuscles will
not be deposited evenly over the floor.
The Thoma-Zeiss hsemoeytometer is in most general
use for the enumeration of the blood corpuscles on the Con-
tinent and in America. As in Gowers' haemocytometer, the
essential parts of the instrument consist of a counting-chamber
and of a measuring pipette, which serves the double purpose
c?l?nMng%hB o^ taking up the required amount of blood and of enabling it
blood oor- to be mixed with a definite quantity of the diluting fluid.
The counting-chamber is formed of a glass slide supporting a
square glass cell with a central circular aperture. Within this is fixed
OB
Pig. 19. — Ca-
pillary tube
(Thoma-Zeiss
THE CLINICAL EXAMINATION OF THE BLOOD
445
a smaller disc of glass ruled on its upper surface into a series of microscopic
squares ; the thickness of the disc being such that, when an accurately
ground cover-glass is lowered over the aperture of the square cell, an
interval of exactly O'l millimetre is left between the adjoining faces of
cover-glass and disc.
The little moat which separates the internal edge of the cell wall and
the periphery of the disc serves to catch any excess of fluid for which
there may not be room in the space between the disc and the cover-glass.
The size of each square is the -^^ of a square millimetre, the individual
lines being exactly Jj- of a millimetre apart. The area over each ruled
square has then the- value of ^rrsTj- o^ ^ cubic millimetre. The small
squares are marked into groups of sixteen by means of more thickly ruled
Pig.
"
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Fro. 21
Thoma-Zeiss apparatus for counting blood corpuscles.
Pro. 22.
lines ; these larger squares being very useful in reckoning the white
corpuscles.
The diluting pipette consists of a thick-walled capillary tube which
towards its upper end expands into a bulb, above which the pipette has
again its capillary bore. Contained within the bulb is a small bead of
glass for the purpose of facilitating the admixture of blood with the
diluting solution. The lower extremity of the pipette is bevelled to a
point and polished so that any excess of blood, or other fluid, clinging to
it can easily be wiped off with a soft cloth. The portion of the pipette
below the bulb is ruled off by cross lines marking tenths from 0"1 to 0'5
and 1 ; while above the bulb the mark 101 is found.
When using the apparatus the point of the pipette is applied to a
drop of blood obtained in the manner previously described. By gentle
suction, through an indiarubber tube attached to the upper portion of the
pipette, blood is drawn up to the 0'5 or the 1 mark ; after which the
diluting solution is also drawn up until the mark 101 is reached, by which
a dilution of the blood of 1 in 100 or 1 in 200 is obtained, according to
whether the half or the whole of the capillary portion of the pipette has
SYSTEM OF MEDICINE
been filled with blood. The pipette is then gently rotated in the fingers
for about a minute in order to ensure thorough admixture of the contents
of the bulb, the process being aided by the presence of the little bead of
glass. It is a matter of some little difficulty to draw up into the pipette
exactly the amount of blood required. For this reason it is well to
employ the dilution of 1 in 200, as in case the amount of blood obtained
at the first attempt should reach slightly above the 0"5 graduation, the
quantity in excess can be got rid of again by gently blowing through the
tube ; whereas if the higher mark should be exceeded and blood escape
into the bulb it is useless to continue the operation until the whole
pipette has been most carefully cleaned out and dried. Moreover, if the
blood be of fairly normal quality, the number of red corpuscles in it will
be so crowded over the surface of the ruled squares as seriously to
interfere with the ease and accuracy of the counting.
Professor Sherrington finds that the greatest amount of. accuracy in
the enumeration of the blood corpuscles is to be obtained by the use of
the Abb6-Zeiss counting-chamber in conjunction with the pipette made by
Hawksley, instead of the one (devised by Thoma) which is usually sent
out with the instrument.
According to Sherrington, the objections to the Thoma pipette are the
large internal surface relatively to cubic content, the difficulty of drying
the bead in the mixing- chamber quickly enough for use in successive
observations, and the presumption that leucocytes will adhere to the bead.
These objections are obviated in the new form of pipette containing no
bead, and possessing a wider bore than the Thoma instrument. Sherring-
ton also lays much stress on the importance of counting both chromocytes
and leucocytes in the same film of the diluted blood j and of enumerating
in the same film the representatives of the various leucocytes distinguish-
able when this step is considered necessary. And there can be no doubt
that this plan is much preferable to that of counting the chromocytes in
one film, the leucocytes generally in a second, and of determining the
numerical proportion of their different varieties in yet another. It must,
however, be borne in mind that it may not be possible to obtain Ehrlich's
colour reactions with a living film.
When counting the leucocytes with the Thoma-Zeiss apparatus it is
usual to dilute the blood ten times only ; under which conditions the
chromocytes must be rendered invisible in some manner, as otherwise
their number tends to obscure the leucocytes. This difficulty may be
overcome by employing Thoma's 0'3 acetic acid solution for diluting the
blood ; this having the effect of " laking " the chromocytes.
After a time, however, the leucocytes are also affected by the acid, so
that it is better to dilute the blood to a larger extent and to enumerate
both chromocytes and leucocytes at the same time. With care and
practice this can be done if the dilution is carried out in the proportion
of forty-nine parts of solution to one part of blood. In order to render
the leucocytes more obvious I have been accustomed for many
years past to dilute the blood with normal saline solution just tinged
THE CLINICAL EXAMINATION OF THE BLOOD 447
with a few drops of a watery solution of some aniline dye ; but for this
purpose the mixture devised by Sherrington (p. 442) is preferable, as
the blood corpuscles remain entirely unaltered in it for considerable
periods.
When the leucocytes are enumerated in a fifty-times diluted blood, as
suggested, it is well to obtain an additional basis for calculation, not only
by counting those lying on the squares, but also those over the whole of
the floor space as far as the ruled lines extend. The area of this enlarged
space must previously have been calculated, as it varies somewhat with
each instrument.
V. Estimation of the reaction of the blood. — Under normal con-
ditions the reaction of the blood, as tested by litmus, is invariably alkaline.
Slight variations in the degree of alkalinity can indeed be demonstrated
in connection with such physiological processes as the digestion of food,
in which the alkalinity of the blood tends to become increased ; or as the
after-effects of severe muscular exertion, by which, on the other hand, it
is for a time somewhat diminished. Even under pathological conditions,
however, it is unusual to find any extreme departure from the normal
range ; and although such variations as have been observed in the course
of those diseases in which systematic investigation of the blood reactions
have been carried out, show that change is usually in the direction of a
fall of alkalinity, it is doubtful whether an acid reaction has ever been
demonstrated during life. It is a somewhat curious fact that the reaction
of the blood is, for the most part at any rate, dependent on the presence in
it of sodium hydrogen carbonate (NaHCOg) and sodium hydrogen phosphate
(NOjHPO^), both of which, chemically speaking, are acid salts. As, how-
ever, these salts are formed of bases very loosely combined with acids,
they are readily dissociated when brought into connection with a substance,
such as litmus, which is capable of withdrawing the bases and uniting
with them to form a distinctively coloured salt ; this colour production
serves, therefore, as a test not only for free bases, but also for bases which
are combined with weak acids. This latter power is not possessed by
certain other substances which are sometimes employed as indicators in
alkalimetric investigations, such for instance as phenolphthalein ; for
this reason they cannot be employed in observations on the reaction of
the blood. Fortunately, however, we have in carefully prepared red or
neutral litmus an indicator sufficiently delicate (according to the observa-
tions of Wright and others) to show an immediate and distinct colour
change with normal human serum which has been diluted as much as
forty-fold. In all the various methods that have been proposed for the
estimation of the reaction of the blood litmus has been employed as an
indicator. In the earlier qualitative methods of Leibreich and Schafer,
slabs of plaster of Paris in the one case, and sheets of glazed paper in the
other, impregnated with litmus were used, the intention being to retain
the blood corpuscles on the surface, from which they could afterwards be
washed in order to bring any colour-change into view ; meanwhile the
448 SYSTEM OF MEDICINE
fluid portion of the blood, soaking into the substance of the slab or paper,
was thus enabled to react with the previously absorbed litmus.
If it be desired to estimate quantitatively the degree of alkalinity of the
blood, it becomes necessary to employ not only an indicator, but also a
standardised solution of some acid. In the titration methods first intro-
duced phosphoric acid was employed for this purpose by Zuntz, tartaric
acid by Lasser and Laiidois, oxalic acid by Drouin. Although convenient
to prepare, solutions of these organic acids tend to weaken after a time
as the result of exposure to light and air ; for this reason they have been
discarded in favour of suitably dilute solutions of sulphuric acid. Landois'
method, as improved by Drouin, is probably that which has been most
extensively employed ; but it possesses the serious disadvantage that, in
order to obviate a difficulty introduced by the presence of the red
corpuscles, the blood has to be considerably diluted with solutions of
sulphate of soda, by which the estimation of the exact neutral point is
rendered somewhat difficult. This objection cannot be advanced against
the methods now to be described.
Hayeraft and Williamson's method.^ — This method is a development
of the qualitative test originally introduced by Schafer. The alkalinity
is estimated by a graduated series of red litmus-papers.
To prepare the papers, place over-night a dozen half-sheets of cream-laid
notepaper under a tap of running water, in order to remove the acid
generally present. Soak the papers in strong neutral litmus and -dry
them. Neutral litmus-papers may be purchased if desired. Pour a pint
of normal (7 c.c. per 1000 c.c. of water) sulphuric acid into a shallow basin,
plunge into it for half a minute a sheet of litmus-paper, withdraw it, blot
it, and dry it ; this is the strongest acid paper.
Now dilute the normal sulphuric acid with an equal volume of water,
soak another sheet of litmus-paper, blot, dry, and mark it. Dilute the
acid again and again until eight or ten papers are prepared. These
should dry in the horizontal plane so that the acid does not gravitate to
one border of the paper.
When prepared, the papers must be glazed by passing them between
steel rollers. Any large stationer will do this, and the papers are then
ready for use. Each sheet may be cut up into strips, or these may be
cut off as required.
The method is to cleanse the finger of the patient and to puncture it
with a broad-tipped stilette ; the blood must not be squeezed from the
finger. A paper, say D, is brought in contact with the drop for ten
seconds, and then dipped in water. If there is no blue stain try E, and
if there is a blue stain try C. The operator will soon find out the paper
which just gives a reaction with normal blood, and he will be able in
other cases to judge roughly if deviations from the normal are present.
This method does not pretend to great exactitude, and may be classed
in this respect with some other clinical methods, such as the estimation
of chlorides in urine by the subsidence of the precipitate.
^ Communioated by Professor Hayeraft.
-J HE CLINICAL EXAMINATION OF THE BLOOD 449
Undoubtedly Haycraft's method possesses the merit of simplicity, but
it has undergone severe criticism at the hands of Hutchison, who has
stated that the results afforded by it are apt to show an extraordinary
divergence from those obtained by means of the titration method. Thus
he finds that the alkalinity of the blood in anaemia, as tested by the
method of Haycraft and Williamson, is invariably above normal; and
often, apparently, to an excessive degree. On the other hand, when the
titration method is employed it is, according to this observer, as invariably
found that the alkalinity of the blood is reduced. Hutchison explains
this apparent contradiction between the results afibrded by the two
methods on the ground that the alkalinity of the plasma alone is ascer-
tained by the glazed litmus-paper method, the alkali contained in the
corpuscles which are left on the surface of the paper not being estimated,
as in the titration method, during the performance of which the breaking
down of the corpuscles liberates their contained alkali. Moreover,
Hutchison concludes, as the results of experiments, that the more watery
the blood the more readily the plasma percolates into the glazed litmus-
paper. Under these circumstances the contained acid is more readily
neutralised, and a fictitious value is given to the amount of alkali present
in the blood. This difficulty cannot be surmounted by allowing the drop
of blood to remain for a longer time in contact with the paper, for, as all
observers are agreed, the alkalinity of the blood diminishes rapidly after
its removal from the body. But the titration method of Landois, which,
according to Hutchison, affords an estimate of the total amount of alkali
in the blood, requires considerable care in its performance, if this result
is to be obtained ; since, as Loewy has shown, it is only when the blood
is titrated very slowly at body temperature that all the corpuscles are
broken down.
With reference to this point, however, it has always appeared to me
that since it is the plasma of the blood and not the corpuscles that come
into direct relation with the tissues, it is the estimation of the alkalinity
of the plasma rather than that of the total blood which is of more
immediate interest from the clinical point of view. I have been ac-
customed, therefore, for the purpose of observations on the reaction of the
blood, to employ specimens of plasma (or serum) obtained by centrifuging
a few drops of blood in capillary U-shaped tubes, after the manner
originally employed by Sherrington and myself when working at the
subject of specific gravity. Treated in this manner, a few minutes suffice
to separate entirely the corpuscles from the plasma (or serum), portions
of which taken up and measured in capillary tubes should then be mixed
with exactly similar quantities of varying dilutions of normal sulphjiric
acid ; the reaction in each case being tested by means of sensitive litmus-
paper.
Wright's method. — This is a titration method also in which, as is now
almost invariably the case, litmus is used as the indicator, and normal
sulphuric acid, in appropriate dilutions, to neutralise the alkali of the blood.
Unlike Hutchison, however. Prof. Wright maintains that, as the result of
VOL. V 2 G
450 SYSTEM OF MEDICINE
his own observations, as also of those of Drouin, "changes in the
alkalinity of the circulating blood invariably manifest themselves in
changes of the alkalinity of the serum." Acting on this assumption,
therefore, he prefers for hsemalkalimetric observations to employ serum,
and preferably that which has exuded from a blood-clot, rather than
fresh plasma " contaminated " with red blood corpuscles.
As is, however, agreed on all hands, the alkalinity of blood undergoes
a gradual diminution after removal from the living vessels ; and conse-
quently Wright thinks it well to postpone the estimation for some hours-
until, as he believes, a condition of stable equilibrium is reached.
It will be obvious, therefore, that the results obtained by him, although
they may be comparable among themselves, do not afford an accurate
estimate of the alkalinity of the freshly-drawn blood. On the other hand,,
if, as I have suggested, the blood be centrifuged, an estimation can be
made within a few minutes of its withdrawal ; and, in the absence of
red corpuscles, the fall of alkalinity, if indeed it occur, is at anyrate
much less rapid than is otherwise the case, and so may be neglected.
In Wright's method five progressive dilutions — twenty, thirty, forty,,
fifty, and sixty-fold — of normal sulphuric acid are employed in the titration.
This is performed by first drawing up into a fine capillary tube about
one-sixth of the amount of serum available, followed by an equal amount
of dilute acid. Accurate measurement is ensured by marking the pipette
at the point reached by the serum, tilting it so as to include a bubble of
air in the bore, and finally filling it up to the original mark with the acid
solution. The exactly equal amounts of serum and acid thus obtained
are next blown out into a watch-glass, thoroughly mixed and tested by
transferring a series of separate drops to the surface of a strip of red
litmus-paper.
If the twenty-fold diluted acid solution has been employed, it will
probably be found that in working with normal blood the mixture will
show an excess of acid. In this case it will be necessary to proceed, in
precisely similar manner, to titrate with each other equal volumes of
serum and the thirty-fold diluted solution. Intermediate degrees of alka-
linity can be estimated by mixing, in a clean watch-glass, equal volumes
of, say, thirty and forty-fold diluted normal acid, and titrating with the
resulting thirty-five-fold acid solution. If this dilution should suffice to
neutralise the acidity of the given sample of serum exactly, the result is-
expressed by the fraction ^. Prof. Wright found, as the result of a.
number of estimations of apparently normal blood, that the serum has an
alkalinity which varies between the values ^ and -^, the average being,
about -jy.
It has been shown that during health the constancy of the level at
which the alkalinity of the blood is maintained is so great as to suggest
that some regulating mechanism must be continuously at work to secure
it. And in many diseased conditions the action of this regulating
mechanism is disturbed in so slight a degree that no appreciable departure.
THE CLINICAL EXAMINATION OF THE BLOOD 451
from the normal slight phasic variations is demonstrable. Under certain
circumstances, however, marked alterations may be found; this being
specially so in the specific fevers, in the various forms of ansemia, includ-
ing leukaemia, in diabetes, particularly if coma be about to supervene, in
uraemia, gout, and jaundice, and in certain cases of poisoning, as for
instance by carbonic oxide or potassium chlorate. The alteration that
occurs under these conditions is almost invariably in the direction of a
lowering of alkalinity, due, as it would appear, to the presence in the
blood of various acids, such as lactic, uric, oxybutyric or bile acids respec-
tively, according to the particular disease under consideration. In anaemia,
however, and markedly in chlorosis, an increase of alkalinity is usually
present, this being the more obvious if it be the reaction of the blood
plasma which is estimated rather than that of the total blood.
VI. Determination of the coagulation time of the blood. —
When first shed, blood appears to the naked eye as a homogeneous red
fluid ; but at a longer or shorter interval, after removal from the body, it
gradually separates into two portions, consisting of a semi-solid coagulum
or clot, which still remains red — though the colour gradually becomes
somewhat darker — and a clear straw-coloured fluid, the serum, the amount
of the latter gradually increasing as more of it is squeezed out of the
interstices of the contracting clot.
The clot consists of a fine meshwork of interlacing filaments of fibrin ;
the red colour and the chief bulk of the clot being due to the entangle-
ment of the red blood corpuscles amid the threads of fibrin. Fibrin may
be obtained free from corpuscles by washing the clot thoroughly under a
stream of water until the washings are no longer coloured : the grayish-
white, stringy mass which remains is fairly pure fibrin. If coagulation
take place more slowly than usual the corpuscles will have time, before
the separation of the serum, to sink towards the lower portion of the
vessel into which the blood is received; and in such case the upper
layer of the clot which eventually appears will be more or less devoid of
colour : this portion is what is known as the " bufiy coat."
In certain pathological states, such as haemophilia for instance, the
rate of coagulation is important both in respect of the disease itself and
of the results of treatment. For clinical purposes the " coagulation time "
can be ascertained by allowing a few drops of blood from a finger-prick
to fall on a glass slide, taking care that the individual drops remain
isolated from one another, and are fairly equal in size. If now a fine and
carefully cleansed needle be drawn through one drop after the other at
short but regular intervals, the moment at which coagulation begins will
be found by observing the lapse of time between the reception of the
drops of blood upon the glass slide and the drawing out of a filament of
fibrin from a drop by the needle.
More accurate information may be obtained by means of the instru-
ments devised by Professor Wright and by Drs. Brodie and Eussell. In
Wright's method the blood coagulability is determined by aspirating
452
SYSTEM OF MEDICINE
blood into a series of tubes, and by then blowing down tube after tube in
succession until coagulation takes place ; when of course blood can no
longer be blown out of a tube. The lapse of time since the blood was
shed is known as the " coagulation time." The necessary apparatus, as
seen by reference to the figure, consists of a water-tin surrounded by a
leather jacket lined with flannel, and constructed with a series of pockets
between the layers of flannel ; each pocket being just sufficiently large to
admit a coagulation tube. One of the pockets is reserved for a glass
thermometer comparable in diameter with the coagulation tubes in the
remaining pockets.
Professor Wright's instructions are : — {a) That the capillary tubes be
of equal calibre, 0'25 mm. being proposed
as a standard diameter ; (6) that in each
tube the column of blood be of approximately
equal length (5 centimetres) ; (c) that the
blood be aspirated for some little distance
up the tube to prevent its desiccation at
the orifice ; {d) that before filling them the
tubes be warmed to blood heat by pouring
water at about the normal blood temperature
into the central tin ; and (e) that this
degree of heat be maintained as constant as
possible — ^by further additions of hot water
if necessary — until coagulation is complete.
This precaution will ensure an optimum
temperature, and will render uniform the
results obtained during the observation or
series of observations. It is desirable to
allow about half a minute to elapse between
the filling of successive tubes ; and in
ordinary cases the condition of the blood
in the first tube should be tested within
three or four minutes from the time of
filling. If then, on testing the first tube,
the blood be still liquid, a longer time must
be allowed before examining the blood in
the second tube. If, on the other hand, the
blood in the first tube is clotted, the next
one should be tested at a somewhat shorter
interval after filling. The first traces of
clot may be most easily detected by blowing out the contents of a tube
upon a piece of white filter -paper. By this method information is
obtained as to (a) the shortest time which is required for complete clotting
in a coagulation tube, and (6) the longest time during which blood can
remain unclotted in a coagulation tube : the mean between these results
will afford a close approximation to the true coagulation time of the blood.
Normal blood-clots form in these tubes in from three to five minutes.
Fig. 23.— Wright's coagulometer, show-
ing the tubes arranged round the
■water-tin.
THE CLINICAL EXAMINATION OF THE BLOOD
453
It is obvious that, if need be, this method may be employed to
investigate the action of various therapeutic agents, such as physiological
styptics, on the blood.
After use the tubes are best cleansed by passing a fine brass wire
through them, and then washing out with distilled water. By drawing
up a little absolute alcohol any remaining water may be got rid of ; and
in its turn the alcohol may be removed by ether. When the last traces
of ether have been volatilised, a process which may be hastened by blowing
a current of air through the tubes, these are again ready for use.
Bpodie and Russell's method. — In certain respects this method pos-
sesses superior advantages, and the necessary apparatus is by no means
complicated. One advantage is that a minimal quantity of blood suffices
for each estimation, and that the readiness with which the instrument can
be cleansed enables a number of such estimations to be carried out in a
comparatively short time.
r
1
w
p
B
r-c
A
W
1
1 ^- — -
A
T
w
Fig. 24.— Brodie and Russell's coagulometer,
•
The instrument consists of a deep air-chamber AA, closed below by a
glass plate E, upon which lies a layer of water M. It is closed above by
a movable glass slide G-, to the centre of which is cemented an inverted
truncated glass cone C. The whole is surrounded by a water-jacket
WW. Inflow and outflow tubes to the water-jacket (not represented in
the diagram) enable us to vary the temperature of the air-chamber at will.
A metal tube T pierces the water-jacket, and to its interior is fitted a glass
tube D which tapers to a fine orifice at P. This orifice lies below the
lower surface of the cone C, but is directed towards it.^
In using the apparatus the glass plate and cone are removed, and the
lower surface of the latter, after thorough cleansing, is dipped carefully
into the drop of blood, so that the whole of this surface, but the surface
only, is wetted by the blood. This precaution ensures that the drop
which is taken up shall always be approximately of the same size. The
hanging drop is then brought into the air-chamber, the whole process
being carried out as rapidly as possible. The instrument is next placed
on the stage of the microscope, and the drop of blood observed under a
low power, when, on blowing air gently through the tube D, the con-
tained corpuscles will be set in motion, a weak and short current of air
being sufficient for the purpose.
' The apparatus is made by Mr. A. E. Dean, jun., 73 Hatton Garden, E.C.
454 SYSTEM OF MEDICINE
Observation should be confined to' the edge of the drop, as the layer
of blood here is thinnest, and the view of the corpuscles consequently
better than in the deeper layers. It is at the free edge also that clotting
is always first noted, the process gradually extending inwards at a rate
which depends, to a large extent, on the surrounding temperature.
At times it is found that at the very edge of the drop the corpuscles
remain quiescent, but this is exceptional. Ordinarily they move freely
right up to the edge of the drop, such movement consisting in changes in
their position relatively to one another, as well as in a rotation of the
whole mass. On the other hand, as soon as the rim at the edge becomes
solid, blowing simply causes an indentation of this rim without causing
rotation of the corpuscles.
This stage it is which should be observed, as it is much more diflBcult
to judge with any accuracy the time at which the whole drop becomes
coagulated throughout.
In order to obviate any chance of fallacy as far as possible it is well
to avoid unnecessary agitation of the drop of blood. We must blow very
softly, and only for brief periods of time. In the following tables it wiU
be seen that the method is capable of afibrding fairly concordant results
in a series of observations.
The coagulation times here set out were obtained from the blood of
normal individuals, the experiments being carried out in each instance at
a temperature of 30° C.
(1) 3-33 (1) 3-10 (1) 3-24
(2) 3-30 (2) 3-00 (2) 318
(3) 3-30 (3) 3-50 • (3) 3-30
(1)
(2)
(3)
(4)
The first two sets of observations were taken on successive days in
the same individuals.
VII. Spectroscopic examination of the blood. — It will occasionally
happen that information of value from the clinical point of view may be
gained by means of a spectroscopic examination of the blood, which could
not be easily obtained by any other method. This will be especially
the case in poisoning by carbon monoxide and coal gas, or by such sub-
stances as amyl nitrite and potassium chlorate. In certain diseases also
information may thus be afforded of the approaching onset of coma. I
have been able to foretell the probable appearance of this dangerous
complication in several cases of uraemia and diabetes on finding evidence
of the presence of methsemoglobin in the blood. Methsemoglobin has
also been found in severe cases of cholera and leukaemia.
The discovery of haematoporphyrin has been recorded in some
eventually fatal cases of sulphonal poisoning.
4-43
(1) 3-00
(1) 3-25
4-40
(2) 2-55
(2) 3-40
4-00
(3) 3-50
(3) 3-35
4-50
THE CLINICAL EXAMINATION OF THE BLOOD
4SS
Fig, 25.— Browning's micro-spectroscope.
In suspected cases of hsemoglobinuria the diagnosis may be assisted
and confirmed by spectroscopic examination of the serum obtained from a
blister, which, in the event of the recent occurrence of a paroxysm of this
disease, will show the absorption bands
characteristic of oxyhsemoglobin due to
the destruction of red corpuscles in the
general circulation.
Method of examination. — The
ordinary chemical spectroscope is practi-
cally useless in clinical work, the extent
of dispersion being too great, and too
large an amount of blood being required.
These difficulties are obviated by making
use of the micro-spectroscope for clinical
examinations. Both Zeiss and Brown-
ing manufacture small instruments of-
admirable construction which are em-
ployed in connection with the micro-
scope, the micro-spectroscope being sub-
stituted for the ordinary eye-piece. The
fluid to be examined is placed on the
microscope stage, in a tiny test-tube
made by sealing one end of a short
narrow piece of glass tubing, the cell thus formed being supported on a
wooden foot, as at first suggested by Dr. MacMunn. This support serves
also to cut off extraneous light. The upper surface of the fluid is now
focussed with the ordinary eye-piece, which is then exchanged for the
micro-spectroscope. If the amount of material to be examined be ex-
tremely small, the high power objective must be employed. In this way
I have had no difficulty in obtaining satisfactory absorption spectra from
separate crystals of hsemoglobin in a cover-glass specimen of human
blood. It is advisable to use artificial light for illumination, as, if day-
light be employed, confusion is apt to be caused by the presence of the
Praunhofer lines.
The, ahsorption spectra of hmmogldbin and its derivations. — The normal
blood-pigment hsemoglobin is capable of existing in two forms, named
oxyhaemoglobin and reduced hsemoglobin respectively, which differ from
one another in the amount of oxygen in combination, in the colour of
their solutions, and in their absorption spectra. Oxyhsemoglobin, when
examined with the spectroscope, shows two absorption bands be-
tween the D and E Fraunhofer lines, the intensity of which will depend
on the degree of concentration of the pigment and on the thickness of
the layer of fluid examined. Under ordinary circumstances these bands
are readily visible, even in venous blood which contains a certain propor-
tion of reduced hsemoglobin. The single absorption band, which is
characteristic of this variety, and which occupies a position in the
spectrum roughly midway between those of oxyhsemoglobin, is somewhat
455
SYSTEM OF MEDICINE
diffused and of relatively small intensity. In order to see it clearly it is
necessary to treat the blood with some reducing agent such as ammonium
sulphide, by the action of which all the oxyhsemoglobin eventually becomes
converted into the reduced variety.
A third modification of haemoglobin which, as previously stated, has
been found in the blood during the course of certain diseases and in
cases of poisoning, particularly with potassium chlorate, is named met-
haBmoglobin. This contains precisely the same amount of oxygen as
oxyhsemoglobin, but differs from the latter in that its reaction is acid
while the other two forms of haemoglobin are alkaline, and also in its
absorption spectrum. Instead of the two bands of oxyhsemoglobin it
shows four bands, of which one between the C and D Fraunhofer lines
V
p ?
1
-
(•)
^^B
1 1 1
■
!" 3|
(2)
-'M
(3)
i
V
M
t*)
lllipini
Cs)
t j II
f- 1
(6)
{ilH
Fig. 26.- Chart of blood spectra. (1) Oxyhiemoglobm ; (2) redneed hsemoglobin ; (3) methsmo-
globin ; (4) acid hsematin ; (5) alkaline hEematin ; (6) reduced alkaline hsematin.
is most definite. A very similar four-banded spectrum is also presented
by acid hsematin (or hsematin in acid solution), but the two may be dis-
tinguished by the fact that when methsemoglobin is treated with
ammonium sulphide, reduced haemoglobin is produced, while treatment of
acid hsematin with the same reagent results in the formation of reduced
alkaline hsematin (see Fig. 26). The spectrum of Co-hsemoglobin shows
two absorption bands resembling those of oxyhsemoglobin, from which,
however, they may be distinguished by their persistence on addition
of ammonium sulphide.
VIII. Examination of the blood for parasites. — This subject is
fully discussed in the articles dealing with the respective diseases in
which parasites of one or another kind are met with, but it may be useful
THE CLINICAL EXAMINATION OF THE BLOOD 457
briefly to set out certain of the methods employed for their demonstration
which experience has shown to be not only efficient but at the same time
expeditious. Of the more highly-organised parasites met with in the
blood may be mentioned the filaria sanguinis hominis and the Plasmodium
malarice. The ova of the hmmatohium BUharzii have been discovered in
large numbers embedded in the walls of the portal vein, but they have not
been found free in the blood. Both the filaria and the malarial organism
can perhaps be examined best in the fresh blood, for which purpose a
drop of blood should be withdrawn at such time as experience has
decided to be likely to give the best results (vol. ii. p. 1065 and p.
724). A perfectly clean cover-glass is then lightly brought in contact
with the drop of blood, and afterwards carefully lowered on to a glass
slide, so as to produce as thin and even a film as possible. A little vase-
line should be smeared round the edge's of the cover-glass to prevent
evaporation. To stain these organisms, extremely thin films of blood
must be taken on cover-glasses and first fixed as rapidly as possible over
the vapour of osmic acid, or by dipping the cover-glass in a mixture 6f
equal parts of absolute alcohol and ether. They may then be stained in
the eosin and methylene blue mixture originally devised by Canon for
the demonstration of the influenza bacillus.
Canon's stain. — Eosin, ^ or |^ per cent in 70 per cent alcohol, 20 parts j
methylene blue, saturated aqueous solution, 40 parts ; distilled water,
40 parts. Plehn recommends the addition to the staining mixture of ten
to twelve drops of a 20 per cent solution of potassium hydrate. This
same method will serve to demonstrate bacteria in the blood. For this
purpose, however, it will be necessary, especially if cultivations are also to
be made, to obtain the blood with antiseptic precautions ; and it is usually
better to carry out the preliminary fixing of the film by means of heat, or
by treatment with a solution of corrosive sublimate. Staphylococci,
streptococci, pneumococci, gonococci, and the bacilli of anthrax, glanders,
typhoid, and influenza all take up the methylene blue of Canon's or
LoefHer's stains.
Loeffler's alkaline methylene blue stain consists of saturated alcoholic
solution of methylene blue, 30 c.c. ; caustic potash (1 in 10,000), 100 c.c.
When examining for tubercle bacilli it is advisable to make use of
Nielsen's carbol-fuchsin solution. The composition of this stain is as
follows : —
Nielsen's stain. — Saturated alcoholic solution of fuchsin, 1 part ; five
per cfent soluti'on of phenol in distilled water, 9 parts. The cover-glasses
are floated face downwards on this solution, a little of which should
previously have been heated in a watch-glass until steam begins to arise
from the surface. Two minutes will probably suffice for staining. The
superfluous stain is washed off rapidly, and the cover-glass is then
placed in a 25 per cent solution of nitric or sulphuric acid in distilled
water, until all colour has disappeared. The acid is next removed by
thorough washing in water, and the cover-glass is rapidly dried by
pressure between two pieces of smooth blotting-paper. If thought
4S8 SYSTEM OF MEDICINE
■desirable, the specimen may be counterstained by a few minutes' treat-
ment witli Loeffler's solution.
For the methods of making cultivations a treatise on bacteriology
must be consulted.
As a general rule, it is only in the most severe cases that it has been
found possible to demonstrate the presence of bacteria in the blood ; so
that, although such an examination often fails to aiford information of
any diagnostic value, if positive evidence be obtained the prognosis will
be very unfavourable.
This rule has been insisted on by Ely, who has shown that, although
the results of bacteriological examinations of the blood have proved dis-
-appointing as an aid in diagnosis, yet, by affording an explanation of com-
plications in diseases which are usually localised, they are often of value
from a pathological point of view. Thus he found pyogenetic microbes
present in the blood during life in cases of pysemic osteomyelitis, puerperal
fever, erysipelas, and infective endocarditis ; the pneumococcus in pneu-
monia and infective endocarditis; the bacillus coli in cystitis complicated
with a pysemic condition ; the gonocoocus in infective endocarditis after
gonorrhcea ; the tubercle bacillus in tuberculosis, and the Eberth bacillus
in typhoid fever. Block has also put on record a fatal case of typhoid
fever in which the bacillus typhosus was twice obtained during life.
Kohn has obtained very similar results. He states that in cases of pro-
nounced sepsis large numbers of bacteria may be present in the blood.
He also agrees as to the grave prognosis which is indicated by the
■ discovery of the pneumococcus in the blood . in pneumonia ; a series
•of negative results, on the other hand, being distinctly favourable to the
patient's chances of recovery. Thus of nine cases of pneumonia in which
he was able to demonstrate the pneumococcus in the blood, no less than
seven were fatal ; the other two being complicated with empyema and
multiple abscesses respectively. On the other hand, of twenty-three
negative cases eighteen recovered, the fatal termination in the other five
being due to various complications.
The Widal-Griinbaum method for the diagnosis of typhoid fever.
— In this method advantage is taken of the fact that on addition of a
small quantity of blood or serum obtained from a patient suffering from
typhoid fever to a dilute culture of Eberth's bacillus, loss of motility of
the individual microbes is rapidly induced, while at the same time they
tend to mass together into clumps, a process to which the term agglutina-
tion is now genei-ally applied.
The recent researches of Griinbaum, Wyatt Johnson of Montreal, and
of Durham, Wright, and others in this country, have rendered the process
at once accurate and simple, and, as it is now possible to obtain the reac-
tion with a single drop of fresh or even dried blood, the method has become
readily available in clinical work. Wyatt Johnson's modification of
Widal's test is specially applicable to examination of the blood of patients
living at a distance. One or more drops of blood are allowed to fall on
THE CLINICAL EXAMINATION OF THE BLOOD 459
the surface of a small piece of non-absorbent paper, which when the blood
is dry can, if necessary, be sent through the post. To test for the reaction,
the drop of dried blood is removed and dissolved up as far as possible in
distilled water. This blood should then be mixed with varying propor-
tions of a fresh beef-broth culture of the typhoid bacillus (12-24 hours),
or with an emulsion made from a fresh agar culture, in varying propor-
tions, the resulting dilutions of the blood thus prepared ranging from
1 in 15 to 1 in 50. It is advisable that control preparations should be
made with normal blood in every instance, and all the specimens should
be examined under the microscope within a definite period, preferably
half an hour, after preparation.
The serum obtained from a drop or two of blood taken up into a
bulbed capillary tube may be examined in the same manner, or it may
be added directly to a suitable quantity of a recent broth culture.
Griinbaum's original method is as follows: — A U-shaped capillary
tube is filled with a drop of blood from the patient, and the serum
separated by centrifugalising. The free extremities of the tube in which
the serum collects are broken off, and the serum is mixed with sixteen
times the quantity of bouillon. A small quantity of fresh culture of the
typhoid bacillus on agar is distributed in 1 c.c. of bouillon, and a
drop of the resulting emulsion is added to a drop of the diluted serum.
The mixture is then examined as a hanging-drop preparation under the
microscope.
It is of importance that the reaction of the culture medium employed
for the test growth of Eberth's bacillus should be distinctly acid (prefer-
ably 3 '5 per cent acid to phenolphthalein in the case of peptone beef
bouillon, according to Wyatt Johnson), as otherwise a scum is apt to
form at the surface, or a sediment at the bottom of the culture fluid,
which in either case not infrequently contains clumps of apparently
dead bacilli, the presence of which would tend to obscure the reaction.
At present some doubt exists as to the exact value of the test
as an aid to diagnosis, for the reason that it cannot usually be obtained
until after the lapse of several days from the beginning of the dis-
ease. Again, one or two undoubted cases of typhoid fever have been
recorded in which from first to last the reaction could not be obtained.
On the other hand, if suitable precautions be taken, it is possible, in the
great majority of cases, to demonstrate the reaction towards the end of
the first week of the disease, or later. The fact that not infrequently
during convalescence the test fails to afford positive evidence in cases
in which it has previously been obtainable, tends to show that the
specific action of the serum is not dependent on a condition of acquired
immunity.
Blood-Crystals. — Under certain circumstances, concerning which as
yet comparatively little is known, crystals of one kind or another may
form in the blood taken from the body during the course of diseases
in which the character and condition of the blood are especially affected.
46o SYSTEM OF MEDICINE
Among these disorders may be mentioned certain anaemic conditions, more
particularly pernicious anaemia, leukaemia, and the various forms in which
septic infection may manifest itself.
1. Hsemoglobin. — It has long been known that the special blood-
pigment hsemoglobin, although of proteid nature, may be obtained with
comparative ease in the crystalline form from the blood of some of the
lower animals, particularly the guinea-pig and the rat. On the other hand,
the haemoglobin of normal human blood is undoubtedly much more
refractory in this respect, since the ordinary laboratory methods entirely
fail to bring about crystallisation. Some years ago, however, I made the
observation that in specimens of blood from cases of pernicious anaemia,
prepared for microscopic examination, rhombic crystals of haemoglobin not
infrequently formed after the lapse of some hours. This was markedly
so when the blood had been obtained from persons suffering from a severe
form of the disease ; especially if a certain amount of pyrexia were present,
and provided that treatment with arsenic either had not been begun or
had been discontinued for a time. Bond and myself have also noted the
appearance of haemoglobin crystals in blood-films' obtained from cases of
leukaemia ; and the former observer has found that the same phenomenon
can be demonstrated in cases of septicaemia and pyaemia. Human
haemoglobin invariably crystallises in the reduced condition, as may be
shown by the micro-spectroscope, a point of apparent difference between
the blood of man and that of the lower animals. The formation of
haemoglobin crystals in human blood, after removal from the body, is
undoubtedly connected with a tendency to abnormal blood-destruction.
The readiness or the reverse with which crystals appear in blood-films
thus affords some measure of the effect of treatment in restraining such
haemolysis.
The method of obtaining crystals of haemoglobin from the blood in
suitable cases is simplicity itself. A fairly large drop of blood, drawn
from the finger or elsewhere, is allowed to fall on the centre of a glass
slide, and, when sufficient time has elapsed for the edge of the drop to
have dried somewhat, a cover-glass is gently lowered upon the surface of
the drop. The blood corpuscles gradually break down, and crystals of
reduced haemoglobin will become apparent, in from ten to forty-eight hours,
without further preparation.
2. Hsematoidin. — The presence of this substance, a derivative of the
blood-pigment, has been detected in an amorphous form by Von Jaksch
in the fresh blood of a child suffering from hereditary syphilis. It is
frequently found in crystalline form in old cerebral blood-clots, splenic
infarctions, and blood-cysts. Occasionally these crystals, or fragments of
them, are found within the substance of white corpuscles in the circulating
blood under such pathological conditions as obtain in pernicious anaemia
and leukaemia, during the course of which diseases minute haemorrhages
in various parts of the body are of not infrequent occurrence.
3. ChaFCot-Leyden crystals. — Occasionally, as in a ease recorded by
Ord and myself, long colourless pointed crystals have been found in
THE CLINICAL EXAMINATION OF THE BLOOD i.d'i
preparations of leukaemic blood. Their occurrence has not been noted in
freshly-drawn blood, but crystals apparently identical with them are not
infrequently to be found in the sputum, the faeces, and the seminal fluid.
Comparatively little is known as yet of their chemical composition or
pathological import.
Certain other methods of blood examination, of which no detailed
account will be given, demand brief notice, either because they appear
worthy of further investigation, although not yet rendered applicable to
clinical needs, or because, although not considered of special value by
myself, they nevertheless have been authoritatively recommended or some-
what extensively employed by others.
Under the first category may be mentioned the work of Graham
Brown and of Huerthle on the determination of the viscosity coefficient of
the blood. These observers find that even slight alterations of the
" viscosity coefiicient " entail an enormous difference in the work thrown
upon the heart in propelling the blood round the circulation. Dr. Graham
Brown, moreover, has demonstrated the great alteration in the " viscosity
coefficient " produced by a change of only a few degrees in the body
temperature, the blood flowing much more readily at fever temperature
than under normal conditions.
Determination of the isotonic coefficient of the red corpuscles is another
method of blood examination, concerning the clinical significance of which
but little is known. The " isotonic coefficient " is usually measured by the
amount of NaCl which it is necessary to add to distilled water to prevent
it, when added to blood, from causing its usual destructive effect on the
red corpuscles.
The quantity of salt required may, under pathological circumstances,
be either greater or less than the normal amount (0'44-0'48 per cent),
indicating respectively an increased or diminished power of resistance on
the part of the red corpuscles.
The estimation of the number of red corpuscles in a given volume of
blood, if it is to be acciu'ate, involves no little expenditure of time and
trouble. In the hope of obviating this difficulty, certain methods of
indirect estimation of the corpuscular richness of the blood have been
introduced. Thus, in this country Dr. George Oliver has advocated the
use of a hsemocytometer devised by himself, in which the number of cor-
puscles is gauged by the amount of water which must be added to the
blood in order to allow the passage of a ray of light through the mixture.
Considerable fallacy, however, is likely to be introduced by any increase
or decrease in the volumes of individual corpuscles, or by increase in the
number of leucocytes, such as we find, for instance, in leukaemia.
In America the Hedin-Dalland haematocrit has been much used for
the purpose of estimating the number of red corpuscles in the blood. This
instrument is practically a small centrifuge driven by hand with the aid
of a system of multiplying wheels. Each of the two arms of the instru-
ment is arranged to hold a small tube of capillary bore, which is marked
462 SYSTEM OF MEDICINE
off into a hundred equal divisions. In use these tubes (or one of them)
are filled as accurately as possible with blood and fixed in place in the
machine, which is then run for about a couple of minutes. The red
corpuscles thus become packed together at one end of the tube. On
removing the tube and placing it on a sheet of white paper, it is fairly
easy to read off the number of divisions of the scale corresponding to
the dense mass of corpuscles. What is really determined by means of
this instrument is of course the volwne of the red corpuscles, from which
their number is empirically calculated, each division on the scale of the
capillary tube corresponding, in the case of normal blood, to about 100,000
corpuscles. Obviously little or no reliance can be placed on estimations
arrived at in this manner in the case of pathological blood ; especially
when, as in such diseases as pernicious anaemia and leukaemia, there is.
much variation in the size and shape of the corpuscles.
S. MONCKTON COPEMAN.
REFERENCES
1. Ezamination of fresh and dried blood-films ; 1. Cofeman. St. Thomais Hasp.
Reports, vol. xvi. 1886, p. 155 ; unA Lancet, May 26, 1887. — 2. EiCHOKST. Monograph-
on Pernicious Ancemia. Leipzig, 1878. — 3. Gulland. British Med. Journ. March 13,
1897, p. 652. — 4. Gulliver. Proc. of Zoological Soe. of Land. June 15, 1875. — 5.
Howell. "The Life-History of the Formed Elements of the Blood," Journ. of Morph.
vol. iv. 1890. — 6. Lepine and Germont. Gazette mMicale de Paris, 1877, p. 218. — 7.
Quincke. Deutsches Archiv f. Tclin. Med. xx. 1877, p. 1, and xxv. 1880, p. 597. —
8. Ranvier. Traiti technique d'histologie. — 9. Weight and Bruce. British Med.
Journ. Feb. 25, 1893.— 10. Zbnoni. British Med. Journ. Feb. 16, 1895.
2. Leucocytes and leucocytosis : 11. Arnold. Archiv f. mikr. Anat. vol. xxx.
1887, p. 226.— 12. Billings. Johns EopMns Mosp. Bulletin, 1894, No. 42.— 13.
Canon. Deutsche med. Wochenschr. 1892, No. 10. — 14. Dekhuysen. Ve/rhandlung
d. anat. Gesellsehaft, 1890. — 15. Ehelioh. Zeitschrift f. klin. Med. No. 1, 1880, p.
553 ; and Charit4-Annalen, 1884, p. 107 ; also 1887, p. 288, and other papers. — 16.
Evbraed, Dbmoor, and Massaet. Annates de I'institut Pasteur, Feb. 1893, p. 165.
— 17. EwiNG. New York Med. Journ. Dec. 1893. — 18. Fblsen. Archiv f. Kinder-
heilkwnde, vol. xv. 1892. — 19. Guli^nd. Labor. Beports Royal Coll. of Physicians-
Edin. voL iii. 1891 (for Bibliography up to 1890), also Journ. of Physiology, vol. ii.
1894. — 20. Hankin. Gentralbl. f. Bakteriol. vol. xii. 1892. — 21. Hankin and.
Kanthack. Trans. Cambridge Philosoph. Soc. Jan. 1882. — 22. Hardy and Eanthaok.
Proc. Royal Soc. vol. Iii. 1892 ; Philos. Trans. Roy. Soc. 1894 ; Journ. of Physiology, voL
xvii. 1894, Nos. 1, 2, p. 81, and separate papers. — 23. Heidenheim. " Ueber Kern nni
FToto-p]B,sma,," Festschrift f. Kolliker. Wiirzburg. — 24. Eanthack. British Med. Jowm.
June 18, 1892. — 25. KiKODSB. Centralbl. f. allg. Pathol, u. pathol. Anatomic, vol. ii.
p. 109. — 26. KORSCHBLT. Zool. Jahrb. Ablheilung f. Anat. u. Ontogenieder Thiere, vol.
iv. 1889. — 27. Lilienfbld and Monti. Verhandlung d. physiologischen Gesellsch. z.
Berlin. Sitzung am 4 Juni 1892. — 28. v. Limbeck. Archiv f. HeUkwnde, vol. x.
1890, p. 392. — 29. Lowit. Studien z. Physiol, u. Pathol, d. Blutes, Jena 1892 ; andi
Centralbl. f. Patholog. 1890. — 30. Metschnikoff. Lefons sur V inflammation. Paris,
1892.-31. MuiR. Journ. Path, and Bact. vol. i. 1892, p. 133.— 32. Mullee.
Sitzung. d. kais. Akad. Wien, 3, vol. xoviii. 1889. — 33. Okintsohitz. Arckvof.
exper. Pathol, u. Pharm. vol. xxxi. p. 383. — 34. Pick. Prager med. Wochensch. xxiv.
1890, p. 303. — 35. PoHL. Archiv f. eoeper. Paihol. u. Pharm. vol. xxv. 1838, p. 87.
— 36. RiEDER. Beitrage z. Kenntniss d. Leukocytose. Leipzig, 1892. — 37. Schmidt.
Archiv f. d. gesammie Physiologie, vol. xix. p. 353. — 38. Sherrington. Proc. Royal
Soc. vol. Iv. Dec. 1893 ; and Proc. of Intemat: Congress of Physiology. Liege, 1892.
— 39. Theyer. Boston Med. and Surg. Journ. Feb. 16 and 23, 1893. — 40. TscHl-
stowitsch. Berliner klin. Wochenschr. 1891, Bo. Si, p. 8S8. — 41. Tumas. Deutsches:
THE CLINICAL EXAMINATION OF THE BLOOD 463;
Archiv f. Iclin. Med. voL xli. 1887, p. 323.-42. Winteknitz. CeniralU. f. klin.
Med. March, and Dec. 1893.
3. Specific gravity: 43. BusoH and Keee. Philadelphia Med. News, Dec. 21,
1895. — 44. CoPEMAN. British Med. Joum. Jan. 24, 1891. — 45. Landols. BMl-Encydop.
No. 3, 1885, p. 163. — 46. Jones, E. Llotd. Joum. of Physiology, vol. viii. 1897, p. 1. —
47. Hammersohlag. Wien. klin. Wochenschrift, No. 3, 1890, p. 1018. — 48. Hay-
craft. Proe. Royal iSoc. Edin. Jan. 19, 1891. — 49. Boy. Joum. of Physiology, vol. v.
1884, p. 9. — 50. Schmaltz. Paihologie des Blutes, etc. Leipzig, 1896. — 51. Shbe-
RINBTON. Proc. Royal Soc. vol. Iv. Dec. 1893, p. 164. — 52. Sheerinoton and
CoPEMAN. Joum. of Phymlogy, vol. xiv. No. 1, 1893, p. 52 : and Proc. of Physiol. Soc
No. 3, 1890.
4. Hsemoglobinometry : 53. v. Fleisohl. WieTier rued. Jahrbacher, p. 425 ; 1885.
— 54. Gottlieb. Wiener 7)ied. Blatter, ix. 1886, pp. 505 and 637. — 65. Gowbes.
Report of Meeting of Clinical Soc. Deo. 13, 1878. — 66. Haeeelin. Miinch. med.
Wochenschrift, xxxv. 1887, p. 364.' — 57. H^NOOQUB. Notice mr Vhimatoscope. Paris,
1886. — 58. LoviBOND. " Colorimetric Analysis by means of Tintometers," Joum.
Soc. of GhemAcal Industry, 1894. — 59. Oliver. Proceed, of the Physiological Soc.
March. 1896 ; and Crooniau Lectures, Lancet, June 20, 1896, p. 1699. — 60. Sheeelng-
TON. Proc. Royal Soc. vol. Iv. Deo. 1893, p. 164.
6. Enumeration of corpuscles : 61. ABBt. Sitzungsberichte der Gesellschaft fil/r
Med. vmd' Naturwiss. in Jena, No. 29, 1878. — 62. Barton. "Pernicious Anemia,"
Therapeutic Gazette, 1888. — 63. Gowees. "On the Numeration of the Blood Cor-
puscles," iamcei, Deo. 1877. — 64. Lton and Thoma. Virchow's Archiv, Band Ixxxiv.
p. 131, 1881.— 65. Shereington. Proc. Royal Soc. vol. Iv. Deo. 1893, p. 162 et seq.
6. Reaction of the blood: 66. Oalabrese. H Policlin, Feb. 15, 1896. —67.
Cantani. Centralblattf. die medicinische Wissenschaften, Band xxii. p. 785; 1884. — 68.
Drouin. "H^moalcalim^trie et H^moacidometrie," rtoe. Paris, 1892. — 69. FoDOE.
Centralblattf. Bakteriologie and Parasitenkunde, 1895. — 70. Graeee. ".Zur klinisohen
Diagnostik der 'Bhitkia,nk'beiteii,"Haeniatologische Studien. Leipzig, 1888. — 71. Hat-
ceaft and "Williamson. Proc. Royal Soc. Edin. June 18, 1888.— 72. Hutchison.
Lancet, March 7, vol. i. 1896, p. 615.-73. Jacob. Portschrit. der Med. April 1896.—
74. V. JAKSOH. "UeberUrio Academic," ZleMfecAe medicinische Wochenschrift, 1890 ; and
Zeitschrift f._ klin. Med. xiii. 1887, p. 350.-75. Lakdois. Rdal-BncyclopMie, iii. p.
161, 2nd edit. 1885. — 76. Lassbe. Archiv f. die gesammte Physiologic, Band Ixviii.
and Ixxiv. — 77. Liebreich. Berichte der deutschen chemischen OeseUschaft. Band i. p.
48 ; 1868.^78. LoEWT. Archiv f. die gesammte Physiologic, Band Iviii. 1894. — 79.
Spiro. Zeitschrift f. physiologische Chemie, Band i. — 80. Weight. Lancet, Sept. 18,
vol. ii. 1897.-81. Zuntz. Cemtralblatt f. die medicinischen Wissenschaften, Band v.
pp. 531, 801 ; 1867.
7. Coagulation : 82. Beodie and Russell. Joum. of Physiology, xxi. 1897, p. 403.
—83. Hasbbeock. Zeitschrift f. Biologic, 1882.— 84. Horne.— 85. Vibrordt.
Archiv f. Heilkunde, 1878.-86. Weight. Brit. Med. Joum. July 19, 1893, and Feb.
3, 1894 ; and Lancet, Sept. 19, 1896 ; Proc. of Royal Soc. vol. Iv. 1893.
8. Spectroscopy: 87. Bohm. Ziemssen's Sandbuch, xv. 2nd ed. 1880, p. 158. —
88. Copeman. St. Thomas's Hosp. Reports, vol. xvui. 1888, p. 105 et sea.; and
Practitioner, Sept. 1890, p. 177.-89. Hering. Prager med. Wochenschrift, xi. 1886, p.
97. — 90. Hoppb-Setlee. Medic.-chem. Vntersuchungen. Tubingen, 1867-70 ; and
Physiol. Chemie. Berlin, 1881.— 91. Jaderholm. Die gerichaich med. Diagnose der
Xholenoxydvergiftung, 1876.-92. MacMunn. The Spectroscope in Medicine. Lond
1880.— 93. Thudkhum. Jowmal f. praU. Chemie, civ. 1868, p. 257.
9. Bacteriological examination, including serum diagnosis; 94. Bilharz.
Wiener med. Wochensckr. vi. 1856, p. 49.-95. Block. Johns Hopkins Hosp. Bulletin,
Nov. and Deo. 1896, and June 1897.-96. Ely. American Jmm. of Med. Sciences
Oct. 1887.-97. Geunbaum. Lamcet, Sept. 19, 1896, p. 806, and May 1, 1897, p. 1088.—
98. Halm. Archiv f. Hygiene, vol. xxv. p. 105.-99. Inghilleei. Centralb. f.
Bakteriol. May 1894.-100. Johnston and M'Taggaet. Montreal Med. Joum. March
1897.-101. Johnston, Wyatt. Lancet, vol. ii. Dec. 18, 1897, p. 1621.-102. Lewis.
Lancet, i. No. 2, 1873 ; and Centralbl. f med. Wissenschaften, xiii. 1874, p. 771.— 103.
LOEFFLEE. MUtheilnng aus d. kais. Gesundheitsamte, ii. 1884, p. 439. — 104. Ober-
MEYER. Centralbl. f. d. med. Wissenschaften, xi. 1873, p. 145.-105. Widal La
presse mMicale, 1896, p. 268.-106. Also papers by Widal, Wilson, and Westbrook,
Thompson, Block and Mussen, and Swan. British Med. Joum. Dec. 18, 1897, pp.
1773-1778. — 107. Welch. Joum. of American Med. Assoc. Aug. 14, 1897.— los!
464 SYSTEM OF MEDICINE
WiDAL and SiCAED. Ann. de I'instUut Pasteur, No. 5, May 25, 1897. — 109. Weight.
British Med. Journ. Jan. 16, 1897. — 110. Weight and Semple. British Med. Jowm.
May 15, 1897.
10. Blood-crystals: 111. Bond. Lancet, 1887, p. 1076. — 112. Charcot, Robin,
and VuLPiAN. Gazette mMicale, 1853 ; and Gazette hebdomadaire, 1860. — 118. Cope-
man. St. Thomas's Hospital Beports, vol. xvi. 1886. — 114. Neumann. Archiv f.
mihros. Anatcmde, ii. 1866. — 115. Oed and Copeman. "Case of Leuoooythemia,"
Clin. Soc. Trans, vol. xxiv. — 116. Pketbe. Die BlutJcrystalle. Jena, 1871. — 117.
ScHKEiNEE. Liebig's Annalen, cxciv. 1878, p. 68 (gives otlier references). — 118.
Teichmann. Zeitschrift f. ration. Med. iii. 1883, p. 375. — 119. Wagnek. Archiv f.
HeilkvMde, 1862.
11. Manuals which may also be consulted with advantage : 120. Cabot. Clinical
Examination of the Blood. Lond. 1897. — 121. Gkawitz. Klinische Pathologic des
Bliites. Berlin, 1895. — 122. Hatem. Du sang et de ses alterations anatomiques.
Paris, 1889. — 123. v. Jaksch and Cagnbt. Clinical Diagnosis. London, 1893.
— 124. V. Limbeck. Grundrissen klin. Pathologie des Blutes. Jena, 1896. — 125.
Reidee. Beitrdge z. Kenntniss der Leukocytosis. Leipzig, 1892. — 126. Simon. Manual
of Clinical Diagnosis by means of Microscopic and Chemical Methods. London, 1896. —
127. Stengel. "Diseases of the Blood," Twentieth CerUwry Practice of Medicine,
vol. vii. London, 1896.
S. M. C.
CAEDIAC PHYSICS
The Cardiac Valves. — 1. Mechcmism of the aurieuh-ventricula/r valves. —
At each systole of the ventricles the tongue-shaped valve-flaps pendent
from the margin of the auriculo-ventricular orifices are moved together
toward those orifices, and meeting together across them block them. By
this means the blood in each ventricle is prevented from returning into
the auricle, and under the compression of the contracting ventricle is
forced to take its way into the great arteries. Were it not for these
valves not a drop of the blood would enter the arteries, so long as the
pressure in the latter possessed a value near the normal ; but for the valves
its issue would be far easier back into the cavity of the auricles where
the pressures are low. During diastole of the ventricle the flaps of the
auriculo-ventricular valves lie in the cavity of the ventricle with their
long axes convergent toward the central long axis of the ventricle.
Between the valve-flaps and the inner face of the ventricular wall there
is always an interval, and therefore always more or less blood (Baum-
garten, Krehl). Manometric observations reveal no increase of pressure
in the auricle at the moment of closure of the auriculo-ventricular valves.
The discharge of its contents by the auricle into the quiescent and already
partly filled ventricle somewhat stretches the slack walls of this latter,
and, whether by eddy or otherwise, the valve-flaps are raised toward
each other and toward the auricular opening. Then, as the contraction of
• the auricle passes off, the pressure in the now fully -loaded ventricle
becomes higher than in the relaxing auricle. The valve -flaps thus
swing together into position, and are moved to meet across the auriculo-
CARDIAC PHYSICS 465
ventricular orifice, even before the ventricular systole has thoroughly set
in. If the arterial openings of the excised heart be blocked, and through
the auricles a momentary rush of water under about 12 inches pressure
be allowed to play into the auriculo-ventricular orifices, the valve-flaps
rise into the orifice, and come together sufiiciently firmly to allow of the
inversion of the heart without the escape of a drop of its contents.
The valve-flaps would be forced through the orifice back into the
auricle were they not tied down to the ventricle by the chordse tendineee
attached to almost all areas of their under surface. Each valve-flap shares
in a pair of papillary muscles ; these latter are so placed in regard to the
valve-flaps that the resultant of their combined individual directions of
pull lies strictly along the long axis of the ventricular chamber, and
at right angles to the plane of the auriculo-ventricular orifice itself
(Ludwig).
The auricular face of each valve-flap in its position of closure is
convex. The thin contiguous edges of the adjacent valve-flaps are bent
abruptly downward, side by side, tightly apposed ; the tenuous edges of
the membranes bear, therefore, no part of the great strain to which the
valve elsewhere is subjected ; for these edges, projecting into the ventri-
cular cavity, are supported on both sides by the fluid pressure of the
blood in the ventricle. That this is the position of these parts of the
valve is proved by the following among other considerations : the chordae
tendinese which are inserted near the free margin of each valve-flap
are much shorter than those inserted into the midrib of the flap.
Eegarding the use of the papillary muscles, it has been shown (Roy
and Adami) that the papillary muscles begin to contract later than does
the rest of the ventricle ; as the ventricle shortens from base to apex
during systole, the papillary muscles, if they are to afford the chordse
tendinese a suitably placed support, and to prevent retroversion of the
valve-flaps into the auricle, must shorten in order to maintain their
distance from the auricular orifice.
It has been suggested (Porter) that the auriculo-ventricular valve-
flaps and their papillary muscles aid the filling of the auricles with blood.
A considerable negative pressure arises in the auricle during the earlier
part of the ventricular systole; this seems to occur at the time of
contraction of the papillary muscles, and to be due to their drawing down
and flattening the valvular curtains which form so large a part of the
floor of the auricles. If so, the auricular cavity would be enlarged, and
blood drawn into it from the great veins.
It must not be forgotten that an important detail in the mechanism of
the closure of the auriculo-ventricular orifices is the circularly arranged
muscle surrounding those orifices, as a true sphincter. This sphincter
appears to be important, especially for the tricuspid orifice. In the
heart of the bird the tricuspid orifice is unprovided with valve-flaps,
and its closure is effected wholly by a muscular sphincter.
2. Mechanism of the semilimar valves.- — So long as the pressure in the
ventricle is below the pressure in the great arterial trunk leading from it,
VOL. V 2 H
466 SYSTEM OF MEDICINE
SO long will the semilunar valve-flaps meet across the arterial ostium and
occlude it. When examined under a pressure approximately that of the
aorta, the valve-flaps are seen to lie apposed across the orifice ; if one of
the flaps be displaced gently towards its attached border, the other two
cusps foUow it, becoming correspondingly more stretched. The cusps,
therefore, in the closed position of the valve mutually support one
another. When during the systole of the ventricle the intraventricular
pressure becomes higher than the aortic (resp. pulmonary) the valve-
flaps yield, are moved apart, and leave between them a triangular
opening.
When the valve is open, the position of the cusps is with their free
edge convex toward the arterial wall, but the cusp membrane does not
lie apposed to or quite close against the wall. In the open position of
the valve the arc formed by the curved wall of the sinus of Valsalva
may be said to have its chord approximately represented by the free
edge of the cusp. The supposition of Briicke that the cusps when the
aortic valve is open are pressed back against the aortic wall, so as to
block the entrances to the coronary arteries, is completely disproved.
The closure of the valves seems to be brought about in the following
way : — During systole the cavity of the ventricle, where it adjoins the
aortic opening, is narrowed by the bulging into it of the contracted
muscular wall ; it forms, in fact, a narrow channel which ends in the
direction of the aorta in the triangular cleft between the semilunar cusps
in the wide root of the aorta with its triple circumferential bays— the
sinuses of Valsalva. At the place where the narrow stream suddenly
embouches into the wide aortic channel eddies are formed, curving back
behind the valve-cusps, and constantly tending to bring these together.
The cusps are, however, kept apart by the pressure of the blood flowing
between them ; as soon, however, as that flow ceases the cusps rush
together, as it were under the force of a spring. Ceradini's account of
the eddies which come into play on closing the valves is as follows : — If
in a vertical tube containing water, in which visible particles are sus-
pended, a piston at the lower end of the tube be pushed upward, the
water in the axis of the tube is seen to move with nearly twice the
velocity average for the whole column ; along the face of the wall
of the tube the water moves so slowly that the piston overtakes the
particles suspended in it. As this occurs the particles are seen to be
swept from the circumferential zone by a centripetal current conveying
them into the axial stream. Along this they rush upward to the free
surface of, the fluid, where they sweep outward in a centrifugal eddy
to reach the wall of the tube again, there later once more to be over-
taken by the piston and swept inwards in a centripetal eddy (inversion).
If the ascent of the piston be suddenly checked, the above currents in the
fluid are modified to the extent that an actual back flow sets in downward
along the inner face of the tube. The result is that at the moment the
piston stops, the column of water above it is split into two parts — -into
an axial cylinder moving forwards and a peripheral layer moving back-
CARDIAC PMYSJCS 4^7
wards, the two being connected above by a centrifugal eddy, below by a
centripetal (inversion) eddy. To this latter is due the bringing together
into position the cusps closing the aortic opening. The cusps thus
brought together are held so by a mechanical force measurable ia the
left heart by the product of the difference between the aortic and
ventricular pressures into the area of the valve -flap, excluding their
margins. It is probable that the cusps are partly supported imder this
strain by the thick bulging myocardium of the ventricular wall on which
they may partly rest.
The eardiae sounds. — In 1810 WoUaston showed that skeletal
muscle, when it contracts under the will, emits a sound — the muscle-note.
The British Association Committee in 1836 declared the first cardiac
sound to be the muscle-note of the ventricles, but their observations were
not decisive. Ludwig, in 1868, succeeded in proving clearly that when
the heart is so placed as to convey by its mass-movement no shock to any
vibrator, and at the same time is so inadequately filled as to exclude the
possibility of tension of any of its valve-flaps, the first cardiac sound
continues to be distinct.
But it has been shown (Wintrich) by means of resonators that the
normal heart-sound consists of two notes, the lower of which only can be
considered a muscle-tona The higher is due to the vibration of the
auriculo-ventricular cusps and the column of blood they support. This
seems clear from the fact that it can bq heard if these valve-flaps are
suddenly rendered tight in the dissected heart. The first sound of the
heart is therefore found to be due to the vibration of (a) the muscular
wall of the ventricles, (/3) the auriculo-ventricular valves, and (y) the mass
of blood in the ventricles.
The second cardiac sound has been traced to sudden tightening and sub-
sequent vibration of the semilunar valve-flaps. The vibration of the
columns of blood in the aorta and pulmonary artery is also partly
answerable for the sound. If the root of the aorta and its valve be cut
out and tied to the lower end of a vertical tube filled with blood, and the
valve be then rendered slack by gently pushing it up from below, and be
then suddenly rendered tense by removing the support from under it, a
sound is produced. If next the length of the tube and cohimn of
blood be doubled, and the experiment repeated, the sound is lowered in
pitch although the tightness of the valve-flap is increased. Hence the
resonance of the tube and column of blood rather than that of the valve-
membrane is the predominant factor in the sound (Talma). But analysis
proves the sound to be compounded of a lower note due to the vibration
of the column of blood and a higher note due to the vibration of the
valve -membrane. The sudden tightening of the valve-flaps and the
production of the second sound occur not at the closure of the semilunar
valve-flaps, but quickly after.
Of the sounds emitted from the heart the weakest to hear on the
surface of the body is that of the right ventricle ; the loudest that of the
468 SYSTEM OF MEDICINE
left ventricle. The aortic sound is usually not so loud as that of the
pulmonary artery (Vierordt).
Mass movements of the heart. — The diminution in volume undergone
by the heart as its ventricles expel their content of blood is accompanied
by a change in its form. If the diameters of the heart in situ be measured
in the opened chest of a supine animal, it is found that during systole the
side to side diameter diminishes much — more than the front to back.
That is, in systole the heart becomes more or less ellipsoid in cross-section.
Probably in the unopened chest and in the erect position its cross-section
in diastole as well as in systole is nearly circular. In systole the
ventricles are somewhat shortened ; but the apex shifts little ; it is the
base which moves, descending and coming forward towards the apex. This
movement of the base is accompanied by a lengthening of the aorta and
pulmonary arteries. The latter causes descent of the base of the
contracting ventricles, and the descent compensates the shortening of the
ventricles, and retains the apex in contact with the chest wall. The
cardiac impulse is a protrusion of the chest wall over the surface of the
ventricles at the moment just before the expansion of the artery at the
wrist. As the ventricles suddenly become hard their long axis becomes
more horizontal to the vertical plane of the chest, and is tilted against
the resistance of the chest wall. Around the spot where the soft parts of
the chest are protruded by the impulse they are found slightly drawn in
at the time of each systole. This " negative impulse " is caused by the
shrinkage of heart in the air-tight chest as it empties itself, being followed
inward by the lungs and to a small extent by the soft parts of the chest
wall under the pressure of the atmosphere.
Graphic records of the cardiac impulse can be obtained by one or
other of the different forms of cardiographs. Cardiograms, however, in
spite of much attention bestowed on their elucidation, still remain unsatis-
factory, on account of their variability and the difficulty of disentangling
their component factors.
The filling of the heart. — The factors concerned in the filling of the
heart are many. The acceleration imparted by the ventricles to the
blood, both mediately through the elasticity of the arterial wall and
immediately in the heart, gives the momentum of the inflowing blood.
Then there is the excess of static pressure in the great veins over that in
the diastolic auricle and ventricle. Contributory is the aspiration by the
thorax during the act of inspiring, and also the slighter thoracic aspiration
produced by the diminution in volume of the heart itself at each systole.
The circulatory effect of the rhythmic decrease in intra-thoracic pressure
due to these two causes is illustrated by the pulsatile recession of the
brain in the cranial fontanelles. Finally the ventricles and the auricles
during their relaxation period generate within themselves pressures lower
than the pressure in the veins.
Intra - auricular pressures. — The curve of intra - aiu-icular pressure
CARDIAC PHYSICS 469
during the cardiac cycle, when its examination is begun at the outset of
the auricular systole, shows — (i.) a systolic rise of pressure, which is
synchronous with the period of contraction of the auricle ; (ii.) a first
diastolic fall of short duration corresponding with the relaxation of the
auricle and with the earliest part of the systolic rise of intra-ventricular
pressure. It is noteworthy that the closure of the auriculo-ventricular
valves causes not even a transient elevation of pressure in the auricle,
(iii.) The first diastolic rise of pressure is short, and occurs during the early
continuance of the ventricular systole. It may be due to the bulging up
of the partition between the auricle and ventricle vmder the high pressure
in the latter. It is absent when by vagus inhibition the ventricle is
prevented from beating, (iv.) K second diastolic fall occurs while the
intra-ventricular pressure is still rising. It lasts longer than the former
fall, and is more marked. Its cause may be in the pulling down of the
aurioulo-ventricular valve-flaps by the contraction of the papillary muscles,
which, as Eoy and Adami proved, contract somewhat later than the
myocardium elsewhere, (v.) A second diastolic rise occurs as a steady
increase of pressure, which continues until the beginning of the diastole of
the ventricle, (vi.) The third diastolic fall, best marked when the heart
is beating slowly, is due probably to a low pressure generated in the
common cavity of auricle-ventricle by the suction of the relaxing ventricle.
In a particular case the values of the pressures were in the dog's heart
systolic rise 9 mm. Hg. : 5, - 10, 5, -5. The flow from the veins into
the auricle is intermittent, ceasing during the systolic and the first
diastolic rise.
The filling of the ventricle. — As the systole of the ventricle ends and
relaxation of its muscle occurs, a negative pressure is generated in the
ventricle. Moens supposed that in the latter part of systole the
ventricle developed in itself a negative pressure, but his hypothesis is
unsupported by subsequent physiological observations. The negative
pressure is at first considerable, but this degree of it lasts for a very short
time only (Porter), and is over before the auriculo - ventricular valve-
flaps can open; it does not, therefore, help directly to fill the heart.
There succeeds a longer period of much slighter negative pressure ; this
assists, the auriculo-ventricular valves being open, to draw blood into the
ventricle from the auricle, and into the latter from the veins. Its
importance for the filling of the heart is proportional to its duration.
The intra-ventricular pressure. — The rise of pressure in the ventricle
which accompanies the systolic contraction of its muscle proceeds gradually
though rapidly. It closes the auriculo-ventricular valves almost at once,
but for some yfg- of a second, though steadily increasing, it can-
not burst open the semilunar valves. This is the period of " getting up
pressure," the " prosphygmic interval " as Allbutt terms it. The pressure
reaches its maximum in about -^^ of a second, and for more than the latter
half of this interval the semilunar valves have been opened. The pressure
continues to rise, therefore, after the opening of those valves has been
effected ; nor does it recede far from the maximum until the relaxation of
470 SYSTEM OF MEDICINE
the muscle sets in, about -^-^ of a second after the opening of the valves.
The pressure in the ventricle then drops below the pressure in the aorta,
and the semilunar valves close. If the pressure in the arterial system is
high, the pressure in the ventricle runs a course somewhat different from
the above, for instead of reaching its maximum soon after the opening of
the semilunar valves it slowly increases throughout the systole, becoming
maximal immediately prior to relaxation (Huerthle). In both cases, how-
ever, the curve of intra- ventricular pressure is a relatively flat-topped one,
showing a " systolic plateau." As Professor Allbutt wisely says* " It is
the function of a healtliy heart and arteries to promote the maximum of
blood displacement with the minimum alteration of pressures." In the
systolic plateau two minor undulations of pressure are seen ; the
causation of these, which are synchronous with two seen in the aortic
pressure-pulse, is not clear. On the setting in of relaxation of the
ventricle the pressure, in -j-^-g- of a second, falls from between 150 and 180
mm. Hg. to below zero ; and then for ^-^ to y^ remains negative.
The negative pressure generated varies much in amount, but may reach
nearly 20 mm. of Hg. Gradually the pressure rises to a little above
zero, and remains a few millimetres above zero throughout the rest of the
diastole, until the auricular systole occurs and drives it slightly up to
about 10 mm. of Hg.
Sees. Sees.
Systole of ventricle before the opening of the semilunar valves,
while pressure is stiU getting up . . . . "03
Continued contraction of the ventricle and escape of blood into
aorta ....... . "27
Total systole of the ventricle . . . . . ■ — '%
Diastole of both auricle and ventricle, neither contracting
passive interval . . . . . . '4
Systole of auricle (about or less than) . . . . •!
Diastole of ventricle, including relaxation and filling, up to the
beginning of the ventricular systole . . . — '5
Total cardiac cycle . . , . . '8
It is important to note that with a frequent pulse the frequency is
obtained without appreciable shortening of the cardiac systole, and almost
entirely by reduction of the resting period of the heart, the diastole.
Further, with a high arterial pressure the period of complete ventricular
relaxation is somewhat shortened.
The work of the heart. — The heart is a machine which converts
chemical energy into heat, electrical difference, and mechanical work. Only
the last-named form of its output of energy need be considered here. Dur-
ing \ sec. of the ventricular systole the left ventricle exercises a pressiu'e
on its contents often amounting to close on 200 mm. Hg. ; that is, a
pressure of 272 grammes on each square centimetre of its internal
surface ; 100 cubic centimetres is a low estimate of the output of blood.
By Torricelli's theorem, the velocity « of a fluid streaming through an
opening in the floor of a vessel under fluid pressure H is u = \/2</H,
CARDIAC PHYSICS 471
where g is the acceleration of gravitation (9 '8 metres). The kinetic
energy E of this fluid is, if m is the mass of the fluid, mgO.. And mg
= w, the weight of the fluid, so that E = wH. In other words, a drop of
the fluid starting from an orifice in the vessel will have at that orifice the
same velocity as if it had fallen freely from the level of the top of the
fluid ; and the kinetic energy can be measured by the work required to
raise it again to a height equal to the height of the top of the fluid in the
vessel. If the ventricle be assumed to have no external resistance to
overcome in expelling the blood, its work W would be (V being the
velocity which the blood would have under a fluid pressure corresponding
to the pressure exerted by the ventricle) ^ • But the ventricle in
expelling its blood has to do so against a high resistance : only a portion
of its energy is employed in imparting velocity to the blood. The total
pressure is divisible into two parts, I. and II., — I. spent in overcoming
resistance in the tubing of the blood-vessels, II. the flow-producing
pressure or velocity pressure. The mean velocity can be ascertained by
experiment ; its value per second is
Volume of outflow Q , __ V^
or — s_. and II. —
Sectional area x time (seconds) irrH' 2g'
The portion of the work of the heart which is used in overcoming the
resistance is the difierence between the whole work and that quantity
arrived at above for II. This latter amounts to about 1-28 grammetres.
If the velocity of the blood in the aorta be taken at -5 metre per
second, and the quantity ejected from the ventricle at 100 c.c,
and the pressure in the aorta to average 150 mm. Hg., we have the
work of the left ventricle amounting to 204 grammetres done against
external resistance -i- 1-28 grammetres represented by the momentum of
the moving blood : a total of 205-28 grammetres. The work done by
the right ventricle against external resistance may be taken at about
81-6 grammetres. The energy of the muscular contraction directly ex-
pended in imparting velocity to the blood is quite small in comparison
with the amount expended in distending the arterial wall. The arterial
wall, and especially the aorta, is to the heart as a high-pressure cistern to
the pumping-station that replenishes it, as its air-chamber to the fire-
engine, or as the bag to the bagpipes (p. 476). And probably 100 times
more of the heart's work in moving the blood is expended on it indirectly
through the aortic arterial cistern than directly on the blood itself. The
potential energy entering the heart in chemical form is transmuted to the
potential mechanical energy of the heart wall, then to the kinetic energy
of accelerated material, and again to the mechanical potential energy of
the blood-vessel walls, ultimately to be converted into heat. In the
tensions and relaxations of the arterial walls, and in the friction of the
moving blood, the heart's energy is continually being converted into heat.
In this form the contractions of the heart yield about -jLj-th of the total
472 SYSTEM OF MEDICINE
daily heat production. With a pulse frequency of 72 per minute the
work produced by the heart is nearly 25,000 metre kilogrammes in tiie
*24 hours — work more than equal to lifting itself six times in the 24
hours from the sea-level to the summit of Mount Everest.
Experimental observation shows that the heart is a machine which
maintains under varying circumstances — so long as its nervous system
and its own nutrition are not interfered with — a curiously constant
action in two respects ; namely, in the duration of the ventricular systole
and in the quantity of the output of blood into the aorta. To keep
these constant the heart has under varying circumstances to perform
very various amounts of work. When the aortic pressure is high, it is
found by direct measurement that not only is the maximal pressure
produced in the ventricle at each systole much higher than when the
aortic pressure is low, but also that the average pressure in the ventricle
during systole is much higher than when the heart is beating against a
low aortic pressure. The systolic pressure-plateau is much heightened.
High arterial blood-pressure involves, therefore, a greater expenditure of
energy by the heart at each systole. It is interesting to note that a rise
of arterial pressure is in most cases followed by a reduction of "the frequency
of the heart's rhythm. This is in consequence of excitation of the vagus
centre ; the stimul.ition being in part a reflex started from the wall of the
heart itself, and in part a direct effect of the high pressure of the blood
circulating in the brain. An important factor determining the work of
the heart is the distension of the ventricular cavity in diastole. The
pressure on a unit of surface of the cavity remaining the same, the total
intra-ventricular pressure will vary approximately as the square of the
radius of the cavity if the cavity be taken as approximately spherical.
Thus Eoy and Adami have pointed out that distension of the
ventricle means not only increase of the tension of the muscular fibres,
but also increase of the lateral pressure on their surface in pro-
portion as the square of their increase in length. But, as they further
pointed out, the content of the cavity increases as the cube, and the
muscle fibres in order to expel the same constant quantity of blood from
the dilated as from the undilated ventricle need to shorten to a relatively
less extent than was required of them before. The effect of diastolic
distension is therefore, if the output from the ventricle at each systole
remain the same, to leave a larger residuum of blood in the ventricle at
the end of systole. Recent investigations (Roy and Adami, Huerthle)
have shown that to suppose that the ventricle empties itself completely at
each systole is erroneous. Not only does it not do so, but the residual
quantity of blood varies a good deal, and with it varies generally the
amount of distension of the ventricle in diastole. The amount of disten-
sion of the ventricle, in other words, the degree of stretch in the muscle-
fibres, at the moment when they enter into contraction, is an important
determinant of the force of their contraction. All muscles respond by
greater contraction when stretched than when unstretched. This increase
in contraction is seen chiefly in increase of the work done, and the amount
CARDIAC PHYSICS 473
of actual shortening of the muscle is usually less when it is placed under
considerable stretch than when it is not. The work done (lift x load) and
the heat given out are, however, greater. The ventricle when well
loaded, or even excessively loaded, may from our general knowledge of the
effect of tension on all muscular structures be expected to expend more
, energy and do more work at each contraction than when lightly loaded.
But it does not necessarily follow that a largely distended ventricle
is during diastole more loaded, that is, under higher tension than one
only normally distended. The tonus of the heart-muscle is variable,
and its tension will depend on the tonus. Moreover, the heart may be
considered an after-loaded muscle, its load only coming into play during
its contraction. The amount of blopd expelled at each systole will be
increased in a largely distended ventricle, and is found by experiment to
be increased ; but at the same time the nervous system is likely to be
excited to reduce the frequency of repetition of the heart's beat, and in
that way to spare the expenditure of energy by the m.uscle-cells.
The diastolic size of the ventricle also influences the contraction of
the ventricle in another way. The mechanical condition of the contrac-
tion of the ventricular muscle differs in one respect remarkably from
the conditions obtaining in the skeletal muscles : in the skeletal muscle
the contractions are in the execution of most movements approximately
isotonic; that is, while the length of the muscle alters, its tension
remains approximately constant ; broadly taken, it is only in using the
muscles for fixation that the contraction becomes isometric, that is, without
change in length. The contraction of the heart during the time of getting
up pressure is, on the contrary, practically isometric. The muscle-fibres
can only alter their length in so far as the cavity of the ventricle can be
altered in its shape, its volume remaining constant. But the larger the
chamber of the ventricle the smaller the amount of shortening, which, as
explained above (Roy and Adami), is necessary for reducing the size of
the chamber by a given volume. The output of the heart remains fairly
constant for each systole. The amount of systolic shortening of the
cardiac fibres then is less when the diastolic ventricle is largely distended
than when- it is little distended. The contraction in the former case
approximates nearer to the isometric condition than in the latter.
In many morbid conditions increased work is thrown upon the heart.
In mitral and in aortic regurgitation the ventricle is not an " after-loaded "
muscle to the extent it normally should be ; its load in those cases is
applied in diastole owing to the excessive filling of the heart by back-
flow. Similar increased diastolic volume of the heart may be brought
about by compressing the abdomen and the veins therein (Eoy and Adami).
As stated above, a certain amount of diastolic loading is favourable to the
heart's contraction. In aortic stenosis an extra load is imposed on the
ventricle at each systole. The heart is more than normally after-loaded ;
and here again high-tension of the muscle is, within limits, a favourable
condition for output of energy by the heart. But tension beyond a certain
degree, and applied for more than a short period, is harmful here as in the
474 SYSTEM OF MEDICINE
case of other muscles. The heart, as Roy and Cohnheim have so well
insisted, offers remarkable examples of the reserve power characteristic of
the mechanisms of the animal body. By artificially reducing the lumen
of the aorta even greatly, the aortic blood-pressure is but little lowered ;
it is maintained by the expenditure of perhaps a fourfold amount of work
by the ventricle, as has been proved by manometric measurements. And
furthermore increased activity within limits in the cardiac muscle leads,
as in other muscles, to growth and further development of the muscle.
To a certain extent, therefore, the heart possesses not merely a great
temporary reserve power, but in virtue of its reaction of " hypertrophy "
a high degree of permanent reserve power.
The peripheral resistance to the heart. — Our knowledge of the
conditions of resistance offered in the circulation of the blood to the
action of the heart can be satisfactorily dealt with from a physical point
of view only by use of laws which connect together certain measiwable
facts concerning the blood-vessels and the blood. We require to know
the amount of motive force which, as shown above, may be taken to be
the aortic blood-pressure, the velocity of flow of blood, and the resistance
which is overcome by the streaming blood. The last-named — the resist-
ance— is composed of two factors, the one resident in the dimensions of the
channel, tlie other in the p-operties of theftmd — the blood.
It has just been said that of the factor resident in the properties of
the vascular channel the dimensions only are of account. The resistance
which the channel offers to the flow of fluid along it diminishes with
the shortness of the tube and with the increase of the bore of it. The
nature of the material composing the tube is practically without influence
on the flow. A tube of given dimensions offers the same resistance to
a stream of water within it whether it be of metal, of glass, or of any
other material. Every moving fluid streams along in a channel lined
by its own fluid particles, and the layer of fluid immediately next the
wall of the containing channel is practically at rest.
The factor depending on the properties of the blood itself is measur-
able in terms of standard fluids, and is due to what is called viscosity,
its internal friction. Fluid flowing along a channel may, of course, be
considered as though composed of a number of concentric fluid cylinders
ranged round an axi'al thread of quickest stream, and contained within
an outermost sheet where velocity is reduced to zero. In their stream-
ing motion, therefore, the particles of the fluid move over and among
their fellows, and this relative movement is opposed in the fluid by its
speciflc coherence or viscosity. As to its degree, this internal resistance
is largely influenced in one and the same fluid by temperature. Dr.
Graham Brown has proved experimentally that the blood flows with
considerably less resistance along tubes when warmed to fever heat than
it does at normal body temperature. The internal friction of distilled
water is decreased 250 per cent by raising its temperature to blood-heat
as compared with its internal friction at 0'5° centigrade.
CARDIAC PHYSICS 475
Between the dimensions of a channel, the pressure-head feeding it
with fluid, and the quantity of fluid output from it, certain laws of rela-
tion are known. Poiseuille's "law" discovers the amount of fluid
escaping from any tubular channel of known dimensions fed under a
known pressure-head. The output Q in unit time varies, when the
length of the tube is very great in comparison with its diameter, directly
with the fourth power of the diameter d of the tube, and with the feed-
pressiwe h; and inversely with the length I of the tube.
(^- — .
From this, by comparing outputs of various fluids with output of a
standard fluid (distilled water), the coefficient of internal friction c can
be obtained ; so that
Poiseuille's law is in all hydrodynamics perhaps the nearest approach
to accord between theory and practice. It is, however, formulated for
conditions which are not very approximately those existing in the circu-
lation of the blood. It deals with flow along cylindrical tubes under
constant pressure. The blood-vessels are but approximately cylindrical,
and we shall probably never be able to ascertain their particular dimensions
from moment to moment, as, under the influence of the nervous system,
yre know they must be continually changing. Again, they are curved
and complexly branched ; furthermore, the pressure in the blood-channels
is to a large extent a pulsatile one. The last difficulty has been especi-
ally investigated by Huerthle. He finds that, in experiments carried
out with distilled water, a pulsatile pressure resembling that in the
arteries did not seriously upset the Poiseuille law so long as it could be
accurately averaged. The results obtained under the pulsatile pressure
harmonised well with results obtained under an equal average but con-
stant pressure. A further difficulty lies in the blood being not purely fluid,
but a fluid containing semi-solid bodies suspended in it. The inspissation
of the blood, which constantly occurs as an element of " collapse," in acute
cholera, and so forth, probably alters greatly the viscosity coefficient of
the circulating blood.
These circumstances complicate the application of Poiseuille's law to
physiology. It is, however, possible for a given brief period to ascer-
tain certain data which are of use in forming a conception of the amount
of physical resistance which the heart overcomes in maintaining the
circulation. We can determine the fluid pressure in a vessel, the
amount of blood flowing through that vessel, and the viscosity coefficient
of the blood of the animal at the time and at its normal temperature,
also in some cases the diameter and length of the channel. Huerthle
has recently determined the viscosity coefficient. He allowed the blood to
flow direct from the carotid through a calibrated tube, and measured
476 SYSTEM OF MEDICINE
contemporaneously the outflow from the tube and the pressure-head
feeding the tube with blood. The blood was successfully prevented
from cooling, and all fear of interference from clotting was avoided by
reducing the period of flow to less than thirty seconds. The time was
measured in hundredths of a second, the quantity of outflow in cubic
millimetres. In this way the following results were arrived at : —
(i.) The coefiicient of viscosity of the blood is in one and the same
species of animal relatively constant.
(ii.) In one and the same individual animal the viscosity of the
blood when measured by observations with tubes of various size and
with various heights of arterial pressure is found to give an almost exactly
identical coefiicient. From this it would seem that the suspension of the
corpuscles in the blood does not seriously affect the application of
Poiseuille's law to it as a fluid.
(iii.) The average coefiicients of viscosity for the blood of different
species examined were found to be, compared with water at 37° C. as 1,
as follows : — Blood of dog, 4-5 ; of cat, i'l ; of rabbit, 3'2. Of these,
that of the dog probably most closely approaches that of man.
With the data of pressure-head, quantity of outflow, and viscosity
coefficient found, there remain in Poiseuille's formula only two unknown
quantities, namely, (^) the diameter and (Q fhe length of the cylindrical tube-
channel. If d be represented by a definite number, as in certain cases it
can be, then we can solve the equation, in so far that we can determine
the length of a tube through which the same quantity of blood would
flow in unit time — as through the aorta — and in that way obtain a
definite expression of the amount of resistance in the circulation along
the aorta.
Huerthle finds in this way that the aortic cha/nnel of the rabbit offers
to the blood-flow a resistance equal to that which would be offered it by
a cylindrical tube of the same diameter as the aorta and 300 m. in length.
Again, making use of data h, the arterial pressure, and Q the quantity of
outflow of blood from the renal artery, and d the diameter of the renal
artery under a pressure of 100 mm. Hg., Huerthle found the resistance
offered in the vascular path through one kidney. The resistance offered
by one kidney (dog) weighing 100 gram, is equal to that which would
be offered by a tube of the same diameter as the renal artery (of the dog),
namely, 4'6 mm., and having a length of 35 metres. Under the influ-
ence of diuretics this resistance becomes greatly lessened, so as to corre-
spond with a tube of similar diameter, but only 22 metres in length.
One very remarkable conclusion from the above is that the resistances
offered in the aortic channel and in the renal respectively are so greatly
different as probably to indicate a profound difference in function. In
comparing the resistances offered in the two channels, we can express
both in tube-lengths of 30 m. ; but then the diameter of the aorta must
be reduced in the tube that represents it to 4 '5 mm. That is, in other
words, the aorta has a relatively greater diameter than the renal artery. This
leads to the conclusion long ago introduced by E. H. Weber, that the
CARDIAC PHYSICS 477
aorta, with its peculiarly elastic wall, is not merely a channel, but a dis-
tensible reservoir for the blood thrown out by the heart ; it stores up this
blood temporarily for distribution during diastole (p. 471).
In using Poiseuille's law it must be remembered that it cannot be
applied directly to solve the relation between speed of blood-stream and
height of blood-pressure in the animal body, although this is sometimes
done. Inasmuch as the vascular channels are extensible, and their
diameter therefore variable under alteration of blood-pressure, the rela-
tionships that hold good between pressure and velocity in rigid tubes
will only obtain in modified degrees. The innervation remaining un-
altered, we may assume that to raise the pressure twofold in a disten-
sible tube will more than double the velocity.
But the main portion of the work of the heart is expended immedi-
ately, not on moving the blood through the vessels, but in stretching the
arterial wall. The elasticity of this wall is therefore of importance in
physical action of the heart. Wertheim and Eoy examined the elasticity
of the aorta by hanging weights on a strip of uniform cross -sectional
area taken from it. Eoy, by an ingenious apparatus, obtained continuous
graphic records while the load was uniformly increased in weight, and
thus obtained curves in which the weights are represented by the
abscissae, the elongations constituting the ordinates. Both he and
Wertheim agree that the curve obtained (if the strip be fresh and from
a healthy vessel) is an hyperbola. Roy and Zwaardemaker have further
examined experimentally the increment of cubic content of the vessel
obtained under heightened pressure. Starting from a pressure about
equal to that normal in the blood-vessel under examination, they found
that, under successive equal increments of pressure, the increase ob-
tained in capacity is greatest at first ; and as the pressure is gradually
heightened, the increase in capacity obtained becomes less and less. They
found also that as the pressure starting from normal (for example, 120 mm.
of mercury for the carotid of the cat) is reduced by successive equal
decrements, the diminution of capacity follows more rapidly at first than
later. These observers, therefore, find the extensibility at its greatest
at a range of pressures which are frequent and usual in the vessel under
examination. Also that above those pressures the curve of extensibility
is hyperbolic. It is clear, therefore, that with a high arterial blood-
pressure a certain further absolute increase of pressure will distend the
vessel less than will the same absolute increase of pressure under a
lower arterial pressure. Also that the injection by the heart into the
aorta of a certain absolute quantity of blood will raise the arterial
tension relatively more when the pressure is already high than when it
is about the mean or is low. The walls of the smaller vessels have been
proved to be more easily distensible than those of the large, so that any
increase in the amount of blood in the arterial system will locally distri-
bute that blood in the smaller or larger vessels relatively differently under
low thart under high arterial pressures.
It is noteworthy that the rupturing strains of the arteries is proved
478 SYSTEM OF MEDICINE
by experiment to be about twenty times greater than any strain the
body can put upon them ; this is true, of course, of healthy vessels.
Influence of the force of gravity on the heart. — It might at first
sight appear that since the blood in circulation lies practically in a vertical
circuit, the effect of gravity as regards the work to be done by the heart
in maintaining the movement of the blood would not be affected by
gravity, the weights of the blood in the up-stream and down-stream
columns balancing one another. But such a view leaves out of considera'-
tion the efiect of the static pressure of the fluid columns in the vessels in
stretching the walls of the vessels. L. Hill has recently investigated the
results of this for the heart and the circulation generally. In respect of
the former he points out that the force of gravity must be regarded as
a cardinal factor in circulatory problems. The splanchnic vaso-motor
system is entrusted with the important duty of compensating the hydro-
static effects of gravity brought about by changes in the posture of the
body. This action of the splanchnic vaso-motor system is far more
developed in upright animals, such as the monkey, than in rabbits and
dogs; and therefore is probably very complete in man. He proves
that when the power of compensation is damaged by paralysis of the
splanchnic vaso-constrictors, for instance by shock, in asphyxia, or by
chloroform, the blood drains into the abdominal veins, the tonus of the
splanchnic vessels not being sufiicient to resist the hydrostatic pressure
if the upright position be assumed ; in consequence the heart empties and
the cerebral circulation ceases. In the horizontal and in the " feet-up "
position syncope is avoided or recovered from, the force of gravity acting
in the same sense as the heart. To bandage the abdomen firmly has the
same restorative efiect. Chloroform by destroying the compensation for
gravity in the circulation can kill an animal if the posture be one in which
the abdomen is on a lower level than the heart.
C. S. Sherrington.
REFERENCES
The Cardiac Valves : — 1. Marc Si^e. Secherches sur Z'anatomie et la physiologic
du cmv/r. Paris, 1875. — 2. Kebhl. Arch. f. Anat. u. Physiol., Physiol. Abth. 1889,
p. 288. — 3. Sachs. Gesellsch. d. Wiss. 1891, p. 358. — 4. Sahdborg and "Wobm-
MCller. Arch. f. d. ges. Physiol, vol. xxii. 1880, p. 412. — 5. Hesse. Arch. f.
Anat. u. Physiol. 1880, p. 344. — 6. Lttchsinger. Arch. f. d. ges. Physiol, vol. xxxiv.
1884, p. 291. — 7. Ceeadini. Der Meehanismus der halbmondformigen Klappen.
Leipzig, 1872. — 8. MoKus. Arch. f. d. ges. Physiol, vol. xx. 1879, p. 531. — 9. Rot
and Adami. Philosoph. Transactions. London, 1893. The Cardiac Sounds : — 10.
LiTDWiG and Dogibl. Ber. d. Sachs. Gesells. d. Wissens. 1868, p. 96. — 11.
Herrotjn and Yeo. Journ. of Physiol, vol. vi. 1885, p. 290. — 12. Kasbm-Beck.
Arch. f. d. ges. Physiol, vol. xlvii. 1890, p. 56. — 13. Haycraft. Journ. of Physiol.
vol. ii. 1890, p. 486.— 14. Talma. Arch. f. d. ges. Physiol, vol. xxiii. 1880, p. 275.
— 15. ViEROEDT. Die Messung der Intensilat der Herztime. Tiibingen, 1885.— 16.
HuERTHLB. Deutsche med. Wochenschrift, 1894. Mass Movements of the Heart : —
17. Colin. Physiol. Comp. Paris, 1888, p. 420. — 18. Roy and Adami. The Prac-
titioner, 1890, p. 82. — 19. SCHEIBBE. Arch. f. klin. Med. vol. xlvii. 1891, p. 368. —
20. Knoll. Sitzungsber. d. Wien. Akad. d. Wiss. 1890. — 21. Febdericq., Travaux
du labor. 1888. — 22. v. Frey and Keehl. Arch. f. Anat. u. Phys. 1890.—
23. RoLLESTON. Journ. of Physiol, vol. •via. 18S7 . — 24. Hubrthle. Arch. f. d. ges.
CARDIAC PHYSICS 479
Physiol, vol. xlix. 1891, p. 92.-25. EoY and Adami. Phil. Tran. 1892.— 26. Magini.
Arch. ital. de biol. vol. viii. 1887, p. 127. — 27. Stefani. Memoria da Ferrara, 1891.
— 28. FiLEHNB and Pbngoldt. Centralb. f. d. med. Wiss. 1879, p. 482. — 29.
GuTTMAN. Arch. f. path. Anat. vol. Ixxvi. 1879, p. 534. — 30. v. Fbby. Die Uhter-
suchung des Pulses. — 31. Edgken. Skand. Arch. f. Physiol. 1889. — 32. Gad and
Cowl. Gentralb. f. Physiol. 1888, p. 264. — 33. Martitts. ZeitscA. f. Min. Med.
vol. XV. 1889, p. 536. — 34. Btkom Bramwbll and Mtjreay. Prit. Med. Joum.
vol. i. 1888, p. 10.— 35. Feedbeicq. Centralb. fur Physiol. 1891, p. 587. The Filling
of the Heart: — 36. HATCRArT and Edib. Joum. of Physiol, vol. xii. 1891, p. 426.
— 37. Newell Martin and Donaldson. Studies from the Physiol. Lab. Baltimore,
1887. — 38. Stbfani-Ferrara. Cardiovolume, ete. 1891. — 39. Mink. Centralb. f.
Physiol. 1890, p. 569. — 40. Townsend Porter. Joum. of Physiol, vol. xiii. 1892. —
41. Roy and Adami. Brit. Med. Jowrn. vol. ii. 1888, p. 1321. The Work of the
Heart : — 42. Stolnikow and Ludwig. Arch. f. Anat. u. Physiol. , Physiol. Abth.
1886, p. 1. — 43. TiGERSTEDT. Skand. Arch. f. Physiol, vol. iii. p. 1891, p. 145. — 44.
TiGERSTBDT. Die Physiol, des Kreislaufes, Leipzig, 1893, p. 146. — 45. Zuntz.
Deutsch. med. Woehensehr. 1892, p. 109. — 46. Rot and Adami. Philosophical Trans-
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Brown. Royal Infirnwry Reports, Edinburgh, 1893. — 48. Nioolls. Joum. of
Physiol, vol. xx. p. 407. — 49. Huerthle. Deutsche med. Wochenschrift, Aug. 1897.
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London, 1895. — 54. Roy and Adami. Srit. Med. Joum. London, vol. ii. 1888, p.
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1885, p. 467, and vol. xxxix. 1886, p. 371. — 56. Leonard Hill. The Physiology amd
Pathology of the Cerebral Circulation. London, 1896,
c. s. s.
CHLOEOSIS
Syn. — ^Latin, Morbus virgineus (Lange, a.d. 1520); German, Bleichsucht ;
French, Poles coulewrs ; English, Greeri-sichness.
[Professor Stockman tells the author that the name Chlorosis was given
to this disease by Jean Vavandal in A.D. 1620.]
Introductory. — Anemia. — That in the course of many diseases the blood
should vary in composition, chiefly in the direction of impoverishment,
is to be expected. It may thus vary in more than one quality; it
may vary in mass ; in plasmatic value ; and in corpuscular value. In
pining, for example, we note loss of water, loss of plasma, and loss of red
coipuscles; as proteids fail, the water, which is retained more or less
loosely by them, tends to escape ; finally, the corpuscles lose their vigour
and the activity of their growth. We have no means of measuring
the fluctuations of the mass of the blood with any approach to accuracy ;
still it seems certain that the blood does vary in mass ; sometimes in the
direction of excess, more frequently in that of defect. Smallness of
arterial pulse is no guide in this matter ; the artery under observation
may contract upon its contents so as to produce a relative ansemia of
48o SYSTEM OF MEDICINE
a particular area ; or a general arterial anaemia may coexist with a venous
plethora, the mass of the blood not being diminished. It would seem,
however, that in some diseases, such as cancer or exhausting discharges,
and in old age, the mass of the blood is diminished ; the arteries are un-
filled, and there may be no sign of venous distension in any area. It
seems probable also that in the anaemia of young men the mass of the
blood decreases ; in chlorosis it does not fall, and is supposed even to rise
(Rubenstein and James).
Of the variations in the composition of the plasma and in cor-
pusculation we have better evidence as, by methods described in a
previous article (p. 408), we are enabled to submit these constituents
to direct estimation. In the present article we have no concern with
excessive values, our text is poverty of the blood. Moreover, seeing
that anaemia is a factor in many diseases, I must refer the reader to
other articles of this work — as to those on pernicious anaemia, splenic
anaemia, leukaemia, wherein the blood changes are eminent ; or to
phthisis pulmonalis, chronic dyspepsia or diarrhoea, wherein the anaemia
is rather a secondary event — in which certain deteriorations of the
nutritive fluid are particularly described. We have some concern here,
however, with anaemia occurring in the course of temporary deviations
from health as distinguished from that of maladies in which the defects
of the blood are of a secondary kind. Apart from the graver maladies
we are all of us familiar with states of debility and lack of colour
and condition which, at whatsoever time of life they may come on, we
attribute, and often with reason, to a temporary and curable im-
poverishment of the blood. There are certain times of life when we
may be too ready to put down any such flagging of sanguification to
transient causes, as for. instance in boys and girls in whom the demands
of growth and development are extraordinary ; there are other times of
life, as for instance in advancing years, when we are on the alert to see
in the change a herald of organic disease, and may be happily deceived
nevertheless, for old persons too are occasionally prone to fail in the
common task of keeping the blood up to its proper standard ; though
in them this failure is always of more serious meaning than it is in the
young. Again, the blood may be sufficient in mass, and yet deficient
either in nutritive value, or in oxidising power; or indeed in both
these qualities together. For these various states sundry and some-
what uncouth names have been provided, such as hypalbuminosis,
oligocythaemia, and so on ; while defect in the mass of the blood has been
named oligaemia — names not without their convenience. We also hear
of hydraemia as a name for a state of the blood in which the fluid is
said to be unduly diluted with water, and thus, if not diminished in actual
bulk, defective in proteid matter. It is said that the blood of anaemic young
men is not deficient in haemoglobin, and that they are not very pallid; that it
is the quantity of arterial blood, or at any rate of the plasma, in the vessels
which is under the standard : the blood does not spring from the finger
when pricked as it does in the ohlorotic girl. In young men's anaemia.
CHLOROSIS 481
therefore, the specific gravity of the blood may actually rise above the
normal mean (Lloyd Jones). Again, the blood may be defective, or, on the
other hand, unduly abundant in salts. These variations are_less important,
as they are probably integral parts of the former changes : for instance,
the salts probably depend directly upon the quantities of the albuminous
elements of the blood ; the water likewise may rise and fall in part
with the albuminous elements with which it is more or less loosely com-
bined : moreover, it is dependent upon the saline density of the blood.
Intimately speaking, therefore, while the causes of anaemia may be in-
finite, the number of anaemic permutations may be few (19). As I have
said, however, we have in this chapter to deal with ansemia in its
dynamical rather than in its statical aspects ; with anaemia which, under
favourable conditions, admits of more or less rapid readjustment with
recovery of equilibrium.
Anaemias of such kinds may be divided into (a) those in which
consumption of the blood is accelerated ; (i) those in which renewal of
the blood is slow ; and (c) those in which both sources of failure are
combined. Of the first, fever may be taken as an instance ; of the
second, inanition from whatever cause ; and in pulmonary phthisis, if
both appetite and digestion be poor, we shall recognise the mode in which
undue rapidity of consumption may conspire with imperfect renewal.
It need not be said at large that such conditions as these merge by
insensible gradations into health. For example, in growing youth rapid >
use of the blood may not be made up even by good appetite and diges-
tion ; in old age, although the use of the blood may be slow, appetite
and assimilation may be slower still. Again, in direct loss of blood, or
in the infection of the blood by some poison, recovery of health is to
be anticipated. We shall not forget, however, that waste of blood is far
more mischievous and dangerous in old persons ; and in those, whether
old or young, in whom restoration of the plasma and of cell growth is
for some reason imperfect.
Apart from the graver diseases, then, we should expect to find
anaemia more frequent and more obstinate in the young on the one hand,
r.nd in the old on the other. Some persons are anaemic, or have a bent
to ansemia, all their lives long ; but simple ansemia is less apt to occur
in the decades between thirty and fifty, for at these ages perturbations
of nutrition are better resisted. Some persons seem to have a richer
blood store than others, to resist the incursions of injurious agents more
successfully, and to recover more quickly from such incursions.
Symptoms. — Of the symptoms of anaemia I shall say almost enough
under the head of chlorosis, to which these considerations are but intro-
ductory ; stiU the symptoms of chlorosis are not merely those of anaemia;
and it may be well to ascertain how far the phenomena of chlorosis are
peculiar to this state, and how far they are common to anaemia of what-
ever origin. The main distinction in the phenomena is in the condition
of the pulse, which in anaemias of failing quantity is not only quickened
but also feeble and empty. In chlorosis, as we shall see, the pulse may
VOL. ■\' 2 I
482 SYSTEM OF MEDICINE
be full and of good or even of excessive pressure. Another side of this
peculiarity is seen in the action of the heart, which in anaemias secondary
to serious disease may be feeble and almost impalpable, while in chlorosis
it is often irritable and sometimes obtrusive. Fatty changes in the heart
are common in their degrees to all anaemias. In chlorosis the ansemia tells
rather on the respiration and on the steadiness of the heart ; in other
anaemias, or in many of them, the effect is rather marked by slackness of
the cerebral circulation and syncope. Wasting, generally speaking, is
not a very prominent symptom in anaemias, and it is rarely seen in un-
complicated chlorosis. The pathology of ansemia will be discussed inci-
dentally under the chlorosis.
The diagnosis, prognosis, and treatment of anaemia depend upon the
primary malady of which the anaemia is a symptom — as of syphilis,
plumbism, malaria, and so forth. For the most part ansemia is a
symptom rather than a disease ; even in chlorosis there is no doubt some
specific series of antecedents which as yet is hidden from us. On the
other hand, as I have already said, in some persons, in whom the
hsemopoietic capacity is habitually low, anaemia may be the primary
factor ; in these cases the proteid elements of the fluid seem to be as
much in defect as the haemoglobin, yet iron is nevertheless an important
means of cure or relief. Thus it would appear that iron, the specific
action of which in ansemia is hard to explain, does more than feed the
red corpuscle ; it seems to possess some property of stimulating the growth
of the blood as a tissue.
Chlorosis. — Definition. — Chlorosis is a malady of women, and
primarily of young women at or about the age of puberty ; it consists in
defect of the red corpuscles of the blood, a defect partly of numbers,
-.chiefly of haemoglobin ; the plasma being constant, or even enriched.
Under one name or another chlorosis has attracted attention from
early times, yet it was not until the clinical studies of Hoffmann and of
Johann Duncan gave accuracy to the description of the malady that
it took a definite place in nosology. Ashwell was the first physician to
recognise chlorosis as something more than a symptomatic ansemia ; and
Hayem the first to place the disease on a firm pathological basis.
Causation. — It would serve little good purpose to dwell on the
fanciful views of the causes and characters of chlorosis which have pre-
vailed among physicians and poets — views which are adumbrated by the
use of such names as fehris amatoria, icterus amantium, and so forth. We
shall see hereafter that the attribution of chlorosis to perverted or
thwarted sexual impulses is mistaken, except in so far as an emotional
disturbance of whatever origin may contribute to the causation of the
malady. On the other hand, although we may have cleared our minds
of certain false preconceptions, we cannot yet pretend to be in possession
of much more accurate knowledge of the causes of chlorosis. Many and
various are the surmises ; and of these, or of some of them, I will try to
give an account.
CHLOROSIS 483
Heredity. — That cMorosis is hereditary in no small measure seems to
be believed by most observers . of the disease, and certainly accords
with my own experience. In family after family do I remember the
daughters, one after another, as they arrived at puberty, coming for
aid in this disorder. It may be replied that as chlorosis is so common a
malady it will naturally appear in most or all families as the girls grow
up. Still, making all allowance for this confusion and for similarity of con-
ditions, I agree with those who say that chlorosis in its more strongly
marked forms tells especially upon certain families ; and that in such
/ families the girls are hit more hardly and resist treatment more obsti-
y nately than in others. Whether the bent to the disorder may run in a
j latent channel through the fathers, I cannot say ; it seems rather to run
/ through the mothers, as I have found that in families of chlorotic girls
\ the mother commonly says that she and her sisters suffered likewise in
I a notable degree. I regret to say that I am old enough now to see
/ in my consulting-room the chlorotic daughters of women whom years
/ ago I had treated before their marriage for the same disorder. Dr. Lloyd
~ Jones has published certain opinions on the heredity of chlorosis which
I shall more conveniently discuss in the following paragraph : —
Sez. — Between the extreme opinions of Dr. Lloyd Jones and those of
Dr. Simon, the one holding that chlorosis is wholly and peculiarly a disease
of women, and the other that chlorosis is little more than an anaemia of
Dl-thriven young people, there is a great interval. Dr. Jones, in a series of
papers which are remarkable not only for speculative ability, but also for
industrious investigation of the phenomena of chlorosis, expresses some
such views as the following : — In chlorotic women the specific gravity of
the blood falls : on further inquiry it seems that this fall is due to defect
in the corpuscular element, and that when the plasma is tested separately
the specific gravity is not only up to the normal standard, but may exceed
it. In this important respect the blood of chlorosis differs from that
found in ordinary ansemia, in which the specific gravity of the blood
tends to rise while that of the plasma alone tends to fall. Again, the
serum in ordinary ansemia is deficient in quantity, but that in chlorosis
is abundant. The first kind of ansemia (oligsemia) may occur in either
sex indifferently ; the second is peculiar to women in the child-bearing
period. In the treatment of this second kind iron is of specific value, in
that of the first its value is less certain.
Dr. Jones then goes on to say that the ansemia marked by abundant
plasma and deficient haemoglobin — that of chlorosis — is peculiar to
women, and is foimd in women who come of large families, — in women
who have many brothers and sisters. Since these observations were
published I have questioned my own experience, and, so far as impressions
go, I am disposed to think that the author is right in this respect. Dr.
Jones goes one step farther, and asserts that in large families the blood of
the sons as well as of the daughters has the chlorotic bent ; its plasma
is abundant and of good specific gravity. From these facts he infers
that this kind of blood is the blood of .fertility j_ and that chlorosis is the
484 SYSTEM OF MEDICINE
exaggeration of the fertile blood, of blood, that is, which has for its end
the storage of nutritive' material for the foetus during pregnancy. That
• such a leaning should be seen in the blood of women at puberty thus
becomes comprehensible. These opinions are based on a large number of
observations both clinical and pathological, they are coherent and in-
teresting; whether they are true cannot be settled, at present. Mean-
while they hold the field, and they make a good working hypothesis, one
which has this in its favour, that, to close observers, perhaps every girl
passes, as it were, through the outer court of chlorosis in her progress
from youth to maturity. One other point seems to me to be in its favour,
namely, that the causation of chlorosis is probably simple ; the symptoms
being uniform, and general in their incidence on one sex, it is probably
due to some widely acting antecedents of a kind not subject to much per-
turbation. Whether Dr. Jones' hypothesis be true or not, we are prob-
ably near the discovery of some such cause of general operation deflected
but little by contingent causes. For this reason I think that the con-
ceptions of causes of more multiform or incidental activity, which we
shall presently consider, are less likely to be true. Some of ■ Dr.
Jones' results, such as the maintenance of the volume of the plasma,
are corroborated by Rubenstein ; and the persistence of its specific gravity
is verified by Hammerschlag. Dr. C. F. Martin says, on the other
hand, that if a relative fall in hsemoglobin be taken as a test, chlorosis
occurs in men also. He gives four cases, estimated by Fleischl's method
(duly controlled), in which with corpuscles from 4,800,000 to 5,300,000
the haemoglobin fell to 68, 72, 77, 77 respectively; he does not state
whether these men were members of large families. My own experience
is that the occurrence of chlorosis in men is either unknown or very rare ;
certainly no observations to the contrary can be accepted unless a careful
examination of the blood be recorded.
Bace and climate. — We are told that chlorosis obeys no climate, no
latitude, no altitude. Hirsch tells us that it is found in Asia Minor, in
Algeria, in the West Indies (Creoles), and so forth. I have seen it
abundantly in South European races, such as the Italian, and in women
of all builds and of all breeding ; at the same time, without records of
examination of the blood, statements of this kind have but an approximate
value. It is said that anaemia is commonest in blondes ; and Lloyd
Jones adds that blondes are more fertile. I am not satisfied that
chlorosis is commoner in blondes ; the assertion is open to the criticism
that in the blonde it is more conspicuous ; indeed the district with which
the observer is conversant is no small element in his experience.
Age. — Chlorosis is a malady of puberty ; if it occur in later life, as
no doubt it often does, the attack may assuredly be regarded as a
relapse. All authors agree that a first attack rarely appears after the age
C)l[24. Professor Stockman gives 23 as the highest age of his series.
Now in this respect it is remarkable that Leichtenstern found in the
age period from 18 to 25 that the haemoglobin is ordinarily aTjout 8 per
cent less than in the period from 25 to 45 years of age. Sorensen sub-
CHLOROSIS 48s ■
stantially corroborates this statement. Stockman (54), in a series of 63
cases, found that no fewer than 41 lay between the ages of 15 and 20.
Sorensen attributes this diminution of red corpuscles directly to menstrua-
tion ; . Stockman to the demands of puberty in a more general sense,
digestion and appetite being, moreover, often impaired at a time when
menstruation is being established.
Conditions of Zi/e.=— Almost every defect in the circumstances of life
has been regarded as a direct cause of chlorosis; that such defects con-
tinually intensify the disease is admitted by all observers. To work in a
badly ventilated room will keep up chlorosis, or anaemia at any rate, in
spite of remedies. Some overwrought and underfed women only keep
going by taking iron, from time to time, for the best part of a lifetime.
Still, an accelerating cause is not necessarily a principal cause. Mental
strain, again, is rather a favouring condition than a direct cause.
Dyspepsia, with consequent inanition, takes an important place in the
causation. In about one-half of Professor Stockman's cases disorders
of digestion were present ; so that if the primary cause do not lie
in the stomach it is probable that malassimilation is a favouring con-
dition. Dr. Simon lays great stress on the dyspeptic element in
chlorosis; he tells us how capricious the appetite becomes in young
girl^, nay even depraved ; such stuff as slate pencil and the like being
devoured. There is, indeed, an especial proneness in chlorosis to atonic
and perverted gastric functions, if not to actual dilatation of the stomach.
Many young women, as their frames develop, fall into a panic fear of
obesity, and not only cut down their food, but swallow vinegar and other
9,lleged antidotes to fatness. Nearly all chlorotic girls are disposed to
shirk meat and to feed rather on pastry and sweetmeats ; and of the meat
which is eaten, browned and burnt fragments form no inconsiderable
part. If these ingesta do no direct harm, at any rate they conceal a pro-
cess of inanition ; ani_a fall in nutritious food quickly leads to a fall in
red corpuscles. These losses the full-grown woman may recover from
readily ; the growing and developing girl cannot so easily make up the
larger arrears. Yet, after all, as careful observers like Professor Stock-
man record that only about 50 per cent of chlorotic women are dyspeptic,
we cannot regard dyspepsia as a necessary antecedent ; the primary cause
lies deeper. We have only to look at the peasant girls who come with
chlorosis to our rural hospitals, and again at the young maid-servants
in good families, to see at once that chlorosis is in its essence inde-
pendent of food caprices, city life, hard conditions, and indigestion.
The healthy country girls may show the malady less ; it may fall on
them with less average severity the better their conditions of life ; at any
rate, they may recover more quickly ; still chlorosis does not pass them
by. Niemeyer testifies to the numbers of robust peasant girls from
the surrounding villages who were wont to present themselves before
him with chlorosis. Meinert presses this kind of explanation in a special
form : he attributes chlorosis to tight lacing or to the belts worn by
women; these practices, as he alleges, lead in a considerable percentage
486 SYSTEM OF MEDICINE
of women to splanchnoptosis; he records gastroptosis in most of his
patients who suifered from the malady, and in 15 per cent he reported
movable kidney. Surely, of movable kidney, at any rate, this is an ex-
aggerated proportion, and one opposed to the reckonings of all physicians
who have studied these dislocations (vol. iv. p. 342). As regards the
stomach, I feel impelled to surmise that in many cases Meinert must have
taken toneless and inflated stomachs for dislocated stomachs : no reports
on this subject are worth much unless the line of the smaller curvature
be plotted out.
Estimates of the hydrochloric acid present in the stomach in cases of
chlorosis have been made by many investigators. In some this acid
was found in excess, in some in defect ; in others, again, it proved to
be normal in amount. Similar results would probably be obtained in
any group of sickly young persons.
It is a common experience that many girls otherwise healthy and
living under the best conditions of life become chlorotic : perhapsjjo-giri
escapes it altogether ; some, however, show it but little, and recover
rapidly. The secret does not lie in inanition or_ dyspepsia.
- A more potent cause, perhaps, is emotion ; either emotion of a wearing
and long-continued kind — such as love sickness, home sickness, and the
like, or shockp of a more sudden onset. A remarkable case of this kind
came under my notice a few years ago. A young lady became very
chlorotic, and her cure was not so easy as usual ; however, after a little
patience she was apparently cured, and the treatment was continued until
fear of relapse had abated. On a certain evening, soon afterwards, the other
members of her family having gone ouf till a late hour, she went to bed
alone. At midnight she was awakened by a sense of some presence in
the room, and on opening her eyes she saw a iigure in white moving
across it. She lay speechless with terror until the apparition, after some
pacings, passed out of the room again. As it issued from the room she
became aware that the ghost was the butler- in his night-shirt ; and she
sprang out of bed to bolt the door after him. As she did so he returned
towards the door, and, thrusting against it, tried to re-enter the room.
With strength renewed by fear she thrust against him, and after some
effort she secured the door. The man hung about the landing for some
time, and she sat on her bed in an agony of apprehension until her
parents' return home, about four o'clock in the morning. It turned out
afterwards that the poor man was a sleep-walker, and his promenades
innocent enough. On the next day, however, the chlorosis was profound,
and she was brought to see me again in a worse plight than before. I was
assured by the girl's mother that when they left the patient on the evening
of the alarm she was to all appearance well ; by daylight next morning
she was seen to be as I saw her. Other cases of the same kind are on
record. Still, such a mode of causation is uncommon, and probably
depends upon a strong proclivity to the disease.
Generative organs. — The fashion of attributing chlorosis to sexual
disturbances of which the patient may or may not be conscious is passing
CHLOROSIS 487
away. The final extinction of this hypothesis we owe to Eokitansky
and Virchow, who proxedJiyinecrop^es that no constant morbid condition
of the organs of generation is found in these cases : the parts may be
normal ; or this or that abnormality, such as hypoplasia, may be dis-
covered : but all or any are of an incidental kind, and present no common
factor. At the same time, if epithelial debris be found repeatedly in the
urine, masturbation must not be forgotten, and corroborative evidence of
the habit may be detected.
MesoUastie hypoplasia. — Morgagni, Meckel, Eokitansky, and, still more
definitely, Virchow have drawn attention to a peculiar arrest of develop-
ment of the arterial system found after death in certain cases of chlorosis.
[Vide art. "Diseases of Arteries."] Such necropsies are few, for it is only
by accident t|jat cases of chlorosis come to the post-mortem table. In the
cases before us a very strange state of things is revealed. The aorta may
scarcely admit the littie finger, and the abdominal portion of the vessel may
be no bigger than the ordinary iliac or femoral artery. This remarkable
arrest of development is seen to be but a part of a general arrest through-
out the whole arterial system, and is supposed to indicate a like hypo-
plasia of the mesoblastic layer throughout, including the blood-forming
organs ; hence, it is said, the peculiar anaemia. This explanation is
rather of the dead-house than of the bedside. That a disorder so common
and for the most part so curable should depend upon a malformation so
grave and so incurable as this aortic and general vascular hypoplasia is
on the face of it highly improbable. Again, so far as our evidence goes,
the arrest may occur in either sex indifferently (Hayem). It is said,
indeed, that Virchow was not always careful to exclude the cases of con-
genital or slow heart disease with "which a hypoplasia of this kind may
be bound up (Pye Smith). Be this as it may, Virchow's doctrine has a
great vogue in Germany ; and it Ji^ould ill become us to deal lightly with
a well-considered opinion expressed by a pathologist so eminent.
Hemorrhage. — Loss of blood is a common and direct cause of ansemia,
and has been assumed to be the primary cause of chlorosis. It is said
that in many cases haemorrhage is or has been obvious enough ; whether
in the form of menorrhagia, epistaxis, haemorrhoids, hsematemesis, or
otherwise. And it is urged, if haemorrhage be a vera causa, and in a
considerable number of cases an immediate factor, may not haemorrhage
be the general cause ; haemorrhage which, if it issue by some passage un-
observed, or, in repeated quantities too minute to catch the eye, may
often be overlooked ? Such imperceptible oozings have been supposed
to occur into the stomach, for example.
Now we have seen that the ansemia which results directly from
haemorrhage is not quite identical with that of chlorosis; that it is
revealed rather by a diminution in the number of the red corpuscles
than by their defect in haemoglobin; this proposition, however, is far
from established. Yet there can be no doubt that chlorosis occurs
daily in which, after the closest inquiry, no haemorrhage can be seen or
heard of: and in respect of the alleged persistent oozing of blood from
SYSTEM OF MEDICINE
mucous surfaces the contents of the stomach have been repeatedly tested
without the discovery of any reactions due to blood or sanguineous
effusion. That menstruation or other blood loss, even if moderate,
may aggravate chlorosis is certain, and amenorrhoea, therefore, is often a
protective condition ; but on the other hand chlorosis, as we all know,
may occur in girls before the appearance of menstruation. The effects
of haemorrhage on the specific gravity of the blood plasms have yet to be
determined.
Bunge's hypothesis. — A very ingenious hypothesis in explanation of
chlorosis, and of the behaviour of iron in the cure of it, has been pro-
posed by Bunge. I will set forth the hypothesis in the lucid words of
Professor Stockman : —
" Bunge holds that the ordinary preparations of iron, including the
so-called albuminates and peptonates, cannot be absorbed from the
alimentary canal. He points out that ordinarily the iron of the red
corpuscles is formed from the organically combined iron in the food,
which is something like haemoglobin in constitution, and can be readily
absorbed and readily converted into haemoglobin. From milk and yolk
he isolated such an organic combination. But he admits that inorganic
iron preparations are capable of curing chlorosis, and explains this as
follows. In chlorosis digestion is disturbed with formation of sulphur-
etted hydrogen and alkaline sulphides in the bowel. These combine with
and separate out the organic iron of the food, and sulphide is formed, an
inorganic compound which, according to Bunge, cannot be absorbed;
hence the blood loses its necessary supply of iron, and chlorosis results.
When inorganic iron is given, however, it combines with and neutralises
the sulphuretted hydrogen, and thus protects the organic iron of the food,
which, therefore, becomes absorbed, and goes to form haemoglobin. In
support of this view he adduces the received opinion that large doses of
iron are necessary for the cure of chlorosis, and this he says is because
large amounts are necessary to neutralise all the sulphuretted hydrogen
in the bowel. Further, he states on the authority of Zander that hydro-
chloric acid cures anaemia more satisfactorily than iron does, because it is
antiseptic, and prevents formation of sulphuretted hydrogen in the bowel."
Now, as Stockman adds, "the presence of iron in our food, in the
tissues and excretions of the body, its constant ingestion and excretion,
and the small quantities with which we have to deal, apparently place a
complete barrier in the way of rigidly proving by chemical methods that
it is or is not absorbed."
Stockman met these difficulties by other expedients. First, in
certain well-marked cases he removed the problem from the sphere of
the bowel, and endeavoured to bring about the cure of chlorosis by in-
jecting iron subcutaneously. Secondly, he administered sulphide of iron
by the mouth, a preparation which cannot take up more sulphur, and,
being non-astringent, cannot be credited with any tonic effect on the bowel
such as might promote its absorptive activities. Thirdly, he administered
bismuth, manganese, and other drugs which have a like power of neutralis-
CHLOROSIS 489
ing sulphuretted hydrogen, and which should therefore have a like
curative power in chlorosis. The results of these observations were as
follows : both in his own cases, and in the cases of others who had given
iron subcutaneously for other reasons, iron thus administered sub-
cutaneously cured chlorosis, though the method is one which has its
drawbacks ; Dr. Warfvinge of Stockholm cured a series of cases by sub-
cutaneous injection of iron, and found that thus used one-fifth of the
ordinary doses of the metal sufficed : the cure of chlorosis seems then
to be by absorption. Secondly, sulphide of iron proved a satisfactory
means of cure. Stockman also emphasises, what many of us had
noted, that reduced iron cures chlorosis in doses too small to have
any substantial effect in neutralising sulphuretted hydrogen. I may
add that patients have complained to me that reduced iron seems,
indeed, to have the unpleasant property of disengaging sulphuretted
hydrogen in the bowel, so that the drug is sometimes quietly shirked
by the patient. Thirdly, Stockman found that bismuth, which would
absorb even more sulphuretted hydrogen than iron, is nevertheless
quite inefficacious in the treatment of chlorosis. Kletzinsky speaks,
therefore, in paradox when he says that " from all the hundred-
weights of iron given to ansemics during centuries not a single blood-
corpuscle has been formed." Stockman thinks that iron is absorbed as
other salts are, the ferric salts being reduced to ferrous in the intestine ;
and that the building of it into organic combinations, which are of various
degrees of intimacy, is done in the liver. Dr. Mackay stated at the
Toronto Congress in 1897 that iron is absorbed by the epithelial cells
of the villi, the iron- of haemoglobin being taken up as haematin. He
adds that the metal is passed inwards by the leucocytes. Binz has
stated, I think, that an early effect of iron in chlorosis is a multiplication
of leucocytes. That they are increased in total number rather than
drawn from their hiding-places would be difficult to prove ; at any rate
they may be more busily employed. That "inorganic iron" given
as a remedy does no more than stimulate the atonic intestine to absorb
the iron (Kobert) seems improbable. Bunge's ingenious suggestion seems,
then, to be without foundation.
Toxic causers. — That chlorosis is due to the influence of some toxin
in the system is a speculation which must have presented itself to many
minds ; and not a few pathologists have busied themselves with hypo-
theses of this kind, from the inevitable microbe to the mere absorption of
faecal juices from the constipated bowel, or the presence of uric acid in
the blood (Haig). Bunge's hypothesis, indeed, rests upon some such pos-
tulates in respect of toxic agents, though in his view the toxins in the
bowel act indirectly and within the canal. The toxic hypotheses of chlo-
rosis depend for their proof on the discovery of such injurious agents in the
blood or excretions. The simplest of them is that popularised by the late
Sir Andrew Clark, who earnestly argued that the impoverishment of the
blood in this malady is directly due to constipation of the bowels ; this, he
said, brings about an accumuIaAion of the products of decomposition in the
490 SYSTEM OF MEDICINE
alimentary canal which, passing thence into the blood, poison it either in its
prime or at its sources. Stockman, Simon, and other observers who have
tabulated cases with this problem in view, point out that, in the first place,
only about half of the cases of chlorosis present constipation ; while, on the
other hand, constipated people who do not suffer from chlorosis are com-
mon in both sexes. When Clark published his paper I paid close attention
to this point, and accepted no mere routine reply to my inquiries into the
state of the intestinal functions; and I likewise found reason to believe that,
when the cases are excluded in which constipation is attributable to the
iron administered, (;hloroticjwomeii are not more constipated than other
women. We shall see presently that this hypothesis of toxicity is not
without considerable importance in the field of tlefapeutics ; no one
has even pretended to show that chlorosis is to be cured by purgatives
alone, yet, on the other hand, I detect in almost all writers on chlorosis a
temptation to rely on the toxicity of the blood in one direction or another.
Even Lloyd Jones, believing as he does that chlorosis is but an abnormal
intensity of a normal storage process, fortifies himself with an argument
out of the same quiver ; he has tested the ovarian system for such a
poison, so far without success, and still has his eye on the uterus as an
alternative source. Van Noorden (36) and Arcangeli are likewise
-disposed to assume some perversion, absence, or excess of an ovarian
internal secretion as a factor in chlorosis. Chvostek reported that in
twenty-one cases out of fifty-six he found the spleen enlarged ; thirteen
times it was palpable : thus he also is led to support the alleged kinship
between chlorosis and splenic anaemia. Clement, if I understand him aright,
looks for the toxin or infective agent outside the body ; and, partly on
analogy, considers that chlorosis should be classed with the infectious dis-
eases. He tells the story of an epidemy which occurred in a small village,
during which eight young girls were attacked with febrile symptoms and
enlargement of the spleen ; phlegmasia alba, dry pericarditis, and pleurisy
were among the complications. Anaemic these patients were no doubt, but
few readers will be convinced that the malady under which they suffered
was chlorosis. Against these allegations of enlarged spleen I may say
that Simon and Schrott, both of whom had their attention directed to this
point, found this enlargement in one case each \wde " Spleen in Ansemia,"
vol. iv. p. 522 ; and art. "Splenic Anaemia," p. 539 of this volume].
Pick finds the source of the blood-poison in another place, namely,
in a dilated stomach. His cure for chlorosis is lavage. Nothnagel takes
substantially the same view of the matter as did Clark. Now, no
doubt, certain poisons do reduce the blood ; such poisons as lead, arsenic,
syphilis, those of acute rheumatism, Bright's disease, and pernicious
anaemia, and so forth ; but it is a superficial way of looking at things to
say that anaemia here and anaemia there must be due to like causes.
If we are to listen to comparisons of this sort we must have the specific
gravity of the blood-serum in all cases, and from it we must learn
whether these anaemias are all of the same kind ; that is, whether the
blood plasma keeps up to the standard of health, or even rises above it,
CHLOROSIS 491
while that of the whole blood falls. Jones teUs that such is the feature
of chlorosis ; and Hayem, Stockman, indeed all careful students, tell us
that in experiments and observations on this subject regard must be had
to the kinds of the changes in the blood. Chlorosis, as Immermann well
says, " maintains its individuality in the teeth of all the attempts that have
been made to merge it in the great ocean of anaemia."
Again, in anaemia there is, or often is, no evidence of poison in other
parts or excretions of the body. For example, Simon (50) says that
indican is not found in the urine of the chlorotic ; and Eethers, by a series
of important investigations, seems to have shaken the foundations of the
toxic hypothesis, by showing that in 9 out of 18 cases of ordinary and
severe chlorosis the ethereal sulphates were absent ; and that in the re-
mainder there was no uniform or considerable appearance of them. Von
Noorden, who (p. 347) discusses this point clearly, quotes Hennige and
Heinemann to the same effect ; and Stockman adds the testimony of
Morner. The secret of the causation of chlorosis does not seem to lie,
then, in a foul state of the intestine, or in the absorption of some poison ;
the evidence lies in the direction of diminished manufacture and meta-
bolism rather than of accelerated destruction. The very poorness of the
urine in many cases of definite chlorosis, its actual deficiency in colouring
matter, indicates that, instead of an excessive breaking-down of blood cor-
puscles, such as results from the absorption of poisons of the kind under
consideration, the Hfe of the red cells is, on the other hand, prolonged.
There seems to be a certain, though probably not a very intimate,
association between chlorosis and Graves' disease. Ohvostek gives
seven cases of chlorosis associated with Graves' disease. Lloyd Jones
and others also note some fulness of the thyroid in many cases. I
have observed the same coincidence; but without a calculation of the
frequency of some fulness of the thyroid in healthy women it is not easy
to express an opinion on the point. Professor Stockman supposes that
chlorosis depends mainly upon two causes ; namely, on insufficient food at
the age of development, in which conclusion he is supported by Simon, and
on the persistent effects of incidental haemorrhages, menstrual and other,
which may be positively excessive, or relatively excessive in the individual
case. When, however, we regard the many contingencies to which
the operation of these several causes are open, the partiality of their in-
cidence, and the many cases in which these factors produce disorders other
than chlorosis — such as mere emaciation and debility, with a fall in the
proteid value of the blood — I repeat that, in my opinion, we have to look
for a more uniform cause, one more independent of contingencies ; such,
perhaps, as that proposed, rightly or wrongly, by Dr. Lloyd Jones.
I fear Dr. Haig's uric acid hypothesis has little to support it;
against it we find on all hands that the excretion of nitrogen in chlorosis
is rather diminished than increased. Graber, moreover, found the
alkalinity of the blood up to the normal standard, and even above it; and
Von Noorden tells us that Peiper, Kraus, Eumpf, and Dronin corroborate
this statement.
492 SYSTEM OF MEDICINE
Pathology. — In the discussion of the causation of chlorosis we have
dealt incidentally with matters of pathology or pathogeny ; the remain-
ing part of the subject will not detain us long. On pricking the finger
of a chlorotic patient, bloodless as she may appear, the blood springs
forth freely, more freely than in ansemias of other kinds; the colour
also is different ; the red corpuscles being fewer, the blood transmits light
more readily and the colour is brighter ; it is bright red or even borders
on orange. The specific gravity of the blood is easily tested by Roy's
method, but that of the plasma less readily ; for this a centrifugal machine
is required. The specific gravity of the blood is reduced ; that of the
( plasma is steady, or possibly even raised. Dr. Lloyd Jones tells us that
the mean specific gravity of the blood rises in both sexes alike till puberty ;
' at this period, however, that of the man still rises, while that of the
woman falls. Taking the blood of childhood (two to three years) at 1050,
that of a young man of seventeen may be 1058; of a young woman 1055'6.
These observations have been made, of course, under dietetic and other con-
trols. From the age of seventeen, then, Jones finds that the mean specific
gravity in man still rises ; in woman it remains low till twenty-five, after
which age it rises to 1055 or 1056. Coincidently with these changes in
the blood general metabolism is lessened, for the excretion of carbonic
acid and of urea also falls (Landois and Stirling). In the Charts herewith,
which I am enabled by the kindness of Dr. Lloyd Jones to publish, these
changes are well exhibited. Whether the haemoglobin be increased, un-
affected, or decreased during or by menstruation seems as yet undetermined.
I may repeat that Dr. Jones says, speaking generally, that the specific
gravity of the blood stands at a lower mean in women who have many
brothers and sisters ; that indeed the specific gravity may be taken, approxi-
mately, as a gauge of fertility, the change in the blood in chlorosis being
an extreme fluctuation of a physiological quality of the child-bearing
/ period of life. Every girl, Jthgn, may be regarded as potentially chlo-
) rotic, and_perhags_none passes through youiig womanhood without some
phase of the disorder. The boundary between the physiological and the
pathologicaTstafes, if Lloyd Jones' conclusions are to be accepted, is an
arbitrary one.
The specific gravity of the serum differs little, if at all, from that of
health ; if anything, it tends to rise. That of the blood falls as a whole by
the diminution of the volume of the red corpuscles or of their haemoglobin,
usually of both ; changes which are commonly recognised in chlorosis.
In twenty-six cases tabulated by Jones (p. 22) the fall of the number of
red corpuscles comes out strongly, so strongly as to teach us that this fall,
taken together with a like fall in haemoglobin value, is more characteristic
of chlorosis than we are wont to suppose ; at the same time the proteid
value of the blood keeps steady. The alkalinity of the blood, especially
of the plasma, as here said, is usually increased.
The reader thus perceives that the features recognised in chlorosis are
the converse of those seen in some other forms of anaemia, such, for ex-
ample, as ankylostoma and pernicious anaemia.
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CHARr. 4. — Showing- the variations in the
years of age, and the results of observations
gravity of the blood in healthy women, from 2 to 42
upon 120 young women with chlorosis. (Lloyd Jones.)
496 SYSTEM OF MEDICINE
Ir. Professor Stockman's no less careful inquiries the bearing of diet on
chlorosis is estimated. That the iron needed for the blood is absorbed
from the food seems probable, nay, it is proved. -It is certain that
the chick gets iron from the yolk, and the suckling from the milk.
Stockman has estimated our sources of this metal. He takes the issue of
iron daily as -^-^ of a grain, and he found that the daily food of fifteen
healthy persons contained iron at the rate of -^-^ to ^ of a grain ; thus the
supply is equal to the demand : moreover, detained in the liver, there is
a store of disengaged iron, the precipitate of defunct corpuscles, which
acts as a reserve ; in healthy livers Stockman found from 2 j^ to 4f grains
of it. Now if we compare this estimate with the state of chlorosis we
find a derangement of these relations. Although in women, owing to
menstruation and so forth, the reserve iron in the liver is less than in
men, yet their food is apt to contain a smaller supply of the metal. In
the habitual diets of four chlorotic women Stockman found iron in the
respective quantities of -^ to -^-^ of a grain a day ; so that if iron be
escaping at a rate '^f -^^ of a grain daily, the red corpuscles may well
starve. Coppola and other observers fed animals (cocks and dogs) on
food from which all iron had previously been removed ; the haemoglobin
value of the corpuscles soon fell, but was readily replaced on the
administration of inorganic iron. It was found that on a non-ferruginous
diet the hsemoglobin fell 35 per cent. It is to be remembered that the
iron is held in various degrees of intimacy in the articles of diet ; in some
organic molecules, as, for example, in the protoplasm of cells and nuclei,
the combination may be so intimate that ordinary tests fail to detect it ;
and the metal has to be recovered by incineration (Zaleski, Vay). In
ordinary anaemia of an accidental kind — as, for instance, after an occasional
hsetnorrhage — the food iron commonly proves to be sufiicient for the
restoration of health ; although, if 20 grains of iron be lost, the food
may be long in making it up. I have said that the defect of the
blood in chlorosis usually extends to the number of corpuscles as well as
to the hsemoglobin contents. Both Stockman and Lloyd Jones insist on
this defect; Stockman, in his cases, reports a "striking deficiency of
red corpuscles as well as of hsemoglobin." A deficiency down to two
millions may be observed, but it rarely falls lower. Stockman's highest
figure was" 6G per cent, his lowest 20 per cent. In four days after
beginning ferruginous remedies the corpuscles go up with a bound, and
in 1 0 or 1 4 days reach the normal standard ; the haemoglobin rises much
more slowly, and two months after the beginning of treatment may still
be defective. Deformity of the red corpuscles is not a feature of chlorosis
as it is of pernicious anaemia ; but a considerable proportion of them may be
under-sized, even when full allowance is made for the presence of microcytes,
and their vitality is said to be low ; that is, their histo-chemical properties
fall, and they fade before doing full work. The relations of water and of
salts to the serum of the blood are less easy to discuss : the steady specific
gravity of the proteids in the plasma would indicate that there is no
tendency to hydrsemia. It seems probable that the amount of water
CHLOROSIS 497
Stands in some definite relation to the proteid constituents, as its presence
is not a mere dilution, but a combination with these substances : in like
manner the salts are related to the state of the proteids and to the
cell activities. For the present, however, it does not seem that these are
points of primary importance in chlorosis.
Coagulation is slower in chlorotic blood, outside the body, notwithstanding
the tendency to thrombosis within it; the clots are scanty, and the fibrinogen
is less, facts which are not easy to reconcile with such an accident. A slow
venous blood-stream may account for the tendency to thrombosis.
We can only guess at the mass of the blood in any case ; in many ansemias
we have seen that the mass of the blood seems to be diminished, the
blood issues slowly from a puncture ; in chlorosis the fulness of the vessels
seems to point to a persistence of the normal blood mass, and such is the
assumption of most writers. Dr. Lloyd Jones thinks that the dyspepsia
of chlorosis is due to an accumulation of blood in the great veins of the
abdomen, the dilatation of which he attributes to some influence on the
splanchnic nerves. If there be an increase in the mass of the blood, there
may be an actual " plethora serosa," with or without hyperalbuminosis.
If the aorta be small, there may be a relative plethora. In some cases of
prolonged chlorosis there ma;y possibly be some mesoblastic hypoplasia of a
transient kind; and the capacity of the arterial tree may grow with its nutris^.
tion and its contents. In ordinary cases, however, the plasmatic elements
of the blood seem to be sufficient for vegetative growth ; chlorotic girls dp
not lackjize, nor do they fall away from the main lines of development. — '
On the other hand, the heart and vessels are subject to deterioration of
a somewhat serious kind. The arteries, and especially the aorta, near the
, origin of its ascending portion, may present on the inner coat dull yellow
spots and strise; indeed, superficial erosions of some extent may be detected.
The striae may also be seen in the descending portion on its posterior inner
aspect, between the intercostal and lumbar arteries (Virchow). These
patches and streaks, when examined microscopically, are found to consist of
minute dots, each, according to Virchow, being a fatty connective tissue
corpuscle. The heart is commonly of normal size, but it may be moder-
ately dilated. Valvular disease is rare, as is ordinary atheroma ; but fatty
degeneration of the heart is a feature of chlorosis, as of all anaemias. The
change is primary, and is best seen in the papillary muscles, especially of
the left ventricle, as spots and striae; healthy fibrils being mixed with fatty.
Virchow also describes fatty degeneration in the capillaries.
The renal, hepatic, and gastric cells are fatty also, and all the organs
are pale. The atonic stomach may be dilated. The spleen, marrow, and
lymphatic glands are not understood to be abnormal.
Symptoms. — The chlorotic girl is known in every consulting-room,
j public or private. The~a^a^Osrn^o; respecter of T'ank orof fortune, ^
WEeffier'heraspeciTatTiFst sight be indicative of the disease or not, her
I characteristic complaint is dyspnoea. Dyspnoea, due probably to incessant i~^
I stimulation of the bulb by suboxidised blood, is more persistent and
\! incapacitating in chlorosis than in any other disorder, except, of course, in .
VOL. V 2 k
498 SYSTEM OF MEDICINE
advanced organic disease of the heart. Many of these patients bear in their
features the classical sign of their malady, but not so all of them ; many
of them carry some colour (chlorosis fiorida) ; but in my experience all
suffer from dyspnoea, and, however insidiously it creep on — for the disease
may attack acutely or insidiously — the patient is never unaware of it.
If she be asked whether she can trip upstairs as she was wont to do a
few months previously, her answer will bring the physician near to his
diagnosis. I have said that many chlorotic girls carry some colour, indeed
a high colour. In past years this was a little puzzling to me, as no doubt
to others also ; but we have now learned to look below the surface, and I
see that Stockman, Lloyd Jones, and many others deal with this aber-
rancy, and point out why even a high colour may not be incompatible with
chlorosis. It is said that the conspicuous chlorotic is a blonde ; but surely
we see many blondes who in spite of an assured chlorosis have some
carmine in their cheeks, and many brunettes who are pale enough and
green enough to reveal their disorder. Much depends, I suspect, upon the
skin of the individual ; a fair and clear skin takes the alabaster or old
wax colour, a brown and a muddy or thick skin does not. We have
blondes -with bad complexions and brunettes with transparent complexions.
Transparent skins are often seen in the dark women of the so-called
Iberians among ourselves, and chlorosis is manifest enough in them ; on
the other hand, I know many blondes who have not presented the standard
tint of chlorosis, although suffering from it in no slight measure : in
such persons a thick complexion conceals or modifies the characteristic
tints ; grayness or sallowness takes the place of marble or alabaster, and
chloasmic tints may be seen here and there on the temples and about the
knuckles and other joints. Such women do not flush readily or deeply,
and their limbs, often rough and hairy, do not offer a good surface for
the display of the changes of the blood. The upper part of the chest,
bared for the stethoscope, may, however, manifest the peculiar hue ; a
.pallor may be detected also in the lachrymal caruncle, on the under side
of the conjunctiva and the mucous membrane of the mouth ; the
pclerotics may be blue, the pupils dilated, and the ear — ^that useful signal
of variations in the colour of the blood — may be white. The nails, also,
/and the blue veins on the skin may have their story to tell.^ The pupils
^ For the following ingenious method of- measuring the oxidising activity of the blood in
chlorosis I can say nothing of my own experience : I therefore put it into a note. The
passage is translated and a little abbreviated from Henocque, " L'hematoscope," Gaz. hebd.
Oct. 23, 1886, and April 1, 1887. It is quoted by GUbert (10).
The reduction of oxyhemoglobin into haBmoglobin in the tissues can be determined by
spectroscopic exiimination of the blood through the thumb-nail. Thus the first band
characteristic of oxyhaemoglobin may be seen, sometimes the second also. If a ligature be
tied round the phalanx the bands disappear, the yellow on the level of the line D reappears,
which was concealed, and then the bands vanish. The ligature isolates in the thumb a.
certain quantity of oxygenated blood, which for a certain time exhibits the bands of oxyhiemo-
globin ; the latter gives off its oxygen to the tissues, is reduced, and the absorption band is
no longer intense enough to traverse the nail. In the normal state this process occupies 70
seconds, and the quantity of oxyhsemoglobin thus reduced is 0'20 per second. This is taken
as the unit of reduction. In chlorosis the oxidising activity falls to 0'65-0"19 of this unit ;
' the mean fall being 0"44.
CHLOROSIS 499
are often dilated, brightening the eye, though the face is often described as
inanimate and puify ; perhaps this word " pufiy " is not a very accurate
one. If chlorosis be a disease in which the proteids of the blood are not
wanting, and if the mass of the blood be not diminished, the face may
retain its ordinary contours and yet seem, as it were, puffed by contrast
with other signs suggestive of serious ill health. In this kind of chlorosis
epistaxis may occur, even profusely. It is preceded by a sense of fulness
and discomfort, and is followed by a sense of relief. In the anasmias of
malaria, plumbism, or cancer, the vessels are more empty and the face
more shrunken. Chlorotic girls still blush readily enough, and even in the
height of an attack of their malady some of them never lose a vivid carmine
on the malar eminences. There is another peculiar sign to be seen in the
face : Dr. Lloyd Jones says that if a healthy person be asked suddenly to
look up at the ceiling, without moving the head, the eyebrows are raised
and the forehead is thrown into horizontal folds by a contraction of the
anterior portion of the occipito-frontal muscle. Now, in many chlorotic
women this associated movement of the occipito-frontal muscle is wanting;
as Joffroy pointed out also in Graves' disease : yet they can contract this
muscle if they try to do so. Lloyd Jones attributes this lagging to a
lessened irritability of the skeletal muscles, due to lack of haemoglobin ;
and thus it is that the face appears inanimate or even apathetic, the
languid, listless look of chlorotic patients being partly due to want of
facial expression, partly to slackness of the limbs (Hayem). Sydenham
says that " crurum tensiva lassitudo " is a complaint of these patients.
Yawning betrays a like muscular affection, and to the patient is often a
troublesome symptom.
Digestive, system.— -The tongue is pale, moist, indented, and often clean.
At other times it .presents on its coated surface some evidence of disorder
of the stomach or associated organs. The breath likewise in some
patients is heavy in odour. Such patients are often constipated, though
great constipation is consistent with a clean tongue. That constipation,
however frequently seen, is not by any means a constant symptom I have
already pointed out. It seems to be noted in about one-half of tabulated
cases.
The stomach is often the seat of some morbid changes; it may
be permanently dilated, though more often temporary distension and
atony may simulate such dilatation. I am not prepared to say that
dilatation in the formal sense of the name is so common in chlorosis as to
make a part of our ordinary conception of the malady (vol. iii. p. 494);
nor do I regard it as a very common complication : were it so, the cure
of chlorosis would be a matter of more serious difficulty than it is.
Dyspepsia of the subacute or chronic catarrhal kind, or that of flatulence
and atony, sometimes stops the way, but it rarely defies the usual means
of treatment. The appetite may give us more trouble. I have said
that it is often marked by caprices and perversions which put serious
obstacles in the way of nutrition. At the same time these symptoms
are seen in other states, such as neurasthenia — the dislike of meat
500 SYSTEM OF MEDICINE
especially — and are, perhaps, characteristic rather of the kind of patient
than of the kind of disease. In neurasthenia this anorexia or parorexia
leads to emaciation ; in chlorosis this is not generally the case. In
anorexia nervosa (Gull) the wasting is also remarkable ; but the chlorotic
woman eats more : her blood is also richer in proteids, and being short of"
oxygen permits the deposit of fat. The relations of chlorosis to ulcer of
the stomach are dealt with in the article on the latter subject (vol. iii.
p. 519).
Diarrhoea is a rare and incidental occurrence. Hysterical chlorosis is
more compacted of fantasy, bizarrerie, and caprice than the common and
uncomplicated form of the disease ; or tears and melancholy may alternate
with fretfulness and self-importance. " Hysterical or barking cough " is
a very trying feature of these cases ; indeed, I have found it a not infre-
quent feature of chlorosis not otherwise marked by hysteria or neurosis.
Such coughs may be interpreted by an examination of the blood, and
cured by iron ; for indeed they are rather chlorotic than hysterical in
nature.
Circulatory system. — Sydenham describes "pulsus febrilis" as a symptom
of chlorosis ; and later authors, relying on the thermometer, describe a
"febrile chlorosis." Were not such observers as Prof. Osier in their
ranks I should be content to say that " febrile chlorosis " is an aberrant
form of the malady, and the fever may prove to be significant of some
complication. The use of such a name by less experienced physicians
might, for instance, lead to confusion between chlorosis and pernicious
or syphilitic aneemia, or some other ansemia due to a toxic agent. I should
be content to say that the temperature in chlorosis is not subnormal, as in
anorexia nervosa, for instance ; and that it may be apt to rise in trifling
measure under the influence of occasional causes.^ The pulse, however,
as Sydenham said, is generally quickened more or less, and is very im-
pressionable by change of posture and the like. In opposition to some
authors, I am scarcely disposed to admit that in chlorosis the arterial
blood-pressure generally ranges above the normal standard ; though no
doubt it is characteristic of chlorotic anaemia that such a rise may be
observed occasionally ; and as a rule the mass of the blood is not dimin-
ished, the artery is well filled. Immermann seems to have given vogue
to the opinion that in chlorosis the heart increases and arterial blood-
pressure rises. Bihler, on the other hand, who has gone over this ground
carefully, concludes that so far from the blood-pressure being raised it
is usually under the normal mean. Estimations of blood-pressure made
with the ordinary sphygmographs are of little or no value. As, generally
speaking, the mass of the blood is not diminished, the output of the left
ventricle is at least normal in amount, and the arteries are well filled ;
but this does not necessarily or even probably mean increased blood-
pressure. Extension of cardiac dulness is generally towards the right,
not towards the left side. As vascular tone increases, the heart returns
' Dr. Stockman tells me later that he finds that all bloodless people are liable to slight
febrile attacks. The cause of this instability is discussed by Graber and others.
CHLOROSIS SOI
to its normal limits. Chlorotic women are liable to syncopic attacks
which seem to indicate that the blood - pressure, if fairly sustained
as a mean, is nevertheless subject to great or extreme variations.
The arteries often throb in chlorosis ; although often these vessels are
really full, they are much slackened in tone : we may commonly see
pulsation in the epigastrium and in the episternal notch, and both first
and second sounds are very loud in the carotids. The second sound is
often louder at the apex than at the aortic cartilage.
The heart is irritable ; it often palpitates, it may be to the great
distress of the patient. The palpitation makes itself felt rather on
exertion — on the least exertion ; a perturbation due to the call of the
ansemic tissues, probably the muscles, for more blood, that is for more
oxygen ; their supply of proteids is probably sufficient. The heart itself,
on examination, is found to vary a good deal. Although its beat is often
throbbing or laboured, yet not less often it is feeble and ill-defined. That
the heart is dilated is the assertion of many observers; however, the
facility with which modern physicians delineate and record the varying
dimensions of this organ excites my admiration of a skill I cannot hope
to attain ; the conditions of physical diagnosis seem to me indeed to be too
inconstant for such appraisements. For instance, in this and other ail-
ments of young women I have observed (cf. vol. iii. p. 505), and the obser-
vation is by no means confined to myself (34), that the mean volume of
the lungs is often reduced. The respiration in chlorosis is obviously
shallow ; and, although to tight lacing is attributed every mischief which
may befall a woman, yet it is indeed probable that the fashion of femi-
nine garments prevents the full excursion of the diaphragm; thus in
chlorosis the lungs may shrink, and the heart more or less denuded may
offer a larger front to the auscultator. In cases of alleged cure of dilata-
tion of the heart we may have a contrary phase ; the lungs may expand
under this measure or that, and the heart be enyeloped over a larger part
of its surface than before : in view of such changes as these it seems very
difficult confidently to infer, in the one case or the other, that the organ
is much altered in size and shape. That in ansemia, generally speaking,
dilatation of the heart as of the stomach is prone to occur from loss of
tone I have already said, but that in chlorosis the heart undergoes an
enlargement both in substance and in capacity is not proven. We know,
indeed, from the appearance of apex murmurs and the tendency to fatty
degeneration, that the organ may yield a good deal ; yet a case of chlorosis
must be of extraordinary severity to bring the patient to the post-mortem
table. Over-exertion under such cardiac conditions may cause "irrit-
able heart " or " weak heart " — symptoms, by the way, which the ailing
patient may never get rid of.
Venous murmurs. — The murmurs heard in the heart and veins in
chlorosis have been studied with an interest enhanced by the obscurity
of their causation. The phenomena are very common, they are demon-
strated to every student in the out-patient room, and the problem of their
generation is a fascinating puzzle for every ingenious clinician. And
S02 SYSTEM OF MEDICINE
wioso cannot himself explain can select his explanation from the teacher
whose doctrine he prefers.
The venous hums, which, although they may occur in any anaemia,
are very characteristic of chlorosis, may be considered first. These
murmurs — known as hruit de didble by the French, as Normengerdusch ■
or Venensausen by the Germans — the two former names being taken
from the humming-top — are most often heard in the jugular veins,
usually more loudly on the right side. The sound in the jugular
vein is a persistent hum, likened by Sansom to the shell soxind which
Landor has made his own ; Sir Thomas Watson likens it to the hum of a
gnat or to that of the wind sighing through a crevice (47). When this
hum is loud it can be felt; if the left hand be laid on the neck,
grasping it lightly so as to let the thumb rest upon the right jugular,
a vibration in the walls of the vein is perceptible to the touch ;
and by such pressure on the vein as shall stop the venous current the
hum is made to cease. It is heard best in the standing position, being
favoured by gravitation ; and during inspiration. It is clear, then, that
the hum is generated in the vein. If the patient be directed to take a
deep breath, or to rise from a recumbent to an upright position, the
venous current is accelerated and the hum is intensified. The sound is
usually louder in the right jugular, because this vessel, by way of the
innominate vein, enters the vena cava almost in a right line ; whereas
the left cervical veins collect and fall into this channel at a considerable
angle. Under these and other circumstances the pitch and intensity of
the murmur may vary. For the same reason it is sometimes louder
during the cardiac diastole ; and if, instead of suppressing the sound by
stopping the vein, the stethoscope be very lightly pressed on the vessel
the murmur may be increased. To turn the head to the opposite side
may have a like effect; but the sound is a capricious one, and that dis-
position which on one day or in one person seems to intensify it, on
another day or in another person may extinguish it ; often indeed it
varies extremely while under continuous observation. It is not difficult
to suggest an explanation of the hum ; that which is generally given, and
which on the face of it seems most probable, is that the vibration of the
walls of the vein is due to a change in the calibre of the tube at the
root of the neck. The lower portion of the vein is of constant or almost
constant calibre ; this constancy being secured by the adhesion of the
coats to the cervical fascia. Now if by any means, such as a smaller
stream of blood, the vessel be narrowed above, there is a run of the
blood from a narrower to a wider channel, this change in the continents
sets up fluid veins in the contained blood, and the walls of the vessel are
thrown into vibration thereby. Still, although this explanation is
rational in itself, yet we may ask why it occurs in some ansemias and
not in others ? Again, why is it — as I think it is — ^incomparably more
frequent in chlorosis than in other anaemias ? In my experience it is
not usual to get the venous hum in plumbism, in malaria, in cancer and
so forth ; it may be there, but it is not to be foretold, while in chlorosis
CHLOROSIS 503
to foretell it is a fairly safe prophecy. Yet if it be true that in chlorosis
the vessels are not empty as they are in some other anaemias, surely it
is in chlorosis that the hums should be less commonly heard. Perhaps
the tone of the vessels enters into the causation. Moreover, there is
an old hypothesis that the hum is due to the " thinness of the blood,"
the corpuscular contents of which as we know are notably reduced :
this hypothesis has never received much countenance from competent
judges ; but Potain has brought it forward again on the basis of experi-
ment. Potain so arranged a tube in connection with a reservoir that at
one time serum should run down the tube, at another defibrinated blood
■containing the normal number of red corpuscles; on the use of the
stethoscope the murmur was heard to fall in intensity when corpuscular
blood replaced the serum. Whether this observation has been verified
"by other observers I do not know ; if so, it has an important bearing on
the generation of the hmit de diable. The hum, as I have hinted, is to
be heard less certainly and loudly in other veins, in other kinds of
anaemia, and even in some healthy persons. Many years ago in a
foreign hospital I was told to hearken for a murmur on placing the
stethoscope on the eyeball of a chlorotic patient; by this manoeuvre,
which I have often repeated since, the hum, fainter than in the jugular,
can be heard ; but before we can say that it is generated in the cerebral
sinuses we must be sure that it is not transmitted from the jugular
through the bones of the face. Dr. Stockman tells me it may be heard
sometimes over the torcular Herophili.
Cardio-arterial murmurs. — That a systolic murmur- is not infrequently
heard over the subclavian artery, especially on the left side and towards
the outer third of the clavicle, is an old observation which has interested
both elder physicians who have found food for speculation as to the modes
■of its causation and younger practitioners who have been alarmed by what
they regarded as a sign of aneurysm. This murmur was carefully studied
by the late Sir Benjamin Eichardson, but I am not able at this moment
to put my hand on the reference. Eichardson named the murmur the
" carpenter's murmur," as it is not uncommon in these and other labourers.
To pursue this side of the subject would lead us into digression ; but in
chlorosis and other anaemias such systolic murmurs are to be heard in more
than one artery. It is a matter of doubt, indeed, whether the Fystolic
murmurs of obscure causation heard about the base of the heart in
chlorosis are formed in the heart proper, or in greater or lesser part in
the large vessels about the same region. Dr. Sansom offers the explana-
tion that under nervous (vaso-motor) disturbance the arteries may be
unequally affected in their calibre, some lengths being contracted, others
dilated or of normal size ; so that the blood passes from narrower to
wider channels. If this be so, we are in possession of a vera causa,
whether it be the actual cause or not. Eichardson attributed the murmur
in the subclavian, increased by manual labour, to the constricting pressure
of voluminous muscles on the vessel ; but as it may be heard in anaemic
persons whose muscles are far from voluminous, we may find in Sansom's
504 SYSTEM OF MEDICINE
hypothesis an essentially similar explanation. For in anaemia, not in chlo-
rosis only, the murmur is to be heard in vessels, such as the carotids, not
mechanically constricted from without as in muscular men the subclavian
may be. The sound may be generated also in Graves' disease. Sansom
quotes from Roger a case in ■which this murmur was musical, audible at a
distance from the body, and in every accessible artery of the body. No
pressure of the stethoscope was needed to bring it out, and the persistent
noise was a torment to the patient. It seems probable, then, that these
sounds, like the venous hums, are due to vibrations of the walls of
locally constricted vessels; and as they are but clinical curiosities we
may not spend any more time upon them.
Certain murmurs heard in the region of the heart are of more
importance. The humming-top sounds are little more than curiosities, as
they cannot be relied upon even for diagnosis ; but the heart murmurs, if
such they be, may have a more serious signification. Physicians do not
hesitate to say that some at least of the murmurs heard about the heart
in chlorosis are mitral in origin, and significant of the deterioration of
the cardiac muscles which we have already considered (p. 501). It seems
clear, however, that more than one kind of murmur is to be heard in or
about the chlorotic heart ; and, if possible, these are to be distinguished,
for some of them may be of a graver character than others. I am enabled
by the kindness of Dr. Sansom to reproduce the useful diagrams published
in his valuable work on the Diagnosis of Diseases of the Heart, wherein
these problems are carefully discussed. The diversity of explanations of
the cardiac murmurs of chlorosis, suggested by eminent observers, makes
it difficult to treat usefully of the matter except from the mere pheno-
menal point of view ; the moment we pass from phenomena to explanation
we find ourselves not only in the midst of conflicting hypotheses, but also
without any clue to a decision.
A precise appreciation of the phenomena is, then, our first duty. The
murmurs to be heard in or about the heart are as follows : — (i.) First in
frequency are the murmurs to be heard in the region of the pulmonary
artery and conus (Sansom's diagram. Fig. 27). In my student days all
murmurs of chlorosis heard about the upper chest were indiscriminately
referred to the aorta ; to Walsh, I think, we owed the closer description
of these sounds with which we afterwards became familiar. All recent
observers are agreed that the murmur now under consideration occupies
the area delineated by Sansom ; and Sansom says that it is " greatly
influenced" by the posture of the body, being louder as the patient
returns to the recumbent attitude. This reinforcement is largely due, no
doubt, to the retardation of the pulse-rate. In this quality it is to be dis-
tinguished from the organic systolic murmurs most of which are less influ-
enced by this change. Dr. Sansom quotes Handford (14) to the efiect that
this murmur again increases as the patient turns over to the right, and
wanes as she turns prone on the face. It varies with respiration, but in no
constant way. It is to be remarked that in these cases pulsation is often
to be felt about the parts occupied by basic murmurs, namely, in the
CHLOROSIS
505
second and third intercostal spaces, or even lower, and in the episternal
notch. This we have all often observed and demonstrated at the bedside.
Fig, 27.^Area of pulmonary artery and
conns, 59 per cent of cases. (After
Sansom.)
Fig. 28. — ^Area of right ventricle and
conus, 11 per cent of cases. (After
Sansom.)
Fig. 29.— Area of aorta, 11 per cent of
cases. (After Sansom.)
Fig. 30.— Systolic murmurs in pulmonary
artery and at apex coexisting, 9 per
cent of cases. (After Sansom.)
Fig. 31. — Systolic apex murmur only,
7 per cent of cases. (After Sansom.)
Now in respect of this pulsation we shall remember that in Graves'
disease, where these pulsations are very evident, we also hear these
5o6 SYSTEM OF MEDICINE
basic or " pulmonary " murmurs, although the blood may present no change
in the red corpuscles, either in number or colour. Sansom gives a very
definite account of these murmurs ; he says that in twenty-nine of his
own cases murmurs over some part of the cardiac region were heard in
sixteen ; and in eleven they were in the pulmonary area. There is a
large amount of evidence that similar murmurs may be produced by
displacements of an otherwise normal heart : one such case I remember
well in which, after death, the absence of aU cardiac mischief was verified.
Arguments of weight seem to prove that these murmurs about the pul-
monary area are not due to mitral regurgitation (Balfour), nor to pres-
sure of a dilated auricle on the pulmonary artery (Russell, Handford).
Dr. Sansom conjectures that the murmur is due to want of apposition of
the mitral flaps on account of an enfeeblement of the muscular apparatus
of the left ventricle. This is a modification of Balfour's surmise, and open
to similar difiiculties. I lean to the belief that the solution will be found
in some altered relation between the blood and the walls of the vessels,
especially the pulmonary artery and conus arteriosus ; so that an excessive
vibration of the walls takes place ; if this be so, the cardiac murmurs, or
some of them, will fall into Hne with the arterial vibrations of the same
■disease (p. 503) and with the venous hums. The pulsation of the vessels
felt under other like conditions seems to lead us in the same direction. In
Graves' disease this vibratile state of the great vessels is apparent enough.
(ii.) The murmur the site of which is indicated in Sansom's Fig.
28 need not detain us long. No doubt it is substantially the same
murmur as the last mentioned, diverted a little in its area by incidental
circumstances which may be guessed at rather than known. Sansom
found it in eleven per cent of his cases.
(iii.) The next murmiu's to be dealt with are those heard about the
aortic region ; that is, at the -base (manubrium sterni) and at the second
intercostal cartilage (Fig. 29). These murmurs are soft in quality and
•diffuse, not leading in any certain direction. Seeing that we were for-
merly taught that a murmur at the base is a common feature of
chlorosis, it is curious to hear from Dr. Sansom that in his series this
was the rarest of the chlorotic murmurs. From my own impressions I
am prepared to coincide in his opinion. I have also noted that a mur-
mur may be heard in this area as distinguished from that of the pul-
monary region ; the two, however, may coexist, and indeed may be mapped
out separately. Within a few hours of writing these lines I have seen a
case of chlorosis, mild in degree, in which, with the venous hum and some
arterial vibration, a systolic murmur was heard at the second right carti-
lage and in the episternal notch. There was no trace of murmur in the
pulmonary area. The history of the case, as a rule, will prevent any
confusion between this murmur and a murmur of organic disease, whether
due to rheumatism or to degenerative changes ; and a persistently ana-
crotic pulse is decisively in favour of organic disease.
(iv.) Finally, there is the apex murmur in the region indicated in Figs.
30 and 31. This murmur was found by Sansom in sixteen per cent of his
CHLOROSIS 507
cases, and is a more serious matter, for it indicates mitral regurgitation ;
though in the cases we are considering the disorder is usually of a curable
kind. There is no experience of the kind to which we may look back with
more satisfaction than to systolic apex murmurs, which in their characters
corresponded in all respects with those of permanent organic disease, but
which disappeared entirely nevertheless. Loud or harsh murmurs in this
place are not so common, if I may speak for my own experience, as the softer
murmurs ; still, soft or harsh, they arise under like conditions of atony, and
to our repeated surprise — for repetition does not do away with the wonder
of it — clear away altogether on appropriate treatment. These murmurs,
indicative of mitral regurgitation as they probably are, I have frequently
heard in middle-aged men who have indulged too freely in the pleasures
of the table ; men who show perhaps a little sugar in the urine for a
time, or other such sign of slackened health. The like murmur arises
.in Graves' disease, in pernicious anaemia, after haemorrhage in childbed, and
so forth. A certain lecture, published by Dr. Donald MacAlister in 1882,
seems to me to throw light upon this subject. " If an animal be bled
till it is feeble," he says, " a murmur indicative of regurgitation from the
ventricle is heard with the heart sounds. You may inject proper salt
solution to make up the normal quantity of circulating fluid, but still the
regurgitation occurs. As the animal makes blood again, so that its
muscles are properly nourished, the murmur disappears." On the clinical
side such instances are to be cuUed on all sides from medical records ;
some of those recorded by Dr. Sansom, as progressing to dropsical and
other systemic changes and yet to recovery, being among the most re-
markable. Dr. MacAlister gave in his lecture what seems to be the
explanation of this phenomenon ; and about the same time he showed to me
a small cast of the interior of a heart in systole which carried conviction
on the face of it. Eelying in part on his own observations, in part on those
of Ludwig and others. Dr. MacAlister demonstrated the large part taken
by the auriculo- ventricular muscular structures in closing this orifice during
the systole. On inspecting the model, one began to wonder whether valves
were not luxuries rather than necessaries ; for the sphincter fibres, contract-
ing during the systole of the ventricle, seemed to reduce the orifice almost
to an imperceptible chink. This of course is not quite the case, for Hesse
has shown that the amount of reduction thus attained is only about one-
half of the expansion area. We have, then, to call in the known factor
of muscular atony in anaemia to explain that mitral regurgitation is very
likely to take place ; the relaxed muscle fails to do its share of the work,
and the valves cannot quite make up for the defect. Moreover, we know
that the papillary muscles are among the first to sufi"er in impoverishment
of the blood, and that in those cases of anaemia which, by their severity,
bring the patient to the post-mortem table, these parts, vital as they are,
are found in states of more or less fatty degeneration. It is reasonable
to assume, therefore, that these muscles are slackened. The diflSculty is
to understand why dilated hearts occurring in elderly folks and under
other cognate conditions are so often unattended by a systolic miu'mur.
5o8 SYSTEM OF MEDICINE
In the section on Mitral Stenosis in the following volume Dr. Sansom
will discuss the coexistence of chlorosis and the former disease. In this
connection I have only to suggest that as both of these diseases are found
especially in women a large proportion of coincidence must be allowed for.
Potain endeavours with much ingenuity to prove that the murmurs
of anaemia, or the chief of them, are of pulmonary origin. It is impossible
to do justice to Potain's views in this place, and the advanced student is
referred to his memoir (39). Sewall states that all "non-organic" murmurs
at the base of the heart can be stopped by pressure with the stethoscope.
QEdema of the ankles and feet is often very considerable in chlorosis,
and occurs earlier than in other anaemias ; as, for instance, of phthisis or
cancer, when it is a sign of dissolution. In chlorosis it seems to bear little
relation to the apex murmur, which may be present or absent. This sub-
ject is more fully and broadly discussed in a later article, on Dropsy.
Although, as I have said, recovery may be anticipated with some con-
fidence from these conditions, attended by murmurs, and even by further
evidence of cardiac failure which up to a certain point we may regard
as transient, it is an interesting point to decide when the murmurs and
other symptoms indicate more than a dynamic change — when the heart
disorder has entered upon an altered static phase. The hope of com-
plete recovery need not be bounded by the appearance of dropsy ;
in many cases I repeat that aU such symptoms have passed away
entirely. I remember having a serious difference of opinion with a
medical man whom, unfortunately, I had no opportunity of meeting
personally, in respect of a case of chlorosis in a young lady in whom a
mitral murmur was audible at the apex, and in the axUlary and sub-
scapular regions. Her own medical man had assured the parents that
the chlorosis was but a subordinate matter, and a permanent heart
disease the principal evil. For this malady she was put under conditions
which were not in all respects good for the anaemia, including the mental
distress thus entailed on the patient and her friends. I did my best to
root out this disheartening prepossession, but with little immediate
success. However, I accidentally heard, a year later, that the subject of
incurable heart disease was playing lawn tennis vigorously at all the
parties in her neighbourhood. Yet I would not lead the unwary reader
to mistake, let us say, the anaemia of insidious acute rheumatism, with
heart lesion, for chlorosis with but a temporary relaxation and dilatation
of the structures about the orifice.
Hypoplasia of the blood-vessels has been discussed already, and for a
fuller account of these phenomena the reader is referred to the articles
hereafter on " Congenital Malformation of the Heart " and " Diseases
of the Arteries."
Thrombosis. — A remarkable and painful feature of some cases of
chlorosis, happily rare, is the tendency of the blood to form thromboses
in the cerebral sinuses, and indeed in other vessels of less im-
mediate importance. Thrombosis may occur in such a vein as the
femoral, or it may occur in the longitudinal or other cerebral
CHLOROSIS 509
sinus. Professor Ogler quotes a case in which chlorotic thrombosis oc-
curred in the axillary artery, with the consequent loss of the thumb and
part of the fingers. The symptoms of thrombosis of the cerebral sinuses
are dulness, stupor, vomiting, dilated pupils, delirium, and occasionally
double choked disks. In a case under the late Dr. Bristowe tenderness and
swelling of the right internal jugular vein appeared. This was followed
by thrombosis in the right leg, yet the patient ultimately recovered. I
have a vivid recollection of a similar case in the Leeds Infirmary in a
servant girl of some twenty years of age. In other cases, of which I
also remember one, hemiplegia may occur, and cases of this accident in
chlorosis have been published by many observers. In thrombosis of the
sinuses there is no palsy. Dr. Coupland says that this thrombosis does
not occur in pernicious anaemia [art. " Pernicious Ansemia," p. 5 1 9]. Eefer-
ence to cases of thrombosis will be found in the list at the end of this
article, and in Professor Welch's article on " Thrombosis." Twice I have
been much pained to hear of the sudden death from this accident of
patients concerning whose ready recovery of health I had expressed
myself confidently but a few days before.
Phlebitis, especially in the legs, is no very rare event in chlorotic
women, and it is' said to be more often bilateral in them (39, 43, 6,
41). It occurs in grave cases of chlorosis, and has been attributed
to fatigue and chill. Its progress is usually rapid, and, accidents apart,
the prognosis is very favourable.
Genito -urinary system. — In some cases of chlorosis the pelvic organs,
like the arterial, are found ill-developed — the uterine hypoplasia of Vir-
chow. It is difiicult to believe that these cases are ever cured by medical
means, or by any means. They find their way into the museums of
pathology. Amenorrhoea is of course a feature of them.
Amenorrhoea is also usual in ordinary chlorosis, though it is far from
invariable. Amenorrhoea is not only the ordinary condition, but also the
most advantageous ; indeed, it may be called the protective side of the pro-
cess. If I may speak from a few examinations, I would say that in the cases
of chlorosis in which the red corpuscles are numerically much diminished
(say to 3,000,000 or under) menorrhagia or even menstruation in normal
quantity (which is a relative menorrhagia in such persons) is or recently
has been present. I find that Sir E. Gowers has observed falls of 10 to
20 per cent in the number of the red corpuscles after a menstrual period.
These cases are less easy to cure. I need not say that many chlorotic
girls are brought to us in order that the menses may be recalled ; and we
have to explain to the friends that if, by local and specific means, such an
achievement were possible, the step would be rather a misfortune than a
blessing. As an old medical friend of mine used to say to troublesome
mothers, "Madam, when the works are put in order the clock will
strike." In chlorosis a very slight loss of blood will intensify the im-
poverishment of the blood beyond all expectation.
Chlorosis may appear before menstruation has ever shown itself.
Stockman in 63 cases found menstruation scanty or irregular in 29
510 SYSTEM OF MEDICINE
absent in 12, normal in 4, profuse in 10. Three girls (aged 13, 15, and
19) had never menstruated, and in five no note had been made (normal ?).
LeucorrhcBa is not infrequently complained of, and is cured by the iron.
Of the urine I have already spoken ; it is as a rule poor rather than
loaded by products of waste, whether normal or abnormal. In par-
ticular there is an absence of those elements, such as indican and the
conjugate sulphates, which would signify excessive fermentation in the
intestines and absorption of toxins into the circulation. In pernicious
anaemia the urine, like the skin, is usually darkened by the presence of
urobilin in excess.
Nervo- muscular system. — Girls and young men alike, as they are adoles-
cent, often go through phases of temper which are a source of anxiety to
their friends ; more new impressions, more new desires crowd in upon
them than they can set in due order and subordination. It will not do,
then, to put down the caprices, passions, perversities, and apathies of this
season of life to any one of its disorders. They may occur even in the
healthiest of both sexes; and with a little patience and protection from folly
\ will " defsBcate to a pure transparency." Yet chlorosis has, no doubt, some
' fretfulness of its own ; lassitude and irritability meet together, and are due
to want of activity in the nervous centres. There is no staying power; and
although there may be proteids enough for repair, a small quantity easily
provided of an element in which chlorotic blood is not deficient, yet the
oxidation of carbohydrates and hydrocarbons for the supply of energy is
behindhand. Fatigue products, also unoxidised, accumulate in the muscles.
Dr. Sansom is disposed to attribute the fatty and other degenerations of
the heart to a direct influence from the nervous system ; at any rate we
see irritability and loss of control (inhibition) in those higher centres
which are the last to develop and the first to feel the lack of good blood.
With these perturbations neuralgias are common, especially the neuralgias
of the face, and headaches — frontal, temporal, or vertical. G-astralgia and
"min under the left breast are common troubles of the chlorotic; the
latter often coexists with leucorrhoea and disorderly heart, and with
hysteria. Dr. Head has shown that all referred pains, with their accom-
panying tenderness, are apt to spread widely under the influence of
anaemia. Thus widespread " neuralgic " pain and superficial tenderness
may, in anaemia, be due to some simple cause. In the same way the
headaches so common in anaemia are, in the majority of cases, a true
referred pain, accompanied by tenderness, and correlated with pain and
tenderness of a like nature on the chest or abdomen, according to the
laws he has laid down. In a certain number of cases the headache and
neuralgia represent a widespread pain referred from some organ of the
head, such as the eye or the teeth. In extremely few cases, apart from
pernicious anaemia and its allies, is the headache directly originated by
the anaemia, though its wide distribution and prominence as a symptom
are due to this cause. Certain kinds of palsy have been indicated under
the circulatory system.
Optic neuritis is discovered occasionally in chlorosis ; but the nature
CHLOROSIS 511
of its association with this malady is wholly unknown. Sometimes
it appears rapidly as a papillitis, as in many cases of tumour. The
prognosis is probably favourable : I have never come across an instance
of permanent injury to vision in this kind. The sign may, however,
embarrass the diagnosis, especially if headache be present. Choked disk
may be seen in cases of thrombosis.
Diagnosis. — The chief difficulty in the diagnosis is to distinguish
chlorosis from other anaemias, simple or toxic. Gilbert lays much stress
upon the doctrine that upon chlorosis this anaemia or that may be super-
posed, or that two kinds of anaemia may be associated from the first
in one person. Dr. Lloyd Jones also points out the same difficulty.
If this be so, and there is strong reason to suppose that thus it is, the
diagnosis in a given case of chlorosis may be no easy matter. We have
seen that chlorosis is more than a simple anaemia following with uniformity
on the withdrawal of blood, and menstruation, unfavourable conditions
of life or work, or lactation may " superpose " a simple anaemia on the
chlorotic (chloro-ansfemia). I have suggested that such may be the
compound causation of those cases of chlorosis in which the number
of red corpuscles is very deficient (3,000,000 and under). A further
difiiculty, and a far more important one, lies in the possible confusion
between chlorosis and such toxic anaemias as plumbism, rheumatism,
chronic Bright's disease, syphilis, arsenic poisoning, and so forth. Of
all these puzzles we see striking examples. One young lady, Viath a
green pale face and menorrhagia, presented on closer examination a blue
line on the gums. In the drinking-water lead was found in considerable
quantities. In another such case, one which resisted all treatment, after
a protracted search for some external cause, we discovered arsenic in large
quantity in the green unsized wall-wash of her own sitting-room (not
a paper). On the removal of this wash the symptoms gradually
subsided. Syphilis does not give us so much trouble in women as in
men, but is not to be forgotten. The quick efi'ects of its specific
remedies may betray syphilitic anaemia and place the diagnosis beyond
doubt. Rheumatism is often insidious in young people, it is a potent
cause of anaemia, and its murmurs more than " dynamic." To the
anemia of malignant disease I need not refer ; I do not remember any
difficulty in such cases. But in chronic Bright's disease in young persons
I have not infrequently felt a brief indecision. The touch of the pulse
will in all probability put the observer on the right line, and an examina-
tion of the retina and of the urine should settle the diagnosis. It is
stated by some authors, as I have said, that a pulse of high pressure is
apt to arise in chlorosis ; this may perhaps occur in constipated patients.
However, an examination of the urine will rarely fail to indicate the
correct diagnosis.
The anaemia which precedes the appearance of pulmonary phthisis
may create embarrassment in some cases ; the absence of murmurs
may guide us more or less, and the thermometer may come to our
assistance. Dyspepsia may accompany any anaemia; there is nothing
512 S YSTEM OF MEDICINE
characteristic in the dyspepsia of chlorosis ; and if an organic murmur
be also present we may find it impossible to arrive at a certain
diagnosis without delay. Fagge published a case from the records of
Guy's Hospital, in a girl of 18, in whose case the diagnosis of chlorosis
was upset on the post-mortem table ; a large caseous mass of tubercle
was dislodged from the cerebellum, and a few scattered tubercles were
found also in the lungs. The blood was not systematically examined in
those days (1861). The specific bacilli cannot be found in such cases.
For the diagnosis between chlorosis and splenic anaemia, a disease of
the " chlorotic type," the reader is referred to the following article on this
latter subject.
Anchylostoma, we are told, produces a state not always to be dis-
tinguished from chlorosis, not even by examination of the blood. The
blood in anchylostoma, however, is generally said to present the
characters rather of pernicious ansemia than of chlorosis. Pernicious
anaemia is more readily to be distinguished from the latter by the blood,
with the aid, perhaps, of the thermometer, and of an examination of
the urine {vide art. "Pernicious Ansemia," p. 519).
Addison's disease might give us pause for a while. I remember one
such doubtful case in a young woman ; but even in the absence of
pigmentations a careful survey of the symptoms and history of the case
should preserve us from error.
Prognosis.- — Chlorosis has never seemed to me to be the obstinate
disease that it is for some writers. I may have been fortunate in not
meeting with bad cases of it ; still, although my experience' of chlorosis has
chanced to be exceptionally large, I recall few cases which seriously resisted
treatment. The danger is lest the disorder relapse time after time. How
this is to be prevented we shall consider in the subsection on treatment.
Prof. Stockman tells us that of his 63 cases 27 were in the first attack,
11 in the second, and 22 had suffered from more than two attacks.
Many of these, he adds, did not persist in the remedies ordered for them,
and became chronically anaemic. Some persons relapse in spite of all
care ; their blood is perpetually unstable, and iron is a necessary aid even
in middle and later life. Dr. Stockman estimates the time of apparent
recovery at four to six weeks. This period will be considered more
fully under the head of treatment.
I find myself at some disagreement with those who say that phthisis
is to be feared as a sequel of chlorosis. It is impossible to be assured
that a patient weakened by chlorosis, or by any other malady, will not
fall into phthisis; yet in my experience this sequel, far from being a
common result, is indeed somewhat rare. It may be that the
" prephthisical ansemia" has been occasionally mistaken for chlorosis.
Gastric ulcer is more to be feared, though the causes of its association
with chlorosis lie in obscurity. Of apoplexy and thrombosis of the
sinuses I have already spoken. Happily they are events too rare to enter
into ordinary forecasts. I repeat that the thing to be feared is relapse
after relapse of the chlorosis itself. No careful prognosis can be given
CHLOROSIS 513
without repeated examinations of the blood. It is more than possible
that many cases of chlorosis recorded as aberrant or peculiar were not
cases of chlorosis at all.
Treatment. — I may almost paraphrase the words of Professor Osier
in respect of quinine and malarious fever : " The physician who cannot
treat chlorosis successfullj'- with ii'on should abandon the practice of medi-
cine" (vol. ii. p. 742). Physicians who restlessly turn from one prepara-
tion of iron to another, and from one drug to another, in order to find a
cure for unmanageable chlorosis, must meet with peculiar cases. It is
only by a strong effort of memory that I can recollect any cases of
/chlorosis in persons of common sense and reasonable obedience in which
' iron failed to effect a cure. On the other hand, I have had many cases
submitted to me as intractable in which, if time and opportunity were
favourable, there was no difficulty in compassing a cure. How are we
to explain the failures ? The reasons may be two : first, that iron
failed of success because given in insufficient quantity ; and, secondly,
that the treatment was not continued long enough to counteract the
strong bent to relapse which is seen perhaps in all cases more or less,
and in some most doggedly. This latter reason covers, I suspect, most
cases of failure. It is well never to begin ' to treat a case of chlorosis
without telling the patient that the first course of medicine will extend
to no less than three months ; and that for a year thereafter she must
be re-examined, and in all probability submitted to further courses of
ferrugiiiousjtonici, as the signs may indicate. In all cases of severity the
blood should be examined regularly, and this process has the incidental
advantage of keeping the importance of the matter before the patient's
eyes. During the first two or three weeks of ferruginous treatment the
red corpuscles will rise quickly to the normal standard in number; though
not in size, colour, or vitality.
It has been said of late that the first change to be seen is an increase
of white corpuscles, and that these bodies act in some way as carriers of
iron to the red. The manifold conditions on which the increased
apparition if not the increased generation of white corpuscles depends are
so little understood that we cannot be sure when an afflux of them is
other than incidental.
The numerical increase of red corpuscles gives rise to a sense of
relief often so rapid and so great that the unwarned patient jumps to
the conclusion that she is " all right again " ; and may throw medicine to
the dogs. If so, the case may well be an " incurable " one. The increase of
hasmoglobin, and the attainment of full growth by the corpuscles — which
are the essential elements in recovery as are the reverse processes in falling
ill — take place much more slowly. It is no uncommon thing to find
that a return of hsemoglobin to the normal standard takes as long as
three months ; and for this reason three months should be enjoined as
the shortest time in which a cure is to be completed. Even then relapse
is more common than not. When I began practice, iron was given in doses
too small to effect a satisfactory amendment, and gradually it became
VOL. V 2 L
SH SYSTEM OF MEDICINE
apparent that larger doses are required. Now there is a reaction, and
physicians are saying that smaller doses suffice. My own opinion is that
in cases of any severity, if recovery is to be ensured, iron must be given
with a liberal hand ; the quantity of the metal is more important
than the particular preparation. Without returning to what has been
said concerning the mode of operation of iron in chlorosis, I may
remind the reader that, although in anaemia of simpler kind, as for
instance after a haemorrhage, " food iron " is adequate to bring about a
repair, the iron given in medicinal doses in chlorosis must certainly have
some further effect than the mere replacement of that required to rebuild
the haemoglobin ; it must have some stimulant, tonic, or " specific " action
which conspires to the same end. A few grains of the ammonio-citrate
of iron is not a dose to cure chlorosis of any severity ; far more than
this may be needed. It is my custom to use the sulphate of iron alone,
or with aloes, in the form of pill. The addition of an alkaU to the
iron is quite useless, and by making the pUls more bulky is in-
convenient. I generally administer one grain of the sulphate thrice
daily after meals for the first week, two grains in the second week, three
grains in the third ; it is rarely necessary to go beyond this, though some
patients do not respond till five-grain doses are reached ; this, however, is
exceptional. When the dose of three grains is reached, I direct that this
quantity — nine grains daily — shall be continued for two months ; the
dose is then reduced by a grain, and thus administered for a fortnight ;
then one-grain doses are ordered for a month. During this time the
pulse is probably settling to the normal rate, and if for a month before the
end of this course the haemoglobin has been constant at the normal
standard a relapse is not very likely to occur; though of course the
disorder may reappear after a time from the original causes. Recently
I came across some little lozenges containing iron, called " jelloids."
These I have found very successful, partly no doubt because being
convenient and palatable, and arousing no fears of injury to the teeth,
they are taken regularly, partly because they retain their free solubility.
Occasionally the sulphate of iron causes some gastric irritation, the
" jelloids " seem not to do so. I have often suspected that incurable
chlorosis may mean insoluble pills ; pills made up, for instance, with
gum tragacanth and the like become as hard as pebbles and about
as useful to the patient. For the flushed chlorotic patients (p. 4&8) the
laxative iron mixtures are indicated, such as the combinations of tincture
of the perchloride with sulphate of magnesia; or of equal parts of Griffith's
mixture and compound decoction of aloes, a most efficacious medicine and
not so nasty as it looks.
It was an imposing lesson of our youth that iron is not to be given
till the patient is " prepared " for it ; and to this end bottlefuls of soda
and gentian, and so forth, would be prescribed ; far be it from me to
encourage a careless mode of administering any drug, yet nevertheless I
think this so-called preparation was otiose and even mischievous in so far
as it wasted time. I rarely find such preparatory courses necessary. If
CHLOROSIS 515
the tongue be white and sticky and the bowels constipated let a blue pill
and a dose of salts be given ; this done, begin with the iron, and watch the
remainder of the tongue-cleaning process going on fast enough under the
iron. The dyspepsia being in most instances the consequence of the depri-
vation of oxygen, the assimilative changes will improve, without any direct
attention, as the haemoglobin is restored. In exceptional cases, no doubt,
some precautionary measures may be desirable; of these the physician
will judge.
I have tried all or most of the so-called preparations of "organic"^
iron " produced for us by our excellent allies the manufacturing druggists ;
helpful as many of their novelties are, I regret to say that " organic iron " ^
does not seem to be one of them. Perhaps I may make an exception in
favour of an old-fashioned French solution of malate of iron which I have
found that patients with queasy stomachs can take when ordinary ferru-
ginous drugs are ill borne or seem inappropriate. Gilbert has found
the protoxalate very useful ; it is said to be soluble in the gastric juice.
Stockman indeed says that " inorganic iron " is more rapidly effective
than " organic iron."
Of "adjuvants" teachers and friends recommend many to us j ether,
liquor ammonise acetatis, nux vomica, and so forth : but I cannot say
that I have found in any of them more advantage than such as may flow
in the individual case from the ordinary properties of these accessories ;
they may be needed or they may not, usually not. It is well, however,
to add some cordial such as chloric ether or sal volatile to all steel
mixtures.
On pathological grounds much has been made of late of an antiseptic
treatment. In a paper lately read at Cambridge by Dr. Latham, great
stress was laid by the author on the value of the liquor of the perchloride
of iron, because, as he showed at the time, it contains much free chlorine.
Dr. Latham's claims on behalf of this vehicle of iron are probably well
founded, as they are in accord with other observations of the kind. For
instance, Townsend thus tabulated his results in 87 cases : —
Hgbn. incr,
j3-iiaphthol (30 oases) ...... 1'85 per cent
Bland's pills (31 cases) ..... 5'07 ,,
Naphthol first and afterwards Blaud's pills (12 oases) . 6'70 ,,
Bland's pills alone (19 cases) ..... 4'50 ,,
This table shows a decided advantage in favour of the use of
^-naphthol before the pills ; and in another such series, of 28 cases, the
Hgbn. increase was 7-9 per cent. In the Boston Medical Society, to which
body this paper was read, it was generally agi-eed that intestinal antisepsis
combined with iron gives better results than iron alone.
I remember in a few cases, when for some reason the iron did not
take good hold at first, the drug seemed to get a start on the addition of
arsenic or phosphide of zinc ; ordinarily to treat chlorosis with these
drugs is, to say the least, a waste of time.
In the belief that in chlorosis the volume of the serum is increased
S«6
SYSTEM OF MEDICINE
(serous plethora), bleeding and diaphoresis have been recommended as
means of cure. It is not apparent how an operation which reduces the
number of the red corpuscles can be otherwise than injurious. However,
Schmidt treated and tabulated the following eight cases (a " bleeding " was
80 ccm.) : —
i. One Weeding and iron
ii. Iron alone .
iii. One bleeding
iv. Several bleedings .
V. Sweating cure
vi. Bleeding and sweating
Several bleedings, sweating,
and
viii. Several bleedings and sweatings ; no iron
iverage incr,
Hbgn. per
cent.
Weekly incr.
of weight
in kilos.
6-20
0-73
6-18
0-48
2-50
0-92
0-59
■0-51
0-39
0-44
0-36
0-46
0-02
0-04
0-56
0-19
The good eifect in the first case was entirely due, no doubt, to the iron.
While prescribing pharmaceutical remedies the physician will not
forget, so far as in him lies, to rectify such disadvantages of life as he may "
be able to ascertain. Over-pressure at school, unwholesome conditions of
work or amusement, late hours, worry, tight lacing are points to which his
attention vrill be directed ; yet while relaxing overwork, if any, he will
be no less alive to the evil of idleness or desultoriness. As much
time as possible should be spent in the open air and in such gentle y
exercise as the strength and respiratory functions will permit. Quiet |
horse exercise or cycling may be encouraged, and some course of study \
likewise which shall interest and discipline the mind and temper without ;
fatigue. The patient should sleep, if possible, with the bedroom window
open ; if this be prevented by hard weather, the door must be open. A /
cold bath will probably prove more than the deficient heat production can
support, but the rapid application of the wet sheet can usually be prescribed
with advantage ; this is better done in the forenoon two hours after
breakfast, and, during the colder months, in a room with a fire. Excessive
cold, as we see in hsemoglobinuria, seems to destroy the red corpuscles.
If love affairs harass the patient it must be remembered that marriage is ~
no direct cure.
I have said that the deficient powers of heat production often forbid
too bracing a line of treatment ; in a bad case of chlorosis, one in which
perhaps iron is not telling at once, the dissipation of heat and the expense
of muscular activity must be husbanded by a week or a fortnight in bed.
Such a measure often gives an impulse to the curative movement, and proves
to be an economy of time in the end. The facial, gastric, and other neur-
algias, which may be prominent symptoms of the case, are usually relieved
at once by this simple means. A further reason for recumbency is given
by Dr. George Oliver in his interesting little book on Pulse-Gauging.
CHLOROSIS 517
Thus the calibre of the arteries is enlarged, residual blood in the ventricles
is reduced, and dilatation of the heart is prevented or relieved. By his
arteriometer Oliver finds (p. 135) "that from 25 to 100 per cent more
blood is discharged into the tissues in the recumbent than obtains in
the sitting posture . . . the radial calibre . . . increases in recum-
bency, as a rule, in proportion to the severity of the anaemia and to the
need of recumbent rest." As soon as the appetite improves and the
other graver symptoms begin to give way, change to the seaside or to
the hills may be advised ; but cold, I repeat, is injurious in chlorosis,
and at considerable altitudes the deficiency of oxygen would be more and
more sensibly felt.
It only remains now to say the few words which are necessary on the
diet of chlorosis. It_is of the first importance to overcome the common
distaste for meat. Girfs will say that the entry of a dish of Hot meat into
the room makes them feel sick ; kindly and gradually this aversion must
be overcome, and meat must take its due place in the diet. Eggs and
milk if well digested will be included, and sweets and other kickshaws
discouraged. Green vegetables are said to be useful for their chlorophyll,
at any rate they avert constipation. It is desirable, if a fair meal be taken,
that nothing be offered between meals. We are pointedly asked in these
cases of chlorosis whether alcohol in any form is to be prescribed. Of itself
I believe that alcohol is of no direct service. It is possible now and then
that a bad appetite may be coaxed into more activity by a glass of stout,
or of red wine and water ; if so, the use of these aids is justified. Some
young persons dislike pure water ; and indeed it is not well for these
chlorotics to drink much with meals : half a tumbler of milk may be the
table drink, and three hours after meals a glass of hot water will act
beneficially both on the stomach and on the secretions. Careful mastica-
tion of the food is of great importance.
In conclusion I would repeat that to test the blood not only for the
number of red corpuscles and apparent haemoglobin value, but also to
ascertain whether they are equal and of full size, is the only trustworthy
means of gauging the rate and degree of cure; a lowered pulse-rate,
however, is a sign of amendment, as is reacceleration of impending
relapse. Colour generally returns to the face and steadiness to the
breathing long before the cure is established.
T. Cliitokd Allbdtt.
REFERENCES
1. AECANaELi, A. La CUorosi. Roma, 1896.— 2. Bannattne. "The Ansemia
of Rheumatic Arthritis," Lamet, N07. 28, 1896.— 3. Bbcquerel and Rodibe. Gazette
de Fans, 1844, 1846, 1852.— 4. Bihlee. Deut. Arch. /. klin. Med. 1894.-5
BOLLINGBE. "Fall V. Sinusthrombose, " Miinch. imd. Woehenschr. 1887, No 16 —
6. BouKDiLLON. "Phl^bite et ohlorose." TAese, Montpellier, 1891.— 7. Chvostek
TFunerkhn. Woehensch. Nov. 27, 1893.— 8. Clement. Centralblatt f. Gynakoloqie
1895, No. 40.— 9. Coppola. "Sul valore fisiol. e therap. del ferro inorganioo ''
Lo Spervmentale, 1890.-10. Gilbert, A. Charcot et Bouchard, TraiU de '^decine,
1894, t. u. 491.— 11. Gkabee. Klin. Diagnostik d. Blutkrankheiten. Leipzig, 1881 —
12. Halfoed, H. " Anaemia as a Cause of Permanent Heart Lesion," Bnt. Med. Journ.
SiS SYSTEM OF MEDICINE
1892.— 13. Hammersohlag. "Ueber Hydramie," Zeitsch.f. Urn. Med. xxi. 475, 1892.—
14. Handford. "The Heart in Ansemia," Jour, of the Med. Sci. Dee. 1890. — 15.
Hatjt et Mathibtj. "Phlegmasia alba dolens dans le cours de la chlorose," Arch,
gin. de mM. 1877, p. 676. — 16. Hayem. Du sang et ses alterations anatomiques, 1889. —
17. Head, H. Brain, 1893, 1894, 1896. — 18. Hoffmann, F. Dissertatio de
genuina chlorosis indole, origime et curatione, 1731. t— 19. Immermann. "Chlorosis,"
Ziemssen's Oyclopddie, Engl. Trans. 1877, vol. xvi. — 20. Joffrot. Frogris
mid. t. xviii. Dec. 23, 1893. — 21. Jones, Lloyd. Jowrn. of Physiology, 1887,
1891.-22. Idem. Chlorosis. London, 1897.— 23. Kletzikskt. "Ein krit.
Beitrag z. Chemiatrie des Eisens," Zeitseh. d. Oescllsch. d. Aerzte zu Wien, 1854,
ii. 281.— 24. Robert. "Ueber den jetzigen Stand der Eisenfrage,'' St. Peters-
burg ined. Wochensch. 1891, 73.-25. Keugbr. "Der Blut in Anamie u. Leukhamie,"
St. Petersburg med. Wochensch. 1892, S. 203.-26. Labat. " Phlegmatia alb. dolens
chez une chlorotique : Embolus puhnonarius, " France mid. 1879, p. 66.' — 27. Landois
and Stirling. Text-booh of Physiology, 3rd edit. 1888, p. 188.-28. Lauremain.
"Phlegm, alb. dolens bilat." Lyon mid. 1888, p. 205.-29. MacAlistee, D. "On
the Form and Mechanism of the Heart," Brit. Med. Jowr. Oct. 28, 1882.— 30. Maea-
GLIANO e Gastbllino. "Azione del siero del sangue nei globuli rossi," Eiforma
medica, June 19, 1890.-31. Martin, C. F. Brit. Med. Jour. July 2, 1894.-32.
Meinert. "Zur Aetiologie d. Chlorose," Wien. med. Wochenschr. No. 12, 1893.
—33. MoRNBR. Zeitschr. f. phys. Ohemie, xyiii. 1893. — 34. MiJLLER. Berlin, klin.
Woch. 1895, No. 38. — 35. v. NooRDEN. X. Pathologic des StoffwecAsel. Bferlin, 1893.
—36. Idem. "Die Bleichsucht," Spec. Path. u. Ther. Nothnagel, Bd. viii. Th. 2, Wien,
1897.— 37. Oliver, George. Pulse- Gauging. London, 1895.— 38. Pick. "Therapie
d. Chlorose," Wiener med. Woch. 1891, p. 939.-39. PoTAiN. Bull. gin. de
thirap. 1895, p. 307. — 40. Idem. Clinique mM. de la Chariti, 1894. — 41.
Proet. "De la thrombose veineuse chez les chlorotiques. " Thise, Lyon, 1889.
— 42. Rendu. "Thrombose spontan^e de I'artere pumionaire chez une chloro-
tique," Bull. Soc. m6d. des Mp. 1887.-43. Idem. Sem. mM. 30th April 1890.—
44. Rethees. "Beitrage z. Pathologie d. Chlorose," Diss. Berlin, 1891. — 45.
KoMBERG, E. Berl. klin. Wochenschr. June,- July 1897. — 46. Rubenstbin?
"Ueber d. Ursache d. Heilwirkung d. Aderlasses bei Chlorose," Wien. med. Presse,
1893, Nos. 33, 34. — 47. Sansom. Diagnosis of Diseases of the Heart, etc. 1892. — 48.
Schmidt. Munch, med. Wochenschr. Nos. 27, 28, 1896. — 49. Sohrott. Diss.
Miinchen, 1896. — 50. Sevfall, Prof. " Stethoscopio Pressure in Physical Examina-
tion of the Heart," New York Med. Jour. Dec. 4, 1897. — 51. Simon, C. E. Clinical
Diagnosis, Philad. 1896. — 52. Idem. "Study of 31 cases of Chlorosis," Amer. Jour,
of Med. Sci. April 1897. — 53. Stockman, E. "Treatment of Chlorosis," Brit. Med.
Journ. April 29 and May 6, 1893. — 54. Idem. "Summary of 63 cases of Chlorosis,"
Edin. Med. Journ. Nov. 1893. — 55. Idem. " The Causes and Treatment of Chlorosis,"
Brit. Med. Journ. Dec. 14, 1895. — 56. Idem. "The Iron in the Liver and Spleen,"
Brit. Med. Journ. May 2, 1896. — 57. Tovi^nsend. "Chlorosis and Intestinal and
Antiseptic Treatment," Boston Journal, May 28, 1896. — 58. ViRCHOW, R. Ueber die
Chlorose u. Anomalien in Gefassapparate, 1872. — 59. Vat. Zeitschr. f. phys. Chemie,
XX. 577, 1895. — 60. Voges. "Mischung d. Nhaltigen Bestandtheile im Harn bei
Anamie, etc.," quoted by v. Noorden (35). — 61. "Warfvingb. Proc. International
Medical Congress at Moscow, 1897. — 62. Zaleski. Zeitseh. f. phys. Chemie, x. 453,
1886.
T. C. A.
PERNICIOUS ANEMIA 519
PEENICIOUS ANEMIA
Synonyms. — Idiopathic ancemia ; Essential ancemia ; Myelogenic armmia;
Progressive pernicious amemia, ; Ganglionic ancemia ; Ancsmatosis.
Definition. — By "pernicious anaemia" is now generally understood a
variety of primary anaemia, which arises insidiously, and is characterised
by progressive diminution in the number and changes in the form of the
red corpuscles of the blood, together with a similar but generally less
marked diminution in the amount of haemoglobin ; which changes appar-
ently depend upon undue haemolysis combined with inadequate com-
pensatory haemogenesis, — a condition which, in the majority of cases,
passes more or less rapidly to a fatal termination, the progress being in
some cases interrupted by periods of improvement followed by relapse,
but rarely resulting in permanent restoration to health, whatever the
method of treatment.
It is difficult, even in the light of modem research, to frame a
satisfactory definition of this affection — one which shall not be too wide,
nor, on the other hand, too narrow to embrace the varied conditions
under which this severe form of anaemia is known to arise. There is
reason to doubt even the constancy of the "progressive " and " pernicious "
characters which were deemed by Biermer to constitute its most charac-
teristic features. On the other hand, the use of such names as "idio-
pathic" and "essential" anaemia, however appropriate they may have
been when Addison directed attention to this class of primary blood
affection, can hardly be justified now except as an admission that patho-
logical research has failed to discover the source of a disease which
presents such striking clinical features. The difficulty is enhanced by
the fact that the clinical phenomena are not in themselves distinctive,
not even the characters of the blood ; hence, as the advance of knowledge
led to the shrinking of the " idiopathic " area, it seemed reasonable at
one time to admit the existence of secondary forms of pernicious anaemia
side by side with the primary.
However, there is good ground for believing that when all extrinsic
causes are eliminated, there remains a residue of cases of progressive
anaemia, to which the term " primary " may be assigned ; and it is to
this class that we may also assign, at least provisionally, the name
"pernicious." For a primary anaemia may be defined as one dependent
on the perverted relationship between the two great functions concerned
in maintaining the normal composition of the blood. In the active
processes of disintegration and renewal of the blood elements, haemolysis
is balanced by haemogenesis. The balance may be disturbed by excessive
haemolysis on the one hand, or by inadequate haemogenesis on the other.
S20 SYSTEM OF MEDICINE
It will be seen that an explanation of idiopathic ansemia has been sought
in each of these directions severally, but, as stated in the above defini-
tion, there may be defects in both. Whether the definition should be
made more precise by indicating the probable source and character of
the hsemolytic process is a matter which I shall discuss under the head
of " Pathology."
History. — By common consent the credit of the first general account
of pernicious ansemia is due to Dr. Thomas Addison, whose reference to
it in his monograph " On the Constitutional and Local Effects of Disease
of the Suprarenal Capsules " has often been quoted. Although these
passages appeared in 1855 he had been teaching their doctrines for
several years. No account of the condition can be considered complete
without Addison's description of it : —
" For a long period I had from time to time met with a very remark-
able form of general anaemia occurring without any discoverable cause
whatever, cases in which there had been no previous loss of blood, no
exhausting diarrhoea, no chlorosis, no purpura, no renal, splenic, mias-
matic, glandular, strumous, or malignant disease.
" Accordingly, in speaking of this form in clinical lectures, I, perhaps
with little propriety, applied to it the term ' idiopathic ' to distinguish it
from cases in which there existed more or less evidence of some of the
usual causes or concomitants of the anaemic state.
" The disease presented in every instance the same general character,
and, with scarcely a single exception, was followed after a variable period
by the same result.
" It occurs in both sexes ; generally, but not exclusively, beyond the
middle period of life ; and, so far as I at present know, chiefly in persons
of a somewhat large and bulky frame, and with a strongly -marked
tendency to the formation of fat.
" It makes its approach in so slow and insidious a manner that the
patient can hardly fix a date to his earliest feeling of that languor which
is shortly to become so extreme. The countenance gets pale, the whites
of the eyes become pearly, the general frame flabby rather than wasted ;
the pulse perhaps large, but remarkably soft and compressible, and
occasionally with a slight jerk, especially under the slightest excitement.
There is an increasing indisposition to exertion, with an uncomfortable
feeling of faintness or breathlessness on attempting it ; the heart is
readily made to palpitate ; the whole surface of the body presents a
blanched, smooth, and waxy appearance ; the lips, gums, and tongue
seem bloodless ; the flabbiness of the solids increases ; the appetite fails ;
extreme languor and faintness supervene, breathlessness and palpitations
being produced by the most trifling exertion or emotion; some slight
oedema is probably perceived about the ankles. The debility becomes
extreme ; the patient can no longer rise from his bed ; the mind occa-
sionally wanders ; he falls into a prostrate and half-torpid state, and at
length expires. Nevertheless to the very last, and after a sickness of
perhaps several months' duration, the bulkiness of the general frame and
PERNICIOUS ANMMIA 521
the obesity often present a most striking contrast to the failure and
exhaustion observable in every other respect.
" With perhaps a single exception, the disease, in my own experi-
ence, resisted all remedial efforts, and sooner or later terminated
fatally.
" On examining the bodies of such patients after death I have failed
to discover any organic lesion that could properly or reasonably be
assigned as an adequate cause of such serious consequences ; nevertheless,
from the disease having uniformly occurred in fat people, I was naturally
led to entertain a suspicion that some form of fatty degeneration might
have a share at least in its production ; and I may observe that, in the
case last examined, the heart had undergone such a change, and that a
portion of the semilunar ganglion and solar plexus, on being subjected to
microscopic examination, was pronounced by Mr. Quekett to have passed
into a corresponding condition.
"Whether any or all of these morbid changes are essentially con-
cerned— as I believe they are — in giving rise to this very remarkable
disease, future observation will probably decide."
Isolated examples of the remarkable condition thus succinctly
described by Addison had found their way into medical records prior to
the date of his writing. This has been shown by Lupine and Pye-Smith
in their historical summaries of the subject. Thus, the latter author
refers to the records of seven cases which doubtless fall into the
category of "Addison's anaemia"; namely, one recorded by Combe
(1823), one by Andral (1823), one by Marshall Hall (1837), one by
Piorry (1841), one by Pearce (1845), and two by Barclay (1851). It
seems clear, too, that the cases given by Channing of Boston (Mass.),
in a paper, written in 1842, dealing with anaemia in relation to the
puerperal state and in uterine disorders, probably belong to the same
class. However, comparatively little attention was attracted to the
subject for several years after Addison wrote, except, it is right to add,
amongst those who were most familiar with his teaching. Thus, Sir S.
Wilks, in the Guy's Hospital Eeports for 1857, discussed idiopathic fatty
degeneration, in which he referred to the morbid change which is the
most characteristic feature of idiopathic ansemia ; and cases were recorded
by Habershon and others of the Guy's school. The writings of Gusserow
and Biermer of Zurich, especially the memoir in which the latter author
first uses the phrase "progressive pernicious anaemia" (1871-72), did
much to awaken interest in the subject, and, I may add, to ignore the
previous work of Addison ; thus to Biermer was given the credit, which
indeed he himself claimed, of describing for the first time the characters
of a condition not hitherto recognised. It is clear, however, that not
only had he been anticipated by Addison, but it is also probable that
the cases amongst pregnant women to which Gusserow drew attention
were the same as those indicated by Channing thirty years previously,
and by Lebert in a case recorded in 1853 as "puerperal chlorosis."
Nevertheless, the service rendered by Biermer was considerable, both
522 SYSTEM OF MEDICINE
from the clinical and pathological standpoint ; and his choice of the name
" pernicious " directed attention to the fatal character of the disease.
However, we must recognise that, as knowledge has grown, reasons have
increased for believing that many cases included by Addison as " idio-
pathic " or by Biermer as " pernicious " would more strictly find a place
amongst the secondary anaemias. For not only have unsuspected causes
been revealed of progressively fatal ansemias which exhibit all the
characters described by Addison and Biermer (such as anchylostomiasis),
but definite, if minute, pathological difibrences have been shown to exist
between pernicious ansemia proper and certain other cases which some
years ago I regarded as examples of " symptomatic (secondary) pernicious "
ansemia ; for in the predominance of the cardinal symptoms masking the
underlying condition, these latter cases ran a course and exhibited many
characters which resembled those of cases not so associated, and therefore
named provisionally " idiopathic." This is not a mere question of
nomenclature, it concerns the true interpretation of the pathology of the
disease before us, and must be referred to again when we speak of this
branch of the subject. We must constantly bear in mind, therefore, that
a certain number of the cases on record are not strictly to be ranked in
the category of " pernicious ansemia " properly so called.
It is not possible in such an article as this to review all that has been
written during the past twenty-five years upon the subject. Many con-
tributions have been made by physicians of Addison's own hospital,
namely, by Pye-Smith, F. Taylor, and Hale White. Most of their
writings appear in the Guy's Hospital Reports. Dr. Stephen Mackenzie,
again, in a clinical lecture published in 1878, did much to invite attention
to a subject to which he reverted some years later in the Lettsomian
lectures which he delivered in 1891 at the Medical Society of London.
Dr. Byrom Bramwell published a full account of pernicious ansemia
early in 1876, and drew attention to the value of arsenic in its
treatment. To Dr. W. Hunter we owe some of the most profound
studies of the pathology of the disease, studies which have materially
influenced our conceptions of its nature, and have done more than any
other work to give definiteness to them. Other labourers in the same
field have been W. Eussell, Brakenridge, Gibson, Stockman, and Fraser
of Edinburgh ; Finny, Purser and Craig of Dublin ; Mott, Russell, and
James Taylor of London. The disease was studied at an early date in
America, the contributions of Osier, Gardiner, and Howard of Montreal
being amongst the first; Osier is also the author of many subsequent
studies. To Pepper of Philadelphia is due the discovery of changes in
the marrow of the bones, observations speedily confirmed by others.
Musser, Henry, Kinnicutt, and Woods have also contributed to the
subject in the United States. Numerous essays and monographs have
appeared in the Continental schools by Eichhorst, Quincke, Muller,
Neumann, Immermann, Lepine, Hayem, Laache, and others.
Etiology. — To speak of the causation of a disease of which, in the
majority of cases, no adequate cause can be discovered seems paradoxical ;
PERNICIOUS ANMMIA $22,
yet in pernicious anasmia we detect certain remoter antecedents, which, if
not of themselves adequate to give rise to the condition, nor constant in
their occurrence, are yet not without importance. These are among the
more general causes of anemia, for anaemia owns an infinity of causes ;
but they seem to have no bearing on the quality of pernicioushess.
Whenever the anaemia appears to pass beyond the boundary of the
incidental, and becomes so dominating a feature of the illness that, as it
increases, all the symptoms are referable to the anaemia, and none to
the primary affection, then it is legitimate to infer the intervention of some
further agency which has converted the simple into the pernicious type of
anaemia. Thus, for example, haemorrhage is a common cause of secondary
anaemia, and repeated small bleedings may produce a condition which
progresses from bad to worse, and ultimately destroys life. Is such a
state to be regarded as " pernicious anaemia " ? Some have thought so,
and a recent writer (Stockman) has striven to show that the very
haemorrhagic tendency which belongs to severe anaemia may be the
means of its passing by a vicious circle into a pernicious and fatal disease.
Such a view, of course, gets rid of the notion that pernicious anaemia is a
specific disease ; as, thus, any anaemia of sufficiently high degree pro-
vides for its own further progress by the effects which it produces
on the nutrition of the blood-vessels. On the other hand, that cases of
haemorrhage and of diseases involving large haemorrhages, or a continued
repetition of smaller ones, although leading to a chronic anaemia, do very
rarely assume the type under discussion, seems to prove the existence of
other determining factors ; for it does certainly happen that, although a
case of pernicious anaemia may seem to have been initiated by a
metrorrhagia or a gastric haemorrhage, the anaemia advances without any
repetition of the loss of blood, whether from the primary source or from
secondary sources opened by the anaemic state. Thus, even were there
no other distinguishing characters — such, for example, as those of the blood
and urine — we should have to assume the presence of some fresh factor to
account for the course of the disease. The consideration of some of the
more common antecedents of pernicious anaemia may suggest to us where
this tertium quid is to be sought.
Amongst the favouring conditions upon which some stress has been
laid are insufficiency or unsuitability of food in persons subjected to hard
manual labour, or even not so subjected. The conditions of life of the
Swiss peasantry were at one time supposed to determine the many
instances of the affection which rendered Zurich a centre for its study.
Misery and famine are conditions of anaemia ; but unhappily such con-
ditions are as common in the large centres of population as they are in
the rural districts, yet pernicious anaemia is a rare disease by no means
limited to the poorer classes of the community. Moreover, it is mainly
in the writings of the Swiss authors that any reference is made to such
etiological factors. Another class of antecedents most prominently
cited in the writings of Gusserow and Biermer, to account for the excess
of women among their patients, consists of pregnancy, parturition, and
524 SYSTEM OF MEDICINE
lactation ; yet how seldom is this fatal kind of anaemia observed as a
direct sequence of these physiological states. Eeference has already been
made to haemorrhage as an antecedent, and mention must be made of
gastro-intestinal disturbance also, which of all factors seems likely to be the
most nearly connected with the etiology of the disease. Not only are
the earliest symptoms connected with this system in a considerable pro-
portion of cases, such as vomiting, diarrhoea, or irregularities of digestion,
but many cases exhibit also definite changes in the gastric or intestinal
mucosa ; and this to such an extent as to have led some observers to
attribute the fatal anaemia to the atrophy or other lesions which attack
nutrition at its source (Fenwick, Kinnicutt, Osier). Again, it is well known
that patients with chronic gastric disorders, such as ulcer or cancer, are
sometimes anaemic out of all proportion to the amount of haemorrhage
which may have occurred during their illness. Indeed, in some cases
where there are no direct symptoms of the gastric disorder the resemblance
to pernicious anaemia is striking ; and cases have been described where
anaemia apparently pernicious has seemed to establish itself upon the
gastric disease (Eisenlohr). The arguments of Hunter on this point
have much force, his contention being that in all these conditions where
the clinical features of pernicious anaemia are manifested in association
with malignant disease or gastric changes, the lesions essential to the
former have been superadded ; for, as he points out, pernicious anaemia
is a rare complication in malignant disease, whilst the gastric lesions often
occur apart from pernicious anaemia. In commenting on the view,
advanced by Fenwick, that atrophy of the gastric glands underlies pernicious
anaemia. Hunter points out that this observer himself found such
atrophy in a large number of cases of cancer also. "Thus, of fifteen
cases of cancer of the breast, in only four were no anatomical changes to
be found in the gastric mucosa. Some degree of atrophy was found in
every case of cancer of the stomach. If atrophy of the gastric glands is
to be regarded as the essential anatomical change in pernicious anaemia,
it would seem reasonable to expect that pernicious anaemia should be
found frequently associated with cancer of the breast, and almost invariably
with cancer of the stomach. Curiously enough, however, I have not
found a single case recorded in which cancer of the breast has presented
the features of pernicious anaemia ; and as regards cancer of the stomach,
it is the exception and not the rule for it to be marked by the clinical
features characteristic of pernicious anaemia " (Hunter). Similar reasoning
is employed by Hunter to cast doubt on the alleged etiological importance
of the degenerative changes described by Sasaki and by Banti in the
nervous tissues of the intestinal wall ; for such changes, according to the
observations of Scheimpilug, are frequent in wasting and acute infectious
diseases. Banti, regarding the sympathetic nerve lesions as a primary
defect, went so far as to give the name "ganglionic anaemia" to this
aiFection.
Among the influences which have been known to precede a pro-
gressive anaemia must be included those in which the mental and
PEUNICIOUS ANEMIA 525
emotional faculties are concerned. There is authentic evidence that shock,
depression, anxiety, or severe mental strain have been followed by the
appearance of an anaemia which has run on to a fatal issue. The precise
relationship between the disease and such antecedents is, however, quite
obscure.
The hypothesis that pernicious anaemia is due to microbic agencies
has little to support it ; the micro-organisms that have been described in
the blood (Frankenhauser) have not been isolated or cultivated, whilst
the condition of the blood itself is such as readily to lead to errors of
observation in this respect.
Lastly, pernicious anaemia is mainly a disease of adult life, most cases
occurring between the ages of twenty and forty-five. But children are
not exempt from it, cases being recorded in patients as young as seven,
eleven, and twelve years. The sexes are about equally prone to it, but
if all cases of its apparent origin in pregnancy and parturition be excluded,
it would probably be found that the disease preponderates amongst men.
Symptoms. — In the vast majority of cases it is extremely difficult to
fix the date at which the illness began ; its onset being so gradual and
insidious that the patient passed imperceptibly from health to disease. It
does, however, occasionally happen that a debilitating illness, a great loss
of blood, pregnancy, or parturition has been followed immediately by an
anaemia of the ingravescent course characteristic of the disease ; and,
as has already been pointed out, even some unusual mental shock or
emotional disturbance may be directly antecedent to the appearance of the
anaemia. Whether or not we are to include in the present category every
case which seems to have its origin so directly in an ansemiating cause,
it is evident nevertheless that the declared symptoms do not differ in
kind from those which are thus produced. There is hardly a single
symptom of the protopathic affection which is not to be found now and
again in association with profound anaemia clearly due to an ordinary
cause. The earliest indications of the malady are so slight and in-
significant as to be disregarded, and it is often not until the disease is
well advanced that its true nature is recognised. Nor is it possible to
assign any period during which these early and indefinite signs may be
said to last. It is a stage measured mostly by weeks or even months
rather than days, although cases of apparently acute course are on
record. These initial symptoms consist in the main in failing strength,
and in disinclination for exertion, physical or mental ; so that the subject
of the malady becomes possessed by an unnatural lassitude which makes
all labour irksome, and often renders him despondent, low-spirited, and
capricious in temper. Together with this persistent asthenia and loss of
energy the appetite fails ; there may be complaint of discomfort after
food, and the patient will perhaps suffer at times from nausea or even
vomiting. If to these gastric disturbances there be added intestinal
irregularity, it is natural for him and his friends to ascribe his weakness
and depression to some functional derangement of the digestive organs.
Yet, as a rule, there is no falling off in nutrition, but even a noticeable
526 SYSTEM OF MEDICINE
increase in bulk and weight. Gradually, however, the signs of anaemia
are more evident, and, as they become pronounced, his weakness increases,
he suffers from palpitation, perhaps from syncopal attacks, and shortness of
breath on exertion, and at last is compelled to abandon his calling and
seek rest and advice. The symptoms which may now be presented, those,
that is, of the declared disease, may best be described in detail ; they
occur with variable frequency, and some even which may be thought to
be essential and characteristic are occasionally conspicuous by their
absence.
The constant symptom is of course the ancemia. The pallor of the
skin is striking, often in marked contrast with the previous good colour
of the individual. The skin and mucous membranes are almost devoid of
colour, save that the former, especially of the face, generally assumes a
faint yellowish or lemon tint that is wholly different from the whiteness
of the subject of pulmonary tuberculosis, the earthy pallor of the
cancerous cachexia, or the muddy tint of the malarial subject; and is quite
different from the bronzing of the malady discovered by Addison in his
search for an adequate cause of "idiopathic" anaemia. This complexion,
however, is sometimes met with in the chlorotic, in those who have
suffered from internal haemorrhage (as, for instance, in cases of large pelvic
haematocele in process of absorption), in rare cases of chronic gastric
organic disease, and in various toxic anaemias. It cannot be deemed
pathognomonic ; but occurring, as it does, with so few symptoms, or
overt evidence of blood loss, it may lead to the suspicion of the grave
nature of the malady. It is all the more suggestive when it occurs in a
male subject of mature age whose previous health record has been
excellent. There may be some oedema of the lower extremities, often
very slight, sufficient to cause slight pitting on pressure over the malleoli ;
sometimes more extensive, and not seldom entirely absent. Indeed, this
symptom is hardly so frequent a feature of pernicious anaemia as it is of
chlorosis. In the later stages, however, it may become marked, as also
may petechial haemorrhages chiefly on the lower limbs. There is no
constant condition of skin as regards perspiration. Some have noticed
undue sweating in the earlier and later periods of illness, but there does
not appear to be any regularity in this symptom, and it can hardly be
regarded as essential. The skin often assumes the soft and smooth
character to be met with in the subject of fatty degeneration.
The temperature of the body is generally normal, and in advanced
stages subnormal ; but most observers record periods of remark-
able pyrexial exacerbation, which some consider to be peculiar to this
kind of anaemia. This pyrexia is not as a rule severe, the temperature
seldom exceeds 102° or 103°, with morning remissions and marked
irregularity. It may last for a few days and then subside, recurring at
intervals during the progress of the malady ; or it may be of more
continued course. This intermittent pyrexia is possibly related to the
variations in the haemolytic process, and may be taken as confirmatory
of the toxaemic theory of the disease ; another conceivable view is that
PERNICIOUS ANEMIA S-27
it is due to capillary hsemorrhages in the heat-controlling centres of the
brain. Whatever the explanation it is seldom entirely absent ; but then,
it may be remarked, a subfebrile temperature is not uncommon in
chlorosis, and may also occur after severe haemorrhage.
The signs of circulatory disturbance are generally obvious, and may
even lead to an erroneous opinion. The patient may complain of
palpitation from an early period, and at times may be attacked with
faintness or actual syncope. The pulse, generally quicker than normal, is
markedly affected by exertion or emotion, the difference between its
rates as influenced by posture being considerable. It is mostly soft and
fairly full, whilst there may be complaint of throbbing in the neck or a
feeling of fulness in the head. The cardio-vascular signs of ansemia are
pronounced. The impulse of the heart is undulating, and the apex-beat
generally somewhat lower and situated more to the left than normal ;
percussion confirms this evidence of slight dilatation of the ventricles by
revealing an increase of the cardiac area of dulness to the left. An
intense blowing systolic murmur is generally audible over the praecordium,
most marked at the pulmonary cartilage. In advanced cases this murmur
may have a grating character, and be even mistaken for friction. (A
diastolic murmur has been noted, but this is not common.) Its hsemic
origin is confirmed by the presence of a similar murmur in the large
arteries, and a loud hum in the jugular vein. The carotids often pulsate
violently, and a distinct thrill is to be felt over them and the large veins
in the neck.
Examination of the hlood reveals a great departure from the normal.
The bloodless condition of the skin makes it somewhat diflScult to obtain
sufficient for its estimation. The drop has a pale watery appearance,
and the number of red corpuscles is found to be notably diminished.
The degree of this oligocythsemia depends upon the stage and severity of
the disease ; but it is not unusual to find the number of red corpuscles
reduced to 1,000,000 per cub. mm., that is, 20 per cent of the normal ;
and as the case progresses they may fall considerably below this figure,
the lowest estimation on record being 143,000 (Quincke). There is no
parallel diminution in the number of leucocytes ; in late stages they may
exceed the normal amount. With the hsemoglobinometer it will almost
invariably be found that although there is a marked reduction in the
amount of haemoglobin this is not proportionate to the reduction in cor-
puscular richness. Thus in a case in which the corpuscles have fallen to
10 per cent the haemoglobin percentage may be as high as 20 or 25 per
cent. Hence it follows that the individual corpuscles must have a larger
relative content of haemoglobin than in health. The microscopical ex-
amination shows notable changes, which when first observed were thought
to be quite characteristic. In the first place, the tendency for the cor-
puscles to form rouleaux is almost entirely lost, although this is not to be
observed in every case. As a rule the scanty corpuscles either form
irregular masses, or lie scattered over the field ; and it is evident at once
that they exhibit very great variations in size and shape. Thus many
526 SYSTEM Of MEDICINE
are of irregular form, pear-shaped, oval, and deformed, constituting the
condition named by Quincke " poikilocytosis," which, however, is not
distinctive. Some are much larger than normal (megalocytes), and
many, on the other hand, appear as small spherical bodies (microcytes).
Neither of these varieties can be considered distinctive, although some
authors think that the prevalence of the megalocytes is greater than in
any other condition ; others, however, consider that the microcytes are if
anything more characteristic. Besides these forms, which may be re-
garded respectively as immature or overgrown red corpuscles, there are
also to be seen nucleated corpuscles, which suggest a reversion to the
reptilian type ; these, according to their sizes, have been named normo-
blasts, megaloblasts, and microblasts. Lastly, Ehrlich showed that
granular corpuscles which stain with reagents are often present, and are
possibly degenerate corpuscles ; whilst the readiness with which the
haemoglobin accumulates in a mass within a corpuscle gives the latter a
pseudo-nucleated aspect. On the other hand, Dr. Copeman found that
haemoglobin separated from the corpuscles in pernicious anaemia with
abnormal readiness. There is no increase in the number of leucocytes ;
but it has been observed that these are mostly of the smaller (lymphocyte)
variety, and granular masses are present. Thus the changes are mainly
limited to the red corpuscles, which may be considered to exhibit dis-
integrating forms and immature corpuscles side by side.
A tendency to hcemorrhage is a noteworthy feature of the disease.
This may be seen comparatively early in its course, and may aggravate
the anaemia ; but in extent and degree it is too variable to be regarded as
the direct cause of the progressive character of the affection. The
haemorrhages may take the form of epistaxis, of haematemesis, of
haematuria, or of bleeding into internal organs, such as the brain and the
spinal cord. Most commonly, however, they are but small capillary
effusions, and occur most distinctly in the retina. It has been shown by
Mackenzie that these retinal haemorrhages are prone to occur in any form
of prolonged anaemia if of sufficient intensity (below 50 per cent corpuscular
richness) ; and as this degree of intensity is generally attained in pernicious
anaemia their occurrence in this affection is one of its most common
symptoms. The retinal haemorrhage was first pointed out by Biermer,
and may be regarded as a sign of some value. As a rule it does not lead
to any impairment of vision, but cases have occurred where it has been
the cause of amaurosis. Mention has already been made of the cutaneous
haemorrhages which may occur.
Dyspncea is a prominent symptom, the enfeeblement of the heart
adding to the respiratory difficulty caused by the lack of haemoglobin.
As the end is approached this symptom may become more marked and
distressing, and the physical signs' of oedema of lung may supervene.
Otherwise there is comparative freedom from pulmonary disease through-
out, although bronchitis and pneumonia have been observed as serious
complications.
Disturbances of the gastro-intestinal system are among the earliest
PERNICIOUS ANEMIA 529
and most frequent features Of the attack. The pale, flabby tongue
denotes the general ansemia and want of tone of the stomach — condi-
tions indicated by nausea, vomiting, epigastric uneasiness, and flatulence.
The secretion is deficient in hydrochloric acid, in many cases it may be
actually wanting (achlorhydria). Digestion is therefore slow, and the
appetite much impaired. Sometimes irregularity of the bowels is marked
by diarrhoea alternating with constipation, the former being occasionally
profuse. So common and so early is the appearance of such digestive
disorders as to give ground for the belief that they have an important
influence in inducing the anaemic condition ; and the fact that anatomical
changes are frequently found in the stomach of subjects of pernicious
ansemia has led some observers to ascribe the affection to atrophy of the
gastric glands. Jaundice is not common, and when present seldom
intense. Palpation reveals enlargement of the liver, with some tender-
ness over it. The spleen is rarely to be felt. Ascites may be present,
but never in large amount.
The mine, is generally fairly abundant, of normal or diminished
specific gravity, acid, and free from deposit. It is often pale, but even
in the course of the illness it may assume a high colour hardly consonant
with the anaemic state. The chief cause of this coloration was shown by
Hunter to be due to an excess of pathological urobilin, and the significance
of this ingredient is considerable.^ There may be an excess of indican,
and free iron has been observed by some (Finny). Uric acid is generally
in excess, but there is no constant change in the amount of urea.
Occasionally albuminuria is noted, but it is not a prominent feature.
Observers have noted the presence of many another abnormal constituent ;
according to Hunter, the presence of pathological urobilin, renal
epithelium, casts containing blood pigment, and increased excretion of
iron, is characteristic. There may be hsematuria.
The symptoms exhibited on the side of the nervms system have
received especial attention of late years since the discovery of definite
organic change in the spinal cord in cases of profound ansemia. The
functional disorders comprise irritability, a growing inability to fix
attention upon a subject, loss of memory, and often marked insomnia.
Headache is not prominent until the anaemia becomes extreme, when
there may be delirium also, or even more violent mental disturbance. In
some cases the end is ushered in by convulsions passing into coma;
in others a lethargy gradually deepens into coma. But the intellect
often remains unimpaired almost to the close, and death takes place from
mere exhaustion. The occurrence of convulsions and the appearance of
partial or complete hemiplegia, or monoplegia, denotes cerebral hsemdr-
rhage of greater or less extent. Sometimes the paralysis is so slight and
transient as to indicate that the haemorrhage must have been very small ;
in others a definite apoplectic seizure terminates the illness. The spinal
1 GowUand Hopkins, from examination of five cases, was unable to satisfy himself of tlie
presence of " patholo^cal " urobilin, and was incKned to attribute the spectroscopic
mdications to an admixture of urobilin and lisematoporphyrin -
530 SYSTEM OF MEDICINE
symptoms referred to above consist, in the main, in slight disorders of
motility, mostly ataxic in character, sometiSmes spastic ; and they have
been found associated with pronounced changes in the spinal cord. At
the same time some of these degenerative lesions have been met with in
cases that did not exhibit any disorder of function during life.
Morbid anatomy. — At the time of death the body appears, in the
majority of cases, to be fairly well nourished. The pallor of the surface
is striking, and petechias may be distributed over the lower extremities,
which may be somewhat oedematous. The panniculus adiposus is often
of a deep yellow colour, and the dark red tint of the muscular layers
contrasts with the exsanguine aspect of the skin. Some thin serous
effusion may be found in the peritoneal and other serous sacs. The
blood is thin and watery, and the clots in the cardiac cavities small and
pale. The blood serum has been observed to have a yellowish tint from
admixture with haemoglobin readily liberated from the corpuscles, and
even to stain the hands of the . pathologist. The specific gravity of the
blood is lower than normal; in one case it is stated to have been 1028
instead of about 1055. The microscopical characters of the blood have
already been given. The heart is generally well covered by epicardial
fat, and sometimes petechial haemorrhages may be seen on its surface.
The muscular substance is soft, flaccid, and of a tawny, brownish tint,
sometimes compared to that of a faded leaf. The musculi papillares,
especially of the left ventricle, are nearly always variegated by wavy
whitish streaks — the "tabby-cat striation" of Quain. Microscopically
the fibres are found to be in various stages of fatty degeneration, some
wholly converted into fatty granular and oily detritus, others with
accumulated fat granules around the muscle nuclei. The valves are
normal, but small areas of opaque white fatty degeneration may stud the
iutima of the aorta. Similar fatty degeneration has been found in the
arterioles and capillaries, leading often to their rupture in various parts
of the body. The lungs present no notable lesion ; they are, as are all
the viscera, very bloodless ; although mostly the lower lobes present some
engorgement and oedema, and there may be petechiae beneath the pleura.
Occasionally it happens that the disease attacks a subject who presents
some old caseous or cretified tubercle in the lung, and sometimes also an
intercurrent pneumonia terminates life ; but of course neither the old nor
the recent changes are essential. The stomach exhibits a striking pallor
of its mucous membrane, which may further show marked evidence of
atrophy of the glands, with or without excessive thickening of the sub-
mucosa. The liver is nearly always slightly enlarged, and fattily degener-
ated. In definite cases the outer zone of the lobules is pigmented by an
accumulation of free iron (hasmosiderin) within the cells and around the
capillaries. The presence of this substance is revealed by treating sec-
tions with sulphide of ammonium (not a very trustworthy test) or ferro-
cyaniJe of potassium, and its discovery by Quincke led to the hypothesis
of the disease that is now mostly adopted. The gaU-bladder contains
dark bUe. The spleen may be sliglitly enlarged, but often it is quite
PERNICIOUS ANMMIA 531
small ; in colour and consistence it varies, being often pale, sometimes soft,
or again rather indurated. In this organ, too, but never to so marked
an extent as in the liver, granules of ferruginous pigment have been met
with. The pancreas and suprarenals show no changes. The intestinal
plexuses of nerves and the great abdominal ganglia have been found to
exhibit evidence of degeneration. The mesenteric and other lymphatic
glands are not as a rule affected. The kidneys are smooth and pale, but
pigment granules have been found in the cells of the cortical tubules.
As regards the nervous system, there may be subarachnoid haemorrhage
OQ the surface of the brain. The brain itself is strikingly exsanguine.
It is instructive to note that although sinus thrombosis has been observed
in chlorosis, it has not been recorded in pernicious aneemia. Cerebral
haemorrhage, however, may be present. In the spinal cord, even in cases
which have not presented any symptoms of such disease during life, tracts
of sclerosis have been met with in the white matter ; they are irregularly
distributed, sometimes involving the whole of the posterior columns, to-
gether with the lateral and anterior, but generally sparing the nerve-roots
and the gray matter. Another change is that of miliary sclerosis or
minute haemorrhagic foci scattered irregularly throughout the substance
of the cord. Notable changes have been found in the marrow of the
long bones, consisting in a reversion to the foetal type of red marrow ;
when first met with, this conversion was thought to be distinctive, and no
doubt it indicates increase of the haemogenetio function ; but it is also
present in anaemia due to haemorrhage, and may be absent in the disease
under consideration.
Pathology. — The interpretation of the clinical and pathological facts
of so obscure a disease as pernicious anaemia could not fail to arouse
widespread interest, and the attempt to afford a rationaL explanation of
its origin has led to much speculation and to more or less thorough investi-
gation. There is no need to dwell further upon a matter already touched
upon in speaking of etiology, but it may be said that for coherence and
reasonableness of doctrine there has been no more satisfactory exposition
than that given by Dr. William Hunter in his numerous essays upon this
disease in particular and upon the subject of blood-destruction in general.
For, although in some respects it may be necessary to admit certain
modifications in his argument, seeing that some of its premisses are not
yet verified, yet it cannot be doubted that his contention for the
specificity of pernicious anaemia, as a disorder consisting in haemolysis,
affords so far a satisfactory explanation of the phenomena. It has
furtlier enabled us to eliminate from the category of pernicious ansemia
many anaemias which are strictly secondary ; closely as they may simulate
the primary disease in clinical features, blood changes, and visceral lesions.
Nor is it warrantable to include within the class such cases as those of
fatally progressive anaemia, associated with the presence of intestinal
parasites ; unless it can be shown that they depend on the same kind of
haemolysis that underlies the primary malady.
Pernicious anaemia, then, signifies a definite group of clinical and
S32 SYSTEM OF MEDICINE
pathological phenomena dependent upon a special form of blood-destruc-
tion, or haemolysis, induced by toxic agents absorbed from the gastro-
intestinal tract. The grounds for this conclusion may be briefly
summed up as follows : — (i.) There is abundant proof that haemolysis
does take place in this disease. This is shown by the condition of the
blood, its deformed and disintegrating corpuscles, the readiness with
which the haemoglobin escapes from them, and the abundance of micro-
cytes. (ii.) The presence of an excess of pigment in the liver, spleen,
and kidneys ; this pigment being in the form of iron granules very loosely
combined in the cells ; whilst the elimination of iron and occasional excess
of pathological pigments in the urine further support the haemolytic
view, (iii.) This haemolysis takes place within the area of the portal
circulation and not in that of the systemic ; as indicated by the condi-
tion of the spleen, the accumulation of the haemoglobin detritus (hsemo-
siderin) within the hepatic cells of the outer zone of the lobules, and by
the absence of haemoglobinuria. For Hunter's researches prove that
when haemolysis takes place in the general circulation haemoglobinuria
occurs ; but in pernicious anaemia the pigment, if eliminated by the
kidney, appears in the form of granules of iron pigment, or as an excess
of other pigmentary matter variously regarded as "pathological urobilin"
(Hunter, M'Munn) or as a mixture of " urobilin " and " hsematoporphyrin "
(Growlland Hopkins). Moreover, iron granules have been found in the
tubules of the kidney in renal casts and epithelia. (iv.) Such a dis-
integration of the blood can take place in the portal system (possibly
mainly in the spleen), as is shown by Hunter's experiments with such
haemolytic poisons as toluylendiamin. The source of this hypothetical
toxin is reasonably considered to be the gastro-intestinal tract, and that
it is of bacterial origin is almost equally probable.
The conception that has thus been framed of the nature of per-
nicious anaemia is rendered more convincing by the fact that in the
forms of anaemia which most nearly approximate to it — such as those
due to other toxic agencies, to prolonged and repeated haemorrhages, to
blood parasites as in malaria, to cancer, or to syphilis — so marked an
excess of iron in the viscera is never found, especially in the liver, as is
found in this disease. Thus Hunter gives 0'7 as the average percentage
of iron found by various investigators in the liver in pernicious anaemia,
as against 0"078 or 0'12 for other diseases; whilst the late Dr. Beavan
Eake found, from an examination of five cases of anchylostomiasis, that
in this affection (which so closely simulates pernicious anaemia as to have
led to the opinion that, like pernicious anaemia, it may perhaps depend
upon haemolysis in the manner peculiar to this disease) it was only 0"1
per cent. Dr. Eake, it is to be noted, adhered to the opinion that the
anaemia of anchylostomiasis solely depends upon the haemorrhages pro-
duced by the parasite from the intestinal wall.
At the same time, in the present state of knowledge it is impossible to
avoid the conclusion that a haemolytic process closely akin to that of
pernicious anaemia may occasionally intervene in the course of grave
PERNICIOUS ANEMIA 533
organic disease, and especially of chronic gastro-intestinal disease. If
this be so, however, it would be no longer correct to speak of such an
exceptional and, so to speak, accidental supervention of the pernicious
process as a "symptomatic" anaemia. The secondary affection should
rather be regarded as a complication than as a regular feature of the
original disease.
The view of the nature of an%mia alternative to that of increased
haemolysis — one, too, which in point of time preceded the promulgation of
the latter— is that of disordered haemogenesis, as suggested by the remark-
able reversion of the bone -marrow to its foetal condition originally
observed by Pepper and Cohnheim, and since veriiied by many other
observers. The significance of these changes has been materially affected
by the recognition of the part played by haemolysis in the disease, as
well as by the fact that they are not invariably met with, nor differ
in kind, if they do in degree, from the changes in the marrow which
ensue on anaemia experimentally produced by bleeding. It may be that
a place should be retained in nosology for a " myelogenic anaemia," but
if so it must stand apart from pernicious anaemia as now understood.
Whenever these marrow changes are met with side by side with the
characteristic hsemolytic features of pernicious anaemia they are more
likely to be of a secondary nature, indicating an effort on the part of the
haemogenetic organ to repair the waste that is in progress elsewhere.
And that the marrow should exhibit these changes in some cases and
not in others may not be more remarkable than that the spleen should be
swollen and apparently in an active state of haemolysis in some cases,
shrunken and inactive in others. The course of the malady suggests an
inconstant and variable haemolytic activity, and it may well be that this
is paralleled by varying degrees of haemogenetic action. In one of the
most recent and careful studies of these marrow changes in pernicious
anaemia the conditions obtaining in the several stages of the disease are
described ; the earlier changes are similar to those met with after haemor-
rhage, the later are characterised by great abundance of large nucleated
corpuscles peculiar to pernicious anaemia, and suggestive of a reversion
to the embryonic type. But both must be considered secondary to the
anaemic state (Muir). Dr. Muir is careful to add, however, that " whether
or not there are any cases of fatal anaemia, in which marrow lesion is a
primary factor, I am not prepared to say. The question ought to be kept
an open one, and in all such cases the condition of the marrow should be
carefully inquired into, along with any changes in other organs which
point to a process of blood-destruction."
There remains another aspect, ably described by Prof. Stockman, in
which pernicious anaemia has been regarded which, if correct, would de-
throne the disease from the position which it has attained, and relegate
it to that of a sequel or result of any form of anaemia of whatever origin.
It is based on the fact that the ansemic state, if long continued, provokes
fatty degeneration of the walls of the blood-vessels, and thus promotes
a liability to multiple haemorrhages, which in their turn intensify the
S34 SYSTEM OF MEDICINE
anaemia and tlie proneness to bleed ; and further, that the effects of larger
haemorrhage are pathologically indistinguishable from those which in
anaemia take place within the tissues and organs. It cannot be denied
that such an explanation of the nature of pernicious anaemia, if substan-
tiated, would get rid of many of our -present difficulties, for it bridges
over the gap between the protopathic and deuteropathic forms of pro-
gressive anaemia by referring them all to the same immediate cause. Yet
as Addison could find no adequate cause for the production of "idio-
pathic " antemia, so too is it difficult to believe that the capillary haemor-
rhages which characterise pernicious anaemia are in the majority of cases
sufficient to induce the extreme degree of oligocythaemia, and the indubit-
able evidences of haemolysis which the disease exhibits. At the same
time, Stockman's thesis is one which deserves most careful study,
for he does not hesitate to deal with the whole of the pathological
and chemical evidence put forward by the advocates of the haemolytic
doctrine.
This doctrine also assumes the operation of a specific toxic agency ;
and it is interesting to note that those who have studied the degenerative
changes in the spinal cord, which are apparently more common in per-
nicious anaemia than might be supposed from the clinical phenomena,
believe also that these changes are best explained by a toxic influence,
although some of them are manifestly the result of capillary haemor-
rhages. In accordance with the prevalent views upon the subject, the
nature of pernicious anaemia is expressed in the classification of anaemic
disorders put forward by Grozier Griffith and Musser. The anaemias
are divided by them into two main groups — the cytogenic and the non-
cytogenie. Of the latter there are two classes — the haemolytic and the
oligocythaemic. The hcemolytic comprise — (i.) Pernicious anaemia; (ii.)
other toxic anaemias ; (iii.) chlorosis ; (iv.) parasitic antemias (some forms).
The oligocythcemic include — (i.) Parasitic anaemias (some forms) ; (ii.) post-
haemorrhagic anaemia ; (iii.) anaemia from loss of albumin ; (iv.) anaemia
from malnutrition. Such a division is only provisional, but it recognises
at least that pernicious anremia is entitled to a distinctive place in
nosology.
Diagnosis. — The diagnosis of pernicious anaemia does not rest
upon any very certain basis, for although, generally speaking, this
diagnosis may be justified in the presence of a case of progressive
anaemia, arising insidiously, without adequate discoverable cause, and
exhibiting the characteristic changes in the blood already described, it
must yet be borne in mind, first, that sometimes an adequate cause
does exist, but cannot be discovered, and, secondly, that the blood
changes are not in themselves pathognomonic. At the same time, when
it is considered that the clinical phenomena may be simulated by pro-
found anaemia of secondary origin, no endeavour should be lacking to
ascertain whether there is or is not some underlying disease. The task
is rendered easier as the number of conditions which are known to give
rise to so grave an anaemia are not large. The most likely are malignant
PERNICIOUS ANEMIA 535
disease, especially of the stomach, and advanced syphilis. In such cases
attention to the course of the symptoms and the history of the patient
may assist in effecting a separation. The anaemia which is sometimes
so marked a feature of chronic parenchymatous nephritis is seldom likely
to he mistaken for pernicious anaemia, in view of the predominance of
definite signs of the renal affection. Malignant endocarditis is more
likely to be mistaken for pernicious ansemia, for here anaemia may be
pronounced, whilst the cardiac murmur, and even the pyrexia and the
cutaneous or other haemorrhages, may be looked upon as indications of
pernicious anaemia. But an examination of the blood will determine the
true character of the aifection. Purpura and haemophilia are hardly
likely to be mistaken for pernicious anaemia.
From chlorosis, which shares with pernicious anaemia the title of a
protopathic anaemia, the differences are fairly well marked. Between
the two affections the clinical diagnosis, apart from considerations of age
and sex, is to be made by examination of the blood. In chlorosis
the reduction in haemoglobin is always vastly greater proportionately
than the reduction in the number of corpuscles ; the chlorotic blood does
not show such marked evidence of poikilocytosis, or so many microcytes
as that of pernicious anaemia. More difficulty may be experienced in
discriminating the anaemias due to intestinal parasites, such as the
anchylostomum or the bothriocephalus, for there are no distinctive
features either in the blood or in the symptoms which would serve to
distinguish them. It is possible that the urine might afford means for
the diagnosis, but it is by no means certain that all cases of pernicious
anaemia exhibit that excretion of " pathological urobilin " which is held
to characterise the affection. In fact, nothing but a thorough examina-
tion of the faeces for the detection of the ova of these parasites can
suffice to exclude them, and the fortunate issue of anthelmintic treat-
ment may clinch a diagnosis so made. From splenic anemia the
diagnosis is to be made by the marked and progressive enlargement of
the spleen in this disease, as well as by the comparatively small degree
of oligocythaemia. In leukaemia the blood condition is manifestly the
diagnostic criterion.
Prognosis. — The outlook in a case of established pernicious anaemia
is very grave. It would, however, be too much to say that it must
necessarily end fatally, for cases are recorded where the patients were
restored to health and remained in health for years afterwards. It is
nevertheless only too true that what has often been regarded as recovery
has proved to be but a temporary rally, however remarkable in degree ;
the oligocythaemia almost disappearing and the distressing symptoms
entirely passing away. Such apparent recoveries often, after an interval
of months, give way to relapse, and the end may come in the first or
some subsequent recurrence of the illness. This character is so common
a feature, after more than one method of treatment, as to raise doubts
whether the rally is wholly attributable to the latter, whether, that is,
there may not be a " relapsing " form of the disease.
536 SYSTEM OF MEDICINE
Treatment. — Pernicious anssmia then, as its name implies, tends or-
dinarily to run a downward course, often uninfluenced by any treatment
that may be adopted ; and frequently, too, when marked improvement has
followed the use of certain remedies, a relapse has occurred in which the
same means are no longer successful. As a recent writer (Dieballa) points
■ out, it may be that much depends on the amount of recuperative power
still residing in the blood-forming organs. If the blood-destruction can
be arrested, or if the hsemogenetic function can be stimulated, then there
is hope that the blood will be restored to the normal by the natural
power of regeneration. So far as can be judged, most of the therapeutic
efforts that have been attended by success, temporary as this may have
been, have had for their aim the second of these two conditions ; but
treatment based upon the theory of intestinal intoxication has not been
wanting.
The general principles of the treatment of ansemia naturally apply in
this disease with especial force. Eest, bodily and mental, and the avoid-
ance of excitement are not only essential, but are often spontaneously
sought by the patient, who is disinclined for exertion of any sort.
Removal to pure air and healthy surroundings, when the conditions of
the patient's ordinary life are without these benefits, are too obvious to
require mention ; whilst for the well-to-do much benefit may accrue, if
the disease be not advanced, from a winter sojourn in a more equable
and brighter climate than this country affords. The matter of diet
is one of the greatest importance. The anorexia, nausea and tend-
ency to diarrhoea, which often mark the early stages, make this
a matter of difficulty. Experience proves that nitrogenous foods are
ill borne, and the dietary therefore must in the main be limited to
milk, vegetable and farinaceous foods. It may be necessary to have
recourse to peptonised and other easily digestible preparations. "When
tolerated, pounded raw meat or meat juice and bone-marrow may be
taken in small quantities, on bread or toast, with advantage. But the
disinclination for food of any kind may be so great as to render it very
difficult to supply adequate nourishment. Small quantities of alcohol in
the form of claret or burgundy may prove of value as aids to digestion.
In a disease which is primarily dependent on destruction of the
elements of the blood, haematinic remedies may reasonably be adopted.
It is remarkable, however, that the chief of these — iron- — is in the great
majority of cases quite inoperative. In this respect the difference between
chlorosis and pernicious ansemia is so striking as to suggest at once that
the pathogeny of these two forms of primary ansemia is totally different ;
evidence of the inefiicacy of iron in the latter is probably to be found
in the fact that the system still retains its iron; in greater amount,
indeed, than can be properly utilised. At the same time, there are a few
cases on record in which iron seemed to do good ; the free and frequent
administration of the perchloride has been especially advocated. It is
possible, however, that the value of this preparation may not depend
on the ferruginous element {wde p. 515).
PERNICIOUS ANALMIA 537
Very different is the experience of the value of arsenic, the intro-
duction of which in the treatment of pernicious anaemia we owe to Dr.
Byrom Bramwell. Administered in gradually increasing dose, it is
generally well tolerated by these subjects, and although by no means
invariably successful in causing improvement, yet this does often follow,
and can hardly be ascribed to anything else than the specific action of
the drug upon hsematogenesis. On the other hand, if there be a natural
tendency in the disease towards a temporary rally, it is difficult to
estimate the precise share in this which is to be ascribed to the action of
the remedy. At the same time, the improvement, when it does take
place, follows too closely upon the adoption of the treatment to afford
room for scepticism. Although of all remedies arsenic has proved to
be most often followed by manifest improvement, yet even in cases
where the benefit has been striking, relapses have occurred sooner or
later ; and it often happens that on the second occasion the drug seems
to have lost its efficacy, and other measures have to be devised. The
arsenic may be given in the form of Fowler's solution, or of the liquor
arsenici hydrochloricus, beginning with doses of 2 to 3 minims, which
are gradually increased to 18 minims, according to the tolerance of the
subject. The arseniate of iron pill is a convenient form. It is well
to continue the drug for some time after the signs of improvement are
manifest.
Cases of recovery have also been recorded after the use of antiseptic
drugs, such as salol, ^-naphthol, salicylate of bismuth, and the like;
their efficacy being ascribed to their direct antagonism to the supposed
fermentative processes which yield a haemolytic poison in the intestine.
A notable instance of rapid recovery, which, moreover, was sustained for
a long time, has been recorded by Dr. Gibson; it followed the pre-
scription of ^-naphthol, after the failure of arsenic. In another case,
where for nearly four months a variety of remedies had been vainly tried
in turn — namely, ferratin, bone - marrow, oxygen, arsenic, iron, and
quinine— the administration of salol (continued with occasional inter-
missions for three months) produced a restoration in the corpuscular
richness which seemed to have been due to the change of remedy
(Dieballa). ^ ^
Other isolated cases of similar good results from this line of practice,
including that of lavage of stomach and intestinal irrigation, have been
recorded, although not seldom the same methods have led to no good
result.
Indeed there are few maladies in which the results of treatment are
more capricious. It is impossible to prophesy in any given case whether
any given remedy will be useful or not. Dieballa, in commenting on
the case of recovery after the administration of salol, points out that the
comparatively, slight diminution of leucocytes and the persistence of a
normal proportion of eosinophilous cells in the blood, as shown in that
case, may afford a clue to the integrity of the blood-forming organs, and may
justify expectation of adequate recovery if the hemolysis can be arrested.
538 SYSTEM OF MEDICINE
We have yet to discover the reasons for the frequent failure of a remedy
in one case and for its success in another. Thus the success attending the
use of red marrow, introduced by Prof Fraser, has been repeated by some
physicians, but never attained by others. A like diversity of experience
is to be found in the records of cases treated, often, no doubt, in the last
resort, by blood transfusion or saline injections. Excellent and even
remarkable results of transfusion have been published — amongst others
by Quincke, Brakenridge, and Affleck — results which often seem quite
out of proportion to the amount of blood injected ; as if the healthy
serum had exerted some specific effect, either in stimulating haemogenesis
or, as some think, possibly by exerting an antitoxic influence upon the
(assumed) hsemolytic virus. Yet in very many cases this measure has
proved futile.
Thus in pernicious anaemia, where the therapeutical results are so
varied and conflicting, it is impossible to frame any uniform plan of pro-
cedure ; and the inconstancy of therapeutical results may be taken as
evidence that there is much yet to learn of the intimate pathology of the
disease. All that can be done in the presence of the progressive blood-
destruction is to make trial of each of the several remedial measures
that have been found at times to be efficacious ; of these I would place
first the administration of arsenic, and next to it that of intestinal
antiseptics.
Sidney Coupland.
REFERENCES
1. Addison, T. On the OonstUutional and Local Effects of Disease of the Suprarenal
Capsules, 1855. See Collected Works (New Sydenham Society). — 2. Affleck, J.
Edin. Med. Jour. 1892. — 3. Andral. Clinique midicale, t. iii. 1823. — i. Banti, G.
Lo Sperimentale, 1881. — 5. Babolay. Med. Times and Gaz. 1851. — 6. Biermer.
Correspondenzhl. f. Schweizer Aerzte, 1872. — 7. Bowman. Brain, xvii. 1894. — 8. Braken-
ridge, J. Edin. Med. Journ. xxxviii. 1892. — 9. Bramwell, Byrom. Edin. Med.
Journ. 1877. — 10. BuER. University Med. Mag. 1895. — 11. Channing, W. "Notes
on Anaemia, particularly in connection with the Puerperal State, and with Functional
Disease of the Uterus," New England Quarterly Jov/mal of Medicine, 1842. — 12. Cohn-
HBIM, J. Virchow's Archiv, Ixviii. 1876. — 12a.. Copeman, S. M. St. Thomas's
Hospital Reports, vol. xx. — 13. Combe, J. Trans. Med.-Chir. Soc. Edin. 1823. —
14. Craig, J. Dublin Journ. Med. Sc. 1897. — 15. Dibballa. Zeitschr. f.
klin. Med. 1896. — 16. Eichhobst. Die progressive perniciose Andmie, 1878; also
Lehrb. spec. Path. u. Therap. 1885. — 17. Eisbnlohr. Arch. f. klin. Med. xx. — 18.
Fbnwick, W. Lancet, 1877, ii. — 19. Finny, J. Brit. Med. Journ. 1880. — 20. Frasee.,
T. R. Brit. Med. Journ. WSi, i. — 21. Gardner and Osler. Gamada Med. Journ. W17.
— 22. Gibson, G. A. Edin. Med. Journ. 1892 ; also International Clinics, vol. iii. 3rd
series, 1893. — 23. Griffith, Crozier. Art. in Keating's Cyclopaedia of Diseases of
Children, iii. 1890 (contains full references). — 24. Gusserow. Archiv f. Gynacologie,
1871. — 25. Habershon, S. 0. Lancet, 1863. — 26. Hall, Marshall. Principles and
Theory and Practice of Medicine, 1844. — 27. Henry, F. P. Ancemia. Philadelphia,
1887.— 28. Hopkins, F. Gowlland. Guy's Sosp. Rep. 1. 1894.— 29. Howard, R. P.
Trans. Centennial Med. Congress, 1876. — 30. Hunter, W. Practitioner, 1888 and
1889; Lanj:et, ii. 1888. — 31. Immbrmann. Deutsehes Archiv f. klin. Med. Bd. xiii. ;
also in Ziemssen's Sandbuch, xiii. 1875. — 32. Kinniotjtt. Amer. Journ. Med. Sc.
1887. — 33. Laaoiie. Die Andmie. Christiania, 1887. — 34. Lbebrt. Handb. der allg.
Path. u. Therap. 1876. — 35. Lbpine, R. Remie mensuelle de mid. et de chir. 1887
(full bibliography). — 36. Limbeck. Cfrundriss einer klin. Path, des Blutes, 2te Aufl.
Jena, 1896. — 37. Lichtheim. Munchener med. JVochenschr. 1890. — 38. Mackenzie, S.
SPLENIC ANEMIA 539
Lancet, 1878, ii. ; also Lettsomian Lectures on Aniemia, Trans. Med. Soc. Land. xiv.
1891.— 39. MoTT, F. W. Lancet, 1889, i. ; also Path. Trans. 1889 ; also Practitimer,
1890. — 40. Mum, E. "On Changes in Bone-Marrow," Journ. Path, and Pact. ii. 1894.
— 41. MuLLEE,, H. JDie progressive pernicioseAn£mie. Zurich, 1877. — 42. Mussbe, J. H.
On Idiopathic Anoemia. Philadelphia, 1885. — 43. Neumann. Berlin, klin. Wochenschr.
1877. — 44. OsLER, "W. Art. in Pepper's System of Medicine, iii. 1885 (full references),
and many other contributions. — 45. Pepper, "W. Amer. Journ. Med. Sc. 1872. — 46.
PuiiSEK. Lublin Journ. Med. Sci. 1877. — 47. Pyb-Smith, P. H. Virchow's Archiv,
Ixv. ; also e«2/'s 5"osp. Jfep. xxvi. 1880 (full bibliography). — 48. Quincke. "Ueberper-
nioiose Anamie," Volkmann's Sammlung, No. 100 ; also Deutsches Archiv f. Min. Med.
1877. — 49. Rake, Beavan. "On Percentage of Iron in Ankylostomiasis," Joam.
Path, and Pact. iii. 1894.— 50. Russell, J. Risien. Brit. Med. Journ. 1894, i.— 51.
Russell. Brit. Med. Journ. 1889, i.— 62. Stockman, R. Brit. Med. Journ. 1895, i.
—53. Tayloe, P. Guy's Eosp. Reports, 1878 ; also Brit. Med. Journ. 1896.-54.
Taylor, J. "On Nervous Symptoms and Morbid Changes in the Spinal Cord in certain
eases of Profound Anaemia," Med.-Chir. Trans. Ixxviii. 1895.— 55. White, W. Hale.
Guy's Eosp. Reports, xlvii. 1890, also International Clinics, vol. i. 4th ser. 1894. — 56.
WiLKS, Sir S. "Cases of Idiopathic Patty Degeneration," Guy's Eosp. Pep. 1857.
The above select list is by no means exhaustive of the very copious literatcire of the
subject, which of recent years has been greatly added to. Nor does it take account
of the numerous articles and monographs upon the various forms of parasitic ansemia,
notably anchylostomiasis and bothriocephalus anaemia.
s. c.
SPLENIC ANEMIA
There is a form of profound anaemia, progressive in character, ending
fatally, generally of no long duration, associated with great enlargement
of the spleen, but without leucocytosis or enlarged glands. Splenic
anaemia is the name by which the disease is best known in this country ;
but it has also been called splenic cachexia, splenic pseudo-leucmmia-,
lymphadenoma splenicum, and spleno-megalie primitive ; under the last name
chiefly it is described in French literature.
To Banti, who wrote in 1882, is due the credit of drawing special
attention to this malady. In 1891 Bruhl published an exhaustive
article on the subject, bringing together all the cases that he was able to
find recorded up to that date. The other contributions consist for the
most part of accounts of isolated cases.
The total number of cases recorded is still small, and probably does
not exceed thirty, including the fourteen cases upon which Bruhl's paper
was founded.
Symptoms and signs.— The disease may be divided into three
stages : in the initial stage the symptoms are those of extreme anaemia,
with great loss of muscular power and some wasting of muscle ; though
usually without emaciation. As in this stage the disease presents no
specific features it can rarely be recognised. The second stage is
characterised by progressive enlargement of the spleen, and by attacks
of severe pain in the splenic region ; the anaemia is more profound, the
54° SYSTEM OF MEDICINE
loss of strength is extreme, and the patients are liable to repeated attacks
of bleeding, especially from the nose ; the temperature is now usually
raised and of hectic character, reaching 102° or more in the evening. It
is in this second stage that the disease is first recognised.
In the last stage the condition is one of progressive asthenia which
ends in death ; there is in it nothing especially characteristic.
Throughout the disease most of the symptoms present but few
peculiarities, for they do not diflfer from those which occur in any form of
profound ansemia. Thus there is general pallor and loss of strength, and
great weakness and dilatation of the heart with its consequences ; namely,
shortness of breath, palpitation and pain, all made worse by exertion,
together with the usual hsemic murmurs. The pulse and respiration are
readily accelerated, especially on effort or excitement ; and there may be
some cedema of the feet.
The haemorrhagic condition in the latter stages is only remarkable in
that it is more than usually pronounced.
This form of anaemia is sometimes said to be of the chlorotic type ;
as there is little or no emaciation, and the reduction in the haemoglobin
is greater than the reduction in the number of red blood cells would
account for.
With a disease so rare as splenic anaemia the best description of the
disease will be an account of a case : —
A man aged thirty-six presented himself with extreme anaemia, raised
temperature, and a large spleen. The case looked like one of splenic leuco-
cythsemia, but examination of the blood showed no increase of white cells.
The patient had been well till twelve months before he came under
observation, when a tooth had been extracted ; this operation was followed by
profuse bleeding, which lasted several days : from that time onwards he became
gradually weaker and tMnner, and suffered from repeated epistaxis.
The patient was extremely pale, cachectic, and somewhat sallow ; his cheeks
were flushed, and the temperature, on the evening of admission, reached 103°.
He was constantly spitting up a little blood, which came from the back of the
pharynx or from the nose. The respiratory organs were normal. The heart
was somewhat dilated, with a blowing, systolic murmur audible over the whole
precordium and loud at the pulmonary area ; there was increased pulsation in
the vessels of the neck ; the pulse was 96, of low pressure, but fair volume.
The liver was somewhat enlarged, extending from the upper border of the
fifth rib to an inch and a half below the costal arch.
The spleen was greatly enlarged, and extended from a point four inches
above the costal arch downwards to an inch above the anterior spine of the
ilium on the left side. It was smooth on the surface, moved freely in respira-
tion, but was tender to touch.
The urine was normal
The left pupil was a little larger than the right. Ophthalmoscopic examina-
tion showed the retinae to be normal.
There was no tenderness of the bones and no enlargement of lymphatic
glands.
On examination of the blood the red corpuscles were found to number
SPLENIC ANMMIA 541
2,055,000, and the white corpuscles 50,000, chiefly lymphocytes ; the haamo-
globin was only 25 per cent of the normal. There was no poikilocytosis or
other changes in the cells, red or white.
Three weeks later another examination of the blood was made. The red
cells had fallen to 1,900,000, while the white corpuscles numbered 58,000 ;
the anaemia had progressed and the strength failed, there had been occasional
attacks of abdominal pain, sometimes in the splenic region, sometimes more
diffuse, but not very severe ; the temperature had remained of a hectic character,
rising to about 103° every evening, as shown upon the chart, and the patient
had one or two attacks of epistaxis. The blood was examined for micro-
organisms, and none found.
A week later the eyes were examined again, and a large haemorrhage was
found in the left retina.
A few days later the patient became very hoarse, dyspnoea increased
rapidly, oedema of the larynx was diagnosed, and tracheotomy performed with
great relief. The temperature remained high, and after the operation reached
105°. There was a good deal of oozing from the incision after the operation,
and five days later a sudden haemorrhage took place from the wound ; blood
was sucked into the trachea, and the patient was suflFocated.
The necropsy showed a large spleen weighing 76 oz. ; it contained one
small infarct. On microscopical examination the Malpighian bodies were seen
to be much diminished in size and badly formed, and there was a slight general
increase in the trabecular tissue. • The liver also was enlarged, weighed 93 oz.,
and was slightly cirrhotic. The heart was dilated and weighed 12 oz. ; all
its cavities contained post-mortem clots ; there was a small vegetation, as large
as a pea, on one of the aortic valves. The muscular substance was not fatty.
The larynx was still somewhat oedematous.
A full account of this case is given in the Transactions of the Medical
and Chirwgical Society, vol. Ixxix.
Williamson's case is also an interesting one to compare wi.th that just
recorded : —
It occurred in a lad aged nine who, for two years, had been growing
increasingly pale and anaemic, and had suffered for the last twelve months from
fortnightly attacks of epistaxis. He was extremely ansemic and had a very
large spleen. The examination of the blood was as follows : red cells,
3,540,000 ; white, 4000 ; haemoglobin, 22 per cent.
Four months later the red cells were reduced to 2,510,000, white 2000.
A month later the following report of the blood was made. There were a
number of poikilocytes, no eosinophil cells, no large mononuclear or granular
cells, but a slight increase of lymphocytes. The temperature for the last six
months of life was very irregular, with marked daily oscillations reaching to
101° and 102° at times. The patient died with an attack of acute peritonitis.
The necropsy showed a very large spleen weighing 40 oz. ; the liver
reached two. inches below the ribs and weighed 44 oz. There was a small
serous effusion in the pericardium, and some recent vegetation's on the mitral
valve. A small ulcer was found in the small intestines, which had perforated
and caused purulent peritonitis.
In the spleen the fibrous trabeculse were increased in thickness, there was
542
SYSTEM OF MEDICINE
an enormous number of large nucleated cells eact containing several red blood-
cells. The Malpighian bodies had undergone fibroid change and the lymphoid
cells were few. There was a slight iron reaction in the fibrous trabeculse and
in the Malpighian bodies, but none in the spleen pulp. Micro-organisms were
looked for and none found.
The liyer showed a little increase of connective tissue, and gave a very slight
iron reaction.
The bone-marrow was dark purple-red in colour, and showed a marked
absence of fat. It contained large cells enclosing several red blood-cells, as in
the spleen.
With these general remarks we may now pass on to the review of
the more special features of the disease.
The affection occurs with much greater frequency in men than in
women; thus, out of 24 cases 19 occurred in men and 5 only in women,
that is, 4 males to 1 female.
In respect of age the affection seems to be fairly equally distributed
through all the age -periods of adult life; thus, of 22 cases 13
occurred between the ages of 20 and 50, and these were fairly equally
distributed within this period. Cases, however, occur in children and also
in old persons ; the youngest on the list was aged 9, and the oldest 72
years.
In infancy and very young childhood I do not know that there is
any undoubted case on record ; and, although anaemia and large spleens
are by no means uncommon in these early years of life — cases which
have been described by some virriters under the name of splenic anaemia
— still a review of these cases and the course they run shows, I think,
that we have to deal in them vyith disease of an entirely different kind.
The, Blood. — The blood shows no pathognomonic changes. The
condition is simply that of profound anaemia. The red cells are
diminished to one-fourth their normal number or less, and their form is
preserved, though they are a little reduced in size ; usually there is no
poikilocytosis. The cells are poor in hsemoglobin, which is reduced to
one-quarter or one-sixth, and the loss is far in excess of the diminution
of red blood cells. Occasionally there is a slight increase in the white
cell, but not more than the fever or some intercurrent malady would
account for. As the disease advances there is a continuous reduction
in the number of red cells, as is shown in the following scheme (taken
from Dr. F. Taylor's paper): —
Red OeUs.
White.
Hsemoglobin.
Sept.
27
3,000,000
no increase
35 per cent
Oct.
4
2,600,000
1 to 300
35 „
,^
17
2,400,000
30-35 „
J,
25
2,200,000
increased
27
1,550,000
1 to70
Nov.
11
1,370,000
1 to 28
28
SPLENIC ANEMIA S43
The blood has been carefully examined in several instances for micro-
organisms, microscopically as well as by cultivation, but without success.
In many of the cases, especially those which were recorded some
years ago, the blood examination was not as systematic as it would be in
the present day. In my own case it was made under the supervision of
Professor Kanthack, and good accounts of the blood are also given in the
cases described by Williamson and Taylor.
Williamson's case is peculiar in the fact that there was poikilocytosis,
which, as already stated, is usually absent.
With reference to the increased number of leucocytes which is some-
times observed, especially where the temperature is high, it must be
remarked that the increase is chiefly due to lymphocytes ; that there is
none of the changes in the eosinophile and other cells which are character-
istic of leucocythffimia, and, finally, that the increase, being due in great
measure to the extraordinary diminution in the number of red blood
cells, is rather relative than absolute.
The Spleen. — The spleen is considerably enlarged and tender, and the
surface usually feels smooth ; but sometimes it may be uneven. Signs of
local peritonitis in the splenic region may be present, or of left basic
pleurisy, in both cases due to inflammation spreading from the spleen.
Some general peritoneal effusion has been also met with.
The spleen may extend beyond the umbilicus and as far as the crest
of the ilium, and be of considerable weight, as will be further described
under the morbid anatomy. The spleen is observed, as the case pro-
gresses, to increase in size, especially during the exacerbations; but
occasionally between the attacks it seems to become for the time smaller.
The recurrent attacks of pain in the splenic region, apparently due to
peri-splenitis, are often the cause of very great suffering.
The Liver.— The liver is often somewhat enlarged also, and may
extend, as in the case described, from the fifth rib in the nipple line to
an inch or two below the costal arch. It is sometimes associated with
slight jaundice, and there may be some pain felt in this region from time
to time.
The Digestive system. — The digestion /is considerably disturbed and the
appetite. lost. There is a good deal of nausea and sometimes obstinate
vomiting; this may occur in such paroxysmal attacks as almost to
constitute crises, and they often coincide with attacks of abdominal
pain. Constipation is usually troublesome ; but occasionally diarrhoea is
present, and this may be almost dysenteric in character, with tenesmus
and discharge of bloody mucus : in one or two instances there has been
free hsemorrhage from the bowels.
Hcemorrhages.—The tendency to bleeding is pronounced : the haemor-
rhages are usually of slight degree and of the nature of oozing ; but they
frequently recur, are very difficult to control, and add greatly to the
anaemia. Profuse hsemorrhages from any part are uncommon, but they
are recorded as occurring both from the stomach and from the bowel, or,
as in my case, from a wound ; in each instance they proved fatal.
544
SYSTEM OF MEDICINE
Epistaxis is very frequent and usually one of the earliest symptoms.
Thougli rarely profuse, it is of importance on account of its frequent
occurrence : it may, however, be so severe as to require plugging of the
nares. Oozing from the gums, again, is by no means uncommon, and
it is most difficult to check.
Haemoptysis and hsematuria have been met with also, but they are
rarer than other forms of haemorrhage.
From the gastro-intestinal organs haemorrhage is rare, and, if in any
large amount, it is probably associated with some secondary lesion. A
case, however, is recorded by Dr. Douglas Stanley, in which, although
profuse and fatal hsematemesis took place, no lesion in the stomach was
found after death ; in another case, however, a gastric ulcer was present.
Miiller records a case of fatal haemorrhage from the bowels, and there an
ulcer was found in the small intestines.
In the skin small petechias on the lower limbs are common, especially
in patients who are not in bed ; but they are of no special significance.
A purpuric eruption of greater degree than this is not described.
Into or behind the retina haemorrhages may occur, no doubt, as they
do in other forms of anaemia; but I do not know any instance of it
except that which I have described.
The Temperature. — Bruhl states that fever is unusual, but in many of
the recorded cases the temperature reached a considerable height. It
has been of the nature of an irregular hectic, rising even to 103° or 104°
every evening (cf. Chart).
IflQnth.
November.
December.
January 1895.
Day.
26
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=
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Chart 5, — Maximum (evening) and minimum (morning) temperature daily.
It is probable that something depends upon the stage which the
disease has reached ; that in the early stages the temperature may not
be raised, or be even subnormal, while in the later stages, when the
disease is actively progressing, it may be high.
At any rate the rise of temperature, when it occurs, appears to be
part of the disease, and not to be connected with any complication.
The nervous system yields no special symptoms.
Urinary changes are indefinite and vary much, but sometimes albumin
is present in small amoimt.
The circulatory system presents only such changes as are common to
all forms of anaemia.
SPLENIC ANMMIA 54S
In the shin, pigmentary changes have been described, but as in the
majority of these cases arsenic had been administered in large doses and
for some time, they were very probably due to this drug.
Morbid anatomy. — The general pallor of the skin and of all organs,
the flabbiness of the muscles, the dilatation and degeneration of the
heart are common to all forms of anaemia.
The panniculus adiposus is usually well preserved ; and in this re-
spect— namely, in the absence of marked emaciation — the body contrasts
with that of malignant disease of the spleen, a still rarer condition, a case
of which, however, has been recorded under the name of splenic anaemia.
The Spleen. — The most obvious morbid change is the enlargement of
the spleen. This organ may be 12 inches long or somewhat more, and
may weigh from 2 lbs. to 7 lbs. It is firm, reddish brown in colour, with
well-marked notches and, occasionally, irregularities on the surface.
It is surrounded by a thickened capsule, which may be adherent either
to the diaphragm or to the parts about. On section it looks as if
there were a general hypertrophy of the organ ; but occasionally there
are one or two haemorrhagic infarcts in it. The surface of the section is
dry and yields little juice ; it shows grayish streaks or fine granulations ;
the former, on microscopical examination, prove to be thickened trabeculae,
the latter fibrotic Malpighian corpuscles. The Malpighian bodies are
stated, in many of the cases, to have been the seat of marked changes,
the central artery being thickened, the corpuscle shrunken and shrivelled,
and sometimes surrounded by a capsule of fibrous tissue. With
the thickening of the trabeculae there has been great disappearance
of the spleen cells and dilatation of the veins. In Williamson's case
many nucleated cells, each containing six to ten red blood-cells, were
found in the splenic pulp; but in the majority of cases.no special changes
are present in it.
The lesions In the spleen then appear to be : (i.) fibrosis of the organ ;
(ii.) disappearance of the pulp ; and (iii.) the cirrhosis and atrophy of the
Malpighian bodies. This last is regarded as the characteristic and
most important lesion, and is the exact opposite of the state found in
leucoeythaemia, in which disease the Malpighian bodies are, as a rule,
hypertrophied.
The Uver is slightly cirrhosed and is much pigmented. The cells are
misshapen, atrophied, and often granular. The iron reaction is usually
absent ; it is only described as present in Williamson's case, and then it
was insignificant in degree.
The pancreas also; in some cases, has been found indurated ; but this
lesion is not constajit, and probably, therefore, stands in no direct relation?
to the disease.
The lymphatic glands are normal.
The bone-marrow also is usually normal ; but in one or two instances
it has been described as red and infiltrated with leucocytes.
The heart is dilated, the muscular substance flabby and occasionally
fatty. In one or two cases minute vegetations have been found upon the
VOL. V 2 N
546 SYSTEM OF MEDICINE
valves ; as in my own case, in Williamson's, and in Striimpel's. In con-
nection with these vegetations may be mentioned the infarcts which have
been found now and then in different organs, notably in the spleen and
in the kidneys.
These vegetations and infarcts deserve attention because undue
significance has been attached to them. They are indeed absent in all
the recorded cases except those which I have mentioned ; and in these
they were obviously accidental and formed no essential part of the
disease.
When haemorrhage has occurred during life the traces of it will be
seen after death ; but, besides this, haemorrhages of small size, petechise
for the most part, may be found very widely distributed in many parts of
the body — in the lungs, pleura, pericardium, and even in the brain ; but
these, again, are of no special significance, for they are found in all cases
of profound anaemia in which the hsemorrhagic tendency has been well
marked. For the most part, no doubt, they arise shortly before death.
Pathogeny. — That these cases of anaemia form a definite clinical
group must, I think, be regarded as fully established. The cause or
pathogeny of the disease is hitherto a matter of hypothesis and opinion.
In the second stage, when the spleen is enlarged, and especially when
fever is present, the cases bear a close clinical resemblance to many
septic diseases, and especially, perhaps, to some forms of malignant ague.
■This would suggest that some parasite or septic organism is present in the
blood. Careful examinations, however, both of the blood and of the
spleen, have been made and have proved negative. In my case the
results were negative, as they were also in two cases investigated by
Sciola and Carta. In one of them, that of a girl aged 13, injections
were made in the spleen of different animals with blood from the spleen
of the patient, and after removal of the spleen with splenic substance ;
in all cases without result. In another case, that of a woman aged 29,
cultivation experiments were made with the extirpated spleen on different
media without result.
So far, then, as our present knowledge goes, bacteriological investiga-
tions have yielded no new facts.
The enlargement of the spleen observed during life, standing in close
relation as it does to the severity of the disease and the peculiar morbid
appearances discovered after death, have suggested that the disease is
directly due to the affection of the spleen itself ; that is to say, to the
peculiar atrophy of the Malpighian corpuscles. So far, however, the
number of cases is too small to determine whether "the peculiar changes
■ described in the spleen are constant, and we must wait until this is
established before we found a hypothesis upon such a pathological basis.
Complieations. — The complications may be divided into two groups :
first, those which are obviously accidental, and, secondly, those which
stand in some possible relation to the disease itself.
In the first group we have instances of death produced by pneumonia
and by bronchitis.
SPLENIC ANMMIA 547
In the second group may be placed peritonitis or abscess in tte
region of the spleen, left -sided pleurisy perhaps, and the severe
haemorrhage from the stomach or intestines which has been recorded in
a few cases.
The eouFse of the disease is usually continuously progressive :
there may be periods of temporary arrest, or possibly even of improve-
ment ; but in the end relapse occurs, and the result is the same.
The duration of the disease. — The disease is not of long duration, from
six months to two years, rarely longer ; yet Miiller records a case which
lasted four and a half years. It is possible that there may be cases of
even shorter duration than six months, for Ebstein records one, under the
name of Pseudoleuksemia splenica, but the nature of these rapid cases is
somewhat doubtful.
Prognosis. — Prognosis in respect of recovery is hopeless ; in respect
of duration of life is bad ; and in respect of the immediate risks to life
must be determined in each case by the condition of the patient.
The mode of death, as a rule, is by progressive asthenia ; though the
end may come suddenly with cardiac syncope, or it may be determined
by hsemorrhage, as in the cases referred to.
Diagnosis. — In the early stage diagnosis is impossible ; in the later
stages it is comparatively easy on account of the enlargement of the
spleen.
1. From pernicious anoemia splenic ansBmia is distinguished by the
enlargement of the spleen, as well as by the condition of the blood ;
though in a clinical sense the anaemia is pernicious, being progressive and
fatal.
It is especially from other forms of profound anaemia in which the
spleen is enlarged that the diagnosis has to be made. Foremost among
these stand leucocythsemia and Hodgkin's disease.
2. In leucocythmmia the diagnosis is determined by the characteristic
blood changes which are absent in splenic anaemia.
3. In Hodgkin's disease the anaemia is usually not so profound, there
is a greater enlargement of the liver, and the lymphatic glands are
affected.
4. In malignant disease of the s/pleen emaciation is a prominent
symptom, arid the wasting advances as the disease progresses ; there may
be secondary growths elsewhere, and there is no rise of temperature.
5. In pernicious ague or mala/rial fever the temperature is of a more in-
termittent and irregular character ; moreover, the presence of the parasites
in the blood and the history of the case will fix the diagnosis.
6. Syphilitic disease of the spleen may possibly cause some difficulty
as in Coupland's case ; but as a rule the history and other evidences of
syphilis will help the diagnosis.
7. With tuberculous disease of the spleen there is generally marked
wasting and the evidence of tuberculous mischief in other organs ; while
as a rule the anaemia is not so profound.
8. In cirrhosis of the liver, with secondary enlargement of the spleen,
548 SYSTEM OF MEDICINE
there is again not so much ansemia, and the ordinary signs and history of
cirrhosis of the liver are obtained.
9. In children ansemia and enlargement of the spleen are not un-
commonly associated. The causes are many, but among them it appears
that splenic anaemia, in the sense in which it is here used, is not to be
reckoned ; for a conclusive instance of the disease under the age of nine
years has not yet been recorded. The course of these cases in children
is also different, for most of them end in recovery, and the hsemophilic
tendency is but rarely seen.
On the whole, therefore, it is evident that though splenic anaemia is
a rare disease, its diagnosis is not generally one of any great difficulty.
Treatment. — The treatment must be symptomatic, and does not differ
from that of other profound anaemias. All the usual remedies have been
tried one after another, but so far nothing has been found to check the
progress of the disease.
Samuel West.
EEFEEENCES
1. Banti. DelV Atuemia Splenica, 1882. — 2. Bruhl. Arch. gSn. de mM. 1891, i.
and ii. (with references to earlier cases) ; Qaz. des hdpitaux, 1891.— 3. Caer. Lancet,
April 1892. — 4. Ebstein. Deut. Arch. f. klin. Med. xliii. — 5. Keating. Diseases
of Children, vol. iii. — 6. Luzet. Th&se de Pa/ris, 1891. — 7. Pel. £erl. klin. Woch.
1885 and 1887. — 8. Potain. Semaine m&lieale, 1887. — 9. Pye Smith. Path. Soe.
Trans. 1875, p. 199.— 10. Renvers. Deut. med. Woch. 1888.— 11. SciOLA and
Carta. Abstr. in Virohow's Jahrb. 1894, ii. p. 39. — 12. Stanley, Douglas.
Brit. Med. Jour. 1895, ii. 1298. — 13. Strumpbll. Arch. d. Eeilk. xvii., xviii. —
14. Taylor, E. Gtuy's Hosp. Rep. Iii. 173. — 15. Toeplitz. Jahrh. f. Kinderheilk.
1897, xxxiii. 367. — 16. West. Med.-Chir. Soc. Trans. Ixxix. — 17. Williamson.
Med. Chron. May 1893.
s. w.
HEMOPHILIA
Definition. — By haemophilia we mean a disease congenital and hereditary,
marked by a tendency to immoderate bleeding on slight causes, lasting
throughout the life of the patient; and further accompanied by a
troublesome tendency to a joint affection, which is often as wearisome to
the patient, as the tendency to external haemorrhages is dangerous.
The name of haemophilia is modern, and seems to have been first
introduced by Schonlein about 1828. "Hemophil" is, however, the
name of one of the dramatis personce in John Ford's Broken Heart, published
in 1633. The disease was not classified or described until the time of
Schonlein, though single observations may be found scattered in medical
literature, beginning with the Spanish Albucasis or Alsaharavius in the
11th or 12th Christian century. The' men who are the subjects of
HMMOPHILIA 549
heemophilia are called "bleeders," a word which appears early in the
nineteenth century in the medical literature of the United States of
America.
Etiology. — Beyond hereditary transmission hardly anything is
known of the causation of haemophilia. It affects especially the male
sex. Though cases in women have been described, it has never fallen
to my lot to see a definite case in a woman, yet the women in the
bleeder families pass on the disease to their male offspring.
The mode of the hereditary transmission of hsemophilia is noteworthy.
In a bleeder family we commonly find all the women free from the disease,
while their brothers suffer. Then these women, if they marry and are
fertile, bear a family some or all of the boys of which are bleeders, while
all the girls escape. But these girls, if they marry, pass the disease on
to their sons ; and so the disease is continued.
This mode of hereditary transmission is not particular to hsemophilia.
It is very well marked in colour-blindness; and in 1881 I published a
genealogical tree showing the descent of this infirmity in a family since
1684. It is also seen in polydipsia, another congenital disorder, as Dr.
Gee has pointed out ; and the same mode of transmission may be seen
now and then in ichthyosis, in the pseudo-hypertrophous paralysis of
Duchenne, and in gout. The disease does not seem to descend from
father to son ; nor through the sons of a bleeder family, free from the
disease, to their offspring. As a general rule, the sons of bleeders, and
the sons of the brothers of a bleeder, who are free from hsemophilia, show
no signs of the disease. But the daughters of a bleeder, like his sisters,
pass- on the disease to their male offspring ; the daughters' offspring often
showing the disorder in a highly aggravated form.
There seems at this moment no evidence that the marriage of near
kinsfolk causes the disease. Nor is hsemophilia pecuHar to any race of
men. I think, however, that it is found more often amongst Jews, in
proportion to the population, than amongst Englishmen. Cases have been
described amongst the aborigines of Sumatra ; and I notice that Japanese
writers have lately begun to describe the disease.
No class in life seems to be exempt from haemophilia ; nor can any
particular geographical distribution be assigned to it.
Symptoms. — As a rule the symptoms of hsemophilia appear during
childhood ; in the large majority of cases before the tenth year. In May
1884, at St. Bartholomew's Hospital, I myself saw a case amongst Dr.
Andrew's patients in which no symptoms had been noticed until the lad
was 19 years old. Other instances have been recorded in which the first
symptoms were seen at the age of 21. But the absence of all early
symptoms of hsemophilia can seldom be proved.
Hsemophilia may even show itself in foetal life. An eight months'
foetus, from a bleeder family, has been found with bruising on the brow :
and a boy when born had large extravasations over both shoulders.
Severe hsemorrhage may take place after ritual circumcision, which is
usually performed on the eighth day after birth; but as a rule th&
550 SYSTEM OF MEDICINE
hsemorrhagic disposition does not show itself until near the end of the
first twelve months of life.
There is a rare affection, one of the chief symptoms of which is a
haemorrhage on the falling off of the umbilical cord. This haemorrhage
rarely occurs in children of bleeder families ; and it is separated from
haemophilia by the fact that when the child recovers it shows no further
disposition to haemorrhage in after-life {vide p. 561).
The joint troubles, which are so prominent in definite cases of haemo-
philia, may appear early in life. In one of Brigstocke's cases an ankle
became distended by effusion a few days after birth ; but as a rule the
joints do not begin to give trouble until the patient be four or five years
of age.
The boys who are the subjects of haemophilia have no external
peculiarities. There is nothing constant about their complexion,
stature, or muscular strength ; nor can it be said that they are always
intelligent, or that they distinguish themselves at school. Physical
examination detects nothing amiss with chest or belly ; neither spleen
nor liver is enlarged, and the urine, in the cases in which I have examined
it, showed the ordinary percentage of urea, and no decided alteration in
its other constituents.
Certain states of the surroundings have been supposed to excite
haemorrhages in a bleeder, or to aggravate his haemorrhagic disposition.
Such are the difference in the seasons, day and night, cold and heat,
changes of the moon, and the like ; but these assertions greatly lack
confirmation. Some have thought that the use of wine provokes haemor-
rhages ; others that the haemorrhagic disposition is increased after- the
first traumatic haemorrhage. This sequence, of course, admits of another
explanation. Anger and other emotions have also been accused. There
can be no doubt, however, that the disposition to haemorrhages in these
patients varies very much ; and the observer must be very cautious in
drawing conclusions as to the action of remedies.
The positive - symptoms of haemophilia may be divided into three
heads: spontaneous bleedings, traumatic bleedings, and the joint affections.
The spontaneous bleedings are said by some observers to be often-
times preceded by distinct prodroma. I have never been fortunate enough
to observe these prodroma, but they are set out at length by Wachsmuth.
They occur three or four days before the onset of the bleeding, and are
mainly signs of plethora : the face is full, the lips and ears swollen, red,
and hot; or the friends remark that the patient is looking remarkably well.
As might be expected, epistaxis is the most common of the spontaneous
haemorrhages, especially in childhood. Few bleeders live to any age
without suffering from some form of nose-bleeding. Nor does it favour
any of the ancient beliefs by flowing more from one nostril than the
other. Bleeding from some part of the mouth comes next in frequency,
though far behind.
As puberty comes on, haematuria and bleedings from the bowels
replace the haemorrhages from the nose and mouth. Very rarely spon-
HALMOPHILIA 551
taneous bleedings are seen from the conjunctiva, the skin, the ears, or
the ends of the fingers.
The amount of blood lost in this way may be very trifling, or it may
be so great as to kill the patient. There may be but a trifling eochymosis
or petechia under the skin, or the whole of the blood may seem to leave
the body. Of the bleedings from the mucous membranes epistaxis is the
most frequent cause of death ; next to that, bleeding from the mouth,
bowel, or lung. Haematuria is but rarely mortal.
On the whole, the traumatic haemorrhages are the most to be dreaded.
A mere scratch is sometimes sufficient to put life in danger. Trifling
injuries, like the scarifications necessary for vaccination, the division of
the fraenum of the tongue, the application of a leech, or ritual circumcision,
have caused death. The taking out of a tooth is an exceedingly dangerous
act ; it is a common cause of death in a bleeder, and should never be
undertaken in a patient of this kind.
These patients vary, however, very much in the amount of injury that
they bear. At one time the same patient will endure injuries the inflic-
tion of which at another time will endanger life ; and in some families of
bleeders the traumatic haemorrhages are, as a rule, nothing like so
dangerous as in others. I have myself seen a tooth drawn in such an
one without any remarkable haemorrhage; but, as a rule, this little
operation is in the highest degree dangerous. Usually the vaccination of
a bleeder is followed by no ill effects ; this is also the experience gained
by the practitioners in the canton of Graubiinden, where there are many
families of bleeders.
The opening of abscesses, either by the surgeon's knife or of them-
selves, is usually followed by a profuse haemorrhage. This is still more
profuse and dangerous when blood tumours or extravasations of blood are
opened.
Death may come on very rapidly, within a few hours ; or the bleeding
may last for weeks. Often the uncontrollable haemorrhage does not
come on with the first infliction of the wound, but some hours or even a
day after the hurt has been given. The quantity of blood lost in a few
hours may be enormous.
Of the composition of the blood thus lost we have no very recent or
exact observations. That first poured out seems to clot naturally, but
after a great deal has been lost, it coagulates feebly or not at all. After
great losses, it looks like water in which meat has .been washed, and
hardly stains the linen. With the microscope a certain increase in the
white coipuscles has been noticed after haemorrhages, as might be
expected.
Symptoms of true anaemia follow the great loss of blood, and the
patient dies bloodless. If, however, the result is to be favourable, the
patient lies long as in a deep sleep, and on awaking he suffers for weeks
and months from pallor and general bloodlessness. The blood lost is
very slowly regained. During convalescence a depraved appetite for
sand, chalk, and the like has been noticed in some few cases.
SS2 SYSTEM OF MEDICINE
It has been said already that in haemophilia the affection of the joints
is more troublesome to the patient than the attacks of external haemor-
rhage. The joints become swollen and painful, and are apparently filled
with iluid ; this disorder is continually recurring, so that some patients
are rarely free from it, and they become cripples from the state of the
knee. The knee is the joint which suffers the most ; after that comes
the ankle, then the elbow, shoulder, and hip joint. The wrist and the
joints of the fingers and toes are seldom affected. When the acute
swelling is over, the joint may recover completely for this turn ; or some
impairment of motion may be left ; indeed after many attacks the joint
at last may be almost destroyed.
The cause of this swelling is, in my opinion, an efiusion of blood into
the joint. Formerly it was thought that its origin was sometimes
rheumatic, but it has been now shown from the necropsies of some
cases that the joints contain blood ; and this seems the most likely
cause of the phenomena in all. Allied are, no doubt, the joint troubles
seen in some cases of purpura which are not rheumatic.
Morbid anatomy. — Morbid anatomy has hitherto given a negative
result in haemophilia. As a rule, nothing but great bloodlessness can be
found ; and a good number of necropsies have now been made by trust-
worthy observers with this as the only result. Schonlein seems to have
laid great weight upon certain changes in the heart, the deficiency of the
muscular fibres in the walls of the septum ; but he may have been
describing only the "unprotected spot" of Peacock. Others have de-
scribed a thinness of the walls of the arteries, but this appearance has
been found in too few cases to justify us in regarding it as a constant
element of haemophilia.
Nor has the microscope anything to tell us in hsemophilia. Dr. Klein
examined for me with the microscope several cases dying in St. Bartholo-
mew's Hospital ; but in no case was he able to detect any disease in the
vessels or tissues. Dr. Percy Kidd observed certain changes in one case ;
but they have not been found in others, and it may be concluded that
they were accidental and not essential to haemophilia.
Of the pathogeny of a disease like haemophilia it is really useless to
speak. It would be mere speculation, and in a work like the present it
would be undesirable to take up space with a discussion of mere
opinions.
On the morbid anatomy of the joints in haemophilia much light has
been thrown of late years. It would seem that the repeated haemor-
rhages into the joints lead up to a state which cannot be distinguished
from chronic rheumatoid arthritis. The first blood efiused into the joint
seems to be reabsorbed, leaving the cartilages free from change. But as
haemorrhage succeeds haemorrhage deep changes make their appearance.
First the cartilages and synovial membrane are slightly coloured from
the presence of blood, but the cartilages remain shining and smooth, and
show no further change. In a further stage the cartilages become deeper
coloured, of the rusty colour so often seen as the result of blood-staining.
HEMOPHILIA 553
and they lose their clear appearance and become clouded and thin. Next
fibrous bands pass from the femur to the tibia, the cartilages are rough
and greatly thinned so that the bone is almost laid bare, and under the
microscope changes very like those observed in the cartilage of chronic
rheumatoid arthritis are observed. There are some specimens of this state
of the joints in the Museum of St. Bartholomew's Hospital (740 a. b. c. d.).
Diagnosis. — When a boy, born in a bleeder family, begins to suffer
from petechise, suspicion is at once aroused ; and if, later, repeated nose-
bleeding, hsematuria, and joint troubles appear, the diagnosis is rendered
highly probable ; if to these be added a long-continued haemorrhage after
slight wounds, there hardly remains room for uncertainty.
Difficulty, however, often arises in practice when a patient presents
himself of whose history little or nothing is known, and the trustworthi-
ness of whose statements is somewhat doubtful. In the first place the
sex is of the greatest importance. I have said that I have never seen a
case of true haemophilia in a woman, and I am inclined to think that the
diagnosis of cases of haemophilia in women is founded on mistaken
observations. Next in importance are uncontrollable haemorrhages after
wounds, especially slight wounds, or wounds that ordinarily give rise
to little haemorrhage; for example, the taking out of a tooth is often
a touchstone in the diagnosis. If no haemorrhage have followed this
operation, the opinion against the diagnosis of haemophilia is materially
strengthened. Then the joint affection in persons already suspected of
haemophilia adds something in favour of the diagnosis, though it must
be remembered that temporary haemorrhagic diatheses, like scurvy and
purpura, sometimes show a joint afiection which appears to be due to
haemorrhages into the joint affected.
In some doubtful cases, especially in children of a bleeder family, it
may be well to wait a few months or even a year till more decided
symptoms show themselves, as nose-bleeding and the like, before giving
an opinion.
It should always be kept in mind that haemophilia is a congenital
general disease, which persists throughout the life of the patient.
Temporary haemorrhagic diatheses, like scurvy and purpura, must not .be
accounted haemophilia ; nor should a long-continued haemorrhage from
one single part have this name given to it, as a German writer, who
ought to know better, has lately done.
There are certain rare cases with umbilical haemorrhage in infants
which may be confused with haemophilia. They have profuse bleeding
from the place of separation at the navel, they are often jaundiced, and
they die after having shown signs of a general haemorrhagic disposition.
Such cases of umbilical haemorrhage, however, do not belong to haemo-
philia. They occur in children of both sexes, and not especially in
bleeder families ; and in those which survive, no tendency to haemorrhage
is noted [vide following article].
Prognosis. — The remote prognosis of haemophilia no longer appears so
serious as was formerly supposed. In Grandidier's figures only 10 per
554 SYSTEM OF MEDICINE
cent attained the age of 21. My own direct experience has been much
more favourable. I have watched the boys of many bleeder families from
childhood ; and they have grown up into manhood, not without pain and
suffering it is true, but they have kept their life, and followed easy occu-
pations by which they gained their bread in a fashion. The patients
whom I have thus watched have belonged mainly to the lower middle
classes. They have known of their tendency to hsemorrhage, and thus
in many instances, no doubt, they have been able to ward off wounds.
With sufBcieiit care, middle age would seem to be within the reach of
many of them.
It is said that with the approach of middle age the tendency to
hsemorrhage may disappear. I have never seen such a case ; but the
fact that it has been noticed by some observers should be remembered.
TFeatment.— First of all it may be well to consider the measures to
be avoided. All procedures by which blood is drawn — blood-letting,
leeches, lancing of gums, scarifications and the like — must be forbidden.
The red-hot iron and even blisters are attended by considerable danger
in many cases. Surgeons should be warned that when the great opera-
tions of surgery have been performed, such as an artery tied in its course,
amputation of a member, or lithotomy, the patient has usually bled to
death of the wound. It is hard to imagine a case in which the use of
the knife would be justifiable.
With traumatic haemorrhages, it would seem best to follow the
ordinary rules of surgery, always remembering the warning given in the
paragraph above. Styptics, it may be noted, are generally worthless.
The use of the hot iron and of the perchloride of iron is specially to be
avoided.
In like manner, spontaneous haemorrhages should be treated accord-
ing to the general rules of medicine. Ice may be passed up the nose in
epistaxis, or into the bowel in bleeding from the rectum, or placed in the
mouth in bleeding from the gums. Whatever may be done will, how-
ever, too often prove ineffectual ; and if the medical attendant have
courage enough for such a line of action, there would almost seem to be
a better chance for the patient if the attendant abstained altogether from
active local treatment designed to check the bleeding. When all the
blood seems to have left the body, and the patient about to die of the
loss of blood, it has not infrequently happened that the hsemorrhage has
ceased and the patient has slowly and gradually recovered.
Transfusion of blood as a last resort has been practised in some cases
with success ; and in desperate cases I should feel inclined myself to
recommend its employment.
During the intervals between the attacks of hsemorrhage, what shall
be done ? The hygienic treatment is of great importance ; all occasions
of hsemorrhage must be warded off; all persons about the boys should be
told of the tendency to hsemorrhage, and of the grave consequences which
may follow the slightest injury. Nearly all the ordinary games of boys,
amongst which are specially to be named cricket, hockey, and football.
HEMOPHILIA SSS
have to be forbidden. Other sports and exercises may be allowed
according to their results.
Cold sponge bathing is useful and well borne. The dwelling-place
should be dry, the air bracing ; during the winter some have seen good
from a removal to a dry and warm climate like that of the Riviera. It
is to be regretted that we have so little experience of climatic treatment.
Warm clothing seems very desirable, as these patients often feel the cold
severely.
As to drugs, a good deal of caution must be exercised in drawing
conclusions even from an experience which may seem to be wide. For
instance, .at the beginning of this century, the American physicians
who had treated families of bleeder children tell us that " the sulphate of
soda was accidentally found to be completely curative of the hsemor-
rhage " in haemophilia. At the present day no such great confidence is
felt in the sulphate of soda. At this moment the chlorides are in greater
favoiu' ; the chloride of calcium has been recommended in these cases
from its supposed power of increasing the coagulability of the blood, and
very favourable results have been reported from its use. I cannot, how-
ever, say that I have seen anything like a complete disappearance of the
heemorrhagic disposition follow even a long-continued use of this drug.
In my own experience I have found very good results follow a course
of cod-liver oil and perchloride of iron alternately.
In the treatment of the acute stage of the joint affections, rest is the
very first, almost the only element in the cure. The joint must be
rendered motionless, as soon as the patient can bear such treatment, by
splints of plaster of Paris or whatever the surgeon may deem suitable.
Pain must be neutralised by opiates ; and there does not seem much
danger in haemophilia from subcutaneous injection of morphia.
J. WiCKHAM Legg.
REFEEENCES
Legg, J. W. Treatise, on HcEmophUia, Lond. 1872, chap. xi. p. 138 ; St. BaHholo-
mew's Eosp. Seports, vol. syii. 1881, p. 317, in which place references to other essays
on this subject will be found.
J. W. L.
5S6 SYSTEM OF MEDICINE
H^MOREHAGES IN NEW-BORN CHILDREN
The haemorrliages which occur in new-born children may be divided into
two groups: (1) Traumatic or Accidental HsBmorrhages, which are
the direct result of injury at the time of birth ; and (2) Spontaneous
Haemorrhages, which occur without any apparent external cause.
The cases of spontaneous haemorrhage are best again subdivided into
(a) Idiopathic cases, where the bleeding is the chief or only symptom —
the so-called " hsemorrhagic disease of new-born children " ; and (h)
Symptomatic cases, where the haemorrhages are secondary to some
serious organic disease, such as congenital malformation of the heart,
congenital obliteration of the bile-ducts, or some grave affection of the
liver. With this group also may be taken the rare cases in which true
haemophilia leads to haemorrhages in early infancy.
I. Traumatic ok Accidental Hemorrhages
The traumatic haemorrhages are mainly due to injuries received dur-
ing birth, either by the pressure of the maternal parts on the child, or
by the artificial means used by the accoucheur to expedite delivery.
They are consequently more frequent in the case of first-born and male
children, in difficult and prolonged labours, and when the presentation is
abnormal. There can be little doubt, also, that increase of the blood-
pressure, owing either to asphyxia from pressure on the cord, or to pres-
sure on veins or compression of some other part of the body, may be
an important cause of their occurrence.
Traumatic cases are of less importance, from the physician's point of
view, than those of spontaneous bleeding. Nevertheless they also are of
interest to him, and therefore worthy of brief mention here because, in
not a few instances, they form the starting-point of serious nervous dis-
ease in later life.
The most important situations in which the effused blood is found
may be stated as follows : — (i.) On the surface of the skull, between the
pericranium and the bone — cephalhaematoma ; (ii.) Inside the cranium
— apoplexia neonatorum ; (iii.) Into the substance of the sterno-mastoid
muscle ; (iv.) Into one or more of the abdominal or thoracic organs.
Cephalhaematoma
Cephalhaematoma is the name given to a swelling on the surface of
the cranium formed by a collection of fluid blood between the pericranium
and the. bone. The condition is due to rupture of blood-vessels under
the pericranium, owing to mechanical pressure during birth ; and it is
HEMORRHAGES IN NEW-BORN CHILDREN 557
met with about once in every 200 births. It is much more commonly
seen after first labours than after subsequent ones, and is especially fre-
quent after diflBcult births in which the head has presented. It occurs,
however, sometimes after breech cases, and occasionally also with com-
paratively easy and normal labours.
In the majority of cases the tumour is situated over the right parietal
bone — this being usually the presenting part. * Less frequently it is
found in the left parietal region ; and sometimes it occurs on both sides.
It is rarely met with over the other cranial bones. The swelling is
generally noticed within the first two or three days after birth. It is
rounded in contour, fluctuating and not apparently tender ; and it shows
no heat or redness. Being under the pericranium it is always distinctly
limited to the surface of one bone and never crosses a suture. For four
or five days it usually goes on increasing in size, and then, after being
stationary for a while, it slowly disappears. When the blood begins to
be absorbed, the bone can readily be felt through the tumour, and round
its margin a raised ring can be made out. This is due to the formation of
bone having gone on under the raised periosteum. Sometimes also from
,the same cause there is a crackling sensation experienced on handling the
surface of the swelling.
Generally the blood tumour is quite absorbed within four weeks of
birth, but it often takes two or three months before all trace of the bony
ridge round it has disappeared. The prognosis in uncomplicated cases is
invariably good, the cephalhsematoma always recovering vnthout any
treatment. It should, however, be remembered that in a certain propor-
tion of cases the external swelling is accompanied by an intracranial
haemorrhage.
Intraeranial Haemopphag'es (Apoplexia Neonatorum)
Intracranial haemorrhages are unfortunately not very uncommon.
They are important, not only because they are a very frequent cause of
still-birth and early death, but also because they are responsible for a
large amount of bodily and mental defect in after-life.
Etiology. — Although the state of asphyxia into which many children
are brought during birth must be regarded as a strongly predisposing
element in the causation of these haemorrhages (Ashby), Spencer's
statistics render it almost certain that they are mainly due to external
injuries. These may be produced either by the pressure of the maternal
parts on the child or by that of the blades of the forceps. Thus he has
found that the frequency of cerebral haemorrhage is greatest with forceps
delivery, less when the breech or foot presents, and least of all with
natural head delivery.
As to the mechanism by which the lesion is brought about, Spencer
suggests that in many cases it is due to displacement inwards of the
lower anterior corner of the parietal bone. This corner directly overlies
the great anastomatic vein, and being driven inwards during birth, clamps
SS8 SYSTEM OF MEDICINE
this vessel so as to cause engorgement in its area of distribution. This
explains, he thinks, the fact that the haemorrhages are often limited to
the parietal region and Sylvian fissure. Compression of the internal
jugular vein by the forceps may also favour cerebral haemorrhage in a
similar way. S. McNutt has shown that hsemorrhages limited to the
convexity are more frequent in breech than in head deliveries.
Morbid anatomy. — In a very large majority of the cases the haemor-
rhage is primarily meningeal, and the injury to the brain itself is secondary
and results from pressure from the surface. In some cases, however, the
bleeding takes place into the brain substance. Effusion of blood on the
inner aspect of the cranial bones, outside the dura mater (internal cephal-
haematoma), is sometimes found along with an external cephalhaematoma.
It is said that this does not occur unless a fracture of the bone is
present (Holt). Generally the blood is poured out into and beneath the
arachnoid and pia.
The lesion is more frequently bilateral than confined to one side ;
and it is much commoner at the base than on the convexity of the brain.
It is also commoner towards the posterior part of the skull than
anteriorly. As has been already mentioned, haemorrhages are frequently
found over the parietal region and in the Sylvian fissure. The ventricles
are sometimes distended with blood.
When meningeal apoplexy occurs, it sometimes lacerates the under-
lying cerebral cortex ; in any case, it is apt to interfere with its
nourishment by tearing through the blood-vessels which pass into it from
the membranes. It also injures it by its pressure, so that softening and
atrophy soon follow. Thus permanent atrophy and arrest of development
of the cortex are set up along with degeneration of the fibres in the
motor tract of the brain and spinal cord.
Clinical features. — If the damage to the brain be very great, the
child will probably be still-born. The haemorrhage may, however, be
tolerably extensive, and yet the infant may survive for several days ; or
it may even recover and grow to adult age, although with a permanently
damaged nervous system.
In many cases where the haemorrhage has been severe the infant
does not at first show any distinctively cerebral symptom, except torpor
and feeble or irregular breathing ; but other indications may be present.
There may be obvious paralysis of one or more limbs, or of tlie cranial
nerves if the haemorrhage implicate the base. If the child live for
some days, convulsions often occur ; and they are more frequent in cases
where the haemorrhage is over the cortex than in those where it is at the
base of the brain (McNutt).
As the child gets older, although the parents are often slow to see
that anything is the matter with him, it will usually soon be found that
the limbs are unnaturally stiff and the knee-jerks exaggerated. Later,
he is backward in learning to hold his head up, in sitting up, and in
walking ; or it may be that he displays a lack of interest in his surround-
ings, which is soon noticed as abnormal. Gradually, as the brain grows,
HEMORRHAGES IN NEW- BORN CHILDREN 559
the extent of the damage to its functions becomes more manifest, and
the case passes off into spastic paraplegia, hemiplegia, diplegia, imbecility,
or idiocy with or without paralysis.
Prognosis. — While extensive hsemorrhages at the base are usually
fatal, comparatively large ones over the convexity are compatible \iath
life. Small cortical apoplexies may, it is said, be entirely recovered from,
but in the great majority of cases more or less permanent injury to the
brain results.
Hsematoma of the Sterno-mastoid (Sterno-mastoid Tumour)
Hsematoma of the sterno-mastoid is a collection of blood which forms
within the sheath of that muscle when some of its fibres have been
ruptured during birth. It is met with most frequently in breech cases or
cross-births where there has been diflSculty in delivering the head ; often
also in difficult forceps cases, and sometimes after labours which are said
to have been quite easy. It is probably caused more often by a sudden
twisting of the neck than by simple traction on it. In nearly 300
autopsies on children, who were either still-born or had died soon after
birth. Dr. Spencer found this lesion in fifteen.
The swelling may occur at any part of the muscle, but most fre-
quently it is situated about its centre. The muscle of the right side is
much oftener affected than that of the left. The tumour is not usually
noticed until the second or third week, and often it does not attract
attention till much later. This is due to the fact that the swelling
caused by the effusion of blood is generally small at first. It is not
until the injury to the muscle has occasioned a considerable growth of
fibrous tissue (" muscle callus ") round it, that it becomes too obvious to
be overlooked. It may reach the size of a pigeon's egg, but it is generally
smaller. The swelling remains stationary for weeks, and then slowly
diminishes. It usually takes six or seven months to disappear ; but it
may have quite gone by the third month, or it may last more than a
year (Pollard).
The connection between hsematoma of the sterno-mastoid and so-called
congenital wryneck is certainly a very close one, but it is difficult at
present accurately to define it. Out of 106 cases of haematoma which
Mr. D'Arcy Power collected from medical records, marked wryneck had
resulted in twenty-one at least, while only in fourteen had it been specially
looked for and not found. Dieffenbach and other older writers on the
subject assumed that the wryneck was the simple result of the injury to
the sterno-mastoid muscle at birth ; but this explanation has of recent
years been much disputed (Golding-Bird, Petersen, Koettnitz). The
chief difficulty in accepting it lies in the fact that in most if not all of
the marked cases of congenital wryneck there is a very decided arrest of
growth of all the structures of the face on the affected side, and it is
difficult to imagine how any lesion of the neck only could bring this
about. What cerebral lesion could cause it, however, is as yet un-
56o SYSTEM OF MEDICINE
determined. The fact remains that this characteristic facial asymmetry
along with wryneck not uncommonly appears as a sequel of hsematoma
of the sterno-mastoid (I have recently watched this sequence in three
instances). Usually little can be effected in the way of treatment
owing to the age of the child ; but it is probable that judiciously applied
massage and manipulations may sometimes be of use.
Hsemorrhages into Abdominal and Thoracic Viscera
As Dr. Spencer points out in his valuable paper, haemorrhages into the
abdoihinal and thoracic viscera are much more frequent after breech
cases than after those in which the head has presented. They may occur
into any of the organs, being seen frequently in the lungs, liver, kidneys,
suprarenals, and intestine, and comparatively rarely in the spleen.
In most cases of internal haemorrhage the diagnosis is impossible
during life for lack of symptoms. Pulmonary infarctions, however,
sometimes betray their presence by causing physical signs of consolida-
tion of the lung. They are the cause of death in many cases of children
who live for a few days only, and in these the fatal issue is apt to be
attributed to congenital heart disease on account of the degree of cyanosis
which is present. If the infant live long enough, pneumonia may result.
Haemorrhage into the pyramids of the kidneys may cause death
within a few days, with symptoms of suppression of rffiiie ; and Spencer
records one case in which a large haemorrhage into the caecum caused
complete intestinal obstruction.
II. Spontaneous Haemorrhages
(a) Idiopathic Cases (the Hsemorrhagic Disease of New-born
Children)
DeseFiption. — The haemorrhagic disease of new-born children may be
described as a passing morbid condition of the system which shows itself
mainly by a tendency to spontaneous bleeding. The haemorrhages may
occur either from the umbilicus, from the stomach or bowel, from the
blood-vessels in the subcutaneous tissue, or from other parts ; and their
occurrence is probably due to poisoning by the toxin produced by any
one of a variety of micro-organisms.
The condition is a very rare one. Cases of gastro-intestinal haemor-
rhage, which is its commonest form, are said to occur once for every
500-1000 births (Eunge, Hermary, Kling) ; while umbilical haemorrhage
is only met with once for every 5000 confinements (Ribemont).
Clinieal features. — In the great majority of cases no family history
of bleeding is to be obtained. The sexes seem to be affected in about
equal proportions. This point is of interest when we remember the
very much greater frequency with which the male sex is affected in
HEMORRHAGES IN NEW-BORN CHILDREN 561
haemophilia — the proportion being stated by Grandidier as eleven boys to
one girl (wde art. "Haemophilia," p. 549).
Sometimes the patient is in weak health before the bleeding sets in ;
being premature or feeble, or perhaps the subject of congenital syphilis.
Generally, however, he appears quite healthy until the hsemorrhage
begins. This takes place usually within the first week of life, and rarely
after the end of the second ; the exact date varies, partly according to
the situation whence it comes.
The site of the hsemorrhage may vary considerably. In the majority
of cases it comes either from the alimentary tract (mouth, stomach, or
bowel), or from the umbilicus. It may also take place into the^ sub-
cutaneous tissue, or from the nose, conjunctiva, or ears, or into almost any
of the internal organs. The bleeding may come from one situation only,
as often happens in the slighter cases, or many parts may be affected,
either at one time or successively. Thus, of 50 cases reported by
Townsend, the umbilicus was affected in 18 (alone in 3); the intestine in
20 ; the mouth in 14 ; the stomach in 14 ; the nose in 12 : subcutaneous
eochymoses occurred in 21 ; bleeding from an abrasion of the skin in 1 ;
from the meninges in 4 ; cephalhaematomata appeared in 3 ; haemorrhages
into the abdomen in 2, and into the pleura, lungs, and thymus in 1
each.
The amount of blood lost at a time is usually small ; but the loss is
generally so frequently repeated that pallor, chilliness, and prostration
with failure of the pulse are very soon produced. In some cases the
temperature is high, in others it is normal or subnormal throughout. In
the cases of recovery the bleeding usually lasts one or two days ; in the
fatal cases death often occurs within twenty-four hours, and rarely later
than three days from the beginning. Sometimes diarrhoea appears, and
towards the end convulsions not infrequently set in.
In children who recover the convalescence is apt to be prolonged
and tedious, although the health is not permanently damaged.
Gastro-intestinal hcemorrhages (Melcena neonatorum). — The blood in
these cases is more frequentljr passed by the bowel than vomited. When
vomited it is sometimes bright red, often dark brown in colour. Its
amount varies greatly in different cases. Sometimes the haematemesis
occurs only on one occasion ; more frequently small quantities are brought
up repeatedly. When passed by the bowel the blood is generally very
black and thoroughly mixed with the motions. Sometimes, when it
comes from the lower part of the bowel, it is red, and it may be in
clots.
The blood is most frequently seen for the first time on the second
day of life, or at least before the fifth ; but occasionally the hsemorrhage
may begin as late as the second week.
Spontaneous umbilical hcemorrhage usually takes the form of a steady
oozing from the point where the cord has separated or is about to
separate. The bleeding does not generally come from any visible blood-
vessel ; it is often intermittent ; sometimes it is alarmingly free. Some-
VOL. V 2 0
562 SYSTEM OF MEDICINE
times it takes place into the substance of the cord, or from fissures on
its surface.
It generally begins about the fifth day of life, but it may occur
earlier, and it may be deferred till the seventh or even the ninth day.
It does not generally last more than three days, but in rare cases it
may go on much longer. It is often fatal within twenty-four hours.
Subcutaneous ecchymoses may occur at any part of the body, and are
as common on protected areas as on those which are exposed to pressure
and friction. They are often of small size, but occasionally they become
very large. If they occur without any hsemorrhages from other situa-
tions the prognosis is generally good.
Bleeding from the female genitals occurs occasionally in cases of
multiple hsemorrhages. It is, however, much more frequently met with
as an isolated symptom ; and, when this is so, it is generally the result of
some trifling local disturbance and has no serious significance. The
haemorrhage begins usually within the first six days of life, rarely
after the twenty-first (Busey). The external genitals appear quite nor-
mal, but there is a more or less constant oozing of blood from the
vaginal orifice, which lasts from two to five days, or sometimes a little
longer. Owing to the trivial nature of the ailment very few oppor-
tunities have occurred for investigating its morbid anatomy. Billard
asserts that the blood comes from the uterine mucous membrane, and
Eross in one case found acute hsemorrhagic catarrh of the fundus uteri.
Only in rare cases does it recur, so that it cannot be regarded as of the
nature of menstruation.
Morbid anatomy. — ^In most cases of children who have died from
haemorrhage there is nothing to be discovered at the autopsy but
the traces of the effused blood and a general pallor of all the organs.
In a considerable proportion, however, of the cases of melaena (40
per cent according to liomme), more or less ulceration of the mucous
membrane of the stomach or duodenum has been found. The ulcers are
usually multiple, and may either consist of superficial abrasions or be of
a perforating character. In one case (Landau) a clot was found obliterat-
ing the blood-vessels which supplied the area in which the ulcers were
situated, but this is not usually the case. In some cases of melsena
cerebral haemorrhages have been found (Pomorski and v. Preuschen),
but these also are by no means constant. In syphilitic cases endarteritis
of the small and middle-sized vessels in the submucous tissue of the
alimentary tract has been described (Mracek).
A considerable variety of micro-organisms has been found in the
blood and in the tissues in cases of haemorrhage, and especially in those
of melaena. The first to record an observation of this kind was Klebs,
who, in 1875, described a micrococcus which he had found in large
quantities in the organs of nine new-born children who had died of
haemorrhage. This he injected into young rabbits, and succeeded in
producing haemorrhages in them. His results were confirmed in the
following years by Weigert, Eppinger, and Rehn. Since then various
HEMORRHAGES IN NEW-BORN CHILDREN 5^3
micro-organisms have been discovered in these cases by competent
observers. Thus, streptococci have been found by Baginsky, Babes, and
Bar ; bacillus pyocyaneus and staphylococci of various kinds by Neumann,
Bar, and SchafFer, and bacterium lactis aerogenes by Neumann and
Schaffer. Further, Babes found in one case an organism with all the
characters of the diplococcus pneumonise, and Dungern one which re-
sembled in every way Friedlander's pneumococcus. In Dungern's case
it is also recorded that, while the child was in the ward, three other
infants died of severe pneumonia.
In 1894 Gartner published an account of two fatal cases of melsena
in which he found a short bacillus. Cultures of this organism were made
and injected into the peritoneal cavity of young puppies, and they set
up fatal gastro-intestinal haemorrhage. In one of Holt's cases a similar
organism was found.
Etiology. — A number of very different hypotheses of the causation
of this condition have been framed. The following deserve mention : —
1. Von Preuschen and Pomorski have published cases where melsena
and pulmonary infarction of an apparently spontaneous origin were
found after death to be associated with traumatic haemorrhages into the
cerebral peduncles and the fourth ventricle, damaging the vaso-motor
centre. They therefore maintain that many if not all of the cases of
spontaneous haemorrhage are secondary to cerebral injury. They were
able to strengthen their position by means of experiments on animals ; for
they succeeded in producing melsena in a considerable number of rabbits
by puncturing the cerebral peduncles and the walls of the fourth ventricle.
While these observations are certainly interesting and important, they
cannot be held as explaining the occurrence of most cases of tHis disease.
Cerebral haemorrhages have only been found in a few instances.
2. Other writers have laid great stress on the local morbid condition.
Thus, for example, in dealing with melaena they have given mechanical
explanations to account for the presence of ulceration in the stomach and
bowel in these cases. The most remarkable of these hypotheses is that
put forward by Landau. He noticed that the condition often occurred in
premature and weakly infants in whom the function of respiration was
established with some delay and difficulty. He accounts for this by
supposing that the delayed inspiration favours stagnation and clotting of
the blood in the umbilical vein. Then, he further supposes that, from
the thrombus so formed or from that in the ductus arteriosus, an embolus
is separated and carried through the circulation until it becomes impacted
in one of the arterial branches which supply the stomach and duodenum,
and ulceration results. In one case of gastric haemorrhage he was able
to satisfy himself that the artery supplying the area from which the
blood came contained a clot.
Emboli of this sort have not been found by other observers who have
looked for them, and Landau's theory has- not, therefore, been generally
accepted. It must be remembered in this connection that the formation
of ulcers in the stomach and bowel is a frequent result of general infection
564 SYSTEM OF MEDICINE
with organisms of various kinds, and even of poisoning by toxins
(Demelin).
3. Considerable stress has been laid by some authors on the fact that
many of the patients in these cases are syphilitic or otherwise weakly ;
and it has been supposed that the bleeding might be attributed to some
disease causing special fragility of the blood-vessels.
Evidence of vascular disease, however, has not usually been found;
and it seems more probable that debilitated states of the system act as
remote causes only ia so far as they prepare a suitable soil for the growth
of micro-organisms.
4. Of recent years there has been an increasing tendency to regard
the spontaneous haemorrhages in these cases as a manifestation of a
micro-organismal disease ; and, although this view can scarcely as yet be
said to be thoroughly established, there are a great many facts in favour
of it. It is well known, for example, that many pathogenetic organisms
have the property of producing a tendency to haemorrhage. As already
mentioned, a large number of different organisms, known and unknown,
have been cultivated from the blood and tissues in these cases ; and some
of them have even been found to cause haemorrhages when injected into
animals. Further, the symptoms of the cases and their short course
point to the disease being an infective one, as do also the facts that they
are more frequently met with in hospital than in private practice, and
that they have been known to occui- as an epidemic.
Diagnosis. — Spurious melsena, that is, the vomiting or passing by the
bowel of blood which the child has swallowed during birth, or has sucked
from fissures in the mother's nipples, often causes needless anxiety if
mistaken for this disease. It is more frequently met with than true
haemorrhage. Or the child may have epistaxis or haemorrhage from
an ulcer in the mouth or throat, and the blood may be passed with the
motions and cause a diagnosis of melaena. Such mistakes are not usually
difficult to avoid. If, however, the haemorrhages be confined to the
internal organs, they are very apt to be overlooked in the absence of
characteristic symptoms.
The occurrence of spontaneous haemorrhages — especially ecchymoses —
has, it should be remembered, some interest from a medico-legal point of
view, as they may be regarded erroneously as evidence of violence.
Progrnosis. — The condition is always a very dangerous one. In Town-
send's cases the mortality was 62 per cent. In cases of umbiKcal haemor-
rhage it is even larger than this, being variously stated by authorities at
from 65 to 84 per cent ; while in melaena it is usually estimated at from
50 to 60 per cent. Should the infant be syphilitic or otherwise con-
stitutionally feeble, this fact naturally renders the prognosis more
unfavourable.
Treatment. — Great encouragement to prompt and persevering treat-
ment of these cases is to be gathered from the fact that the disease is so
brief in its duration. The treatment is to be conducted on general
principles, and too much reliance is not to be placed on drugs. It is
HEMORRHAGES IN NEW-BORN CHILDREN S^S
especially important that everything possible should be done to con-
serve the child's vitality. He should be kept perfectly quiet, and pro-
tected from cold by wrapping in cotton wool; he should also be surrounded,
if necessary, with hot-water bottles. French writers recommend the use
of a couveuse (Dusser, Oui). He should not be allowed to suck, but
at short intervals by a spoon or medicine-dropper should have small
quantities of his mother's milk, or diluted peptonised milk, cooled with
ice. Small doses of ergotin may be given by the mouth, or, if the bleeding
be severe, subcutaneously. If there be much collapse, it may be necessary
to give alcohol by the mouth or ether as a hypodermic injection.
In melaena injections into the bowel are to be avoided. They
are probably worse than useless, as they stimulate the intestinal
movements. In umbilical haemorrhage intelligent and patient digital
pressure on the bleeding part is probably the best means of treatment.
The actual cautery, nitrate of silver, and the application of plaster of
Paris have also beeo successful in some cases. If other means fail, the
base of the bleeding spot should be transfixed by a hare-lip pin and a
ligature applied round it.
■
{b) Symptomatic Cases
Description. — Spontaneous haemorrhages, similar in most respects to
those we have been considering, are frequently met with as a symptom of
various diseases. Thus we find them occasionally occurring in children
with congenital malformation of the heart, rarely in infants who inherit
true heemophilia, and frequently in cases of congenital obliteration of the
bUe-ducts and other serious diseases of the liver accompasnied by jaundice.
The tendency to haemorrhage met with in these morbid conditions
differs from that seen in the haemorrhagic disease of new-born children in
that it is permanent. With few exceptions it lasts as long as the child lives.
Children with congenital malformation of the heart do not often suffer
from spontaneous bleeding ; and although haemophilia generally manifests
itself for the first time in childhood, it is very rare indeed to find it as a
cause of haemorrhages as early as the first year of life. Out of 576
eases of haemophilia, of which Grandidier collected details, the bleeding
occurred in early infancy in 12 only.
In congenital obliteration of the bile-ducts,- however, and in all other
forms of disease which cause lasting jaundice in young infants, haemorrhages
are a common and characteristic symptom. Thus, more than two-fifths
of the cases of umbilical haemorrhage collected by Jenkins and Grandidier
occurred in icteric infants ; while in 65 cases of congenital narrowing or
obliteration of the bile-ducts tabulated by myself, haemorrhages were noted
in more than half of the number of infants which had lived more than
a few days. A similar haemorrhagic tendency is of course well known
to occur sooner or later in all cases of continued obstruction of the
common duct ; and is almost equally characteristic of a number of very
different morbid conditions, all of which are accompanied by jaundice ;
S66 SYSTEM OF MEDICINE
such as acute yellow atrophy, yellow fever, phosphorus poisoning, and so
forth.
Clinical features. — The places from which the bleeding occurs in
these cases are just the same as those observed in the case of idiopathic
hsemorrhages. Their onset, however, is generally later. Thus in
Grandidier's cases of umbilical haemorrhage the average date of onset was
about the sixth day in the non-icteric and about the tenth in the icteric
cases. In the case of gastro-intestinal hsemorrhages this difference is very
much more marked ; for, although jaundiced infants sometimes show a
tendency to haemorrhage from the very first, they often do not begin
to bleed until several months after birth. When once established the
tendency seems rather to increase as they grow older.
Etiology. — The causation of the hsemorrhages in cases of jaundice has
never been satisfactorily explained, although many hypotheses have been
proposed to account for them. By some they have been attributed
to impoverishment of the blood (Budd, Murchison.) ; by others it has
been supposed that they are due to bile acids circulating in it, and
either acting on the corpuscles (Leyden) or setting up a diseased state of
the blood-vessels (Wickham Legg).
It seems, however, more probable that the hsemorrhagic tendency is
caused in some way by the presence in the blood, not of bile acids, but of
ptomaines or some similar organic poisons. These are formed in the
process of ordinary digestion, and the diseased liver is not able to render
them innocuous, as it would do if it were in a state of health. The
following facts seem to support this hypothesis. It has been found by
Roger that the function of the liver, in virtue of which it neutralises
the organic poisons formed in the alimentary canal, as well as others,
is closely connected with the amount of glycogen it contains. Thus, when
the liver contained little or no glycogen, he found that a very much
smaller dose of these organic poisons was required to produce a given
result than was necessary if the organ were healthy in this respect. It
has also been demonstrated by Dr. Wickham Legg and others that the
obliteration of the bile-ducts by ligature is followed in animals by dis-
appearance of glycogen from the liver. It would appear that the retention
of bik interferes with the proper discharge of the function of glycogenesis
in the hepatic cells.
In the light of these observations, it seems not improbable that in
congenital obliteration of the bile-ducts and other serious forms of
jaundice a process of auto-intoxication is set up. If this be so, the
poisons which come thus to circulate in the blood will probably induce
hsemorrhages in the same way as do those toxins which are produced
by the action of micro-organisms in the idiopathic cases.
Owing to the serious nature of the diseases present in these cases the
pFognosis is much worse than in the idiopathic group, and the treatment,
which is to be conducted on the same lines as in the others, is even less
likely to be successful.
John Thomsox.
HAEMORRHAGES IN NEW-BORN CHILDREN 567
EEFERENCES
A. Traumatic Hsemoirhages ; — 1. Ashby. Brii. Med. Joum. 1890, vol. i. p. 281.
— 2. Ashby and Wkioht. Diseases of Children, 3rd edit. 1896. — 3. Dieffenbaoh.
Theor.-praM. Hmidbuch der Chirurgie, Ui. Berlin, 1830. — 4. Golding-Bikd. Guy's
Hasp. Rep. 1890, vol. xxxii. — 5. Koettnitz. "Ueber Beokenendlagen, " Volkmann's
Sammhmg, No. 88, 1893. — 6. MoNutt, Sakah J. Amer. Joum. of Obstetrics, Jan.
1885.— 7. Pbteksen, Feed. Centralbl. f. Gynakol. No. 48, 1886. — 8. Pollakd,
Hilton. Clinical JouttmI, July 29, 1896. — 9. Powee, D'Akoy. Trans. Med.-Chir.
Soc. Bond. vol. Ixxvi. 1893. — 10. Spenoee, Hbeeekt E. "On Visceral Haemorrhages
in Still-bom Children," Trails. Obstet. Soc. Zand. vol. xxxiii. 1891. — 11. Idem. "On
Hsematoma of the Sterno-mastoid Muscle in New-born Children," Joum. of Path, and
Bacteriol. vol. i. 1893.
B. Spontaneous Haemorrhages ; — 12. Babes. Bakter. TJniersuch. uber sept. Proc.
1889. — 13. Baginsky, A. Virchow's Arch. 1889, Bd. oxv. — 14. Bae. Bev. g&n. de
din. etdeth&r. Nov. 29, 1893. — 15.'BiLLAB.D. TraitS des maladies des enfwnts nouveau-
nAs et a la mamelle. — 16. Busey. Amer. Joum. of Obstet. vol. xxiii. No. 5, 1890. —
17. Demelin, L. Granoher's Traiti des maladies de I'enfance, 1897, t. ii. — 18.
DuNGEEN. Centralbl. f. Bacteriol. 1893, Bd. xiv. No. 17, S. 547. — 19. Dtjssee.
"Des h^morrhagies gastro-intestinales ohez les nouveau-nes." Th^se, Paris, 1889.' — 20.
EppiNGEE. Prager med. Wochenschr. 1877, No. 39. — 21. Eeoss. Archiv f. Kinder-
heilk. Bd. xiii. 1891, S. 172.— 22. Gaetnee, F. Archiv f. Gynak. Bd. xlv. S. 272.—
23. Geandidiee. Jowrnal f. KinderkranTcheiten, May 1859, S. 380. — 24. Hermaky.
Joum. de din. et tMr. infant. 4th March 1897. — 25. Holt, L. Emmett. Diseases of
Infamcy and Childhood, 1897, p. 93. — 26. Jenkins, J. F. "Report on Spontaneous
Umbilical Haemorrhage of the Newly-born," Trans, of the Amer. Med. Assoc, vol. ji.
1858. — 27. Klebs. Arch. f. experiment. Pathol, und Pharmakol. Bd. iv. S. 473. — 28.
Klino. "Ueber Melaena Neonatorum." Diss. Miinohen, 1875. — 29. Landau. "Ueber
Melaena Neonatorum." Diss. Breslau, 1874. — 30. Legg, "Wiokham. Bile, Jaundice,
and Bilious Diseases, London, 1880, p. 315. — 31. Leyden. Beitrdge zur Pathol, des
Icterits, Berlin, 1866, S. 100.— 32. Maokay, J. G. H. Arch. f. experiment. Pathol,
und Pharmakol. Bd. xix. 1885. — 33. Mkaoek. Vierteljahresschr. f. Dermal, u. Syphilis,
H. i. 1887.— 34. Neumann, H. Arch. f. KinderUilk. Bd. xii. 1891, S. 54.-35. Oui.
Rev. prat, d'obstit. et de pcediat. Jan. and Feb. 1897. — 36. Pomoeski. Arch.f. Kinder-
heilk. Bd. xiv. 1892, S. 165. — 37. v. Pebuschen. Centralbl. f. Gyndkol. 1894. — 38.
Kehn. Centralbl. f. Kinderkrankh. 1878, S. 227. — 39. Eibemont. " Des h^morrhagies
chez le nouveau-n6." Thise, Paris, 1880. — 40. RoGBE. Gaz. des h6p. No. 66, 1887,
p. 525. — 41. KoMMB. Archives de tocologie, 1895, p. 25. — 42. Eunge. Krankhsiten
der ersten Lebemtagen, 2te Aufl. 1893. — 43. Sohaffee. Centralbl. f. Gyndkol. No. 22,
1893.-44. Thomson, J. Edin. Med. Joum. Jan. 1892, p. 614.— 45. Townsend.
Arch. ofPediat. 1894, p. 657.-46. Weigeet. Oesterr. Jahrb. f. Padiatr. 7ten Jahrg.
1876, S. 98. J e>
J. T.
S68 SYSTEM OF MEDICINE
PURPUEA
Definition. — Spontaneous extravasations of blood into the skin, mucous
membranes, and internal organs of the body, sometimes accompanied by
free haemorrhages from mucous surfaces.
Etiology and Pathology. — Morbid anatomy simply reveals the exist-
ence and extent of distribution of hsemorrhagic eflusions, often accom-
panied by evidences of anaemia. In a minority of cases in the mucous
membranes, and more rarely in the skin, erosions or ulcerations are met
■with in connection with the haemorrhages, but these are clearly the effects
and not the cause of them ; in mucous membranes the moisture of the
part, and in some organs the digestive property of the secretions, tend
to produce this result. In the hollow viscera blood may be found in con-
siderable quantities, and the serous cavities may contain blood-stained
serum. Besides the skin and mucous membrane, haemorrhage occurs in
the solid organs and in the serous membranes. They are found in the
lungs, kidney, spleen, liver, brain, and retina ; indeed, there is no part
in which haemorrhages may not occur. In the brain, from the delicacy
of its structure and feeble resistance, the haemorrhage may reach con-
siderable magnitude, and may be fatal. The pleura, pericardium, peri-
toneum, and pia-arachnoid are often dotted over with small extravasa-
tions. The haemorrhages vary in size from a pin's head to a patch as
large as the palm of the hand. On post-mortem examination the most
important changes found, other than haemorrhages, are in the kidneys
and lungs. Slight degrees of diffuse or parenchymatous nephritis are
relatively common. Congestion and oedema of the lungs are frequently
present, and are often the determining cause of death. Ulceration of the
intestine and enlargement of the solitary and agminated glands are some-
times present.
With regard to the mode of escape of the blood in this as in other
conditions in which spontaneous haemorrhages take jjlace, it may be
by rhezis — ^by rupture of blood-vessels, or by dia^pedesis — ^by the escape of
blood corpuscles through unbroken vessel walls. The former is most
probably the process in the great majority of cases. Though many
observers have failed to discover rupture of blood-vessels at the seat of
the extravasations, Unna and his pupil Sack (20) have shown they are to
be detected by certain methods of examination. According to Unna, it is
the veins that give way; and he has pointed out that the laceration
occurs especially at the junction of the superficial part of the subcutaneous
tissue with the lower part of the cutis. At this point, which he regards
as one of less resistance, the vessels lose their well-marked adventitia,
and lack the support of the highly elastic cutis. The extravasated blood
from its seat of origin percolates the epidermis, and occasionally tho
PURPURA 569
sebaceous and sweat glands ; in some cases sero-hsemorrhagic extra-
vasations take place also in the subcutaneous and intermuscular tissues.
The causes that lead up to and actually determine the escape of blood
are probably many and complex. Search has naturally been made in the
walls of the blood-vessels for changes apt to cause them to give way.
In some cases inflammatory changes have been found, and naay in such
instances have been the cause of the ruptures. In the majority of cases,
however, the inflammation is the result of the violence to which the
coats of the vessels have been subjected, an inflammation which may
extend to vessels at some distance from the rupture. A hyaline degenera-
tion, either of the intima or of the adventitia, or both, has been found by
some observers. In the well-known case recorded by Wilson Fox a
lardaceous change was found in the vessels of a syphilitic subject.
Unna properly remarks, and experience of these changes in other cir-
cumstances confirms his opinion, that these hyaline . and lardaceous
changes would rather have a tendency to restrain than to encourage
hsemorrhage. Venous thrombosis, as in so-called "purpura thrombotica,"
has been met with occasionally ; but probably it stands in the relation of
eff'ect rather than of cause. Capillary emboli have been found in sar-
coma (Hilton Fagge), in leucocythsemia, and in pyaemia, and may have
a direct causal influence; but numerically such cases are very infre-
quent, and afford no explanation of the majority of cases of purpura
in which they are absent. In recent years great attention has been
devoted to the search for micro-organisms in the blood, in the blood-
vessels, and in the tissues. Various bacteria have been found by differ-
ent observers in some cases, but in other cases the same observers
have failed to discover them. The presence of micro-organisms in the
" blood-vessels, even in large numbers as in diphtheria or anthrax, does
not necessarily give rise to hsemorrhage ; moreover, apart from the
negative results of the search for bacteria, the circumstances in some
cases in which purpura occurs make it unlikely that its causes are of
this kind. Though thus not necessarily leading to rupture of vessels or
diapedesis, they may nevertheless affect the vessel walls indirectly, by in-
ducing some chemical change in them, as suggested by Watson Cheyne
and Unna. Further, as Watson Cheyne has pointed out, the presence
of bacteria does not necessarily imply that their entrance into the
blood is the starting-point of the disease ; the alternative view, however,
may be entertained that, although the primary cause may be of quite a
different nature, the result may be such an alteration of the fluids of the
body that, of the innumerable organisms present in the mouth and in-
testinal tract, certain species may be enabled to penetrate into the blood
and to live in it. It is quite possible, also, that some poisonous toxin or
albumose formed in other parts of the body may be absorbed, and act
chemically upon the blood-vessels, or on the vaso-motor nerves, produc-
ing variations of blood-pressure which at the weakest points they are un-
able to resist. In the whole class of specific diseases, whether in those in
which micro-organisms have been demonstrated, or in those in which so
S70 SYSTEM OF MEDICINE
far they are only assumed, the bacteria or their products must play an
important part in the production of the cutaneous haemorrhages which are
an occasional feature of nearly all members of this group of diseases.
The fact that purpuric phenomena are not uncommon in certain of them,
such as scarlet fever and measles in which no specific micro-organisms
have as yet been demonstrated, should make us chary of denying the
possible existence of bacterial influence in the purpura of other diseases
in which up to the present no micro-organisms have been found.
It is certain that cutaneous haemorrhages are sometimes determined,
and in all probability primarily caused by nervous influences ; as in the
case of purpura occurring in the situation of the lightning pains of tabes
(Strauss, 1 9), and in connection with certain neuralgias (Weir Mitchell).
The mechanism of the hsemorrhage in such cases is hitherto purely con-
jectural ; but it seems most probable that, by acting on vaso-motor centres,
it produces variations of vascular pressure under which the blood-vessels
give way in the situation already indicated at the points of least resist-
ance. Though purpura is one of the manifestations of haemophilia,
the histopathology of the latter need not be fully discussed here (see
"Haemophilia," p. 552), nor would it materially elucidate the pathology
of the majority of cases of purpura. Haemophilia is believed, however,
by some authors to be due to a congenital defect in the vascular walls.
It is quite possible that in some cases of purpura a hsemophilic taint
may be an element in the haemorrhagic tendency.
Venous stagnation plays a part in the production of purpura. Though
not of itself a sufiicient explanation of hsemorrhage, it is evidently a
factor of importance, as in nearly all cases of purpura the haemorrhages
begin and are most marked in the lower extremities, the veins of which
have to support a longer and heavier column of blood than those of other
parts. As a rule, however, something more than stagnation is necessary
to bring about rupture or diapedesis. When hyperaemia co-operates with
stagnation the conditions are favourable to haemorrhage (Unna).
Next, in relation to the escape of blood from the vessels, we have to
consider the influence of the quality of the blood. The changes in the
composition of the blood in purpura may be of the most varied kind : (i.)
deficiency of the red corpuscles as in pernicious and other severe forms of
anaemia, (ii.) excess of white corpuscles as in leucocythaemia, (iii.) deficiency
or excess of some of the saline constituents of the blood as in scurvy, (iv.)
alterations in the reaction, (v.) alterations in the specific gravity, (vi.)
deficiency in the fibrin-forming elements may all play their parts in
the initiation of changes in the vessel walls and in their permeability.
Lastly, the presence in excess of some organic matters such as bile, urea,
and other products of metabolic changes as in jaundice or uraemia, or
the addition to the blood of extraneous matters, have all a tendency to
promote some chemical or vital changes which render the vessels liable
to rupture or increase the permeability of their coats. In the latter
category we have important evidence of the efifects of certain chemical
substances. The observations of Prussak, confirmed by Wickham Legg,
PURPURA 57 1
have demonstrated that chloride of sodium injected into the vessels or
subcutaneous tissues of the frog gives rise to diapedesis of coloured
corpuscles which, under the microscope, may be seen to pass through the
intact walls of the blood-vessels (9). Similarly, in certain persons, iodide
of potassium, as well as other drugs, give rise to purpura. Though the
exact mode of operation of such agents has not been worked out, we
must ascribe some influence, direct or indirect, to chemical action on the
walls of the blood-vessels.
Finally, it must be pointed out that a diminution of support to the
blood-vessels by the tissue immediately surrounding them may lead to
their rupture. Thus purpura occurs in those who have wasted much
from severe or protracted diseases (convalescence purpura) ; in the wast-
ing, loss of elasticity, and vascular degeneration of the aged (senile pur-
pura), and in the newly-born (purpura neonatorum).
Keviewing briefly the pathological condition's under which purpura
occurs, we may arrange them as follows : —
I. (a) The infective diseases, in nearly all of which, but especially
in small-pox, measles, scarlet fever, cerebro-spinal fever, syphilis, and
malaria, purpura is an occasional incident.
(6) Eheumatism, which may be placed temporarily in this class, but
requires separate description.
(fl) The various conditions under which certain organic matters pre-
sent in excess in the blood — such as bile, urinary constituents, or certain
adventitious organic poisons, such as snake venom — may gain access to
the blood.
(5) The presence in the blood of extraneous chemical substances,
such as phosphorus, mercury, mineral acids, salicylic acid, iodide of
potassium. For clinical purposes group (A) should be considered apart
as " toxic " or " drug " purpura, but pathologically it fits in here.
(«) Conditions in which some constituent of the blood is wanting, as
in scurvy.
(/) Alteration in the formed elements of the blood, as in anaemia and
leucocythsemia.
To Series I. the term " Vascular purpura " may be given.
II. (a) Conditions that offer an impediment to the circulation,
general or local; as in diseases of the heart and large vessels, and
tumours compressing them, thrombosis, temporary vascular spasm or
paralysis ; as in convulsive seizures, whooping-cough, or angina pectoris.
(6) Want of mechanical support of blood-vessels, as in wasting, in
the newly-born, and the aged.
Series II. may be designated "Mechanical purpura."
III. Conditions in which the direct influence of the nervous system
can be traced, as in tabes, neuralgia, and the like. To this series the
name " nervous purpura," or purpura of nervous origin, inay be applied.
IV. Congenital imperfection of the blood-vessels, as in haemophilia —
" haemophilic purpura."
In the absence of a common cause, of a definite clinical course, of
572
SYSTEM OF MEDICINE
lonstant pathological changes, it is obvious that purpura is not a con-
sistent or uniform symptom group, but is itself a symptom entering not
into one only but into many groups.
The best notion of the circumstances in which purpura occurs will be
conveyed by an analysis of 200 cases from the records of the London
Hospital. They were not selected, but taken consecutively, so far as
the records permitted. They are given in the following table : —
Table of 200 Cases of Purpura in the London Hospital, arranged
as regards probable Causes or associated Conditions.
Males.
Females.
Total.
Rheumatism . • .
33
28
61
Doubtful rheumatism
7
3
10
Bright's disease
7
2
9
Heart disease .
3
5
8
Ansemia ....
3
3
6
Leucooythaemia
1
0
1
Scurvy ....
6
0
6
Privation and dietetic
3
2
5
Pyasmia ....
0
2
2
Ulcerative endocarditis
2
0
2
Malaria ....
0
1
, 1
Rickets ....
1
0
1
Whooping-cough
0
1
1
Congenital syphilis .
1
1
2
Tuberculosis
3
1
4
Alcoholism
2
0
2
Toxic (drugs) .
3
0
3
Cirrhosis of liver
1
0
1
Convalescence .
2
0
2
Injuries ....
2
0
2
Haemophilia
0
1
1
Varicose veins .
0
1
1
Peripheral neuritis .
1
0
1
Unexplained
31
37
68
Totals
112
88
200
This table does not present any instances of purpura in con-
nection with the specific fevers, for these, with the exception of enteric
fever, are not admitted. Nor are there any cases of P. neonatorum or
P. senilis.
Age incidence will be best shown by the subjoined table : —
PURPURA
573
Table of 200 Cases of Purpura arranged in Decades.
Up to 10
years.
11 to 20.
21 to 30.
81 to 40.
41 to 60.
61 to 60.
61 to TO.
Totals.
Males
Females
24
25
29
28
31
17
13
10
9
7
2
1
4
0
112
88
Totals
49
57
48 •
23
16
3
4
200
From these figures, which fairly represent the condition in which
purpura occurs, apart from the eruptive fevers and in the newly-born,
it will be observed that purpura is more common in the male than in the
female sex, in the proportion of 14 males to 10 females — not quite \\
males to 1 female. This holds good for aU ages with the exception of
the first decennium, in which the females exceed the males by one. It
will also be observed that the greatest number of cases occur in the first
three decades, 77 per cent in persons under 30 years of age. In the fourth
decade the numbers rapidly fall to less than half of those in the third
decade ; still fewer cases occur in the fifth decade, and only 7 cases occur
in persons of either sex over 50 years of age.
The number of cases here dealt with is probably larger than in any
published series ; but it will be seen how comparatively rare purpura
is when I say that 200 cases represent the number occurring amongst
63,834 medical cases in \^\ years. They only amount to 0-3 per cent of
the medical cases, and this is probably a fair calculation of its occurrence
in purely medical practice.^
The great variety of supposed causes or associated conditions is
sufiiciently striking. Still more so is the fact that in one-third of the
cases tabulated no explanation was afforded for the purpura, though in
several of the cases a necropsy was made. It will thus be seen how
extremely complex is the pathology of purpura. All we can do in the
present state of our knowledge is to accumulate further information,
and to exhaust every means — ^histological, bacteriological, and chemical
— in the investigation of cases. It will be observed that in by far the
majority of cases in which anything definite can be ascertained as to the
causation of purpura this is of a vascular character — some known or
probable alteration of the blood, or some condition which brings about
a change in the blood-vessels ; and, arguing from the known to the un-
known, it seems probable that, in those in which no definite causation can
be ascertained, purpura is due to one of these two kinds of change.
Symptoms. — Certain phenomena are common to most cases of
purpura.
^ A very few cases, too few to affect the calculation, were omitted as the notes were
incomplete.
574 SYSTEM OF MEDICINE
Chwnges in the extravasated blood. — Eecent extravasations appear of a
more or less bright red or crimson colour. They are usually oval or round,
but may occur in lines or streaks — vibices. In a short time they become
of a dull purple, and later of a brownish red tint ; lastly, a brownish stain
persists for a considerable time. In some cases a bluish green colour is
present. In quite superficial haemorrhages, spots, as they fade, present
a yellowish hue, passing into a faint brown. As regards the changes in
the blood effused, when the haemorrhage takes place into the cutis, there
begins, according to Unna, very soon after the occurrence of the bleeding
solution of the haemoglobin, which is partly reabsorbed with the blood-
plasma, and partly crystallised in the tissue (precipitated). Where large
masses of blood corpuscles are closely packed, they break up, without
previously giving up their haemoglobin, into yellow or brownish flakes,
which are gradually converted into pigment granules, and as such are
partly taken up by the connective tissue cells.
Pyrexia. — A certain degree of fever is present in more than half the
cases. In the majority it is slight and transient ; in others the disease
runs a moderately febrile or highly febrile course (P. febrilis), and
hyperpyrexia has been known to occur. The decidedly febrile cases are
nearly always characterised by a greater severity, and are therefore
attended with greater danger than those which are non-febrile ; other-
wise no important differences are noticeable.
Albuminuria, apart, of course, from cases in which it is plainly secondary
to Bright's disease, is of rather frequent occurrence in purpura ; it occurs
in both febrile and non-febrile cases, and corresponds with the statement
(p. 568) that in fatal cases the kidneys are frequently found diseased.
Digestive system. — Derangement of the stomach and intestine is
common. Apart from anorexia, which is frequent, colic in severe paroxysms,
vomiting and difl,rrhoea are so pronounced in some cases as to have been
constituted into a special form of the disease (Henoch's purpura).
Haemorrhages. — Haemorrhage may occur from any of the mucous
surfaces. Epistaxis is the most common; next, haemorrhage from the
gums and throat, and, following these in frequency, from the intestines,
urinary passages, stomach, lung, and sexual organs. Intra- visceral and
interstitial haemorrhages also occur ; and haemorrhages in the retina may
be detected during life by the ophthalmoscope. Eetinal haemorrhages
are, however, rare in purpura.
On account of the variety of circumstances in which purpura is met
with, some classification in the investigation of cases is absolutely neces-
sary. Dr. Eadcliffe Crocker's classification has a pathological basis ; he
makes the following varieties : (i.) Certain blood alterations ; (ii.) visceral
disease ; (iii.) want of support to the vessels ; (iv.) sudden changes in
the circulation ; (v.) diseases of the nervous system.
Dr. Pringle makes the following classes : A. Symptomatic purpura :
(i.) Mechanical, due to increased blood-pressure ; (ii.) dependent on changes
in the blood or walls of blood-vessels ; (iii.) toxic ; (iv.) due to disordered
innervation ; (v.) the result of a specific infective virus ; (vi.) cases which
PURPURA 575
cannot be considered as belonging to any of the foregoing classes, and
which must provisionally be classified as idiopathic. B. Purpura sim-
plex. C. Purpura hsemorrhagica.
Professor Osier gives a very good provisional grouping of the varieties
of the condition. A. Symptomatic purpura : (i.) infective, (ii.) toxic, (iii.)
cachectic, (iv.) neurotic, (v.) mechanical. B. Arthritic purpura : (i.) a
mild form known as P. simplex, (ii.) peliosis rheumatica, (iii.) Henoch's
purpura. 0. Purpura haemorrhagica.
The following kinds will be described here :— (i.) Purpura simplex,
(ii.) purpura hsemorrhagica, (iii.) purpura rheumatica, (iv.) iodic purpura,
(v.) Henoch's purpura.^ There is no fundamental distinction between
P. simplex and P. hsemorrhagica ; the former is a mild form of purpura,
the latter a severe purpura with haemorrhages from mucous surfaces. Both
are symptomatic of a great variety of causes.
Purpura simplex. — With or without preceding constitutional disturb-
ance, hsemorrhagic extravasations make their appearance in the skin.
They frequently begin in the lower extremities, but become generally
disseminated over the whole surface. They may present a rough sym-
metry, or have a random distribution. The spots are generally circular
or rounded, but may occur in streaks ; they vary in size from mere petechise
to extravasations as large as half a crown or larger. The attack may be
ushered in by a slight rise of temperature, or febrUe disturbance may
arise in the course of the attack. Many cases are non-febrile throughout
their course. The disease is most common in young persons. The
patient may be ansemic, or may present a healthy appearance, and be well
nourished. There may be some malaise, digestive troubles, and other
constitutional disturbance; or these may be wanting. The first spots
fade, passing through the changes of colour described, and new ones ap-
pear ; so that all varieties of colour are present. After lasting a variable
and indefinite period, usually a week or two, no fresh spots make their
appearance, the old ones fade, and the attack comes to an end, leaving
pigmentation of the skin where the hsemorrhages have been present, for
some weeks or longer. '
Purpura hsemorrhagica (Morhus maculosus Werlhofii). — The etymo-
logically meaningless name P. hsemorrhagica — for all purpura is hsemor-
rhagic— is applied to cases in which not only cutaneous extravasations are
present, but in which hsemorrhages take place from mucous surfaces also.
It represents the more severe and dangerous kind of purpura. No more
than P. simplex is it to be regarded as a uniform symptom group, for it
occurs under a variety of conditions.
' Neurotic purpura, or purpura of nervous origin, cannot be made into a well-defined
variety ; but the name neurotic purpura may be applied to cases in wbiob the hsemorrhages
can be confidently attributed to nervous influence. Dr. Weir Mitchell has described cases
of neuralgia in which hemorrhages occurred in the skin about the penis ; Strauss (16) and
others, purpura in connection with tabes. Purpura is also met with in angina pectoris,
meningitis, whooping-cough and epilepsy. In the latter categories the immediate mechanism
is probably vascnlar, and consists in a local increase of blood-pre sure.
576 SYSTEM OF MFDICINE
It may begin witli more or less constitutional disturbance — headache,
debility, gastric pain, and vomiting, and be followed by extravasations
into the skin and mucous membrane, and free haemorrhages from the
latter. Or it may begin as P. simplex and later become P. hsemorrhagica,
as bleedings take place into and from the mucous surfaces. The haemor-
rhages vary in size as in P. simplex, but tend to be larger, and are often
accompanied by hsemorrhagic oedema in large patches — as large as the
hand or larger— appearing in certain parts, raised, reddish, or purple-blue
in colour, and pitting on pressure. The orbits, the penis, and scrotum
occasionally become extremely swollen, and the skin tense and of a livid
colour. The appearance may suggest a fear of sloughing, and indeed the
fear may be justified. The cutaneous haemorrhages pass through the same
stages as in P. simplex, but appear in rapid succession, and are often of
large extent. Haemorrhages in severe cases are usually met with in the
mucous membrane of the mouth and throat ; and in this situation they
may give rise to alarming symptoms, and even occasion a fatal issue. In
several recorded cases haemorrhages have taken place into the palate
and tongue. When occurring in the latter organ acute swelling of
the tongue, resembling acute glossitis, has been produced, necessitating
incisions for the relief of the consequent dyspnoea. In one or two cases
sloughing of the tongue, with shedding of its apex, has occurred.
Of the haemorrhages that take place from the mucous membranes
epistaxis is the most common ; haemorrhages from the mouth and throat
are also very common : in some cases haemorrhages occur from tho
stomach, intestines, lungs, and genito-urinary organs. The bleedings
from the mucous membranes may be very severe and frequently re-
peated, and in some cases are uncontrollable. Though in some cases
anaemia may not be present at the outset, it rapidly makes its appear-
ance, which is not surprising when we consider the large amount of
blood lost from the mucous surfaces and into the skin. Von Laache has
recorded a case in which, eighteen days after the beginning of the disease,
the red corpuscles numbered only 2,680,000 per c.mm., and the haemo-
globin was 0'067 per c.mg. In another, a woman twenty-one years of
age, the corpuscular richness was 2,091,900. When the disease has
lasted some time, and, as would be anticipated, when copious internal
hseaiorrhages have taken place, the blood richness, in numbers and
colour, shows still greater reduction. Hayem has recorded a case in
which the red corpuscles fell below 1,000,000 ; Quinquand a case with
only 740,000 per c.mm. ; and H6rard a case in which the cor])uscular
richness was 1,885,000, when first counted, but fell to 620,<i00 per
c.mm. I have recorded a case (10) in a child eleven months old, in
which the red corpuscles just before death numbered only 290,000 per
c.mm., or 5-8 per cent, with one white to fifteen coloured corpuscles. In
this case the great debasement of the blood was due to uncontrollable
epistaxis, and the patient died quite exsanguine. The blood that exude.-.
in such cases of extreme ansemia is only tinged with red, appearing a 3
a thin serous exudation.
PURPURA 577
Fever is present in the majority of cases of P. haemorrhagica. It
may reach a high grade — 104° F. or higher, and maybe hyperpyrexia! —
105'5° or higher. Such cases with high fever, extensive extravasations,
and copious and repeated haemorrhages from the mucous membranes,
may run a very rapid course, and end fatally in the course of a few
days. Such cases have been described as P. fulminans. In severe cases
haemorrhages may take place into the brain, and may occasionally be
seen during life in the retina. In P. haemorrhagica pains are often
present in the joints and linibs, even in cases in which there is no reason
to believe the condition to be of rheumatic nature. Schebey Buch has
drawn attention to effusion into the joints in non-rheumatic cases.
Albuminuria, with, or without blood, is often present in cases of P. hsemor-
rhagica. In fatal cases pulmonary oedema, often associated with haemor-
rhage into the lung due to exhaustion, is commonly the determining
cause of death.
In cases which pursue a favourable course, or which do not end
fatally, the haemorrhages into the skin and from the mucous membranes
recur from time to time over a period of days, or, more usually, of weeks,
in a fitful manner, and eventually cease ; the patient being left extremely
weak, anaemic, and often much wasted.
PuEPUKA EHEUMATICA (Schonlein's Peliosis rhewmatica). — This kind
has gradually gained increased recognition, though twenty or fifteen years
ago it was scarcely ever diagnosed. Schonlein's description is worth
reproducing, as differences of opinion have arisen as to the meaning of the
name he used.
" The patients have either already suffered from rheumatism, or rheu-
matic symptoms accompany the attack ; slight periodic throbbing pains
in the joints (in the ankles and knees, rarely in the hand and shoulder-
joints), which are cedematously swollen and tender on pressure. The
characteristic spots of the disease in the majority of cases first appear on
the extremities, especially on the lower extremities, and here only as
high as the knee (rarely on the upper). The spots are small, of the size
of a lentil to that of a millet seed, bright red, not raised above the skin,
disappearing under the pressure of the finger [italics not in original] ; they
gradually become dirty brown or yellowish, the skin over them slightly
desquamates with a branny scale. The eruption comes out in crops,
often during several weeks. Ever so slight a change of temperature, as
for example passing into a colder room, may occasion a fresh outbreak.
The eruption usually appears with some fever, of a remittent type.
Towards evening the symptoms are at their height, -^th a recession in
the morning. There is frequently a deposit in the urine." It is clear
from Schonlein's own words that he described an erythema papulatum,
for he expressly notes the colour " disappearing under pressure." Further,
in discussing the diagnosis, he gives the diagnostic criteria from Werlhof 's
disease (P. haemorrhagica). The majority of writers, following Schon-
lein, regard purpura rheumatica as a purpuric erythema, though this is
VOL. V 2 p
578 SYSTEM OF MEDICINE
scarcely justified from his description that the colour disappeared on
pressure. Some go farther and appear to regard all purpura as erythe-
matous in nature. Though an allied process, I believe it better to keep
the two conditions distinct, and in the following description of purpura
rheumatica I shall restrict the name to a condition which is purpuric from
the beginning, and in which the spots do not disappear on pressure at any
stage. In other respects Schonlein's description of tie eruption coming
out in crops, and of the aggravation of diseasein the evening, is singularly
apt.
The disease occurs with about equal frequency in the two sexes, and
is most common in the second, third, and fourth decennia (from eleven to
forty) ; it is rare before ten years of age and after forty. In some cases
the purpuric eruption makes its appearance whilst the patient is suffering
from acute or subacute rheumatism. More commonly the arthritic
symptoms arise coincidently with the purpuric eruption ; in a few cases,
in which arthritic symptoms are doubtfully present in the attack, or are
entirely absent, an attack of arthritic rheumatism may appear at some
subsequent period, thus revealing the rheumatic nature of the purpura ;
or, perhaps, to be more exact, thus demonstrating that the patient is a
rheumatic subject. Apart from cases in which acute or subacute rheu-
matism ushers in the purpura, the very characteristic onset and course of
the disease is as follows : — The patient has pain in the lower extremities,
which may be of a dull aching character, but frequently and character-
istically is a sense of tension — a " sensation of bursting " in the parts
affected, as patients frequently describe it ; often there is itching. When
these symptoms are present (and patients who have had a previous attack
know well their meaning), bright red spots, which do not disappear on
pressure, are seen on the legs. In the majority of cases when they
first make their appearance they are raised (P. papulosa). The erup-
tion and its accompanying discomforts usually make their appearance
in the later part of the day, afternoon or evening. The knee and
ankle joints are usually painful and often swollen and tender, some-
times the skin over them is slightly reddened. A slight degree of oedema
of the lower part of the leg, of the ankle, and of the dorsum of the foot
is present in nearly all cases. By the following morning the pain remits,
and inspection shows that the spots are now of a purple or dull red
colour, and no longer raised. On the second evening, or after an interval
of two or three days, the same phenomena are repeated — the aching of
the legs, the pains in the joints and oedema, and the appearance of
another crop of bright red spots similar to those first observed. The
spots pass through the usual stages of discoloration characteristic of
haemorrhages into the skin, and if the patient is seen after the occurrence
of two or three outbursts, and at a time when a fresh crop has recently
appeared, we observe: — 1. Bright red raised spots, varjring in size from
a millet seed to a threepenny piece or larger, not disappearing on pres-
sure. 2. Spots of a similar size of dull red or purple colour, but not
raised above the surface, and unaffected by pressure. 3. Yellowish brown
PURPURA 579
stains. The affected limbs are tender to pressure and slightly oedematous.
In most cases, as already stated, there are pain and swelling of the joints
of the lower extremities, and in some of the elbows and wrists ; even in
cases in which the skin of these parts is not affected by haemorrhages. The
joint affection often persists between the outbursts of haemorrhages,
though exacerbations of pain and swelling occur in the attacks. The first
outburst of hsemorrha'ges is usually confined to the lower part of the legs
and feet. In subsequent outbursts there is a tendency to an extension
of range, so as to involve the upper part of the legs, and, later still, the
thighs and buttocks. In slight cases the eruption is limited to the lower
extremities, but in more severe cases the forearms and arms are affected
also. Usually when the thighs are affected the skin above and below
the elbow is the seat of haemorrhages. The eruption is so far sym-
metrical that if one leg is affected the other leg is affected also ; and if it
attacks the upper extremity both will be attacked. The eruption shows
no marked predilection either for the flexor or extensor surfaces of the
limbs. In the great majority of cases it is confined to the extremities ;
but in the more severe cases, especially those in which the arthritis and
pyrexia are great, the trunk and face also are affected. Haemorrhages
into and from the mucous membranes are rare, but in a few cases small
haemorrhages may be seen in the buccal mucous membrane ; and in rare
and very severe cases extensive haemorrhages may take place into the
tongue (intra-muscular) and throat In about one -third of the cases
some degree of pyrexia is present, and probably, if careful thermo-
metric observations were made in the evening at the time of the erup-
tion, some elevation of temperature would be found in nearly all of
them. Sweating is not a marked symptom unless the arthritis be pro-
nounced. The amount of constitutional disturbance is variable, this being
slight in the majority of cases; but in some malaise and debility are
present. The majority of patients are able to walk about stiffly in the
early part of the day, but locomotion is very difficult and painful in the
later day, especially at the time of the outbreaks of haemorrhages. Any
exertion tends to bring on an attack. The department for diseases of
the skin, of which I have charge, is open in the morning, and patients
tell me they had a bad attack in the afternoon or evening of the days
when they had been to see me. Exertion seems to me to determine
attacks much more than changes of temperature, to which Schonlein
referred them. The eruption usually lasts an indefinite time, unless
treatment of a certain kind is adopted for several weeks, or months ; I
have known it to persist for two years. The disease is occasionally,
though extremely rarely, fatal. Usually it is a benign affection. It
is very apt to recur.
The assemblage of symptoms is very definite and characteristic. The
occurrence of haemorrhages — usually confined to the extremities, appearing
in crops, usually in the latter part of the day — the arthritic pain and
swellings, and its protracted course, distinguish it from other forms of
purpura, and from erythema exudativum multiforme. It has undoubtedly
S8o SYSTEM OF MEDICINE
close clinical alliances with the latter, which also, in a large proportion
of cases, is of a rheumatic nature, and the two may occur in the same
subject ; but in the cases to which I would restrict the name purpura
rheumatica the eruption from first to last is purpuric, and not ery-
thematous. The evidence of its connection with rheumatism is, in the
majority of cases, extremely distinct. The arthritis, which is present
in many cases, is characteristic, and may precede the purpura ; so that
the diagnosis of acute or subacute rheumatism is already made. In
other cases the patient has previously suffered from rheumatic fever.
In a considerable proportion of cases valvular disease, usually mitral
incompetence, is present ; and in a few it may arise during an attack.
Many patients have had other affections belonging to the rheumatic
series, such as tonsillitis, endo- and pericarditis, pleurisy, chorea ; and a
family history of rheumatism is very common. I have seen two brothers
with purpura rheumatica at some years' interval. The second one died
of heart disease a few years later. In a certain number of cases the
arthritic symptoms in the attack are equivocal or absent ; but the com-
plex of symptoms described have been definite and identical with those
in which the rheumatic nature was beyond dispute ; so that when the
symptoms above described are present, I am of opinion that we are
justified, even in the absence of arthritis, in diagnosing purpura rheu-
matica. I have seen a case in which no arthritis accompanied the
purpura, yet (at an interval of a year or more) an attack of rheumatic
fever subsequently appeared. In the list I have given of the ascer-
tained causes of purpura, rheumatism, it will be observed, stands very
high, giving in the 200 cases 30 '5 per cent, exclusive of doubtful but
still probably rheumatic cases.
Iodic purpura. — ^Fournier was the first to give a good descrip-
tion of this form of purpura. The eruption is generally confined to the
lower extremities, and in the majority of cases to the parts -below the
knee. The eruption consists of discrete miliary hsemorrhagic spots,
bright red when recent, not elevated, not obliterated by pressure, un-
attended with heat, pain, or swelling. The eruption comes out at an
early period of the iodide treatment, and continues to appear for two or
three days. It remains for a certain time as a staining of the skin, the
blood undergoing the changes of colour usual in cutaneous hsemorrhages,
and finally disappears by the end of two or three weeks. During its
progress a renewed attack may sometimes be induced by augmenting the
doses, and then the bright red recent haemorrhages contrast very
markedly with those that are fading. Though usually confined to the
legs, it may affect the trunk and the face, as in a case I have recorded.
The purpuric spots are usually more pronounced in the anterior than in
the posterior parts of the legs. Successive outbreaks are usually less
profuse than the original one. It may be accompanied by some oedema
of the legs, but this is not usually the case. The various salts of iodine
seem all to produce purpura, but exceptions to this rule are met with ;
PURPURA 581
some persons can take sodium or ammonium iodide witliout inducing it,
whilst potassium iodide is operative ; or potassium iodide may fail to pro-
duce it, whilst ammonium iodide may be operative. As potassium iodide
is the salt most frequently prescribed, purpura is most frequently met
with in patients taking this preparation. It is held by Besnier that pure
iodine will not cause the haemorrhages, and he has illustrated this fact in
the person of a man who had purpura in the lower limbs every time
he took iodide of potassium ; yet, although tincture of iodine caused
symptoms of iodism in him, no purpura appeared (1 2). Purpura is a very
rare consequence of the administration of potassium iodide. Usuall}' it
is quite a benign and unimportant affection, but one to be borne in mind,
lest it be misinterpreted. Occasionally, moreover, the salt may give
rise to very grave symptoms and even prove fatal ; as in a case I have
recorded. In this case fatal purpura followed a single dose of %\ grains
of potassium iodide in an infant five months of age. In prescribing
iodides to young children a small dose should be first given, and if
tolerated, the dose may be augmented.
The reaction is clearly due to idiosyncrasy, as it occurs in a very
small minority of persons. It does not depend on the debilitated state of
the patient, whose nutrition may be quite good. It is possible that
syphilis favours its occurrence ; but the frequency with which iodides are
administered for syphilis and the rarity of iodic purpura show that
personal peculiarity or idiosyncrasy is the determining factor. It is
probable that the cause of the iodide purpura is some chemical action of
the drug on vaso-motor centres producing variations in pressure in the
area in which purpura appears ; but it is possible that the drug may have
a selective action on particular vascular areas, rendered more vulnerable
than usual by incidental influences.
Henoch's purpura.— Though Willaip (21) many years previously had
described a case of this kind very graphically, it was not until Henoch
published a series of cases that attention was prominently directed to
this form, often called " Henoch's purpura " (6). Gouty recorded a number
of cases which he recognised as similar in nature to those described by
Henoch ; and Osier, who takes a more general view of purpura than I have
done in the present article (including it under erythema exudativum), has
particularly directed attention to the visceral complications.
The marked feature of this disease is the association of abdominal
symptoms (vomiting, colic, intestinal hsemorrhage) with purpura and
arthritic swellings. The attack may begin with rheumatic pains and
swellings of the joints, and be followed by purpura and colic with vomit-
ing and blood in the stools. Or it may begin with gastro-intestinal
derangement, and the purpura and articular swellings and pains follow.
What is especially characteristic of it is the occurrence of repeated out-
breaks of colic, vomiting, and hsemorrhage from the bowels, with purpura
and pains and swellings in the joints. The illness generally consists of a
series of such events over a period of some weeks or months ; but intervals
582 SYSTEM OF MEDICINE
of months may occur, and fresh outbreaks then take place. Recurrence
is one of its most characteristic features.
The colic is generally of a very intense character. The abdomen is
usually tender, especially over the colon. The vomiting is often severe
and protracted, frequently bilious, occasionally but not frequently bloody.
The stools contain more or less coagulated blood, but in some of the
attacks no blood may be passed. In some cases albuminuria is pre-
sent, and well-marked symptoms of nephritis set in which may prove
fatal; or this complication may slowly subside. Epistaxis, hsematuria,
haemoptysis may occur, but are not frequent. In the majority of cases
the eruption is purely haemorrhagic, but in others, in addition to the
purpura, purpuric oedema, exudative erythema and urticaria may be
present. Most commonly the eruption is confined to the extremities,
but it may involve the face and trunk ; and haemorrhages may occur in
the mouth and throat. In the attacks the joints are usually affected.
There may be only pain and stiffness, or there may be effusion and redness
of skin over the articulations. The dorsa of the feet are often swollen,
as in purpura rheumatica. There is as a rule little pyrexia, and it may
be entirely absent. In one of Osier's cases great coldness of the feet was
a prodromal symptom of the attacks, and in one case the spleen was
enlarged. Silbermann has published a fatal case (7) ; a child, aged ten
years, was attacked on December 15, 1887, with fever and pains in the
knees. On the 16th there was an outbreak of purpura, with colic,
hsematemesis, and melsena, and after persisting for three days the symptoms
disappeared. The attack recurred in January with great severity, and on
the 20th, 21st, and 22nd there were signs of peritonitis. The autopsy
showed an acute peritonitis, which had resulted from a perforation at the
fundus of the stomach. There was no ulceration in the bowels, but the
mucosa was swollen and congested. There were necrotic foci in the stomach
and intestines, and thrombi wer^ found in some of the blood-vessels.
Henoch's purpura is relatively most common in childhood, but it
occurs in adults also. As to the nature of such cases the evidence is
inconclusive, and whether the colic and vomiting stand in relation to the
haemorrhage from the bowels and stomach as cause or effect is uncertain.
Silbermann's case, however, suggests that haemorrhage is the primary
event and may lead to ulceration and perforation ; as haemorrhage is an
exceedingly rare or almost unknown event in colic of the most severe
degree, as in lead poisoning. Some of the cases appear to be of a
rheumatic nature — the patients, as in some recorded by Henoch, having
previously had a rheumatic attack without purpura or colic. Couty
regards the disease, by the exclusion of other causes, as of nervous
origin, affecting the vaso-motor nerves.
Diagnosis of Purpura. — It must be reiterated that purpura is rather a
symptom than a disease. It is not sufficient, therefore, to recognise purpura,
but the nature of the process in the individual case must be ascertained. To
recognise the symptom purpura is an extremely easy matter. The occur-
rence of haemorrhages in the skin and mucous membrane is demonstrated by
PURPURA 583
an eruption of blood-colouring matter not of traumatic origin, the colour not
disappearing under pressure. In many forms of exudative erythema there
is blood extravasation, but this is accompanied by overfilling of the blood-
vessels, which may be emptied by pressure, the colour returning when
the pressure is removed. To this condition the name purpuric erythema
may be applied ; but the name purpura should strictly be applied to cases
in which the haemorrhages are primary, unattended with erythema, and
not due to injuries.
Having decided that purpura is present the observer has next to
search for its cause. It is for this reason that some clinical classifioation
is not merely desirable, but absolutely essential. The first step is to
ascertain whether the purpura is an expression of one of the specific
diseases prone to be attended with haemorrhage. Small-pox, scarlet fever,
measles, pyaemia, syphilis, and rheumatism have especially to be borne
in mind. The diagnosis of purpura rheumatica has been sufficiently given.
Next, the various primary blood diseases have to be considered — per-
nicious anaemia and leucocythaemia in particular. The appearance of the
patient may afford a clue, but the most important matter is the examina-
tion of the blood. In the next place the possibility of scurvy must be
remembered. In this disease, in addition to the cutaneous haemorrhages,
subcutaneous and intra-muscular extravasations occur, producing brawny,
blood-stained patches in the hamstring muscles and calves of the legs,
and in the skin over the patches; and the gums are swollen and
bleeding. Evidence of insufficiency of fresh vegetable or animal food is
generally obtainable. In doubtful cases the effect of treatment will assist
in the diagnosis, as scorbutic cases rapidly improve when treated with
fresh vegetables and meat juice. It must be remarked, however, in this
connection that in certain cases of pernicious anaemia the gums may be
swollen and bleeding as in scurvy. To these cases the name " scorbutic
anaemia " has been applied. Scurvy being excluded, the possibility of
some poison having been accidentally or intentionally taken must be
considered — phosphorus, mercury, mineral acids, etc., being borne in mind ;
or some medicinal substance, especially iodide of potassium. Nor must
the possibility of a nervous origin be forgotten ; the history of the case,
and an examination of the nervous system, will determine whether this
cause be in operation.
Finally, in a considerable number of cases no definite cause can be
ascertained for the purpura, and such cases are indicated by the name
P. idiopathica. They must temporarily be relegated to the class purpura
simplex or purpura haemorrhagica, according to the symptoms presented.
It must be remembered, however, that this indefinite name serves but
to remind us of our ignorance ; and the observer must ever be on the alert
to discover the cause which will immediately remove the case to its own
category.
Ppogmosis. — Most cases of purpura end in recovery. The mortality
is probably about 14 or 15 per cent. Thus of the 200 cases above
analysed the mortality was 28, or 14 per cent. Sex does not appear to
584 SYSTEM OF MEDICINE
exercise any decided influence — the mortality in males, in the 200 cases,
being 14'2, -whilst in females it was 13-6. Age exercises some influence,
the gravity appearing to increase, on the whole, with the age of the
patient. But in the 200 cases analysed the mortality in the first decade
was 16 per cent ; in the second decade, 10 per cent ; in the third decade,
1 4 per cent ; in the fourth decade, 1 3 per cent ; in the fifth decade, 2 5 per
cent ; in the seventh decade, 25 per cent. It is thus seen that the greatest
mortality occurs in patients under 10 and over 40 years of age. Cases of
P. simplex almost invariably end in recovery ; but, on the other hand,
purpura simplex may be the beginning of a severe and fatal case of
purpura hsemorrhagica. The gravity of the case is generally stamped early
upon it. The severity and frequency of the cutaneous haemorrhages, the
occurrence of haemorrhages from mucous surfaces, the degvcn, of pyrexia,
the constitutional depression, the degradation of the blood, as ptoved by
the hsemoglobinometer and hsemocytometer, and the occurrence of marked
albuminuria, will draw attention to the danger attaching to the case. At
the same time it must be borne in mind that the most severe and
apparently dangerous cases sometimes end in recovery.
Treatment. — The patient in all kinds of purpura should be confined
to bed. Whenever a definite cause for the purpura is discoverable, a clue
to the treatment will be supplied. In the infective diseases it invariably
indicates a very grave condition, and calls for support by nourishing fluid
food and stimulants ; whilst at the same time some of the hsemostatics to
be subsequently mentioned, especially turpentine, should be administered.
In syphilitic purpura iodide of potassium should not be given, for it appears
in some cases to increase or to initiate the haemorrhages. In many eases
of P. rheumatica oil of turpentine appears to act as a specific ; it should
be given in ten or twenty minim doses in capsules, or suspended by means
of tr. quillaise saponariae or mucilage. The following mixture I have
used in numbers of cases with the happiest results : — 01. terebinth
TTL X., quillaise sapon. TTl^ x., aquam cassise ad §j. To be given three
times a day. Prof. Boeck of Christiania recommends antifebrin in five
or ten grain doses in these cases. Salicylates, in my experience, as well
as in that of Prof. Boeck, have little or no influence for good.
In cases in which no discoverable cause can be ascertained, as well as
in many in which there is a recognised cause, turpentine is, on the whole,
the best remedy. Ergot and hamamelis may be tried, but they have not
proved very efficacious in my hands. Calcium chloride, suggested by
Dr. Wright of Netley, is indicated when deficient coagulability of the
blood is proved or suspected, and certainly should be tried when other
remedies fail. It should be given at first in twenty-grain doses, every
three or four hours, the dose being reduced later to fifteen or ten grains ; as
when given in excess it diminishes the coagulability of the blood. Iron,
as preparations of the perchloride or persulphate, appears useful in some
cases in the attack, and should be given in convalescence to remove the
anaemia which so commonly results in severe cases. In Henoch's purpiu-a
Henoch himself has seen benefit from an ice-bag applied to the abdomen ;
PURPURA 58s
in chronic cases he recommends perchloride of iron. Osier in two
cases saw beneiit from arsenic, which appeared to control the tendency
to recurrences. In other cases, however, it failed.
PetechijE. — Minute haemorrhages in the skin, the size of a flea-
, bite. Such haemorrhages vary in colour from bright red, dark red, to
purple ; and have this characteristic, that the colour does not disappear
on pressure. Peteehise may be one of the expressions of purpura, in
which case they will be almost invariably associated with larger haemor-
rhages in the skin, and in these circumstances own the most varied causes
(see Purpura). Or they may be caused by the bite of the common flea.
In the latter case, when recent there is a small circular spot of
erythema with a pin-point haemorrhage in its centre. The erythema dis-
appears on pressure, to return when the pressure is removed, whilst the
central punctum remains, as it does also when the erythema spontaneously
subsides. When due to flea-bites, recent lesions, with the above
characters, will almost invariably be found afi'ording a clue to their
nature. Their position, on covered parts of the skin, as well as the
evidence of want of personal cleanliness of the patient and clothes, will
be of assistance in determining their nature. There is some evidence
that cachectic conditions and want of food favour the persistence of the
minute haemorrhages due to flea-bites, and their abundance undoubtedly
implies neglect. When associated with pyrexia they may cause mistakes
in diagnosis, especially as regards typhus and measles ; so that the subject
is not unimportant. Care with regard to the. above points will enable
the observer to avoid errors in diagnosis. The term petechial is applied
to diseases, especially fevers, accompanied by haemorrhages.
Stephen Mackenzie,
references
n }' -9^^™"^' Watson. Patholog. Soc. Tram. 1884, p. 412.— 2. Coutt. Gaz. hebd.
1876, Noa. 36-40.— 3. Crockeb, R. Diseases of the Skm, 2nd edit. p. 339.-4. Fournier
&vue mensuelle, Sept. 1877.— 5. Fox, Wilson. British and Foreign Med.-Chir
Eemew, 1865, p. 480.— 6. Henoch. "Ueber eine eigenthumliche Form von Purpura "
Berlin. Mm. Wochenschr. 1874, and Lectures cm Children's Diseases.— 1. Henoch's F^t-
schnft for 1890, quoted by Osler, " On the Visceral Complioations of Erythema Exuda-
tiTum Multiforme, ' Amer. Joum. Med. Sci. Dec. 1895.— 8. voN Laachb, L. Die
Anamie, Chnstiania, 1883, p. 41.-9. Legg, Wickham. St. Bartholomew's Hasp.
Keports, vol. xix. — 10. Mackenzie, S. Bntish Med. Journ. Sept. 1, 1883—11
Mitchell, Weir. Trans. College of Phys. Philadelphia, Anierican Journal of Med. Sci.
vol. Ivm. p 116—12. Morrow on Drug Eruptions, New Sydenham Society, 1893 :
footnote by P. Colcott Fox, p. 497.-13. Osler, William. The Principles and Praetice
of Medimm 2nd edit. p. 343.-14. Pbinolb. Fowler's Dictionary of Medicine, p.
'i^:~^°-, Pbussak. Sttsungsberichte der math, naturw. Classe der Icaiserl. Akad. der
Wissensehaftm, Wien, 1867, Bd. Ivi. Abth. 11, p. 13.— 16. Quoted bv DU Castel. Des
dnerses espices de purpura, Paris, 1883.-17. Schonlbin. AUgemeine und spec.
Path und Iherap. Freiberg, 1837, vol. ii. p. 48.-18. Soheeet Buch. Deutsch. Archiv
fur Mvn,.Med. Band xiv.— 19. Strattss. "Des ecehymoses tab^tiques \ la suite des
°? «' ne donlours fulgurantes," Archives de neurologic, 1881.-20. The Histopatholoqv
qf the Diseases of the Skin, translated by Norman Walker, p. 50.— 21 Willan
Robert. Cutaneous Diseases, 1808, p. 457. ' '
S. M.
586 SYSTEM OF MEDICINE
SCUEVY
Synonyms. — ^Lat. Scorbutus ,■ Ft. and Germ. Scorbut ; It. Scorbuto ;
Euss. Zinga.
Scurvy is a general apyretic and non-contagious disorder consisting of
mental depression, extreme debility, a tendency to syncope, and special
lesions of the mouth, skin, and muscular system, indicative of a morbid
change in the composition and properties of the blood. Of these lesions
the most frequent and most marked are swollen deeply congested and
softened gums, petechias and diffused livid patches on the surface of the
skin, and swelling and rigidity in the hams. In severe and advanced
cases there may be bleeding from the mouth and nose and from internal
organs, and rapid breaking down of ulcerated, injured, or scarred skin.
Scurvy is still endemic in certain small districts in the north-east
of Europe and in Asiatic Eussia. It has occurred from time to time
on land in epidemics, differing in extent and severity in different in-
stances, but invariably produced under analogous conditions. The disease
seems to have preserved the same type, and the records of recent out-
breaks show that it is capable now of presenting characters equal in
virulence and intensity to those recorded in past ages. The history of
land epidemics proves clearly that it is very seldom met with save in
times of war and famine, or under circumstances of neglect ; and that it
should always be dreaded in besieged towns, in armies in the field, after
a widespread failure of crops, and in badly-provisioned and overcrowded
public institutions. These conditions being present, scurvy will not spare
the members of the most advanced and civilised communities. Paris
suffered severely during the last siege, and both the French and English
armies were much stricken in the Crimean War. Of about 110 records of
epidemics of scurvy in the course of the present century, collected by
Hirsch, 11 occurred in Great Britain.
It is chiefly from its former prevalence at sea that scurvy has excited
the most interest. To the recorded experience of naval medical officers
the profession is indebted for most of its knowledge of the nature of the
disease, and, from their successful efforts to banish this grievous scourge
from the service, it has learnt not only how to treat, but also how to prevent
it. The oft-quoted passages from the history of Lord Anson's expedition
in 1740 gave but a partial idea of the ravages caused by scurvy in the
Eoyal Navy in the course of the past century. According to Lind, it
killed more men than did the hostile French and Spanish armies ; and in
1795 the safety of Lord Howe's fleet was seriously endangered by an
outbreak of this disease. From this date, when, at the recommendation
of Sir Gilbert Blane, lime-juice was introduced into the Navy, scurvy has
gradually decreased; and during the past fifty years, except in some few
SCURVY
587
outbreaks arising under exceptional circumstances, it has become so rare
as to be practically abolished as an important disease (Bryson).
Notwithstanding' this example and the striking results from the
adoption of so simple a preventive measure, scurvy, until quite recently,
prevailed to a very unsatisfactory extent in merchant ships. In 1864
it was pointed out by Dr. Barnes that, during the twelve years fol-
lowing 1851, 1058 cases of scurvy had been admitted into the hospital
ship DreadrumgU. The following table, giving the numbers of cases
subsequently admitted into this institution, shows a gradual but inter-
rupted decline, which, during the past six years, has reached such a
point as almost to justify the hope that this disease will soon be
practically extinguished in the British merchant service as well as in
the Eoyal Navy : —
Table of Cases of Scurvy treated in the Seamen's Hospital,
Greenwich, from 1864 to 1896.
Tear.
Cases of
Scurvy.
Fatal
Cases of
Scurvy.
Tear.
Cases of
Scurvy.
Fatal
Cases of
Scurvy.
1864
74
1881
36
1865
101
2
1882
28
1866
96
5
1883
15
1867
90
a
1884
6
1868
64
1885
8
1869
31
1886
5
1870
30
1887
12
1
1871
24
1888
10
1872
30
1889
2
1873
7
1890
3
1874
18
1
1891
4
1875
15
1892
0
1876
30
1
1893
3
1877
24
1
1894
1
1878
30
1895
0
1879
21
1896
3
1880
46
Of the 302 cases admitted in the course of the past twenty-two
years, 240 were brought from British and 62 from Colonial and foreign
Scurvy may occur in any climate ; and neither extreme heat, nor
extreme cold, nor excess or absence of humidity, is to be regarded as an
essential factor in the causation of the disease. Though more frequently
observed in northern and cold regions it has at times prevailed severely
in India and China, and amongst exploring parties in Australia. It
attacks in the same way both white and coloured subjects, and no race
is exempt. Its greater prevalence amongst adult males is doubtless due
to incidental circumstances, as in extensive epidemics on land neither
sex nor age affords immunity or even resistance against attack.
Etiology. — There can be no doubt that this disease, though almost
S88 SYSTEM OF MEDICINE
invariably associated with circumstances of privation, is the result of a
defective quality of food, and not merely of a reduced supply. The
large majority of those who have had actual experience of scurvy, and
have carefully studied the records of its epidemics, are convinced that the
defect consists mainly in the want of vegetable matter, which forms part
of every ordinary and adequate dietary. Whether, as it is held by some,
scorbutic symptoms may under certain circumstances be due to the absence
of fresh animal food is still an unsettled question, and so must necessarily
remain until more is known of the essential nature of the disease.
Notwithstanding the doubts of Immermann and Mah^, and the expression
of opinion by the medical members of the Arctic Survey Committee, in
1877, that scorbutic disease may be due to an absence of fresh meat,
it seems difficult, on a review of the evidence that has accumulated since
the middle of the last century, to resist the conclusion, first formulated
by Bachstrom, that the primary and only cause of this disease is an
absence of vegetable food. The question is one of purely scientific
interest, and need not at present be brought to bear on measures of
prevention and treatment. Whatever may be the differences of opinion
as to the causes of this or that epidemic, there is an absolutely unanimous
agreement, amongst both medical men and ship's officers, that the only
sure and effectual means of preventing this disease, and of curing it
when it has shown itself, is the supply of fresh succulent vegetables or
■fruits, or of a pure vegetable juice. As the introduction of lime-juice
into the Eoyal Navy in 1795 was speedily followed by a practical
extinction of scurvy, so in recent years a like result has been attained
in the merchant service by securing for seamen a good supply of this
antiscorbutic, and by a general adoption of a dietary of increased vegetable
and reduced animal food.
If further evidence, beyond that collected and reviewed by Dr.
Buzzard in 1870, were needed in support of the conclusion that scurvy
is exclusively caused by the absence of vegetable nutriment, it would be
found in the accurate and carefully prepared records of subsequent
outbreaks. The appearance of scurvy in Paris in the winter of 1870-71
was due, as Delpech and Bucquoy showed, to a failure of vegetable and
not of animal food; and in the thorough inquiry into the causes of
scurvy in the Arctic Expedition of 1875-76, the outbreak was unanimously
attributed by the members of the Admiralty Committee to the absence
of lime-juice from 'the sledge dietaries. The latest official returns of
scurvy on board British merchant ships also support the same conclusion.
It is necessary to bear in mind that the manifestation of scurvy, as
of other constitutional disorders, especially those of a cachectic character,
may be much favoured, though not directly caused, by such conditions as
are likely to impair physical vigour, and to disturb the maintenance of
good health. Amongst the host of such indirect and remoter causes
mention may be made of exhaustion by hard work, poor diet, previous
disease, faulty hygienic conditions such as bad air and water and over-
crowding, deprivation of sunlight, monotonous diet, and an almost
SCURVY 589
exclusive use of salt meat. In instances of scurvy on board ship, debility
from previous disease, especially dysentery and malarial fever the most
frequent penalties of tropical service, often plays an important part ; and
very frequently the first manifestations of a scorbutic taint are excited
by extreme cold, or by a sudden transition from warm to cold and rough
weather. The latter conditions probably exert in most cases a mixed or
indirect influence, as cold and bad weather at sea usually necessitate
increased work and exhausting or prolonged muscular exertion.
On the other hand, such conditions as a more or less varied diet,
freedom from severe physical labour, a good standard of health and
vigour, and fair hygienic surroundings will enable those who have been
long deprived of vegetable food to resist and even to escape an attack of
scurvy. Although it is not strictly true that this disease is exclusively
one of the forecastle, there can be no doubt that even in the most severe
outbreaks of scurvy at sea the number of ofiicers affected is relatively very
much less than the number of men. The existence of absolute immunity
from scurvy under a very long-continued or habitual deprivation of vege-
tables has yet to be proved. It is not impossible, however, that in in-
dividual instances immunity may exist from scurvy as from acute infectious
disease and many forms of organic poisoning. This quality of immunity,
on which so much stress has been laid by some, does not affect the
validity of the generally recognised rule as to the causation of scurvy ;
for, as was pointed out by the. Arctic Commission, "although a deficiency
or entire absence of fresh vegetable food is an invariable antecedent of a
scorbutic attack, it does not follow that the disease invariably -occurs
during this deficiency or absence."
General pathology. — Inquiries into the general pathology of scurvy
have hitherto consisted in attempts to determine on the one hand the
changes in the blood and urine of scorbutic patients, and, on the other
hand, the special chemical element of food the absence of which results
in the appearance of scorbutic symptoms. Experimental researches on
animals, as might have been anticipated, have failed to throw any light
on this subject. The experiments of Strieker and Prussak on frogs seem
to have been made in ignorance of the physiological peculiarities of these
animals ; and those of Hoffmann, quoted by Ealfe, have but an indirect
bearing on the question.
No satisfactory information has yet been attained by the examination
of blood and urine. The statements, as a rule, are very contradictory, the
results of one observer being diametrically opposed by those of another.
This is doubtless due to the difiiculty of obtaining a sufiScient quantity of
either of these fluids for the purpose of strict scientific investigation. At
the present day it would be considered unjustifiable to treat a scorbutic
subject by bleeding; and the composition of the urine is always rapidly
changed by the dietetic and remedial measures which, in a case of well-
marked scurvy, it is necessary to prescribe without delay.
The next questions to be asked are what elements of nutrition are
withheld in the absence of vegetable food, and to which of these, whether
59° SYSTEM OF MEDICINE
singly or in combination, the normal immunity from scurvy is to be
attributed. We have been taught by wide experience that the most
efficient of so-called antiscorbutics are fresh green vegetables, succulent
and acescent fruits, and the juices of the latter, especially of the lemon
and lime. Of vegetables in common use the most trustworthy are those
represented by the lettuce, cabbage, potato, yam, onion, cress and other
cruciferous plants. The most prized and useful fruits are such as are
juicy, particularly those belonging to the order of Aurantiacese. Apples
also are good antiscorbutics, and their use has done much to protect
American seamen against scurvy. Vegetables retain their antiscorbutic
properties when preserved, though to a diminished extent. Probably
of all forms of preserved vegetable sauerkraut is the best. As sub-
stitutes for succulent fruits lime and lemon juice appear to be by far the
most efficient. Malt liquors, spruce beer, and claret possess antiscorbutic
properties, and probably cider also, which has certainly had a good reputa-
tion in this respect.
It seems to be quite clear that vegetables do not owe their anti-
scorbutic properties to their free organic acids. Citric and tartaric acids
have been found practically worthless as antiscorbutics ; indeed the use
of the former as a substitute for lime-juice on board British ships has been
legally proscribed. Though these acids are present in large proportions
in the most succulent fruits, they exist but in small quantities in many
antiscorbutic vegetables; and the potato, so it is said, contains no
vegetable acids at all.
The simplest hypothesis of the causation of scurvy — which hypo-
thesis, however, necessarily admits the antiscorbutic action of animal as
well as vegetable food — is that based by Sir Alfred Garrod on the
following conclusions which were published in 1848 : —
1. That in all scorbutic diets (salt meat, leguminous vegetables, rice,
bread, etc.) potash exists in much smaller quantities than in those which
are capable of maintaining health.
2. That all substances proved to act as antiscorbutics contain a large
amount of potash.
It seems strange that the well-known table on which these conclusions
were founded has not been extended by further analyses of other articles
of diet, especially of fresh vegetables and fruits. As it stands at present,
the support it was to give to the hypothesis that scurvy is caused by a
deficiency of potash in the food is much shaken by the fact that its data
are opposed to those of common and repeated experience. Potatoes and
lime and lemon juices are certainly excellent antiscorbutics, and contain
large quantities of potash ; but it is no less true that for the prevention
and treatment of scurvy a vegetable diet, even though it may not contain
these articles, is, to say the least, far superior to animal food ; and that
onions, for instance, possess far more active and useful antiscorbutic
properties than salted or even fresh meat. Another and probably more
serious objection is that, except in the case of potatoes, the arrangement
of the few vegetables given in the table bears no relation at all to their
SCURVY 591
comparative value as antiscorbutics. The administration of nitrate of
potash, regarded by Dr. Buzzard as a crucial test, has failed both to
prevent and to cure scurvy.
Immermann, who, following the late Professor Hirsch and other con-
tinental writers on scurvy, favours the potash hypothesis, tries to overcome
these difficulties by suggesting that the scorbutic disorder may be due, not
to an insufficient supply of potash to the organism, but to an absence or
deficiency of this base in the tissues. An insufficient supply in the food,
according to this author, is certainly one way, but not the only possible
way, in which this absence of potash in the tissues can be brought about.
In the first place, the potash combination may be supplied to the blood by
the food in sufficient quantity, but in a form ill adapted for assimilation.
Green vegetables and potatoes contain potash in easily assimilable form ;
whilst meat, leguminous vegetables, and bread contain the same alkali in
a form less capable of decomposition and assimilation within the body.
In the second place, a deficiency of potash in the tissues may arise in spite
of an abundant supply in the food, when the food is prevented by in-
testinal disturbances, such as dysentery and diarrhoea, from entering the
circulating fluid in sufficient quantities. In the third place, the absorption
of the circulating potash by the tissue elements must also be influenced
by those weakening agencies, such as deprivation of fresh air and hght,
want of exercise, excessive heat, and the like, which lessen the trophic
energy of the ceUs, and diminish their capacity for appropriating the
potash from the blood. The first of these explanations seems to be a very
suggestive one, and hkely, if it can be made good by further chemical
investigation, to remove some of the most serious objections to Garrod's
hypothesis. The second and third are opposed by the well-known clinical
fact that in ordinary cases of scurvy a supply of fresh vegetables will
speedily remove the purely scorbutic symptoms notwithstanding the per-
sistence of associated diseases and other unfavourable conditions.
The view now in most favour with English authors, and one which
seems capable of accounting for these numerous discrepancies, was expressed
in a suggestion, made many years ago by Dr. Buzzard, that the anti-
scorbutic element in vegetable food is not potash alone nor the organic
acids alone, but a combination of the two. Thus scurvy is to be attributed
to the absence of organic salts of citric, tartaric, malic, and, as seems
probable from an interesting Arctic record by Dr. W. H. Taylor, of
oxalic acid also ; especially of the potash salts, which are present in the
growing leaves of plants and in fruits and their juices, and which in the
organism are converted into carbonates. This view, as further explained
and elaborated by Chalvet, whilst recognising the important part played
by potash in the production of scurvy, solves many of the difficulties
of Garrod's hypothesis. Potash in combination with citric, tartaric,
malic, and (very probably) oxalic acids is readily absorbed, because the
organic salts thus formed, being unstable, are converted into carbonates
which are taken up into the organism, the potash being absorbed by the
tissues, and the gas eliminated. In fresh meat and dry leguminous
592 SYSTEM OF MEDICINE
vegetables, on the other hand, the potash, though abundant, is much less
useful for purposes of nutrition, as it is present in more stable forms such
as those of chloride and phosphate. Thus, he says, mutton containing
a given weight of potash fails to protect against scurvy, whilst lemon juice,
containing not more of this base, acts as a most efficient antiscorbutic.
That this, however, is not the final and only possible view of the
matter was shown by the late Dr. Ealfe, who, in an able paper on
the general pathology of scurvy, endeavoured to extend the suggestions
of Dr. Buzzard yet further. Ralfe, from observations on the results
attending abstinence from fresh succulent vegetables and fruits, and from
the analyses of urine from scorbutic patients, came to the following con-
clusions : — " The primary alterations in scurvy seem to depend on a
general alteration between the various acids, inorganic as well as organic,
and the bases found in the blood, by which (a) the neutral salts, such as
the chlorides, are either increased relatively at the expense of the alkaline
salts, or (6) that these alkaline salts are absolutely decreased. This
condition produces diminution of the normal alkalinity of the blood ;
and it is suggested that this diminution produces the same results in
scurvy patients as happens in animals when attempts are made to reduce
the alkalinity of the body (either by injecting acids into the blood or
feeding with acid salts) ; namely, dissolution of the blood corpuscles,
ecchymoses, and blood-stains on mucous surfaces, and fatty degeneration
of the muscles of the heart, the muscles generally, and the secreting cells
of the liver and kidney."
From the results of his investigations Ralfe was led to surmises rather
than to positive conclusions concerning the changes in the blood and urine
of scorbutic patients. These surmises, however, are very suggestive, and
likely to prove of much value as indicating the lines on which further
researches of this kind should be carried out.
Symptoms. — Scurvy, as a rule, comes on slowly and insidiously ;
and the appearance of its external lesions is usually preceded by a pre-
liminary stage of extreme physical weakness and mental apathy. In this
stage the nature of the illness is indicated by shortness of breath, fleet-
ing pains in the back and lower limbs, and a peculiar sallowness of the
skin. As the morbid condition is displayed and the characteristic
signs of scurvy manifest themselves, the following symptoms appear : —
The patient is listless and weary ; the skin is dry and rough, and
marked by small purple spots (petechiee), which are most abundant
on the thighs and legs and, in many instances, are met with on the lower
limbs exclusively. In addition to these spots there are livid patches of
A'arying size and shape, which resemble bruises. Here and there, most
frequently in the soft parts of the ham and calf, and behind the ankle,
firm subcutaneous swellings may be felt which are widely diffused, are
not well defined at their margins, and are very tender. The eyelids are
slightly swollen, and the conjunctivae often marked by bright red patches
of ecchymosis. In some cases the eye is covered by the swollen and
purple lids, and the conjunctiva presents the appearance described by
SCURVY 593
Dr. Buzzard as "tumid and of a brilliant red colour throughout." The
lips are pale and anaemic, and the gums of a deep red colour, very soft
and vascular, and much swollen. The tongue is moist and clean. There
is a peculiar and characteristic foetor in the breath. The patient suffers
from breathlessness, which is increased by the slightest muscular exer-
tion ; he sleeps well and retains a fair appetite. The urine is scanty, and
the bowels are usually constipated.
Of these characteristic symptoms of a mild and ordinary scorbutic
attack, the earliest and most frequent are those presented on the surface
of the skin. In the primary stage, and when all other signs of scuivy
are absent, there will be found almost constantly a dirty and pale yellow
stained skin, and a decided dryness of the epidermis with a tendency to
desquamation. Duchek has directed attention to the frequent presence
of a roughness over the extensor surfaces of the limbs caused by elevation
of the follicles. The petechial Spots, each of which is formed by a small
and circumscribed effusion of blood around a hair follicle, are smooth,
level with the surface of the skin, and persistent under digital pressure.
The centre of each is Usually traversed by a hair. These spots are in
most cases confined to the lower limbs ; but in a severe' and prolonged
attack they may arise on other parts of the body, with the exception of
the face. The patches of ecchymosis which usually appear later than the
petechial spots; and are not constant, are likewise met with most frequently
in the lower limbs : although within these limits they have no special
seats of election, they often occur just over or near a large subcutaneous
swelling. Like the patches of ecchymosis observed in the subjects of
hasmophilia, they are probably due to slight injuries. The tender
subcutaneous swellings which occur so frequently in the popliteal space
and the muscles of the calf, and which are sometimes met with in the
sheath of the rectus abdominis muscle and the armpit, usually succeed
the more superficial lesions.
The affection of the ^ms and the subcutaneous indurated swelling
are the two especial lesions of scurvy. The former, though generally
regarded as a test Symptom, is by no means constant. In most cases it
is an early and well-marked symptom ; but sometimes, even though all
the other lesions may be present in a severe and advanced form, this may
be altogether absent, and the guins may remain smooth and regular, though
very anaemic, and of a pale blue colour. The swelling and discoloration
may come on suddenly and increase rapidly at an early stage of a scorbutic
attack, or may advance very slowly whilst all other symptoms are well
marked. The intensity of the gum affection, though, as a rule, most
marked in very severe arid advanced cases of scurvy, often fails to bear
any proportion either to that of the general condition or of the other
, local symptoms. The first indications of the gum affection are usually
redness and swelling of the tongue-shaped extensions of gingival tissue
between the teeth. Afterwards the gums along the dental arches, both
in fi-ont and- behind, form soft and pulpy swellings of a deep red colour
which are tender and bleed readily when rubbed. Where any teeth arc
VOL. V ' 2 Q
594 SYSTEM OF MEDICINE
absent, there is little or no swelling; and in very old or young subjects
who are edentulous the morbid alteration of the gums is reduced to a
minimum, or may be quite absent. The swelling is most marked about
the necks of carious and broken-down teeth ; but certainly it is by no
means always absent from the gums of those scorbutic patients who retain
a perfect set of teeth.
If the disease be allowed to progress and to acquire an intensity
which fortunately is now very rarely seen, the patient rapidly becomes
weaker and more lethargic. He suffers much from shortness of breath
and palpitation, and the heart's action is so weak that any muscular
exertion, such as an attempt to sit up in bed, may cause fatal syncope.
The muscular pains in the back and legs still persist and render him more
or less helpless. There is decided emaciation and wasting of the muscles,
whilst the feet and ankles become oedematous, and the face and eyelids
bloated. The petechial spots and patches of ecchymoses become more
livid, and make their appearance on the trunk and upper extremities.
The indurated swellings increase in size and become more painful, the
affected limb, usually the leg, being kept in the flexed position. The
swollen gums form large, vascular growths which surround and often
hide the teeth, and occasionally project from the mouth and distend the
cheeks. These growths break down into large and deep ulcers, which
may cause wide destruction of the gingival structure, free exposure of
bone, and loosening of the teeth. No other portion of the oral mucous
membrane participates in these morbid changes.
At this stage there is a general tendency to effusion of blood or
sanguineous fluid. Thus a tender subperiosteal swelling — the so-called
scorbutic node — may be formed in front of a long bone, most frequently
the tibia ; the breathing and heart's action may be suddenly disturbed
by the pouring out of fluid into the pleural or the pericardial cavity ; or,
again, all the symptoms of pulmonary gangrene may be caused by the
occurrence of heemorrhagic foci in the lung. 'Scorbutic effusion into a
large serous sac or into a large joint is usually of an inflammatory nature,
as indicated by pain and rise of temperature. A marked peculiarity of
severe scurvy is the readiness of the skin to ulcerate ; not only will any
existing sore suddenly thus alter its character, but an old scar, a recent
wound or scratch, or even a portion of apparently sound and intact
integument may become the focus of a rapidly spreading scorbutic ulcer,
the characteristic feature of which is a dry black slough which, when de-
tached, reveals sharply cut edges and a base of large livid granulations
from which there, is a profuse and continuous discharge of ichorous fluid.
The formation of large vesicles distended by blood-stained fluid, which,
according to Immermann, may result in ulceration of the skin, probably
occurs only in malignant and very advanced forms of scurvy ; it is very
rarely, if ever, met with in the milder and ordinary forms of the disease.
The tongue still remains moist, except in cases of visceral complication
or extensive ulceration of the skin, but it is usually more or less swollen.
There is now a tendency to diarrhoea. The stools in simple cases consist
SCURVY S9S
mainly of partly digested food and blood-stained fluid, but in a dysenteric
patient, or in one who has been treated by strong purgatives, it may be
mixed with large and abundant clots.
Notwithstanding the evident gravity of the lesions presented by
scorbutic patients, and the profound morbid changes produced in almost
every part of the body, this disease, in the form known to modern
observers, is not only attended with remarkably small mortality, but
yields at once to medical treatment and even to a suitable change in diet.
Of the 790 cases admitted into the Seamen's Hospital since 1864, 15 only
were fatal — a death-rate of 1'89 per cent ; and of 182 received during the
past seventeen years (1896-7), only one was fatal. A frequent cause of
death in the forms of scurvy to which reference has hitherto been made is
syncope. In many cases of death, whether during the attack or after the
disappearance of most of the special scorbutic symptoms, the fatal result is
due either to extreme weakness from pre-existent disease, or to a complica-
tion with dysentery, malarial fever, or some other such exhausting malady.
In an uncomplicated case of scurvy, even though very severe, a supply of
lime-juice and suitable vegetable food, together with rest, good nourish-
ment, and healthy conditions, is speedily followed by the disappearance of
most of the symptoms and by rapid restoration to perfect health. The
external lesions usually, though not always, disappear in the following
order :— first the firm subcutaneous swellings, next the swellings of the
gums, and finally the petechise and the cutaneous ecchymoses.
A knowledge of the clinical phenomena presented in the final stage of
an attack of scurvy in its worst form can only be obtained by reference
to the writings of the older authors of this subject. According to Lind,
it was not easy to conceive a scene of more diversified wretchedness than
that beheld in the third and last period of this disease. Then the swollen
legs were covered with livid and fungous ulcers ; there was a profuse dis-
charge of altered blood in the stools and urine, and also from the lungs,
nose, and stomach ; there was a tendency to effusions into the chest and
abdomen, and towards the dose of the attack there was much oppression
of breathing and extreme dyspnoea ; there was a troublesome cough with
expectoration of foetid and blood-stained sputa ; the gums were black and
gangrenous ; the teeth became loose and fell out ; the skin was covered
by cold and clammy perspiration ; there was a constant involuntary dis-
charge of stools ; the urine was retained, and the patient, unless carried
off by a sudden attack of dyspncea, gradually sank from asthenia.
Although in many of the scorbutic outbreaks recorded in the last
century scurvy was often confounded with typhus and other infectious
diseases, there can be no doubt that the disease itself was then attended
by a very high rate of mortality. The ships of the East India Company
in their voyages round the Cape often lost nearly one-half of their crew ;
and in Lord Anson's voyage round the globe 380 out of 510 seamen
perished from the disease.
In scurvy it is difficult to draw the line between the ordinary symptoms
on the one hand and the complications on the other. Formerly many
5c6 SYSTEM OF MEDICINE
lesions were regarded as specially scorbutic which were certainly due to
casual and extrinsic causes ; of late the tendency has been to reject even
the least variable and most characteristic signs, and to reduce scurvy to a
simple cachexia associated with much mental depression and muscular
weakness. Thus the petechise are attributed to the rubbing of clothes,
the swollen gums to the irritation of carious or dirty teeth, the livid
patches and subcutaneous swellings to pressure and injury, and the
pleural and pericardial effusions to catarrhal inflammation. There can be
no doubt that, from the peculiar circumstances under which it is produced,
scurvy must almost always be associated with other morbid conditions
due to insufficient as well as to unsuitable food, to overcrowding, to mental
depression, and to exposure to cold ; as occurred in the siege of Paris, in
1871, from the failure of fuel during an exceptionally severe winter. As
the late Dr. Ealfe truly asserted, simple dietetic scurvy is seldom seen,
even afloat. In many instances on board ship it is really a secondary and
complicated affection in men laid up from injury or some other disease,
subjected to the most unfavourable hygienic conditions, and probably
unable to obtain lime-juice. In such cases one would expect to find the
patient suffering from diarrhoea the result of dysentery ; from stomatitis
the result of syphilis, or rather of its treatment ; from affections of the
bones and joints the result of tertiary syphilis ; and from one or more
fungous ulcers of the legs the result of the chronic ulceration of the lower
limbs frequent in seamen. It is very doubtful whether scurvy can exert
any particular influence on fractured bones. In the form now observed
it never causes the absorption of old callus ; and in recent fractures,
though like other weakening diseases it may retard union, it is rarely, if
ever, followed by a permanent pseud-arthrosis. Indeed, notwithstanding
the frequent occurrence of fractiu-e on board ship non-union is very rarely
met with amongst seamen.
Much attention has been directed to the frequent association of night-
blindness with scurvy. This association may occur in epidemics on land,
but has been most frequently met with amongst the large crews of war-
ships cruising in tropical waters. Many instances have been recorded by
English and French naval surgeons in which a large proportion of men
suffering from an outbreak of scurvy also suffered from night-blindness.
Some of these writers go so far as to regard this disturbance of sight as a
symptom of scurvy, whilst others reject the notion of any connection
between the two affections. Mr. Donald Gunn, ophthalmic surgeon to
the Seamen's Hospital, to whom I am indebted for much information on
the subject, expresses the latest and most rational view, in stating that
night-blindness has no more to do with scurvy than with any other
exhausting disease, except that instances of the eye affection were first
observed in scurvy patients. Night-blindness is a functional disorder
depending primarily on exhaustion of the retina from prolonged exposure
to bright light. Any cause that lowers the general vitality will tend to
accelerate the incapacity of the retina to respond to less than the strongest
stimuli. Scurvy would be the more likely to act in this indirect way,
SCUJi VY S97
as the special conditions which give rise to it are often associated with
exposure of the patient to bright light. That the retinal and not the
general state is the cause is shown by —
(i.) Perfectly vigorous well-fed men, if exposed to sufficient glare,
become night-blind ; as in the snow-blindness of Alpine travellers, which is
quite independent of the associated conjunctivitis.
(ii.) A man, however depressed by scurvy, or any other disease of mal-
nutrition, will not show night-blindness unless he be also exposed to very
bright light. It has been asserted, as the proof of the retinal, or, at any
rate, functional origin of the trouble, that if one eye of a nyctalopic patient
be bandaged, this eye will recover sufficiently to enable the patient to get
about at night, while the other eye remains quite blind.
Blood and Urine in scurvy.— In scurvy, according to Duchek, the blood
in the heart and large vessels is fluid, of a dark red colour, and contains
soft ruddy clots ; thus resembling the blood in enteric fever. In anaemic
bodies, after long protraction of the disease and extensive haemorrhages, it
is lighter in colour, but still coagulable. When taken from a living
scorbutic patient it differs but slightly from healthy blood. Microscopical
examination has failed to reveal any definite change in it. Hayem found in
blood taken during life that the number of white globules was normal,
and that there was no alteration in the appearance of the red globules.
On the other hand, Laboulbene found the number of white globules or
leucocytes considerably increased, — a condition, however, which he con-
sidered of no special importance with regard to' scurvy, as it is observed in
many other pathological conditions. The statement of Mr. Busk, in 1841,
that the amount of fibrin in scorbutic blood is increased, though opposed
by Andral on the strength of a very doubtful observation of scurvy, and
afterwards by Becquerel and Rodier, has been fully confirmed by more
recent observers. Chalvet, who has made very careful analyses of blood
taken from scorbutic patients, agrees with Busk that the blood globules
are diminished and the amount of albumin increased. As a result, no
doubt, of the impossibility of obtaining suflacient quantities of blood for
such purpose, no endeavour has been made to determine the relative
quantities of the different inorganic constituents. The assertion of
Becquerel and Rodier, that there is an increase of chloride of sodium and
other salts in the serum of the blood, has been disproved by the later
investigations of German chemists.
Haematuria seldom occurs in scurvy, even in the severe cases. The
urine during the course of the scorbutic attack is scanty, dark-coloured,
clouded, and in severe cases from time to time slightly albuminous. As the
symptoms pass ofl^ and the patient becomes convalescent, it increases in
quantity and becomes paler. The specific gravity increases during the
attack, and decreases after it. In correspondence with these changes
Duchek found a decrease of the solid constituents, except phosphoric acid
and potash, in the first stage ; and subsequently a restored relation between
all the solid elements. In a more recent investigation, to which allusion
has already been made. Dr. Ralfe found in the urine of scurvy patients
59^ SYSTEM OF MEDICINE
(i.) an increase of uric acid ; (ii.) a diminution of the acidity of the urine ;
and (iii.) a reduction of the alkaline phosphates.
The following are the complications most frequently observed in scurvy :
— (a) Inflammatory effusion in the pleural cavities ; (b) Pneumonia and
gangrene of the lungs. These affections were very prevalent amongst
scorbutic patients in the Crimea. It would have been interesting to
trace their association with ulceration of the gums, as the excellent
descriptions of the pulmonary symptoms given by Haspel and Buzzard
seem to indicate an infective rather than a catarrhal origin of these
lesions, (c) Pericarditis with abundance of sanguinolent effusion, (d)
Diarrhoea usually of the simple irritative form, but in severe land epi-
demics and amongst seamen, often of haemorrhagic character, in consequence
of the presence of dysentery. («) Dropsy: dropsical oedema of the foot
and ankle is a very frequent complication ; rapid effusion into the whole
of the lower limb on one side was occasionally observed during the epi-
demic at the siege of Paris. Ascites rarely occurs, and when present is
probably the result of renal or hepatic disease. Hydrothorax and hydrar-
throsis are not infrequently met with.
In scurvy there is not, as is generally supposed, any marked tendency
to bleeding from internal organs. Epistaxis occurs more frequently than
any other form of haemorrhage ; melsena is met with occasionally as a
result of dysenteric ulceration or of the action of strong medicine;
hsematuria and haemoptysis occur very rarely.
Pathological anatomy. — Our knowledge of the pathological changes
produced by scurvy still remains very imperfect, notwithstanding the
researches of Duchek and the careful observations made by French
pathologists in 1871. One important point, that has been well established
by the latter, is the exemption of the blood-vessels from morbid change.
Another point which, if confirmed by further investigations, will also prove
no less important, is the observation made by Leven of a general fatty
degeneration of the organs. According to this writer, the striated fibres
of the voluntary muscles, and of the muscles of the heart, are destroyed,
and are replaced by fatty granulations. This fatty degeneration also
invades other organs, such as the kidney, the liver, and the lungs ; the
blood-vessels alone remaining free. It is very probable, however, that these
changes, which have escaped the notice of many competent pathologists,
are due to cachectic or other general morbid conditions associated with
scurvy but not dependent on it.
The condition of the body after death from scurvy is such as might
be expected in a case of cachectic disease marked by a tendency to
hsemori'hagic effusion. An interesting fact, to which attention has often
been directed, is that, except in protracted and very severe cases, there is
very little wasting of the subcutaneous fat and the muscles. De-
composition sets in rapidly, and the petechiae and ecchymotic patches
observed in the skin during life are soon obscured by post-mortem
lividity. The subcutaneous tissue, especially in the lower limbs, is
suffused by blood-stained fluid, and here and there are collections, varying
SCURVY 599
in extent, of effused blood, some quite black and others of a paler colour,
from cherry-red to yellow. In the indurated swellings, such as those so
often met with at the back of the thigh and knee, the muscles and tendons
will be found embedded in a thick and firm clot, and the muscles within
their sheaths studded with hsemorrhagic foci, which, like the extra-
miiseular effusions, are soft and ruddy when recent, and pale, tough, and
scar-like when of long standing. Similar deposits, though of much less
extent, may be found in connection with bones, in most instances the tibia,
just beneath the periosteum ; and also, as Immermann asserts, . within the
bone, especially in the midst of spongy tissue. Effusions are sometimes
found between an epiphysis and the shaft of a long bone in a young
subject ; and also between the ribs and their cartilages. Many of these
effusions do not consist merely of altered blood or sanguineous fluid, but
of a fibrinous and plastic material which, after a time, is traversed by
minute vessels which may be readily injected. In most cases of mild and
uncomplicated scurvy the viscera present but few morbid appearances.
The lungs, except at their lower lobes, are usually collapsed, pale and
anaemic. The cavities of the heart are sometimes empty ; at other times
they are distended by dark-coloured blood containing soft and gelatinous
clots. The organ itself, as a rule, is small and flabby. In many oases the
only marked indications of a scorbutic taint are hsemorrhagic spots scattered
over the pleura and over the roots of the large vessels of the heart. The
changes observed in cases of grave inflammatory lesions which may
involve the pulmonary organs in scurvy have been fully described by
Buzzard. Of these the most considerable are complete engorgement
of the lungs; a diffusion of ecchymotic deposits which compress and
obliterate little by little the pulmonary tissue, and often form large
fluctuating tumours composed of fluid blood and gangrene. Many
medical men versed in severe scorbutic attacks have made mention of
effusions of more or less blood-stained serum into the pleural and
pericardial sacs. Such effiasions, it seems, take place rapidly, are
generally abundant, and always associated with fever and other indica-
tions of inflammation. Mention has been made also of similar effu-
sions, which, however, are not so frequent, into the abdominal cavity,
together with ecchymotic spots and patches on both the parietal and
the visceral peritoneum. The abdominal lesions observed in seamen
are usually such as are due to tropical diseases ; to dysenteric ulceration
or pigmentation of the large intestine ; a swollen spleen ; and a swoUen
and an engorged liver. Although transient albuminuria is not of infrequent
occurrence in scurvy, no constant morbid change nor any special scorbutic
lesions have been observed in the kidney. All pathologists agree as to
the rarity of any intracranial lesions in scurvy. It has been pointed out
by Dr. Buzzard that, considering the delicate structure of the brain, it is
remarkable that scorbutic lesions occur by no means so commonly in this
organ as in other and less vital parts of the economy. Here clinical and
pathological data are in correspondence ; as in even the most severe cases
of scurvy the intellect remains clear to the last. In considerino- the few''
6oo SYSTEM OF MEDICINE
records in which paresis and analgesia are recorded as scorbutic lesions,
it would be well to take into account the possibility of confounding scurvy
with beriberi, especially in coloured men.
Diagnosis. — Under ordinary circumstances no difficulty will be met
with in the diagnosis of. scurvy^ Most of the symptoms are very
characteristic : the pulpy and swollen gums and the subcutaneous in-
durations are not features of any other disease. In a large majority
of instances the scorbutic symptoms are observed in several persons
living together who have been subjected alike to the influence of a diet of
insufficient quantity and deficient in vegetable food. In some few cases,
however, the nature of the disease may be readily overlooked, or cannot
be determined. Sporadic scurvy may occur on land in consequence of
abstinence from vegetables through extreme poverty, of aversion to such
food, or of too much zeal in enjoining or in carrying out medical instruc-
tions. In such instances an absence of one or more of the special lesions
of scurvy might give rise to uncertainty; The gums may remain quite
healthy, the lower limbs be free from swelling, and only those symptoms
be present which scurvy possesses in common with other diseases. The
chief points to be taken into consideration in a doubtful case are the
nature of the patient's diet, the presence, both before and during the illness,
of cachexia and extreme debility, the absence of continued fever, and the
effect on the symptoms of the addition of fresh vegetables, lime-juice, and
other antiscorbutics to the patient's diet. The following clinical pheno-
mena may be regarded as indicative of scurvy : the multiplicity of lesions,
— not of the skin only, but of the gums, muscles, bones, and some of the
viscera also ; occasional sudden and brief attacks of fever followed by
equally sudden and very abundant effusions of an inflammatory character
into large serous sacs (pleural and pericardial).
There is very probably but one disease attacking several persons at a
time, which is likely to be confounded with scurvy. On board ship,
particularly with coloured men in the crew, it might be found difficult
in case of an outbreak of cachectic disease to distinguish between scurvy
and beriberi. The latter interesting malady presents many symptoms
resembling those of scurvy, and indeed Morehead was thus led to attri-
bute to beriberi a scorbutic origin. It is a cachectic disease causing much
muscular weakness ; it is associated with severe muscular pains ; it gives
rise to breathlessness, and often causes sudden death from failiu-e of the
heart's action. The patient is often dropsical, especially in the legs {^e
vol. ii. p. 443). It certainly presents in general neither petechial spots
nor livid patches ; but these are signs of scurvy which, even if sought for,
would be difficult to make out in a black subject. In beriberi, however, it
should be borne in mind that the oedema usually begins in front of the
tibisB, and not in the foot and ankle ; the gums are not swollen, and,
generally, decided symptoms of peripheral neuritis — such as numbness
and paresis of the limbs, and tenderness of the muscles — are present.
Although there is at first sight a strong resemblance between scurvy
and purpura, particularly that variety known abroad as Werlhoff's
SCURVY 60'
disease, there are well-marked distinctions between the two affections.
Purpura is not due to any special defect in diet, nor is it relieved by an
increased supply of antiscorbutics. It is characterised by plethora rather
than anaemia, and shows a marked tendency to epistaxis and bleeding from
internal organs ; it affects chiefly the mucous membrane and the skin,
whilst the muscles, bones, and subcutaneous soft parts remain free. There
is no swelling of the gums. The ecchymotic spots and patches are more
vivid in colour and more generally diffused than those of scurvy.
It would hardly be possible to mistake sporadic scurvy for haemo-
philia ; the latter being a chronic affection of a congenital and hereditary
character, met with usually in young subjects, and presenting signs of
haemorrhage froni time to time, usually after injury. Three other haemor-
rhagic affections have in the diagnosis of scurvy to be taken into con-
sideration. These are leucocythsemia, splenic anaemia, and pernicious
anaemia, which affections, like scurvy, are preceded by cachectic con-
ditions. Leucocythaemia, indeed, in some rare instances, presents haemor-
rhagic swelling of the gums. Scurvy would, however, be set aside at once
by the presence of glandular swellings,, of splenic enlargement, and of
definite excess of leucocytes in the Wood. . With regard to pernicious
anaemia, which resembles scurvy in many respects, the distinction should
rest upon the chronic course of the foi:mer disease, the absence of any
special dietetic fault, a marked difference between the waxy pallor of
those affected and the sallow hue of the scorbutic subject, and the exami-
nation of the blood (art. p. 408). [For " Splenic Anaemia," vide p. 539 ;
"Infantile Scurvy," p. 604.]
Prognosis. — The prognosis of a case of scurvy is favourable if the
attack have not lasted long, if there be no visceral complications, and if
the patient can be supplied at once with efficient antiscorbutics and
placed under other good hygienic conditions. In cases of prolonged
scurvy death may occur from prostration and general loss of power.
Abundant inflammatory effusion into the pericardial or pleural sacs must
be regarded as serious ; although, as a rule, such effusions disappear with
remarkable rapidity under the influence of an improved and antiscorbutic
diet. Dysentery is a serious complication ; if it do not lead to a fatal
result it '(vill certainly retard convalescence. Notwithstanding the low
mortality that has attended scurvy during the present century, care
should be taken in every case not to give too favourable an opinion ; as,
even under the most promising conditions, and at any moment in conse-
quence of a moderate muscular effort, — such, for instance, as that of sitting
up in bed, — fatal syncope may occur. Persistence of a normal tempera-
ture, a tendency in the haemorrhagic spots and patches to fade, an in-
creased flow of urine, and a clean tongue are all to be regarded as
favourable signs. On the other hand, scanty and high-coloured urine,
an increased tendency to local haemorrhages, an occasional elevation of
temperature, diarrhoea, difficulty in breathing, signs of cardiac failure,
are all to be' regarded as indications of the steady persistence of the scor-
butic attack.
6o2 SYSTEM OF MEDICINE
Prevention. — If, as has been concluded, scurvy is invariably caused
by a much diminished supply or a total absence of vegetable food, then
the means for the prevention of the disease must consist mainly in cor-
recting this fault, and in ensuring a full and mixed diet. On land this
question, which, except in children, very rarely presents itself in
times of peace and plenty, becomes one of pressing urgency in war ; and
then forms one of the greatest difficulties in military hygiene. In long
sea-voyages it is always necessary to take the matter into consideration,
and to endeavour to make good the enforced deficiency of fresh vegetable
food by the supply of preserved vegetables and fruits, and of some anti-
scorbutic preparation. Of these substitutes for natural nutriment the
former, though not the more efficient, are certainly the more convenient and
trustworthy. Lime-juice, when taken day after day, becomes distasteful,
and often disagrees with those who take it ; as it is not an article of food
there is no certainty of its being regularly consumed except under such
conditions of discipline as exist in the Royal Navy and in large mail
steamers : moreover, in spite of all precautions it may deteriorate after
long storage on board ship. Notwithstanding the improved means of
preserving vegetables, and the undoubted value, as antiscorbutics, of
preserved potatoes, cabbages, carrots, and so forth, they are still much
inferior in this respect to vegetables and fruits that are quite fresh. For
this reason short voyages are an important factor in the prevention of
scurvy. Dr. Curnow, alluding to the decrease of scurvy in merchant
ships in correspondence with the increase of steam shipping and the
decline in the number of sailing vessels, justly points out that more rapid
voyages mean more frequent supplies of fresh food, and thus eventually
lead to the practical extinction of this disease.
Whenever the ship touches at a port no opportunity should be
neglected of supplying the crew with fruits and fresh vegetables, and in
taking an abundance of these on board. A good supply of preserved
vegetables and of lime-juice on board ship would not justify any neglect
of this precaution.
To the above-mentioned antiscorbutics, which are strictly of vege-
table origin, may be added milk, which contains all the elements required
for the nourishment of the body ; and also certain beverages such as
malt liquors and light wines, especially claret, tea, and very probably
cider which was regarded by Lind as the best of all. These beverages are
remarkable for the large quantity of potash which they contain in com-
bination with organic acids. Alcohol not only fails to act as an anti-
scorbutic, but, when taken freely, is undoubtedly an active contingent
cause of the disease.
It is necessary, also, to take into consideration the means by which, in
the absence of efficient antiscorbutics, an outbreak of scurvy may be
averted. These should consist in removing, as far as possible, all other
conditions that interfere with the maintenance of good health ; in an
endeavour to supply good and nutritious food, particularly fresh or well-
preserved meat ; to avoid exposures to extreme heat and cold ; to j^romotc
SCURVY 603
moderate but not excessive exercise ; to afford suitable clothing, and to
maintain good ventilation and other favourable hygienic conditions.
Treatment. — The treatment of scurvy, provided the attack be free
from complication, is very simple. The chief indications to observe are
the supply of those elements of food which have hitherto been wanting,
to restore strength and vigour, and to relieve the more severe local
lesions. In most cases all these indications may be fulfilled by strictly
dietetic means ; the scorbutic taint being removed by the free use of fresh
vegetables, and the general weakness overcome by nourishing and readily
assimilable food. Under such treatment the more serious symptoms,
such as those of pleural and pericardial effusions, will, in most cases, dis
appear together with those that are less grave and more superficial. In
dealing with a scorbutic patient care must be taken to avoid such articles
of diet as might intensify any complicating affection, particularly dysen-
tery ; and, in the second place, by keeping the patient in the recumbent
position, to prevent syncope or sudden death. The local lesions, even the
most severe, usually disappear with singular rapidity, and by the end of the
second week the patient may be restored to his former state of health.
The diet should consist of a free supply of fresh vegetable (potatoes, green
vegetables) with oranges and other succulent fruits, and eggs, fresh milk,
strong soups, and beef tea ; to these, as the health improves and the diges-
tive organs become stronger, may be added chicken and lean meat. There
is no need, as a rule, to give medicine ; nor, if a good supply of vegetables
be at hand, even lime or lemon juice. In complicated cases only will
it be found necessary to resort to medicinal treatment. Dysenteric
diarrhoea must be met by appropriate remedies; and in a case of extensive
pleural or pericardial effusion it may be advisable to remove the fluid by
aspiration. The gums, if much swollen and ulcerated, should be touched
with solid nitrate of silver or sulphate of copper ; or be brushed over with
a solution of one part of chromic acid in five parts of water. If there be
any scorbutic ulceration, the swollen and sloughing sore should be
douched three or four times a day with cold sterilised water, or salt and
water, and be dressed in the intervals with some iron lotion, or boracic
ointment. The petechise will disappear rapidly and need no local treat-
ment. The indurations, if they remain tender and show but little
tendency to diminish, should be treated by gentle massage and the com-
pression of a flannel bandage.
W. Johnson Smith.
REFERENCES
1. Aemstkong. Observations on Naval Hygiene and Scurvy, 1858. —2. Bach-
STKOM. Observationes circa Scoriuium, 1734.— 3. Baknes. Sixth Report of the Medi-
cal Officer of the Privy Council, 1863.— 4. Becquekel and Rodiek. Gazette mddicale,
24-31, 1852. — 6. Blanb, Sir Gilbekt. Observations on the Diseases of Seamen, 1873.
—6. Bkyson. Ophthalmic Hospital Reports, }-a\y 1859.— 7. Buoquoy. Le scorbut a
I'hdpital Cochin, pendant le siige de Paris,. 1871.— 8. BuDD. The Library of Medi-
cine (Tweedie), vol. v. 1841.— 9. Buzzard. A System of Medicine (Russell Reynolds)
vol. i. 1866.-10. Chalvet. Gazette hebdomadaire, 1871.-11. Christison. Edin-
burgh Monthly Journal (f Medical Science, June and July 1847. — 12. Donimet and
6o4 SYSTEM OP MEDICINE
FuASBR. Report of the Admirally CommHtee on the Causes of the Outbreak of Scurvy
in the Arctic Expedition of 1875-76, 1877. — 13. Ducuek. Handbuch der allgemeinen
und speciellen Chirurgie- {Fitha. and Billroth), Einband 2, Band 1, Abtheilung 2,
Heft 1, 1870. — 14. FoNSSAGKiVBs. Traits d'hygiine navale, 1856. — 1,5. Garkod.
Monthly Journal of Medical Science, Jan. 1848.— 16. Hayem. Gazette hebdomadaire,
Nos. 14-18, 1871. — 17. HiRsCH. Handbook of Geographical and Historical Pathology,
Sydenham Society, vol. ii. 1885.^18. Immeemann. Handbuch der speciellen Patho-
logic und Therapie (v. Ziemssen), Band xiii. 1876. English Translation, vol. xvii.
1878. — 19. Kkebel. Oeber die Erkenntniss und Heilung des . Scorbuts, 1838. — 20.
LAsfeGUE and Legrosex. Archives g&nirales de mSdecine, July 1871. — 21. Leach.
Report on the Hygienic Omidition of the Mercantile Marine, 1867. — 22. Lbven. Gazette
mM,icale de Paris,, 1871, No. 39. — 23, Lind. Treatise on the Scurvy, 1752, 57-72.
— 24. MAHfi. Dictionnaire encyelopddique des sciences midicales. (Raige-Delorme and
Dechambre), troisieme serie, tome viiii 1880. — 25. Maoleod, G. H. B. Notes on
the Surgery of the War in the Crimed, 1858. — 26. Parkbs. British and Foreign
Medieo-Chirurgical Review, vol. ii. 1848. — 27. Parliamentary Return of Copy of Reports,
Correspondence, and Papers relating to cases of Scurvy on board British Merchant Ships,
March 20, 1876. — 28. Ralfb. Inquiry into the General Pathology of Scurvy, 1877.
— 29. Idem. A Dictionary of Medicine (Quain), vol. ii. 1S94. — 30. Rby. IHction-
naire (nouveau) de mMecine et de chirurgie pratiques (Jaccoud), tome xxxii. 1882. —
31. Trottbr. Observations on the Scurvy, 1786-92. — 32. "Wales. System of Practical
Medicine (Pepper), vol. ii. 1885.
W. J. s.
INFANTILE SCUEVY
Syn. — Scurvy Rickets.
Definition. — The scurvy of childhood, like that met with in adults, is a
morbid condition of blood and tissues due to defect of diet. It is char-
acterised by great and progressive anaemia, tendency to syncope, cachectic
earthy complexion, marked muscular debility, mental apathy and depres-
sion, sponginess of gums, and haemorrhages into various structures,
notably under the skin and periosteum and into the muscles, especially of
the lower limbs.
The disease has a definite dependence upon the privation of fresh
food : in the case of adults usually of fresh meat and fresh vegetables ;
in the case of infants of fresh milk or other fresh food which supplies the
same antiscorbutic property ; in both it is immediately relieved and
rapidly cured by the administration of the fresh elements which have
been wanting.
History. — The existence of sciu'vy in young children, in sporadic
form, apart from its occurrence in common with adults under the special
conditions of epidemics, has only been recognised within a comparatively
recent period. It appears from the researches of Dr. Barlow that isolated
cases of similar character had been observed and recorded in Germany
from the year 1859 to 1873, by Mohler, Bohn, Hirschspring, and Senator,
as examples of acute rickets. The first suggestion of their real nature
seems to have been made by Dr. Ingelev, a Swedish physician, in recording
INFANTILE SCURVY 605
a case which came under his care in 1873. The first case observed
in this country was recorded in the Pathological Transactions by Mr. T.
Smith, in 1876, under the provision's,! title of Hsemorrhagic Periostitis,
but the condition was not recognised as scorbutic. In 1878, in a clinical
lecture on three cases in young children, published in the Lancet, I
identified the affection as true scurvy, and traced it to the want of anti-
scorbutic element in the food ; and similar cases were reported by me again
in 1879 and 1882. In 1880 Dr. Dickinson noted cases of hsematuria in
children which he recognised as scorbutic, and . described in his work on
Renal and Urinary Disease. Other cases, distinguished by swelling of the
lower limbs, attracted the attention of Dr. Gee, in 1881, who described
them in the St. Bartholomew's Hospital Reports under the designiition of
Osteal and Periosteal Cachexia. In 1883 Mr. Herbert Page recorded a
case of subperiosteal haemorrhage which he judged to be scorbutic. The
credit of completing the investigation of the disease and adding the final
proof of its nature belongs to Dr. Barlow, who in the same year published,
in the Medico- Chirurgical Transactions, an account of 31 cases, with an
exhaustive description of the morbid changes found on post-mortem
examination, and showed that the lesions found were identical with
those met with in the so-called sea or true scurvy of adults. Since that
time these conclusions have been fully confirnied by later observers.
Many cases have been recorded by Dr. Barlow, Dr. Gee, Dr. Goodhart,
and others in this country ; by Dr. Eehn and Professor Heubner in
Germany ; and by Dr. Northrop, Dr. Louis Steer, Dr. Fruitnight, and
others in America. In the latter country no less than 106 cases were
reported to the New York Academy of Medicine in the year 1894.
These later observations fully confirm the general conclusions pre-
viously arrived at as to the nature of the afi'ection and the dietetic causes
which give rise to it.
Symptoms. — The occurrence of infantile scurvy is almost limited to
the period between 6 and 18 months. In rare instances, under special
conditions, it may arise earlier or later ; but as a rule it appears within
the period stated, and most often towards the middle or end of the first
year. The onset of infantile scurvy has been regarded as sudden,
because the most characteristic symptoms may be manifested somewhat
rapidly. There is, however, an antecedent period of pallor, anaemia,
and debility; and, although the child may be sufficiently fat, it is
soft, and its muscles flabby and feeble; this muscular feebleness is a
significant and marked feature. In the majority of instances there is
some evidence of rickets, often limited to slight enlargement of the
epiphyses and beading of ribs ; in others there is in addition projecting
forehead, thickening or rarefaction of skull bones (cranio-tabes), large
fontanelle, delayed dentition, head-sweats, and attacks of laryngismus.
But the degree of rickets is rarely extreme, and in some cases the dis-
tinctive signs are entirely absent. The first symptom usually noticed is
that the child is curiously fretful and uneasy, and that it cries incessantly
and violently when being washed or dressed or handled, although toler-
6o6 SYSTEM OF MEDICINE
ably quiet and contented when left at rest and undisturbed by move-
ment or pressure. The legs especially are tender ; the child no
longer kicks them about, but keeps them drawn up and still. As the
condition advances, the tenderness becomes extreme ; the child screams
out, not only on the least movement, but on the approach of a hand to
touch it; and the lower limbs lie splayed out, and absolutely motionless,
as if paralysed. This extreme dread of touch and movement, this quasi-
paralytic stillness of the limbs are together almost diagnostic. On
examining the legs, swelling of the periosteum will probably be found
along the shaft of one or both tibise above the ankle ; the thigh bones
may be affected in the same way, and there may be oedema of the dorsum
of the foot. In some instances this periosteal swelling is slight and not
apparent at first sight ; in others it is palpable and at once attracts
observation. With the subperiosteal changes are associated, in severe
cases, deep-seated haemorrhages into the muscles themselves, causing
puffy swellings and brawny indurations. In certain cases these are
so great as to excite the suspicion of abscess, and they have led more
than once to surgical exploration, which has, however, revealed nothing
but blood-clot. There is no heat or redness of the surface, no sense of
fluctuation, and no rise of body temperature : the temperature is normal or
subnormal, except in a few instances where the haemorrhages are large and
recent, when it may run up to 100° to 102° for a period of a few days.
The upper limbs may be unaflFected, but there is often some swelling
and tenderness of the forearm above the wrist ; and more rarely on the
humerus. Occasionally other bones are invaded ; similar swellings have
been observed on the ribs, on the scapulae, and on the skull. In one
instance under my own care the chief periosteal swelling was on the
malar bone. The joints proper escape, although periosteal changes near the
epiphyses cause a fulness just above them, which at first sight appears to
be connected with them, and is not infrequently mistaken for that of
rheumatic arthritis. At these joints also, occasionally, crepitus due to
separation of the epiphysis from the shaft may be detected ; or more
rarely fracture of the shaft itself. In some instances the same fractures
are found close to the juncture of the ribs with the cartilages, giving rise
to a curious depression of the sternum and costal cartilages connected
with it, as if it had been driven forcibly inwards towards the vertebral
column. A similar deformity is sometimes observed in rickets without
known scurvy ; in such cases there is no fracture of the rib bones, but
acute bending only.
As these signs of affections of bones and periosteum are manifested,
the anaemia progresses also, and the complexion assumes the sallow
earthy hue so characteristic of true scurvy, due probably to diffusion
or deposit of altered haemoglobin. With this the debility increases, the
patient becomes more limp of body and weak of back, and cardiac power
grows more impaired. Other characteristic signs also begin to appear,
notably the one which is really pathognomonic ; namely, sponginess of the
gums;
INFANTILE SCURVY 607
Spongy gums are swollen, soft, boggy, purple, hsemorrhagic. In
severe cases, when the teeth have come through, they become so swollen
as to protrude between the lips in livid bleeding lobulated masses, some-
times so large as to hide the teeth altogether. These spongy excrescences
bleed freely, .soon begin to ulcerate, and exhale the horribly putrid odour
met with in sea scurvy. T'he teeth become loose and frequently fall out.
In some instances the gums are so tender that a child can only be made
to take food with difficulty. The change in the gums is not, however,
invariably present. If the incisors have appeared there is almost always
some purple discoloration to be seen at their base. If the teeth have
not appeared, but are approaching the surface, the same purple colour is
found over the gums which cover them, or minute eccbymoses appear
there. As Dr. Barlow has aptly pointed out, the manifestations of this
condition of the gums depends not upon the severity of the disease only ;
it has also a definite relation to the number of the teeth ; and that this
is strictly analogous to the sea scurvy of adults, in which disease where
the teeth have fallen out the portion of gum in relation to them does not
become spongy, although in that portion in relation to existing teeth the
condition is fully established. To undergo this change the gum must be
in functional relation to the teeth. Another marked and characteristic
feature in severe cases of infantile scurvy, as in that of adults, is the super-
vention of haemorrhages of various kinds into different tissues and organs ;
in some cases as petechial spots on the skin, occasionally as larger sub-
cutaneous haemorrhages, especially on the'trunk and lower extremities ;
sometimes there is extravasation into the loose areolar tissue below the
lower eyelid. In one case under my own care the supervention of a well-
marked black eye, which suddenly followed a fit of crying, decided a pre-
viously doubtful diagnosis. The fragility of the capillaries in these cases is
further illustra,ted by the readiness with which discoloration and' bruise
marks are produced upon the skin by slight injury ; such as the pressure
of handling or the blow of a slight fall.
Occasionally a curious phenomenon appears in the shape of sudden
proptosis of one eye, with slight discoloration of. the upper eyelid and
redness of the conjunctiva, due to hsBmorrhage under .the periosteum of
the orbit. The haemon'hagic tendency of the disease is further marked
in some cases by hsematuria, which is occasionally the first or the principal
sign of the supervention of the scorbutic state. In addition there may
be epistaxis, or haemorrhage from the bowel ; but these occurrences are
not common, and the loss of blood is seldom or never very copious. In
some of the slighter cases the symptoms of the disease may be limited to
one or two signs, the significance of which, when occurring alone, may
be overlooked or misinterpreted. In some instances hematuria may be
almost the only manifestation in addition to ansemia and muscular
debility ; in others orbital haemorrhage and proptosis may be the only
prominent features. More frequently, perhaps, there is merely slight
purple staining over the gums of the erupted or pushing teeth, with some
tenderness of limbs and general anaemia and cachexia.
FIG. I.
Infantile Scuhvt
Showing spongy gums, proptosis of right^ eye, external strabismus due
to post - orbital hsemorrhage, witb eccbymosis and oedema of right upper
eyelid. t'
H. D., set. 9 months. Sole diet for previous six months, condensed milk
and malted farinaceous food. Drawn from life, July 26, 1895.
MO. 1.
5.'v^
/>■.'/.-■ &• D(,nklssan, IM., ,UL mt Nnt. «. r/„,,„
o
FIG. II.
Infantile Soubvy
Showing swelling in front aspect of tibia from subperiosteal hsemorrhage,
just above the ankle, with oedema of ankle and foot.
From the same patient as Fig. I. Drawn from life, July 26, 1895.
FIG. III.
Poat-mortem appearances presented by the femur and surrounding tissues
in a fatal case of infantile scurvy, namely, haemorrhages and masses of blood-
clot under the periosteum, which is vascular and thickened ; haemorrhage and
serous infiltration into the deep muscles adjacent ; hfemorrhage into the
central canal of the bone, and fracture of the shaft near the epiphysis.
Sketched from a preparation in the Museum of the Hospital for Sick
Children, Great Ormond Street. From a case of Dr. Barlow's.
VOL. V 2 R
6io SYSTEM OF MEDICINE
There are no doubt cases slighter still, where the only symptoms
are tenderness of limbs evidenced by irritability and intolerance of
handling, with perhaps some signs of rickets, to which the symptoms are
referred. The fact that in many instances these conditions, so closely
associated with scurvy, rapidly disappear upon antiscorbutic diet, while
those more particularly identified with rickets are little affected by it, is
very suggestive of their real nature.
This characteristic group of symptoms, in well-marked examples of
infantile scurvy, accurately correspond, not merely individually but as a
composite whole, with the series of phenomena met with in the epidemic
form of the disease. The pallid, earthy complexion, the progressive
anaemia, the excessive muscular feebleness, the tendency to syncope, the
various haemorrhages and their seat, the hsematuria and albuminuria, the
oedema, the swellings of periosteum and of muscle, the extreme tenderness
of limb, the special implication of the lower extremities are the same
in both. The fact that the bones suffer somewhat more severely in
proportion to other tissues is explained by the great formative activity
which pervades these parts in infancy. The symptoms are indeed
practically identical with those of the adult with, in most cases, the
signs of an underlying rickets ; such as beading of the ribs, enlargement
of the epiphyses, head-sweats, and laryngismus. In most instances,
however, these signs are slight, and in some no indication of rickets can
be discovered.
Course of the disease. — The course of the disease varies according
to the degree of its intensity and development, and the conditions under
which it arises and under which the patient remains. If the defects of
diet in which it has its origin continue unchanged, and the hygienic
surroundings are unfavourable, the patient grows steadily worse, the
debility and anaemia increase and become extreme, and the cachexia
profound. In this state the child may die suddenly from haemorrhage
into some vital organ, or from syncope, or from more gradual exhaustion ;
or from some intercurrent affection such as bronchitis or pneumonia, or
diarrhoea ; or again, an acute infectious disease may prove rapidly fatal
to the enfeebled organism. Occasionally, without special treatment, slow
amelioration of the disease takes place after a time ; some change of
food in the ordinary advance to a wider and more varied dietary, as the
child grows older, leads to a gradual improvement in the condition, and
the symptoms after some months may disappear. Relapses often
occur ; and in any case the disease, when uninfluenced by treatment, runs
a chronic and protracted course, unless cut short by some fatal accident
or complication. If, however, the nature of the affection is recognised,
and proper antiscorbutic treatment adopted, improvement is immediate,
anil recovery so marvellously rapid that the child may be practically
well in from two to three weeks. The swelling of the limbs subsides,
tenderness and the dread of movement disappear, the child begins to
move its limbs again voluntarily and to sit up once more, the haemor-
rhages cease, and the anaemia and cachexia and asthenia quickly decline.
INFANTILE SCURVY 6n
Some wasting of the muscles of the affected limbs remains, and for some
time afterwards hard thickening can be felt round the shafts of the
affected bones. If fractures have occurred, they are repaired without
obvious deformity, except in rare cases, when they take place in the
middle of the shaft of a long bone ; then much thickening may remain
for a time. In the end, however, the recovery is final and complete ;
although, where accompanying rickets exists, the signs of this condition
may long persist. As already observed, however, the rachitic complica-
tion in these cases is usually slight, and but rarely severe of degree.
Morbid anatomy. — For an accurate knowledge of the morbid changes
which are associated with the signs and symptoms described, we are
chiefly indebted to the careful investigations of Dr. Barlow, who, in a
paper published in the Medical and Ohirurgical Transactions for 1883, has
given an exhaustive account of the appearances met with after death,
and has shown conclusively that in this respect also the conditions
observed are identical with those found in the true epidemic or sea scurvy
of adults. These conditions have been further examined and confirmed
by other observers in this country and abroad, and again by Dr. Barlow
himself, who has set forth the results in the Bradshaw Lecture for 1894.
The details of morbid changes given below are largely drawn from this
source.
As will have been gathered from the previous account of the
symptoms, the principal lesions found after death are due to increased
vascularity and extravasations of blood into various tissues. The most
extensive and important of these are found in connection with the
periosteum, the bones, and the muscles. These changes are most common
and extreme in the lower limbs ; but they are met with also, although
less frequently and in minor degree, in connection with the bones of the
upper extremities, and of the skull.
The periosteum of the long bones of the leg and thigh is highly
vascular, and blood is effused more or less extensively round the shaft
beneath it, detaching it from the bone and forming a thick sheath of
blood-clot between periosteum and shaft ; the tibia and femur are usually
most affected in this way (Pig. II. of Plate). The extravasations corre-
spond with and account for the exquisitely tender and sensitive swellings
observed during life. In some cases similar haemorrhages occur under
the periosteum of the humerus, of the scapula, of the ribs, and of the
cranial bones, corresponding to the swellings described there. One of
the most characteristic of these, when it occurs, is the extravasation into
the loose tissue which connects the roof of the orbit with its periosteum,
and accounts for the curious proptosis which has been described in
some cases, the eyeball being thus pushed downwards and forwards.
Haemorrhage is also found sometimes in the loose tissue of the upper
and lower eyelids, causing the black eye of which mention has been
made. A thin layer of newly-formed osseous material is occasionally
found beneath the upraised periosteum, forming a bony sheath round the
shaft of the long bones, or a similar formation of delicate bony film
6i2 SYSTEM OF MEDICINE
under the periosteum of the flat bones, such as the scapula. Hisemor-
rhages also take place, in some cases, into the medullary cavity of the
long bones of the limbs and of the ribs, forming masses of blood-clot
there ; the medulla itself being soft and reddened. The muscular swellings
(Fig. III. of Plate) are due to deep-seated extravasations, especially in the
muscles of the lower limbs, which are also sodden by serous effusion, wasted,
flabby and pale. In rare instances hsemorrhages have been met with in
some of the joints, and under the dura mater of the skull ; and the purpuric
blotches and bruises which are liable to follow handling are also, of course,
hemorrhagic in nature. Similarly, extravasations have been observed in
the pleura, the lungs, spleen, intestines, kidney, and mesenteric glands.
In one fatal case under my care, in addition to the spongy, bleeding gums,
there were extensive haemorrhages into the lung, and smaller extravasa-
tions and ecchymoses into the intestinal mucous membrane and into the
lymphatic glands ; the bones and muscles being free. Similar cases have
been observed by others. When haemorrhage into the central canal of the
long bones occurs, the bone itself sufiers so that the compact tissue of its
wall becomes absorbed and rarefied, and is reduced to a thin shell. A
similar condition is found in the ribs.
Another characteristic feature of the morbid changes in the bones in
scurvy is the occurrence of the fractures before alluded to. These take
place especially in the rarefied imperfectly ossified portion of the long
bones connecting the shafts with the epiphysis, and sometimes a little
above this ; the two extremities of the femur and the upper end of the
tibia are the most frequently affected in this way ; occasionally the
upper end of the humerus shows a similar fracture. The ribs again,
as previously noted, are occasionally broken away from the costal
cartilages. The fractures are due in part to the weakening of the shaft
by the detachment of the periosteum by the haemorrhage into the
medullary canal, and by the extensive absorption of the trabecular
structure.
In the mouth the gums are seen to be spongy, swollen, and sodden
with serum ; and perhaps clotted with blood. The teeth, if present, may
be loose and on the point of falling out.
The viscera show no morbid changes beyond those caused by the
haemorrhages which have been detailed, and the well-marked anaemia.
The muscles likewise are anaemic, soft, and wasted, while those of the
limbs most affected usually show the local haemorrhages so often alluded
to. The blood is watery. In the majority of cases, but not in all, the
bone changes of rickets are found in addition to those of scurvy.
It will be seen that, in like manner with the symptoms observed
■during life, the morbid changes discovered after death in infantile scurvy,
namely, the various haemorrhages and their seat, the rarefaction of bones,
the fractures, the formation of bony plates under the periosteum, differ in
.no respect from the similar changes found in the epidemic scurvy of adults.
Etiology and general pathology. — It will be gathered from what
"has gone before that the general pathology of infantile scurvy, occurring
INFANTILE SCURVY 613
sporadically, is, in its symptoms and morbid anatomy, in all essential
points the same as that of the scurvy of adults. The original view of
the earlier observers in Germany that this affection is an acute form
of rickets has proved erroneous, and is generally abandoned. It was
based upon an imperfect acquaintance with the morbid anatomy of the
disease, as well as of the exact dietetic conditions under which it arises.
Although, as has been stated, a certain degree of rickets is usually
present, this is not a constant and invariable accompaniment ; there is
no relative correspondence or proportion between the degree of rickets
and the degree of scurvy, nor indeed between it and the supervention of
scurvy at all. In severe and advanced cases of rickets where the bone-
changes are extreme and there is marked cachexia, with head-sweats,
laryngismus, and aH the signs of severe and progressive disease, the gums
are not spongy, there are no subperiosteal haemorrhages, no muscular or
subcutaneous extravasations, no hsematuria, no haemorrhages elsewhere.
Eickets is not in itself haemorrhagic in any degree, so that the scorbutic
features are not a mere manifestation of severe or acute rickets. More-
over, signs of rachitic implications may be altogether absent, as in two cases
under my own observation recently, and in a similar instance, recorded by
Dr. Northrup of New York, in which no rickety change of any kind could
be detected on post-mortem examination.
It had been thought possible that the condition might be one of purpura
hsemorrhagica, or hsemophilia concurring with rickets. The lesions found
after death and the course of the disease, however, are widely diiFerent, and
no family history of hsemophilia can be traced. Moreover, as has been
shown above, the underlying basis of rickets is not always present. Again,
the disease is not simply the purpuric state which is liable to supervene in
the late stages of wasting disease, for the subjects of it are not merely not
marasmic but in some instances fat and full tissued ; nor is it the hsemor-
rhagic stage of lymphadenoma or leukaemia, for there is no enlargement
of lymphatic glands or spleen ; nor is it a phase of congenital syphilis,
the signs and history of which have been wanting in all the cases seen by
myself, although some instances have been recorded in which this condition
was concurrent. The evidence of the real nature of the disease is com-
pleted by the effect of full antiscorbutic treatment, and this, added to that
drawn from the dietaries of the children affected, and the pathological
changes found after death, is conclusive. There is nothing in the whole
range of medicine, not even excepting the effect of thyroid extract in
myxoedema, more striking and remarkable than the immediate and rapid
recovery which follows the administration of fresh vegetable material and
other fresh elements of food in these cases of infantile scur%7^. Simple
rickets is no doubt influenced by dietetic treatment, but it is not especially
influenced by antiscorbutics ; moreover, the effect of diet is gradual and
follows slowly, in marked contrast to the instant and immediate ameliora-
tion which follows in the case of scurvy. Lastly, diet is powerless to
arrest the haemorrhages of purpura and haemophilia, or those of lymph-
adenoma or leukaemia.
6i4 SYSTEM OF MEDICINE
Sporadic infantile scurvy, then, like the epidemic affection, the so-called
true or sea scurvy, consists essentially in an altered and depraved condition
of blood, which gives rise to an enfeebled and fragile state of the capillaries,
so that serum readily transudes and the vascular wall easily ruptures.
Hence follow the serous infiltrations, fibrinous exudations, and haemorrhages
which have been described. The exact nature of this defect in the blood
which is the immediate cause of the softness, permeability, and fragility
of the capillary walls, has not been ascertained with certainty. It would
appear, however, from the researches of Busk, Garrod, Ralfe, and others,
that the alkalinity of the blood is diminished ; probably because neutral
salts such as the chlorides are increased at the expense of the alkaline
salts, or else that the latter are absolutely and not only relatively
diminished. The defective alkalinity leads to dissolution of the blood
corpuscles, ecchymoses, and fatty degeneration of muscles and secreting
cells. The source of the defect in the blood has been clearly traced to
lack of fresh food and notably of fresh vegetable food.
"Whatsoever the exact nature of the antiscorbutic element, it is clearly
supplied by this kind of food, and the lack of it sets up the disease.
The scorbutic state arises under conditions of life which involve such
privation ; as on long voyages, expeditionSj shipwrecks, the campaigns
of armies, sieges, or famines : and it is intensified and fostered by
conditions of malhygiene, by hardship, exposure, foul air, want of light,
and probably also by the prolonged use of salt provisions.
In the case of children the cause has been traced with equal certainty
to this deficiency of the fresh element in food. The natural ordinary food
of infants is milk alone. Instances of children becoming scorbutic when
at the breast ard limited to epidemic scurvy, and no case of the kind has
ever come within my own cognisance.
With the exception of one or two doubtful cases, of which the
details of breast feeding and diet are imperfectly given, the only instances
of scurvy arising in sucklings are those when the nursing mother has been
suffering from scurvy at the time. Similarly no case has come under my
observation in which scurvy supervened on an ordinary diet of fresh cows'
milk unaltered by peptonisation, or by the prolonged heating of a sterilis-
ing process.
Fresh milk must necessarily contain the antiscorbutic element, what-
ever the exact nature of this element may be ; for milk is the source
from which it is supplied to the infant organism. A careful examina-
tion of the conditions of diet in a large number of cases confirms this
inference, and establishes the prime fact that the children who become
affected with scurvy have been brought up upon a diet deficient in fresh
milk. In 37 cases under my immediate observation, in which the details
of feeding could be ascertained with exactness, it was found that in the
great majority — namely, in 27 — no fresh milk at all had been given
for a long time before the attack. In the majority of these none had
been given at any time ; and in the rest only at the commencement of
hand-feeding, having been quickly and finally abandoned because it did
INFANTILE SCURVY 615
not agree. In the 10 remaining cases a very small quantity of fresh
milk had been given ; in 4 of these, however, for a few weeks only, the
children having been previously brought up entirely on dried or patent
foods. In 2 cases only out of the whole number of 37 had the defect of
diet been in any degree compensated by the addition of fresh elements
in the form of a small quantity of raw meat juice. In a few cases the
food was entirely limited to some dried farinaceous preparation made
with water only. In the greater number of instances, however, the
scorbutic condition arose upon an exclusive diet of one or other of the
proprietary preserved foods, consisting of malted flour mixed with dried
animal matter, and prepared by the simple addition of water, without
fresh element in any form.
Next to these in frequency come the cases where the diet has been
restricted for a considerable period to one of the predigested foods, more
particularly the pancreatised farinaceous foods, in which the milk added is
pancreatised in the process of preparation ; or upon a prolonged diet of
peptonised milk, especially peptonised condensed milk. Simple condensed
milk is responsible for a certain number of cases. In a larger number
still, however, the disease had arisen after the continued use of the com-
mercial preparation of so-called " humanised " milk — that is, milk deprived
of a portion of its casein and sterilised by heat or other methods to make
it keep.
It is clear that the process of peptonisation or pancreatisation of milk
greatly impairs its antiscorbutic property ; and this is also the unmistak-
able result of prolonged heating at high temperatures, as in the process of
preparing condensed or desiccated milk. Although no cases of scurvy
arising upon a diet of simple sterilised milk have actually come under
my' notice, it is highly probable that its antiscorbutic virtue is lessened
by the process; and leading physicians both in Germany and America,
where it is more largely used than in this country, deprecate on this
ground permanent feeding on milk sterilised in this way. The mere
raising of milk to the boiling-point for a few moments appears to have no
serious deteriorating influence, although it is probable that its antiscorbutic
power is lessened in some small degree by this minor process.
The antiscorbutic power even of fresh untreated milk is comparatively
feeble, far less than that of fresh vegetables ; and it probably varies to
some extent according as the animal from which it is drawn is fed on dry
food, or grass or roots. The imperfect power of milk in this respect was
long ago noted by Dr. Parkes, who investigated the point ; his conclusion
was generally that in the case of adults one pint to one pint and a half
was not always sufficient to prevent scurvy in the absence of fresh
vegetable food.
The relatively slight antiscorbutic virtue of milk is further exemplified
by its slow and imperfect curative power when used as an antiscorbutic
agent in the treatment of scurvy. To be effective it must be given in large
quantity. This fact seems to explain the occasional occurrence of the
disease in children who have milk in small amount, and the deleterious
6i6 SYSTEM OF MEDICINE
effect of any impairment of its properties by peptonisation or over-heating.
In addition to the cases which occur in infancy, instances are recorded
in older children which throw additional light on the etiology. In five
cases of typical scurvy in children after infancy, observed by Dr. Barlow,
the cause was traced to a curious morbid antipathy to vegetables and
to meat.
In accordance with the fact that the majority of cases of scurvy occur
in children fed upon patent foods and peptonised and other forms of
prepared milk, comes out another curious fact ; namely, that the disease is
met with chieily amongst the children of the better classes. Although
the children of the poor are by no means exempt, the disease is much less
common amongst them than amongst the children of the well-to-do.
Of the thirty-seven cases under my immediate observation during the
last ten years, thirty-one occurred in private patients, and only six in hospital
patients ; and the experience of others is in accord with this statement.
The unequal incidence is partly explained by the consideration that the
artificial foods which are without antiscorbutic properties are chiefly used
by the well-to-do. They are too expensive for the poor. The poor,
however, use largely condensed milk and farinaceous materials, such as
corn-flour and other farinaceous preparations ; the first is feeble in anti-
scorbutic power, the latter destitute of it altogether. The reason
why scurvy does not follow more frequently on diet of this kind
is to be sought in the fact that the children of the poor begin to share
the food of their parents at an earlier age than the children of the rich ;
thus they get a more mixed diet, of which potatoes, one of the mo.'^t
powerful of all antiscorbutics, usually form a chief part. The disease would
appear to be growing more prevalent, in response, no doubt, to the more
extended use of the dried and peptonised fopd preparations which now
prevails. The experience of the American physicians is to a like effect.
It is interesting to observe, in respect of the relation of scurvy to rickets,
that this prevalence of scurvy amongst the rich, as compared with the
poor, is the exact converse of the position of rickets in this respect ; for
rickets is most prevalent and most severe amongst the poor. The children
of the poor grow rickety, the children of the rich scorbutic. The co-
existence of rickets in the majority of cases of infantile scurvy is due to
the fact that most of the foods — as notably the farinaceous and dried
milk foods — are ricket-producing foods also, deficient in fat and proteid
and phosphates of animal origin, as well as wanting in the fresh anti-
scorbutic element. It is possible also that the physiological activity of
]ieriosteal bone growth in infancy, and its vascularity, may be another
factor in the meeting of scurvy and rickets.
Diagnosis. — The recognition of a case of infantile scurvy is not
difficult when the typical signs of periosteal tenderness and swelling, and
spongy gums, are present. When the latter sign is wanting, as may be
the case in very young subjects in whom the teeth are not yet
pushing, and the periosteal affection not pronounced, the condition is
apt to be overlooked, or regarded as one of rickets, of rheumatism, or
INFANTILE SCURVY 617
of simple aiiseniia and debility. Even in severe cases, the tenderness and
swelling of the limbs leads not seldom to a mistaken diagnosis of
rheumatism, from which, however, scurvy may be distinguished by the
facts that the joints are free, and the part affected is the shaft of the bone
above it, in addition to the other symptoms of scurvy present. Another
common error lias its origin in the motionless state of the lower limbs,
which the child dreads to move on account of the pain ; this inhibition of
movement is frequently mistaken for paralysis, so that in many cases
infantile scurvy is diagnosed as infantile paralysis. In other instances,
again, in which the tenderness and dread of movement attract attention,
the condition is regarded as one of tuberculous affection of the hip and
knee joint. In another group of cases, in which hsematuria or albuminuria
are the symptoms iirst observed, the affection is regarded as a form of
Bright's disease.
Even in cases where the gums are fungous, swollen, and bleeding,
this local symptom has been regarded as the sole ailment, and the case
judged to be. a severe form of stomatitis. Similarly cases of proptosis
due to scorbutic hemorrhage may be regarded as cases of orbital tumour.
In all these conditions a full examination will seldom fail to reveal the
true nature of the afiiection. Even if there be no sponginess of gums,
the periosteal swelling, the exquisite tenderness of the limbs, the extreme
dread of movement,, and the earthy pallor and possibly haemorrhages
under the skin or elsewhere, added to the diet history, are sufficiently
distinctive. If the gums be affected also, the evidence is complete, and
the diagnosis may be quickly and finally confirmed by the test of anti-
scorbutic treatment.
All doubtful cases, especially those of rickets in which there is some
limb tenderness, should be tested in this way.
The prognosis of infantile scurvy is almost uniformly favourable. If
the disease is duly treated before extreme symptoms have arisen, recovery
is rapid and certain. Before the nature of the disease was generally
recognised the rate of mortality ran high. In. the first series of thirty-
one cases collected by Di'. Barlow seven proved fatal, or upwards of
21 per cent. Since that time, however, the death-rate has fallen
remarkably. Out of thirty-nine cases under my immediate observa-
tion three only have ended fatally. Of these patients one was in a
condition of extreme debility; the child took food with difficulty, and
died from hsemorrhage into the lung three days after admission to
hospital. In the second case the, condition was also far advanced ; the
child was fed with difficulty, and died shortly after admission. In the
third case the disease was not diagnosed at first, and the patient was
treated surgically, for a supposed abscess of the femur. It is to' be noted
that all the deaths, occurred in hospital patients of the poorer class, in
whom the disease had reached an extreme degree, under unfavourable
conditions of life, before they came under treatment. In two, moreover,
the difficulty of treatment was greatly enhanced by the fact that the
curative agent could only be taken sparingly, owing to the extreme
6i8 SYSTEM OF MEDICINE
prostration of the patient ; and death took place under these circumstances
before sufficient time had elapsed for the amelioration of the disease.
In the third case, in addition, the nature of the disease not being re-
cognised, special antiscorbutic diet was not administered.
Danger to life exists, however, in all cases, both from haemorrhages
and from syncope, until the condition is controlled. In no instance
within my knowledge has a fatal issue occurred after a week of anti-
scorbutic diet.
Treatment. — Prevention. — Since the disease arises from the persistent
use of farinaceous dry foods or prepared foods containing no living or
fresh element, or an insufficient amount of it, the obvious means of pre-
vention lies in the avoidance of such foods, and in the use of some
aliment of which fresh milk or other fresh material, forms at least the
chief part. Experience proves further that milk cannot with safety be
submitted for any great length of time to predigestion, to prolonged heat-
ing at high temperatures, or to the process adopted in preparing preserved
"humanised" milk. But to raise the milk to the boiling-point for a few
moments, in what is called " scalding," does not appear to impair its
nutritive value or its antiscorbutic power materially.
If therefore in any case the milk of the mother or of a wet nurse
cannot be obtained, and diluted fresh cows' milk cannot be digested,
the food in use should be replaced gradually by fresh milk, or some
equivalent of fresh living material should be added. If, that is, it should
be found absolutely necessary, on account of digestive troubles or other
urgent reason, to place a young infant upon peptonised milk, humanised
milk, or pancreatised food, or on any patent dried food, this should be
regarded as a temporary expedient, and should not be continued for more
than a few weeks. The prolonged use of such foods is a fruitful source
of impaired nutrition in many ways, and especially of scurvy ; it should
be replaced by fresh milk by a system of gradual substitution. This can
generally be effected by mixing fresh milk with the food used, in small
quantity at first, and then slowly increasing it. Should the child be
unable to digest a sufficient amount of the fresh milk in the course of a
week or two, the lack of fresh elements may be supplied, and disaster
averted, by the addition of raw meat juice, or by a small quantity of beef
or chicken tea in which potatoes and carrots have been boiled and
strained out. Similar precautions should be adopted in the case of older
children when from illness or other cause they are placed upon a diet of
peptonised or sterilised milk, or predigested food in any form, or upon
any dried food to which fresh milk has not been added.
Cure. — The treatment of infantile scurvy consists almost entirely in
the administration of fresh foods which possess the antiscorbutic virtue
in high degree. The child should, if possible, be placed on fresh milk,
which maybe raised to the boiling-point, but not sterilised or "humanised."
Fresh milk, however, as pointed out previously, possesses only moderate
antiscorbutic properties, and is insufficient alone to effect the rapid cure
of scurvy ; just as it is insufficient to prevent it if given in small quantities.
INFANTILE SCURVY 619
For effective antiscorbutics we must have recourse to vegetable juices.
Fresh green vegetables, more particularly the cruciferse so efficacious in
the scurvy of adults, are not available in the case of young infants of
from six to eighteen months old, the period during which the disease
usually appears. A most efficient substitute is, however, available in
potato, which Dr. Baly, in his experience during the epidemics of scurvy
at Millbank Penitentiary, proved to possess such remarkable antiscorbutic
power. Even young children can usually take potato, properly prepared
and administered, without digestive disturbance. It should be well
steamed and reduced to light floury powder by rubbing through
a fine sieve. This should be well beaten up with boiled milk until
it is of the consistence of thin cream, and should be added to the
regular food, beginning with a small teaspoonful to each bottle. The
quantity may be gradually increased to a dessertspoonful, or even a
tablespoonful in the case of children above a year old, if it agrees.
Another effective plan, although less rapid than the preceding, is to
administer the vegetable juices through the medium of beef tea or
chicken tea, in which potatoes and carrots have been boiled and sub-
sequently strained out. A small cup of this may be given once or twice
a day.
The fresh element in diet should be further strengthened by the
addition of the juice of raw meat, which possesses antiscorbutic power,
although, like milk, not in high degree ; and similarly it is unequal alone
to effect the rapid cure of scurvy, or to prevent it when a small quantity
is the sole addition to an otherwise scurvy diet. This comparative feeble-
ness of raw meat juice and milk in antiscorbutic power have sometimes
led to erroneous conclusions as to the nature of the disease, when it arises
where milk or raw meat juice has formed a small portion of the diet,
or has failed quickly to relieve it. Milk and raw meat juice are, in fact,
only efficient when given in large quantity, and even then 'are much
less active than vegetable juices. Raw meat juice has, however, a special
value in these cases from its haemic virtue. It contains iron in the
most assimilable form in its haemoglobin, and is the most powerful of
all remedies for the anaemia constantly present and often extreme. The
juice should be prepared by macerating the finely-minced pulp of raw
beef in an equal quantity of cold water for half an hour, and then
expressing all the liquid through fine muslin by twisting it. The strain-
ing is necessary to avoid danger of tapeworm by removing possible
hydatids. It should be freshly made at the time of using, for it quickly
undergoes decomposition, and, if kept, acquires poisonous properties.
Grape juice, orange juice, lemon juice, baked apples, are useful
adjuncts, especially in the case of children above a year old. When
potato pulp and raw meat juice are given and well borne, the result is
immediate and almost magical. If the gums are spongy and swollen, all
sign of this disappears in the course of a few days, the swelling of limbs
goes down, tenderness subsides. In the course of a week or ten days
the child no longer dreads handling or moving, and in a fortnight or
620 SYSTEM OF MEDICINE
three weeks is practically well — in strildng contrast to the slow progress
of simple rickets under similar dietetic treatment. In addition to
antiscorbutic diet, fresh air and sunlight, as in the case of adult scurvy,
are useful aids, although diet alone is certainly and rapidly curative.
Little local treatment is required beyond wrapping the limbs affected in
cotton wool, keeping the child absolutely at rest on a soft pillow, and
preventing the movement of the limbs, which causes pain, and therefore
wear and tear. The tenderness may be relieved, especially if the limbs
are hot and uncomfortable from recent periosteal or muscular extrava-
sation, by the application of warm compresses. As a rule, however, no
local applications are required, and such measui'es as massage or stimulat-
ing applications are actively injurious.
Drugs are not required; diet is all-sufficient. Depressing remedies, such
as iodide of potassium, often given with the mistaken view of aiding the
absorption of the effused material of the subperiosteal swelling, are dis-
tinctly harmful ; and iodide of iron is little less objectionable. Like all
the iodides it is depressant, and if pushed far enough it eventually pro-
duces in children a cachectic purpuric condition.
Cod-liver oil and steel wine are useful in the later stages for any
underlying rickets which may exist. In the active stage of scurvy they
are better omitted, as they are apt to interfere with the ample ingestion of
fresh food. In these cases raw meat juice is better than any iron prepara-
tion of the Pharmacopoeia, and the cream of fresh milk is more potent
than cod-liver oil.
"W. B. Cheadle.
REFERENCES
1. AsHBT, H. Practitioner, 1894, liii. p. 412 ; and G. A. Wmght. Dis. of Children,
1896, ,p. 401.-«-2. Ball, J. B. Proc. W. Lcmd. Med. Glin. Soc. 1884-6, Lond. 1887, ii. p.
94.-3. Baklow, T. Med.-Chir. Trans. 1883, Ixvi. p. 159 ; £rU. Med. Journ. 1894, iL 1029.
—4. BOHN. Jahrb. f. KinderUilk. 1868, N.F. 1. Hft. ii. p. 201.— 5. Bkttsh, E. F.
Journ. Amer. Med. Ass. Chicago, 1892, xix. p. 735. — 6. Carr, W, L. Med. Bee. Jf. V.
'l892, xlii. p. 419 ; Ibid. 1894, xlv. p. 811.-7. Cassel. Arch. f. KinderheilTc. Stuttg.
1892-3, XV. p. 350.— 8. Cheadle, W. B. Lancet, 1878, ii. p. 685 ; Brit. Med. Journ.
1879, ii. p. 987 ; Lancet, 1882, ii. p. 48.-9. Dickinson, W. H. Dis. of Kidneys, Ft.
iii. (1885), p. 1287.— 10. Forster, R. Jahrb. f. Kinderheilk. 1868, N.F., 1. Hft. iv.
p. 444 ; Feroffent. d. Gesellsch. f. Eeilk. in Berl. Pddiat. Section (1880), 1881, iv. p. 89.
—11. Fox, T. CoLOOTT. Trans. Path. Soc. Lond. (1886-7), 1887, xxxviii. p. 275 ; Illust.
Med. News, Lond. 1888-9, i. p. 25.— 12. Feuitnight, J. H. Arch. Pediat. N.Y. 1894,
xi. pp. 486, 573.-13. FiJRST, L. Jahrb. f. Kinderheilk. 1882, N.F. xviii. No. 11, p.
210 ; Arch.f. Kinderheilk. 1895, xviii. p. 50.-14. Gee, S. St. Bart. Hosp. Rep. 1881,
xvii. p. 9 ; 1889, xxv. p. 85.-15. Goodhart, ,T. F. Dis. of Children, 1894, p. 639.— 16.
Goss, F. "W. Boston Med. and Surg. Journ.. 1892, cxxvii. p. 619. — 17. Green, W. E.
PractUimur, 1885, xxxv. p. 171. — 18. Heubner, 0. Jahrb. d. Kinderheilk. 1892,
xxxiv. 13, p. 361. — 19. Hirschsprung, H. Eosp. Tid. Kjobenh. 1894, 4, R. ii. pp. 869,
898, 934.— 20. Hoffmann, F. A. Lehrb. d. Constitutionskrankh. Stuttg. 1893, p. 145.
—21. Holt, E. E. New York Polyclin. 1893, i. p. 16. — 22. Jugeisler, V. Hosp.
Tid. Kjobenh. 1871, xiv. p. 121.-23. Jallanu, W. H. Med. Times and Gaz. Lond.
1873, i. p. 248.-24. KiJHN, A. Deutsch. Arch. f. klin. ited. Leipzig, 1880, xxv. p.
123.— 25. Leonard, C. H. Tra.ns. Rhode Island Med. Soc. Providence, 1889-93, iv.
p. 538. — 26. LiND, J. A Treatise of the Scurvy. Edin. 1753. — 27. Marfan. Bull.
mM. Paris, 1895, ix. p. 75.-28. Mather, W. H. New York Med. Journ. 1873,
HEMOGLOBINURIA 621
xvii. p. 102.— 29. Mollek. Konigaherger med. Jahrb. 1859, Bd. i. p. 377 ; 1862, Bd.
iii. p. 135.— 30. Nokthkup, W. P. Med. Record, N. V. 1889, xxxvi. p. 305 ; Arch.
Pediat. N. ¥. 1892, ix. p. 1 ; Starr's Dis. of Children, 1894, p. 405 ; and others, Arch.
Pediat. N. Y. 1894, xi. p. 227 ; and F. M. Ceandall. New York Med. Journ. 1894,
lix. p. 641. — 31. Oppenheimee. Beutsch. Arch. f. Min. Med. 1882, xxx. p. 87. — 32.
Oed, W. LaTicet, 1894, ii. p. 1483.— 33. Owen, E. Lancet, 1884, i. p. 246.-34. Page,
H. W. Med.-Ohir. Trans. 1883, Ixvi. p. 221.— 35. Paekes. Med.-Okir. Rev. Oct.
1848, Art. viii. — 36. Peteone, L. M. Ann. wniv. di med. chi/r. Milano, 1881, cclv. p.
539.— 37. PoLiTZEE. Jdhrb. f. Kinderheilk. \%59,'&A. ii. ^. 159.— Si,. Pott. Munehen.
med. Wochenschr. 1891, xxxviii. p. 805. — 39. Railton, T. C. Lancet, 1894, i. p. 332.
— 40. Rehn, J. H. Veroffent. d. Oesellsch. f. Heilk. in Berlin, Padiat. Section, 1879,
p. 178 ; Berlin, klin. Wochenschr. 1889, xxvi. p. 11 ; Verhandl. d. X. Internat. med.
Cong. 1890, Berlin, 1891, ii. 6. Abth. 57.-41. Rogees, 0. F. Boston Med. and Surg.
Journ. 1892, oxxvii. p. 617. — 42. SoHlPPEES, 0. Nederl. Verreu. u. Pcediat. Vooedr.
Utrecht, 1894, iii. p. 31 (Disc.).— 43. Smith, T. Trans. Path. Soc. Land. (1875-6), 1876,
xxvii. p. 219. — 44. Sutherland, G. A. Brain, Pt. Ixv. 1894, p. 27 ; Practitioner, 1894,
Iii. p. 81.-45. Taylor, H. L. Arch. Pediat. N.Y. 1894, xi. p. 648.-46. Thomson, J.
Lancet, 1892, i. p. 1292.-47. Toedens, E. Clinique Brux. 1887, i. p. 237.-48. Whit-
come, G. H. Arch. Pediat. PhUa. 1891, viii. p. 7«0.
W. B. C.
HEMOGLOBINURIA
Synonyms. — Paroxysmal hmmatinuria ; Intermittent hcematinuria ;
Intermittent hcemogiobinuria ; Paroxysmal mdhcemoglobinuria.
Definition. — Hsemoglobinuria is the name given to a disorder of
which the most prominent symptom is the occurrence in the urine of
haemoglobin or methsemoglbbin resulting from the destruction of red
blood corpuscles in the general circulation. Various other names, as
above, have been employed for the same pathological process. .
Causation. — Destruction of the blood corpuscles, giving rise to the
appearance of blood pigment in the urine, occurs under various
circumstances : —
(i.) Exposure to extremes of temperature ; as in cases of sun-stroke,
severe burns, or frost-bite.
(ii.) The absorption of certain poisons into the blood through the
alimentary or respiratory systems, or through the skin. Among these
substances are sulphuric, nitric, hydrochloric, pyrogallic, and oxalic
acids; arseniuretted and phosphoretted hydrogen, phenol, naphthol,
quinine, nitro-benzine, poisonous fungi, and, perhaps more important than
all of these, chlorate of potash.
(iii-) Transfusion, especially when the blood of an animal of one
species is conveyed into the circulation of an animal of another species.
In such cases the red corpuscles of the transfused blood are broken up
during their passage through the blood-vessels of the animal into the
circulation of which they are received.
(iv.) The disease occasionally occurs also as a complication of certain
622 SYSTEM OF MEDICINE
specific infectious disorders, such as scarlet and typhoid fever ; as a result
of certain blood diseases such as septicsemia, pysemia, purpura, and
scurvy; and of some unknown pathological condition of the blood-
forming organs.
(v.) It occurs, again, as a primary disease, the so-called paroxysmal
hsemoglobinuria, which is generally believed to be due to a previous
invasion of the system by syphilis, malaria, or gout.
Raynaud's disease. — Hsemoglobinuria is not infrequently found in
association with Eaynaud's disease ; even in comparatively mild cases
deadness of the patient's fingers or toes and occasional " mottling " of the
skin have been observed from time to time. On the other hand, many
cases of Eaynaud's disease have been recorded in which at no period of
the affection could blood pigment or albumin be detected in the urine.
Notwithstanding their frequent association, it may be doubted whether
there be any relation between them other than that the paroxysms of
both are apt to be induced by the same cause ; namely, exposure to cold.
In the one case the nerves and walls of the blood-vessels suffer, in the
other the blood and possibly the blood-producing organs.
Condition of the urine. — This malady is to be carefully distinguished
from heematuria, in which blood, as such, is found in more or less intimate
admixture with the urine. In hsematuria, according to the amount of
blood present, the urine will be smoky, or even quite opaque ; and under
the microscope, blood corpuscles will be found in considerable numbers,
particularly in the sediment which is deposited on standing. If the
quantity of blood be large, coagulation will take place, giving rise to the
formation of a definite clot in the urine. In hsemoglobinuria, on the
other hand, the urine is generally clear when first passed, although on
standing it may become more or less turbid. Its colour ranges from a
light pink to a deep scarlet, brown, or black colour, according to the
amount and state of the pigment present. In severe cases the colour may
be as dark as that of porter. Its reaction is for the most part strongly
acid, and on standing it deposits a thick precipitate of lithates, with which
a quantity of haemoglobin in an amorphous form is usually mixed ;
occasionally a very few blood corpuscles may be detected. The presence
of blood, however, forms no integral part of the disease ; it is merely the
result of slight congestion of the kidneys, due to the irritation of the tubules
by the passage of the disintegrated haemoglobin. ' Occasionally the pre-
cipitated blood pigment is present in the urinary sediment in the form of
minute yellowish, rounded masses which may be aggregated into the
form of chains or bunches. Definite casts of the renal tubules com-
posed of this material are sometimes found, but in all probability true
hyaline casts do not occur. On rare occasions the haemoglobin (or h^matin)
has been present in the crystallised form, and the occurrence of crystals of
oxalate of lime has also been noticed.
Should there be any doubt as to the true nature of the extraneous
colouring matter in the urine the various tests for the presence of blood
or its derivatives may be applied. Examinations by means of the micro-
HMMOGLOBINURIA
623
scope will determine the presence or absence of the red blood corpuscles ;
although it is well to remember that their shape and consistence may
vary considerably with the reaction and specific gravity of the urine. If
the colouring, be not very intense, special search should be made for the
corpuscles in the sediment deposited on standing. If none be found, the
guaiacum test for blood pigment may be applied; but the test is somewhat
fallacious, as the same colour i;eaction may be obtained in the presence of
pus or mucus., . The only really trustworthy evidence will be afforded by
the spectroscope, by which not only can the presence or absence of blood
pigment be determined, but also the actual form in which it is present.
In making the spectroscopic examination care must be taken to use only
such a strength of solution that the light can easily pass through it. If
the colouring matter is blood pigment, the spectrum of hsimoglobin (Fig. 1,
Fig. 82— Spectra of haemoglobin and its derivatives. (1) Oxyhiemoglobin ; (2) reduced teinoo-lobin •
(8) metlisemoglobin , (4) acid haanatin ; (6) alkaline hiematin ; (6) reduced alkaline hseujatin.
Nos. 1 and 2) or of methsemoglobin (No. 3) may be seen. The latter
is almost identical with the spectrum of acid haematin (No. 4), from which,
however, it can be distinguished by addition of some reducing agent to
the urine. If the spectrum be due to methsemoglobin, the pigment will
become converted into reduced haemoglobin, which gives a single wide
absorption band in a position intermediate between the two bands due
to oxyhsemoglobin. If, on the other hand, the original spectrum were
due to the presence of acid hsematin (No. 4), a single intense band of
reduced alkaline hsematin (No. 6) will be observed on the violet side
of the sodium line between D and E, and, in strong solutions, a much
fainter band still farther towards the violet end of the spectrum.
Owing to the presence of hsemoglobin, or its derivatives, the urine
will generally contain a more or less considerable quantity of proteid
624 SYSTEM OF MEDICINE
which, although when the urine is heated it gives rise to a coagulum
(reddish brown in colour, owing to the pigment entangled with it), is
probably not serum albumin, as in the ordinary forms of albuminuria,
but consists for the most part of globulin, as was first pointed out by Sir
William Gull.
The coagulum formed by heating the urine is also said to differ from
that obtained in like manner in the urine in Bright's disease, in that it
usually floats on the surface of the fluid instead of sinking immediately
to the bottom. The proteid, the presence of which may be demonstrated
in this manner, or by the other general tests for bodies of this nature,
is derived from the splitting up of the haemoglobin present.
This point may be demonstrated by saturating the specimens of urine
with magnesium sulphate, by which reagent globulin is precipitated, but
not serum albumin. The specimens should be left some time to ensure
complete precipitation if possible ; and after filtration the filtrate may be
treated with a further quantity of the salt, and filtered again. If any
serum albumin be present in the filtrate it will be precipitated by
slightly acidifying with dilute acetic acid, and then gradually raising the
temperature to about 80° C. In some few instances a certain amount of
nephritis may be associated with the hsemoglobinuria, in which case, of
course, serum albumin would be present in the urine as well as globulin.
Pathology. — Hsemoglobinuria is probably always the result of the
removal of haemoglobin from the red corpuscles in the general circulation.
That this is so may be demonstrated by cupping the patient and leaving
the blood, in a small cylindrical glass vessel, in a refrigerator for a con-
siderable length of time. The fed corpuscles gradually sink to the
bottom, when, if the blood has been obtained during an attack of hsemo-
globinuria, the serum will be tinged with a more or less deep red tint.
A simpler method of testing for the presence of free hsemoglobin is to
remove serum from a blister and examine it vrith the spectroscope.
Normally, the only absorption band visible when blood serum is examined
is a dim one at the violet end of the spectrum, about the F. line. This
is indicative of the presence of lutein, to which the colour of the serum is
said to be due. If, on the other hand, the serum has been obtained from a
blister at the beginning of an attack of hsemoglobinuria, the characteristic
absorption bands of haemoglobin will present themselves, their intensity
being proportional to the thickness of the layer of serum examined. It
was formerly taught that hsemoglobinuria is primarily a disease of the
kidneys, but no evidence has been afforded to justify this opinion ; in fatal
cases of the disease no definite alteration in the structure of the kidneys
has been demonstrated.
Toxic hj?moglobinuria. — One of the most important, because the
most dangerous, forms of the diseases included under the general name of
hEemoglobinuria is that variety which occurs as a result of poison.
Mention has already been made (p. 621) of the different ways in
which hsemoglobinuric intoxication has been induced : of the mode of
HEMOGLOBINURIA 625
its causation but little is known; especially as, with regard to the
majority of these toxic agents, the recorded instances of their action
are but few in number. It is a remarkable fact that the employ-
ment of chlorate of potash has been followed in a considerable number
of cases by a severe attack of hsemoglobinuria, which has often resulted
in death. Thus it was in no less than 23 out of 27 cases collected by
Hofmeier. This untoward result, indeed, has not infrequently ensued on
the ingestion of unusually large doses of this drug, whether administered
intentionally, as a therapeutic agent or with suicidal intent, or in a
strong solution, intended for use as a gargle, but unfortunately swallowed
by mistake. The urine passed in these cases of poisoning, in that it
contains a large amount of the dark granular debris of the broken-
down corpuscles, resembles that usually seen in other forms of hsemo-
globinuria. The amount of urea present has also often been enormously
increased. The blood pigment present is invariably in the form of
methsemoglobin, which has also been detected in the circulating blood — a
point in which this form of hsemoglobinuria differs from the paroxysmal
variety. Tomaselli has also recently put on record a number of cases in
which symptoms resembling paroxysmal hsemoglobinuria have followed
the administration of quinine to certain patients who were the subject of
chronic malaria ; this is a matter of no little importance, as this drug
is often employed in the treatment of hsemoglobinuria, especially when
attributed to malaria. Tomaselli believes that the method of administra-
tion, and the quantity of the drug employed, have little bearing on this
curious idiosyncrasy, which appears indeed to be more or less trans-
missible, since several members of the same family showed the same
intolerance of the drug.
Symptoms. — In Tomaselli's cases, half an hour to a couple of hours
after the quinine was given, the patients were suddenly seized with nausea
and shivering, accompanied by a considerable rise of temperature. Com-
plaint was also usually made of a feeling of weight in the loins followed
by an imperative need to void urine, which when passed was found to be
" sanguineous." Not infrequently vomiting, diarrhoea, and jaundice also
ensued.
In chlorate of potash poisoning the chief symptoms are very similar,
the patient being seized with rigors followed by vomiting and diarrhoea.
Eventually he becomes collapsed and comatose, and dies after a variable
interval. The fatal dose of this drug has been set down in the adult at
from three to four drachms, or less, in the twenty-four hours ; in the case
of young children about half this quantity has been known to cause death.
Morbid anatomy. — In cases of toxic hsemoglobinuria the kidneys are
generally found to be of a more or less uniformly dark brown colour ;
under the microscope the renal tubules are seen to be plugged with a
brownish granular material which is often found also in the Malpighian
capsules. The colour of this material, and also of the kidneys generally,
is due to the conversion of the pigment into methsemoglobin. No constant
change has been noted in any other organ.
VOL. V 2 S
626 SYSTEM OF MEDICINE
Treatment. — No drug is known to exert a direct influence on hsemo-
globinuria. Treatment must therefore be directed to removal of the
cause, if this be possible. The more disturbing symptoms must be allayed,
and the patient placed under such favourable conditions as warmth and
rest in bed.
Infantile hemoglobinuria. — Occasionally this disorder occurs
among infants ; in some cases it seems to alternate with true hsematuxia.
Usually no general symptoms are present, and the child does not show
any signs of pain ; the only indication of anything wrong is the appear-
ance, at more or less irregular intervals, of blood or blood pigment in
the urine. Even this indication is wont to disappear on admission to
hospital, where equable temperature, regular and proper feeding, and
attention to the digestion effect the patient's cure, at any rate for the
time being. This affection seems to show that an occasional extra-
physiological destruction of corpuscles may be a result of improper feed-
ing, clothing, and the like carelessness, on the part of ignorant or
inattentive parents. The proper method of treatment in such cases is
obviously hygienic.
Now and again, however, more serious outbreaks occur, such as
that put on record by Winckel, which occurred in the wards of a lying-
in hospital at Dresden in the spring of 1879.
Here, during a period of about six weeks, twenty-four newly-born
infants were attacked with a form of hsemoglobinuria ; of these no less
than twenty-three died. In all these cases the symptoms were practically
identical, and were very similar to those met with in the toxic form of
the disease. Thus the children within a few days of birth showed signs
of collapse, and the skin acquired a yellowish tinge. This was followed
by a distinct rise of temperature, and by increase in the pulse and respira-
tion rate. The urine was somewhat scanty and brown, the contained
pigment probably consisting, in part at any rate, of methsemoglobin.
Death ensued in about thirty-six hours from the beginning of the illness.
The necropsies revealed considerable enlargement of the mesenteric
lymph-glands and of the spleen — the latter organ being somewhat
tougher than usual and of a browner colour. The kidneys also were of a
brown colour, and the renal tubules were plugged with masses of haemo-
globin.
The onset of this affection appeared to be due to a more or less
complete disintegration of the red corpuscles of the circulating blood ; but,
though investigation was diligent, no sufficient cause for the outbreak
could be discovered. It is not improbable, however, that some bacterial
infection played a part in the matter. The general symptoms and the
pos1>mortem appearances all pointed to a toxic cause ; and other facts,
which appear to support such a contention, are that in each instance
a period (of incubation ?), of about equal length in all, elapsed between
the birth of the infant and the invasion of the system by the disease ;
that a large number of children were affected within a comparatively
H.SMOGLOBINVRIA 627
short period, thus giving an indication of possible infection; and that
the disease was as sudden in its disappearance as in its first onset.
Paroxysmal hemoglobinuria. — Definition. — A disease, not depend-
ent on any known anatomical lesions, in the course of which the patient is
attacked, at more or less irregular intervals, by severe rigors, followed, after
a longer or shorter period, by a discharge of urine ranging in colour
from a pinkish hue to a bright scarlet, or even black-brown ; such colour
being due to the presence of a quantity of blood pigment in the form
of hsemoglobin, or of one of its derivatives. The disease was first de-
scribed by Dr. George Harley under the name of intermittent hematuria,
and shortly afterwards by Sir William Gull as intermittent haematinuria.
To Dr. Pavy we owe the more accurate name Paroxysmal Haemoglobinuria,
now generally used.
Causation. — In some cases attacks of this disease may occur even in
the height of summer; nevertheless, the most obvious immediate cause
is exposure to cold. Such exposure in the first instance was often,
extreme ; but where the tendency already exists, a comparatively slight
chill is sufficient to determine an attack. As a general rule the patient
is free from attacks during the warm weather ; but with the return of
winter the affection reappears, although even then the malady may
remain in abeyance as long as confinement in an equable temperature at
home or in hospital is observed. The liability to attack may persist for
years without much apparent danger to life ; although a severe series of
paroxysms may seriously depress the vitality of the suflferer for the time.
Exhaustion of any kind, whether mental or bodily, over-work, excesses of
the table or of the sexual functions, or again, want of proper nourishment
of the body, whether resulting from dyspepsia or from the actual depriva-
tion of food, undoubtedly dispose to attack.
The disease is almost entirely confined to men, usually between the
ages of fifteen and fifty or sixty years. Attacks, however, have been
recorded in women ; and in certain instances the disease has been known
to occur, in its most typical form, in children even of quite tender years.
The disease has probably some afiinity to syphilis, whether acquired or
congenital ; a definite specific history has been forthcoming in all the
cases that have come under my own observation.
In many cases there has been a history of malaria also ; although, as
this form of hsemoglobinuria is apt to occur in malarious countries, the
comiection between the two diseases may have been assumed to be more
definite than it really is. Gout and rheumatism have also been placed
among the remoter causes of the disease.
Symptoms. — Generally after definite exposure to cold the patient
is attacked, at a longer or shorter interval, with chilliness of the ex-
tremities, often attended with dead fingers or toes, shivering or actual
rigors, pallor and roughness of the skin, general sensation of cold, and
often severe headache. He may complain of pain or difficulty in swallow-
ing ; although there is usually no loss of appetite, and no evidence of
628
SYSTEM OF MEDICINE
disease either in the thoracic or in the abdominal viscera. In this early
stage the temperature of the body is usually lowered by as much as two
or three degrees. Within from half an hour to three hours a quantity of
urine is passed which is of a somewhat high specific gravity, of a red,
brown, or black colour, clear, acid, and containing excess of urea and
abundant albumin. Occasionally the urine is turbid when passed, and
in any case on standing it deposits abundant sediment, composed for the
most part of a brownish granular matter. Occasionally some of the
blood-pigment is deposited in a crystallised form also. During this period
the patient, if he is in the house, usually crouches over the fire, and feels
sick and giddy, even if he do not actually vomit. A reactionary rise of
temperature now ensues, which may reach as high as 103° F. The
TIME 10 II 12 I 2 3 4 1
Ex. BLOOD
X
c
Ex. URINE
X
X
XX
X
r
r° 101°
100°
99°
98°
97°
96°
95°
94°
93°
S3
o
5r
1
^
s
/
\
\
\
r
\
\
J
>
f*
Ghabt 6. — Chart showing range of temperature during a typical attack of paroxysmal hsemoglobinuria.
whole attack usually lasts for about five hours, after which time the urine
gradually loses its specific characters, and the patient very shortly seems
to be restored to much the same condition as that in which he was before
the onset of the paroxysm.
Similar attacks will recur as frequently as the patient is exposed to
the causes. They may return with great regularity, and sometimes two
or three attacks may occur during a single day ; but they are not char-
acterised by the definite periodicity which is seen so notably in ague. If,
on the other hand, the patient's surroundings be favourable, attacks may
be postponed for an almost indefinite period. In a patient subject to the
disease, the skin, particularly of the face, is generally of a somewhat
sallow colour, which is apt to become intensified after an attack ; so much
so indeed, on occasion, as almost to simulate jaundice. Considerable
ansemia may also be noticeable, the patient sometimes remaining weak and
HEMOGLOBINURIA 629
languid in the intervals of attack ; and it may be possible to observe
capillary pulsation on the lips, such as is often obtainable in other cases
of extreme ansemia, and generally in aortic regurgitation.
Pathology. — One of the most remarkable features of this disease is
the enormous and often extremely rapid destruction of the red blood
corpuscles, such destruction depending apparently on the direct influence
of cold. This is well shown in the series of experiments carried out by
Dr. Bristowe and myself, in which the blood was examined, by means of
the hsemocytometer, immediately after exposure to cold, and before any
blood pigment had been passed by the urine. The results of a number
of cases on which such examinations were made were so far identical
that a large decrease in the number of corpuscles was noticed, varying
from 129,000 to 824,000 per cubic millimetre. The injurious action of
cold on the blood corpuscles was further shown by the loss of consistence
and the variability of size and shape of those which survived ; by the
presence of granular masses of haematin in the plasma, and by the tinting
of the plasma with the escaped haemoglobin of the corpuscles. In the case
of three children who came under my observation at the Great Ormond
Street Hospital, the direct influence of cold was specially obvious, and it
may be mentioned that two adult patients, who remained for a consider-
able time in St. Thomas's Hospital, had no attack while there, save those
which were brought on by occasional exposure to cold.
The extreme rapidity with which the destruction of the corpuscles is
effected was shown in some cases by the examination of the blood
immediately after the patient had been exposed to cold, and before any
of the characteristic symptoms of an attack had been observed ; but there
is also ground for believing that the destruction of the corpuscles goes on
at a diminished rate for some little time after such exposure. The
removal of pigment from the corpuscles does not usually affect the urine
for half an hour or more after the beginning of the exposure.
A proteid is excreted with the pigment which may readily be shown
to be globulin and not serum albumin.
Dr. MacMunn has put the statement on record that the pigment
invariably consists of methseinoglobin ; but if the urine be drawn off
from the bladder by means of a catheter at frequent intervals from the
onset of the attack, it can be shown then to consist of oxyhsemoglobin.
Dr. Druitt, who himself was the subject of this disease, states that his
urine was of a bright scarlet colour on those occasions when, suffering
great pain from the irritability of the bladder, he was obliged to void
urine about every half-hour. On the other hand, if the pigment be
allowed to remain in the bladder for some considerable time in contact
with the acid urine, it may finally become converted into methaemoglobin,
or even into acid haematin. Experiments show, however, that it invari-
ably passes through a preliminary stage of methsmoglobin before con-
version into acid haematin. Some difficulty in distinguishing these
pigments has evidently been experienced in the past, as the spectrum of
methaemoglobin and that of acid hsematin are practically identical, each
630 SYSTEM OF MEDICINE
showing four absorption bands (Hoppe-Seyler) ; although in most text-
books only three bands are given for methaemoglobin. In specimens of
urine obtained from persons suffering from paroxysmal hsemoglobinuria
the four absorption bands are generally -well marked. This fact may
have led to the conclusion that the pigment voided is acid hsematin, even
in cases in which mefchaBmoglobin was present alone. In point of fact,
however, the degree of change appears to depend solely on the length
of delay in the bladder (or perhaps, in part, in the renal tubules) ; so
that, according to the time which the urine has remained there, oxy-
hsemoglobin, methaemoglobin, or even acid haematin is obtained.
Hsemoglobin, the colouring matter of the red corpuscles, is known to
be capable of existing in the three forms of oxyhsemoglobin, reduced haemo-
globin, and methaemoglobin. These differ from one another, not only in
the amount of oxygen in combination but also in the colour of their
solutions, and in their absorption spectra. The reaction of the first two of
these modifications is alkaline. By spirting ap haemoglobin haematin is
produced which also is capable of existing in three forms; one of these,
which is very stable, and has an acid reaction, is known as acid haematin or
haematin in an acid solution ; the two others possess an alkaline reaction,
but difier in the amount of oxygen in combination. Methaemoglobin, on
the other hand, has an acid reaction, and its spectrum, is almost, though not
quite, identical with that of acid haematin. It is readily distinguished
from this body, however, as, when treated with a reducing agent such
as ammonium sulphide, or, better still, sodium hyposulphite, it is
changed into reduced haemoglobin, while acid haematin under similar
circumstances yields reduced alkaline haematin. It is evident that met-
haemoglobin must be nearly related to haemoglobin, although there has
been some diversity of opinion on the subject. Eeeentiy, however, it
has been proved conclusively that it contains precisely the same amoiuit
of oxygen as oxyhaemoglobin, from which, therefore, it differs only in its
closer union with its oxygen, and in its acid reaction.
It is noteworthy that not only, as has been stated, is the destruction
of blood corpuscles rapid and enormous, but that the restoration of blood
corpuscles is also remarkably rapid ; experiment has shown that in the
course of from four to six days after a severe attack their number will
have risen almost to the amount recorded in the previous interval of
health. It appears highly probable, indeed, that paroxysmal haemoglobin-
uria is but an exaggeration of a physiological phenomenon. The red
corpuscles of the blood are constantly imdergoing destruction, the products
of this destruction are used up in the system, and in health they do not
appear in the urine either in the form of haemoglobin or of albumin. If,
however, the destruction oversteps the normal limit, the system is unable
to make away entirely with the products of such destruction, and albumin
appears in the urine. If the destruction be much above the limit, even
for a very short time, then oxyhaemoglobin will appear ; or, if the pig-
ment be retained in the tubules of the kidney or in the bladder for any
length of time, methaemoglobin.
HMMOGIOBINURIA
631
Sir George Johnson, Dr. Mahomet, Dr. Ralfe, and others have called
attention to the fact that temporary albuminuria may follow cold bathing,
or any other form of exposure to cold, in persons apparently healthy ;
and a case has been recorded by myself, in which an attack of hsemo-
globinuria followed a cold bath taken after exertion at tennis, in an athletic
man, apparently in perfect health, who has never bad any symptoms of
renal disease either before or after this solitary attack. Dr. Ralfe also
showed from his own personal experience that albuminuria is apt to
occur in persons otherwise apparently healthy after exposure to cold,
fatigue, or mental worry ; and — excepting that there was no rise of
temperature — with symptoms practically identical with those character-
istic of hsemoglobinuria. Indeed, Ealfe expressly stated that in four of
his cases the attacks of paroxysmal albuminuria occurred in persons who
had been subject to hsemoglobinuria ; and he considered that there is a
TIME 1 2 3 4 5 6 ''A
Ex. BLOOD
X
X
X
X
Ev. URINE
X
,
:x)
:x)
;x;
;x5
■
X)
:x
:x;
:x
:x
-p° 102°
101°
100°
99°
9B°
97°
96°
'
■■
-1
bJ
u
D
II
^
-^
J
^
■*.
, t
-\
\
^
i'^
A
J
V
\
s
s
/
_
N
s
n
Ohabt 7.— Temperature curve m a case of paroxysmal hsemoglobinuria.
definite relationship between the two diseases. It appears extremely
probable that paroxysmal globulinuria (which name appears preferable to
the more usual one of albuminuria, at any rate for those cases which are
brought on by exposure to cold) is a latent form of paroxysmal heemo-
globinuria, being due, as in this latter disease but in less degree, to
abnormal destruction of the red corpuscles in the blood.
That a relationship between these two affections actually exists
appears to be proved by the effect produced on persons subject to
paroxysmal hsemoglobinuria by exposure to slight degrees of cold. Such
exposure is often followed by a marked elevation of temperature, together
with comparatively slight but unmistakable destruction of corpuscles ;
the evidence of which is the appearance of globulin (not albumin) in
the urme. This relationship is well brought out in a series of observa-
tions made by myself in the case of an omnibus conductor, aged 41
who for two years previously had suffered during the winter months from
632
SYSTEM OF MEDICINE
occasional attacks of paroxysmal haemoglobimiria. In the accompanying
Chart 6 it will be seen that, as judged from the temperature curve,
the first exposure to cold, which consisted in the taking of a short walk
in the open air, resulted in less constitutional disturbance than did a second
but shorter period of exposure later in the same day.
At intervals of time, designated by crosses marked on the chart,
examinations of the urine were carried out, the results of which are
shown in tabular form. During the first period covered by these observa-
tions no blood-pigment could be detected in the urine, although albumin
(globulin) was found in easily recognisable amount.
Urine.
Temperature
.
Pulse.
Resp.
Albumin.
Blood-colouring matter.
Before exposure 97 "8°
2 P.M. 96-2°
76
14
None
None
2.15 P.M.
97-3°
82
18
None
2.30 P.M.
2.45 P.M.
3 P.M.
3.15 P.M.
98-6°
98-8°
98-8°
99°
73
85
85
80
17
13
15
14
Trace
Larger trace
Larger trace
One-tenth
No guaiacum re-
action, and no
absorption-bands
3.30 P.M.
99-2°
87
16
Fair trace
3.45 P.M.
99-2°
82
15
Trace
4 P.M.
98-4°
82
14
None
Some time later, after the second period of exposure, the slightly
higher range of temperature which ensued was accompanied by the
additional presence of blood-pigment in the urine.
Pulse.
Besp.
Urine.
Albumin.
•Blood-colouring matter.
4.45 P.M.
98-4°
84
17
None
None
5 P.M.
99-2°
87
17
Trace
Guaiacum reaction
5.15 P.M.
99-2''
76
16
Much
Haemoglobin (spectroscope)
5.30 P.M.
99-8°
84
16
One-quarter
Do.
5.45 P.M.
99-7°
78
17
Less
Do.
6 P.M.
99-4°
73
15
Trace
Do.
6.15 P.M.
99-4°
72
16
Trace
Do.
6.30 P.M.
99-2°
74
16
Trace
Trace
6.45 P.M.
98-0°
74
16
None
None
These results accord to some extent with the experiences of Ponfick,
who has shown that, whilst an injection of large quantities of haemoglobin
into the blood causes hsemoglobinuria, the injection of small quantities
causes no such elimination. It seems a legitimate inference, therefore, that
HEMOGLOBINURIA 633
■when the unwonted destruction of red corpuscles, the cause of which has
been exposure to cold, is comparatively slight, the proteid moiety of the
haemoglobin alone appears temporarily in the urine ; the colouring matter
of the eflfete corpuscles, on the other hand, being used up in the system,
probably by conversion into biliary and urinary pigments. When, how-
ever, the destruction is more extensive, hsemoglobin is discharged as
such.
In the light of these arguments it is not necessary to assume that
either of these affections is dependent upon disease of the kidneys, which
appear to act merely as the organs for the elimination of the excess of
effete products with which the blood is charged.
It must be admitted, however, that, although the destruction of red
blood corpuscles is the most obvious feature of paroxysmal haemoglobinuria,
there is very strong evidence to show that there is some antecedent
peculiarity of the blood corpuscles themselves which renders them unduly
sensitive to the influence of cold, seeing that in the healthy man an equal
degree of exposure is quite incompetent to bring about such a result.
According to Murri, the cause is to be sought in the diseased condition
of the blood-forming organs, which renders the corpuscles less resistant
to cold. This is borne out by the fact that under the microscope the
blood corpuscles do not run together into rouleaux in the normal manner,
even when there has been no paroxysm for some time ; while their con-
sistence seems to be lessened, as, in preparations for the microscope, the
slightest pressure on the cover-glass is often sufficient to make them
assume all kinds of fantastic shapes. One cause for this chronically
diseased condition of the blood-forming organs may probably be found
in the effects of syphilis, as has already been suggested by Murri, Barlow,
and others. As bearing on this point it is of interest to note that in all
my own cases syphilis, either primary or congenital, had been present.
It is hardly possible to look upon such an occurrence as a mere
coincidence.
As far as our knowledge at present extends, paroxysmal hemoglobin-
uria appears to depend on two main factors : —
1. A lessened power of resistance on the part of the blood corpuscles,
due to some defect in the blood-producing organs.
2. A tendency on the part of the corpuscles to break down in the
general circulation under the influence of cold, followed by the appearance
in the urine of the products of such haemolysis.
This tendency to disintegration of the corpuscles is apparently the
result of an imperfect power of production in the blood-forming organs,
caused in turn by the baneful influences of syphilis, or possibly of malaria,
gout, or rheumatism.
Treatment. — Seeing that the paroxysms of this disease appear to be
determined for the most part by exposure to cold, the obvious indication is
to keep the patient as much as possible in a warm and equable temperature.
This is to be done in severe weather by confinement to the house, and by
protecting the body from the effects of possible draughts by means of
6j4 SYSTEM OF MEDICINE
warm clothing, which, especially as regards the under-garments, should be
of wool. Meals should be regular and ample, but the food should be of
an easily digestible kind. Alcoholic drinks, especially wine and spirits,
unless much diluted, should be avoided, as they tend to produce a temporary
dilatation of the superficial capillaries of the skin, which may bring about
a slight lowering of the body temperature. Worry of mind or body
should be avoided as much as possible, and the patient should keep early
hours, so as to escape the imprisonment in heated rooms which appears
almost inseparable from evening entertainments. But only by removal
to a warmer climate than that of England can there be a reasonable
prospect of curing the disease.
The attack will probably be relieved if the patient retire to bed
immediately it threatens. He must be kept warm by every possible
means, such as a sufficiency of bed-clothes, and hot bottles in the bed.
Whether excessive thirst be present or not, a cup of hot soup will prob-
ably be found both pleasant and useful.
Probably but little good is to be obtained from treatment by drugs,
although both quinine and arsenic have by some been vaunted almost as
specifics for the disease. On the other hand, I must repeat that Tomaselli
has shown that, in some instances, the administration of quinine has
appeared to induce an attack of haemoglobinuria. If quinine be employed
it should be given in full doses, but no considerable benefit can be
expected from it in severe cases.
As from the constant drain on the blood system a certain amount of
anaemia is usually present, this symptom should be met by an administrar
tion of iron, either alone or combined with arsenic or digitalis. Seeing
that syphilis is present in a considerable proportion of cases, iodide of
potassium and the various forms of mercury should invariably be em-
ployed, when for this reason their use is indicated ; in some instances,
indeed, permanent cure has followed this method of treatment.
S. MONCKTON COPEMAN.
EEFEEENCES
Toxic Hsemoglobinuria : — 1. Eitnbe. Berlin. IcKn. Woalienschr. 1880. — 2. Hood,
DoKALD. Lancet, Ort. 4, 1890. — 3. Makchand. Firchow's Archiv, Ixxvii. 488,
1879. — 4. ToMASELLi. Clinica Moderna, May 1st, 1879. — 5. Sharp and Summek-
SKILL. Lancet, December 9th, 1893. Infantile Haemoglobiunria : — 6. Baginsky.
Deutsche med. Zeitung, 1889. — 7. Bare and Grandhomme. New York Medical
Journal, March 16th, 1889. — 8. Cnopf. Miinch. med. Wochenschr. May 7th, 189.').
9. WiNCKBi.. Deutsche med. Woch. 1879. Paroxysmal Hsemoglobinuria : — 10. Barlow.
"Eaynaud's Disease," Trans. Clin. Soe. vol. xvi. 1883. — 11. Barton. British Med.
Journal, Nov. 6th, 1889. — 12. Boas. Diss. Inaug. Halle, 1881. — 13. Bollinger.
Deutsche Zeitschr. f. Thiermedicin, 1877, vol. iii. p. 155, and Munch, med. Wochenschr.
1885, No. 3. — 14. Beistowb and Copbman. Proeeedvngs Med. Soc. 1889, vol. xii. ; and
Lancet. — 15. Chauffard. Semaine mM,icale, June 19th, 1895. — 16. Copeman.
Practitioner, Sept. 1890.— 17. Dickinson. Brit. Med. Journal, May 19th, 1894.— 18.
Dresslee. Virdiow's Archiv, \65i, vol. -vi. -p. 26i. — 19. Ehelioh. Zeitschr. f. klin.
Med. 1881, vol. iii. p. 383 ; and Chariti-Annalen, Berlin, 1885, vol. x. p. 142.— 20.
Eioheatjm. Diss. Inaug. Berlin, 1881. — 21. Fleischer. Berlin, klin. Wocheschm.
1881, No. 47.-22. Frohmee. Archiv f. wissenschaft. und prakt. Thierheilk. 1884,
LEUCOCYTHJSMIA 635
vol. J.. Nos. 4 and 5.-23. Gull. Chiy's Hasp. Eeports, 1866, 3rd series, vol. xii. p.
381. —24. Harlet, Gbobgb. Med.-Ohir. Trans. 1865, vol. xlviii. p. 161.— 25.
Hbinbmann. Virchow's Archiv, 1885, vol. oil. p. 517.— 26. Hoppb-Sbylee. Physiol.
Chemie, Berlin, 1881, p. 822.-27. East. DeutscJie med. Woehensehr. 1884, No. 52.
—28. Klempbree. OhariU-Annalen, Berlin, 1895, vol. xx. p. 130.— 29. KtJssNEE.
Deutsche med. Woehensehr. 1879, No. 37.-30. Lbubb. Sitmngsber. der Wurzburger
physiol.-med. Gesellsehaft, No. 20, March 1886.-31. Liohthbim. Vollcmann's
Sammlung Mm. Fortrage, 1878, No. 134.— 32. Mbsnet. "De rhenioglobmuna a
frigore," Archives g&n. de rtiM. etc. May 1881.— 33. Mueei. Delia Emoglohmuna da
Freddo, Bologna, 1880 ; and Rmista clmica, 1884, No. 4.-34. Pavy. Lancet, 1866,
vol. ii. p. 33.-35. Ponpick. Virchow's Archiv, 1874, vol. Ixii. p. 273 ; and Berl. klin.
Woehensehr. 1883, No. 26.-36. Rosenbaoh. Berl. klin. Woehensehr. 1880, Nos. 10
and 11.— 37. VAN Kossem. Acad. Proefschr. Amsterdam, 1877.— 38. Sbcohi. Berl.
klin. Woehensehr. 1872, No. 20.-39. Silbbrmann. Berl. klin. Woehensehr. 1886,
Nos. 29 and 30 ; Zeitschr. /. klin. med. 1886, vol. xi. p. 459.-40. Tetjmpp. Miinch.
med. Woehensehr. May 4tli, 1897.— 41. Vaquez and Maecano. Gompt. rend. soc. de
tiolog. Paris, 1896, vol. x. p. 111.-42. Wickham Legg. St. Barth. Bosp. Reports,
1874, vol. X.
S. M. C.
LEUCOOYTH^MIA
LEUcocYTHiEMiA, or Leuchsemia (Ger. Leukamie), may be briefly described
as a disease in which there is great, and usually permanent, increase in the
number of leucocytes in the blood, associated with greater or less anaemia,
and with peculiar changes in the spleen, bone-marrow, lymphatic glands,
or other organs, these being affected in various combinations. Further,
the leucocytes are not only increased in number, but, taken as a whole,
are altered in character also.
Intpoduetopy.— Though conditions which can now be identified as
cases of leucocythsBmia had been described before, the definition of the
group of symptoms of which it consists dates from the independent and
almost simultaneous publications of Hughes Bennett and Virchow on the
subject. In October 1845 the former recorded a case which, from the
microscopical characters of the blood, he described as one of " suppuration
of the blood, with enlargement of the spleen and liver " ; and a month later
Virchow gave an account, under the title " white blood," of a similar condi-
tion in which he noted the association of splenic enlargement, epistaxis,
and a peculiar richness of the blood in leucocytes. In both of these cases
the important changes were observed after death. Afterwards Bennett
gave the name leucocythcemia to the disease, whilst Virchow called it
leukaemia. A short time after his first case Virchow observed another in
which the leucocythsemic condition of the blood was associated with
enlargement of the lymphatic glands, whilst the spleen was only slightly
enlarged; and in subsequent papers he drew a distinction between a
lymphatic form of the disease in which there is an admixture in the blood
of leucocytes from the enlarged lymphatic glands — " lymphsemia," and a
splenic form in which he believed the excess of leucocytes to be produced
636 SYSTEM OF MEDICINE
in the enlarged spleen — " splensemia " ; the cells in the blood being of
smaller size in the former than in the latter variety. Neumann, in 1870,
not long after his discovery of nucleated red corpuscles in the bone-marrow,
found that this tissue is often profoundly altered in cases of leucocy thsemia,
and this change he regarded as primary. After much discussion of
Neumann's views a medullary form was added. A Considerable amount of
confusion, however, arose from this classification of cases according to the
organs affected, as, according to this nomenclature, most cases were found
to be of a mixed kind.
Eenewed interest in the subject was aroused by the researches of
Ehrlich and others on the characters of the cells in the blood and their
reactions to various aniline stains ; and much of the work in recent years
has been along the same lines. The general result has been a tendency
to take the characters of the leucocytes in the blood in leucocythsemia as
the basis of distinction in different cases, and this method appears to me
to be justifiable.
Within recent years special attention has also been directed to the
more acute forms of the disease; and, in consequence, cases which formerly
would have been overlooked have been identified as cases of leuco-
cythsemia. Though the disease is, as a rule, very chronic, yet there are
instances in which it runs its course in a few weeks after the first appearance
of symptoms. In these the splenic enlargement is often slight, and the
true nature of the condition is revealed by examination of the blood.
Varieties. — Taking as the distinctive feature the characters of the
leucocytes found in excess in the blood, we find that there are two chief
varieties.
A. In the one class, which includes most of the cases generally described
as splenic leucocythsemia, there is almost invariably great splenic enlarge-
ment, whilst there are present in the blood numerous large uninucleated
cells and certain other elements which are believed by many authors
to originate in the bone-marrow. The latter point will be discussed later.
The name spleno-medidlary is often applied to this, the commoner, variety
of the disease, and will be adopted in this article. It might be more
correct to speak of it as medullary or myelogenic leucocythsemia, or
myelocythsemia with splenic enlargement; but the origin of the disease
in the marrow has not yet been proved. Some German writers have
called this form " myelsemia." In it the lymphatic glands are not usually
enlarged, but may be so, especially late in the disease. Though the
great splenic enlargement is almost constant, a few cases have been
recorded in which it was absent or slight ; and these have been designated
as cases of pwre medullary leucocythmmia. Provided that the condition of
the blood be the same, they may be classified with the others.
B. In the second variety the leucocytes in excess in the blood are
chiefly of the small uninucleated class, that is, are lymphocytes. This
will be spoken of as the lymphatic form, though the name lympliocythmmia
might be adopted. In this form the lymphatic glands are usually en-
larged, though occasionally the enlargement may be slight or even absent;
•a
Fio 1 -SDleno-medullary leucocytliaeima. Film of blood, showing the chief forms of cells met with .
(a) Laree uninucleated cells, -marrow cells," one of which (a') shows mitosis ; (S) eosinophile cells ;
MoriiSary leucocytes with multipartite nucleus ; (d) nucleated red corpuscles, showing variety
in form of nucleus ; (e) ordinary red corpuscles, x 1000.
Fio 2 -Lymphatic leucocythaemia or lymphocythsemia. Film of blood showing enonnouB increase
of nnhiucleated leucocytes, many of which are of very small size, with scarcely visible protoplasm.
xlOOO.
LEUCOCYTHMMIA 637
splenic enlargement is the rule, though it is not generally so great as in
the first form : other organs are not infrequently the seat of diffuse
leucocytic infiltrations. It is not possible to infer the origin of the
condition from the characters of the cells in excess, as the lymphocytes
have such a wide distribution in the normal body ; but that in many
cases the disease may originate in the lymphatic glands.
If we attempt to classify cases of leucocythsemia according to the
organs affected, we are met at once by the objection that usually more
than one are affected at the same time ; moreover, we do not find that the
characters of the leucocytes in the blood vary with the organs affected.
In a pronounced case of spleno-medullary leucocythaemia, for example,
enlargement of the lymphatic glands may occur, but this enlargement
is not attended by the appearance of lymphocytes in the blood; so
also the spleen may be very much enlarged in the lymphatic form
(lymphocythaemia), whilst the lymphocytes alone are increased in the blood.
In the latter case the splenic enla,rgement is found to be due to distension
of the pulp with lymphocytes, a change analogous to what may be found
in the kidneys and other organs ; the bone-marrow also may be the seat
of lymphocytic infiltration. As the increase of leucocytes, both in the
blood and in the various organs affected, is the essential feature of the
disease, it is better to take differences in their characters as the
principle of classification ; especially as these differences are of a definite
nature.
Pathological anatomy. — The blood. — The appearance of the blood
may show little change on naked-eye examination, or, on the other hand,
it may be strikingly altered. In cases where the number of leucocytes is
very much increased, it is pale and slightly turbid in appearance, as if
mixed with pus ; and if, in addition, marked anaemia be present, it is thin
and watery and may have a yellowish tint. It usually coagulates less
readily than normal blood, especially when there is much anaemia.
On microscopic examination the change is generally obvious at
once, the number of leucocytes being notably in excess. But, as will be
shown hereafter, it must not be inferred that when the increase is
apparently trifiing the case is not one of leucocythaemia. Occasionally
the number may fall very considerably in the course of the disease, or
even towards death.
As the characters of the leucocytes have been taken as the means of
classification, and as they differ considerably in the two forms, they will
be described under these two heads.
A. Spleno-medullary form {vide Fig. 1 of Plate). — In the fresh blood a
large proportion of the leucocytes are seen to be of greater size than those
of normal blood ; namely, 14-16 /i in diameter. Most of these are finely
granular, whilst some contain coarse, highly refracting granules. The
characters of the nuclei may be made visible by the addition of weak acetic
acid, but they are best studied in films of blood prepared by Ehrlich's dry
(or a corresponding) method {vide p. 413), and afterwards stained; for
the study of the granules this is necessary. In such preparations a great
638 SYSTEM OF MEDICINE
variety of cells is found to be present, some of which are not normally
present in the blood. The following are the chief forms :—
1. Large uninucleated corpuscles, which are often called marrow-cells or
myelocytes (" cellules medullaires " of CornU) from their supposed origin.
These are the largest cells present, and form a considerable proportion
(sometimes more than half) of the total number of leucocytes (Fig. 1, a).
The single nucleus is of large size, and is round, oval, or indented at one side
so as to have more or less a horse-shoe shape. It stains rather faintly,
being weak in chromatin, which forms a loose network with granular
thickenings in its interior. The protoplasm is finely granular, and stains
diffusely and faintly with a nuclear stain, such as methylene blue. The
minute granules in the protoplasm have, according to Ehrlich, a " neutro-
phile " reaction — staining with a mixture of a basic and an acid aniline
stain ; according to others, a weak " oxyphile " reaction. Some of these
cells may be found undergoing mitotic division (Fig. 1, a'), though mitotic
figures, as a rule, are not many, and may be sought for in vain. When
examined on a warm stage nearly all these corpuscles are quite devoid of
amoeboid movement, only some of the smaller forms showing traces of it.
2. Eosinophile corpuscles. — These are cells containing coarse, highly
refracting granules, which are called eosinophile, or oxyphile, as they stain
deeply with eosine and other acid aniline dyes (Fig. 1, V). Some of them
are of large size, and differ only from the cells of class 1 by the presence
of the large eosinophile granules. They are larger than the eosinophile
leucocytes of normal blood, and are non-amoeboid, or but slightly amoe-
boid. Others of smaller size correspond to the ordinary eosinophile cells
of the blood, and possess amoeboid movement ; various intermediate
forms are also present. The total number of eosinophile cells varies
much in different cases, but is always increased ; whilst the proportion to
the total number of leucocytes sometimes exceeds the normal, sometimes
not. The relative proportion of eosinophiles in the blood is not to be
relied upon as a means of diagnosis in early cases of leucocythsemia, as
was at one time supposed, since it is sometimes higher in other conditions.
A much more important point is the presence of the above-mentioned
large neutrophile and eosinophile cells.
3. The ordinary "multinucleated" leucocytes, or, more correctly,
those with multipartite nucleus (as the nucleus is usually single though
much lobulated) are also increased in number (Fig. 1, c). Along with the
cells of class 1 they constitute the great bulk of the leucocytes present.
They possess active amoeboid movements as in normal blood.
4. Sometimes leucocytes with " mast-cell " granules are present, occa-
sionally in considerable numbers. These granules are a coarse variety,
and are stained deeply and of slightly violet tint with methylene blue.
They are not found in normal conditions, though they occur occasionally
in diseases other than leucocythsemia ; their significance is not known.
A considerable number of cells with finer basophile granules may some-
times be present.
Such are the main varieties, though some intermediate forms are also
LEUCOCYTH^MIA 639
found. The small uninucleated leucocytes are not increased in number,
and may be diminished ; sometimes several fields of the microscope may
be examined without any being found.
As abnormal elements in this variety of leucocythaemia we must also
mention nucleated red corpuscles. They are practically always present,
and generally in larger numbers than in any other condition in adult life.
Another important point is that their presence does not appear to depend
upon the degree of the ansemia, as they may be numerous when the
number of red corpuscles is but slightly diminished. They are readily
recognised in stained specimens by the very deeply coloured nucleus, and
by the perinuclear portion being coloured like the ordinary red corpuscles.
The nucleus is usually single and circular, though sometimes it is frag-
mented, and there may be two or more nuclei of unequal size (Plate, Fig.
l, d). The nucleated red corpuscles vary somewhat in size, most being
about the size of an ordinary red corpuscle, some considerably larger.
B. Lymphatic form (wc^e Plate, Fig. 2). — In this variety the prominent
feature is the increase, almost exclusively, of uninucleated leucocytes —
lymphocytes and slightly larger corpuscles, such as are normally present
in the blood. In the smaller forms the protoplasm is scanty and hyaline ;
in the larger forms it is relatively more abundant, and often contains
small scattered basophile granules. These corpuscles as a rule are non-
amceboid, though the larger may show slight movement. In some cases
the leucocytes vary greatly in size, from 6 /;., to 12 /i, in others they are
nearly all under 9 /x. Mitotic figures in these cells have rarely been
seen in the blood. The multinucleated leucocytes and the eosinophiles
are not at all increased. Nucleated red corpuscles are usually absent,,
though a few may be found when the ansemia is great. The general
appearance of the blood in this form, as seen in a stained film, differs
much from that in the previous form (vide Plate, Figs. 1 and 2). (A
general reference may be made here to art. " Clinical Examination of the
Blood," p. 408.)
With regard to the amoeboid movements of the leucocytes the general
statement may be made that those leucocytes which are amoeboid in normal
blood are so in leucocythaemic blood also ; but in the first form of the
disease a large number of non-amceboid cells enter the blood, whilst in
the second the cells increased are chiefly of the non-amoeboid variety.
In leucocythsemia the red corpuscles undergo diminution in number,
sometimes to an extreme degree ; the number per c.mm. occasionally reach-
ing 1,000,000, or even less. When the ansemia is marked the corpuscles
vary in size, both larger and smaller corpuscles being present ; they also
show irregularity in shape — ^poikilocytosis. Eouleaux are imperfectly
formed in such conditions.
The total number of leucocytes varies much in diff'erent cases, and
the number relative to the red corpuscles depends also upon the latter.
The relative proportion may be as high as 1 : 3, or even higher ; and
cases have been recorded in which the leucocytes equalled or even
exceeded the red corpuscles in number, though most of these observations
640 SYSTEM OF MEDICINE
were made before the hsemocytometer came into use. The total number
of leucocytes does not often reach 1,000,000 per c.mm. The number
fluctuates considerably from time to time, and occasionally falls greatly.
In a case observed by myself (Osier records a similar one) the number
fell to normal ; but even then the abnormal elements remained in the
blood — large uninucleated non- amoeboid leucocytes, nucleated red cor-
puscles, etc.
According to our observations the ilood-plates are usually very much
increased in the spleno-medullary form, sometimes fourfold ; in the
lymphatic form they are usually diminished in number. We cannot
state this as a general rule, as in most cases recorded by others the con-
dition of the blood-plates has not been stated. Nor can we explain this
difference in the two types, although the coexistence of increase of
blood-plates and increase of multinucleated leucocytes in the spleno-
medullary form, as well as in many diseased conditions attended by
leucocytosis, is worthy of note.
The hcemogloUn is diminished in amount, usually in the same propor-
tion as the number of the red corpuscles, sometimes in rather greater
proportion.
Changes in the viscera. — The morbid changes in the viscera are often
very extensive, though they vary much in diiferent cases ; they chiefiy
depend upon the following processes : — (a) Accumulation and infiltration
of leucocytes within organs, leading to enlargement ; (6) the occurrence
of leucocytic thrombosis ; (c) haemorrhages, which may be of small or
large size; and (d) the progressive ansemia which produces fatty de-
generation and aids in the production of the general oedema which may
be present. We shall afterwards consider whether any of the changes
in the organs are to be regarded as primary in nature.
Spleen, — The splenic enlargement is one of the most striking features
of the disease ; in most cases it is very great, in some cases extreme.
The largest spleens are met with in chronic cases ; the weight of the
organ is often from 5 to 6 lbs., and weights up to 1%\ lbs. have been
recorded. In the more rapid cases the enlargement is not so marked,
and the organ may be less than 1 lb. in weight. The enlargement is
generally uniform, so that the form of the organ is maintained; the
notches in the anterior border are usua,lly so strongly marked as to be
palpable during life. Spleniculi, if present, may share in the enlargement ;
I have seen in one case a spleniculus of 3 inches in diameter. On the
surface of the spleen there may be cartilage-like plates of fibrous thicken-
ing, or there may be fibrous adhesions. On section the organ may have
a fairly uniform red colour varying in depth, and a somewhat dry appear-
ance ; or it may contain infarctions of various numbers and ages : some-
times it is studded with them. The infarctions are of different sizes and
shapes, being usually more or less wedge-shaped towards the surface, and
of irregular outline in the deeper parts ; they vary in colour from a deep
purple to a pale pinkish gray or yellow, the recent ones being dark in
colour. The substance of the organ is usually pretty firm (the more
LEUCOCVTHMMIA 641
chronic the case the firmer it becomes), owing to a general thickening of
the supporting stroma ; nevertheless it is often somewhat friable. The
Malpighian bodies are, as a rule, indistinct, and it may be impossible to
define their outline ; sometimes, though rarely, they are very distinct.
In the more acute cases, which are often of the lymphatic variety, the
organ is generally rather soft, and shows on section a uniform reddish
pink colour.
Microscopically, the change is found to consist in a packing of the
general pulp with leucocytes similar in character to those found in the
blood. Thus in the spleno-medullary form, the large uninucleated cells
can be distinguished, and many eosinophile cells also are usually to be
found; whilst in the lymphatic form the cells are almost exclusively
small uninucleated leucocytes. A general thickening of the reticulum
of the pulp may be present in the chronic cases, and thickening of the
trabeculse and vessel walls is also common, the fibrous tissue often show-
ing a hyaline appearance. These latter changes are, however, no doubt
secondary to the chronic distension of the organ, aided probably by
abnormal metabolic processes ; they occur in all conditions of long-
standing enlargement of the organ. In the cases which run an acute
course, on the other hand, the stroma of the organ may be quite un-
changed. The Malpighian corpuscles usually show no alteration ; they
appear few in number owing to their being separated by the enlargement
of the pulp. The infarctions, when present, show the usual minute
structure.
Bone-marrow. — As indicated above, the changes in the bone-man-ow
are of special importance in relation to the pathology of the disease ; though
further minute histological examination in a large series of cases is still
necessary before a very definite opinion can be formed regarding them.
According to Neumann, the bone-marrow may present one of two appear-
ances : it may be soft and yellowish white in colour, almost like pus —
the " pyoid " condition ; or it may be of pinkish colour and firmer con-
sistence— the "lymphoid" or " lymphadenoid " condition. The former
is comparatively rare, and has only once been observed by me in a case
of spleno-medullary leucocythsemia. In both varieties of the disease the
marrow usually presents the appearance described as lymphoid ; that is, it
has a pale pinkish colour and is moderately firm, though the consistence
varies somewhat in different cases. (The term "lymphoid," however, is
a bad one, as it naturally suggests lymphoid tissue, from which marrow
differs widely both in the cells present and, especially, in the vascular
arrangements.) This pale pink marrow fills not only the spaces in the
small bones, but also replaces the fatty marrow in the shafts of the long
bones, and occasionally causes considerable absorption of the bone. It may
be conveniently removed in pieces from the shafts of the long bones, and
examined by breaking down a little in normal salt solution tinted with
methyl violet, by film preparations, or by means of sections. It is
desirable to use all the methods together.
Microscopically, the marrow in .the spleno-medullary form is found to
VOL. V 2 T
642 SYSTEM OF MEDICINE
contain very much the same cellular elements as are found in normal
marrow. The marrow - cells, neutrophile and eosinophile, are very
numerous, and, as already stated, closely resemble the cells present in
the blood. Nucleated red corpuscles are also fairly numerous, and some
of them may be of larger size than usual. Cells containing red cor-
puscles in various stages of disintegration may also be present, but these
are often met with in the marrow in a great variety of other conditions.
In sections it is usually found that the fat has been completely replaced
by a richly cellular tissue which has the structural arrangements of an
active marrow ; here, however, there is an excess of the colourless cells.
The vascular channels are badly defined, the blood -stream percolating
between masses of cells loosely held in position. Grian1>ceUs, generally
of smaller size than usual, may be scattered through the section in con-
siderable number. The change may be described in general terms as a
hyperplasia of the marrow with excess of the colourless elements.
Recently special attention has been directed to the presence of mitotic
figures, indicating indirect division of the marrow-cells ; and these have
been found by some observers to be very numerous. I have found
mitoses specially abundant in one case out of four examined — a case of
spleno -medullary leucocythsemia in a child aged 14 months. The
amount of cellular multiplication taking place, however, at the time of
death will probably vary very much in different cases. It would be of
great importance to examine a portion of marrow removed during life,
but an opportunity of doing so rarely occurs.
In the lymphatic form, in which the marrow may present very much
the same naked-eye appearances as in the other variety, there is found a
large proportion of small uninucleated leucocytes, which displace to a
considerable extent the cells proper to the marrow. The nucleated red
corpuscles are few in number. The condition is really a lymphocytic
infiltration of the bone-marrow, this tissue being secondarily affected in
the same way as other organs {mde infra).
Lymphatic glands. — Enlargement of the lymphatic glands is not
uncommon if we take all the cases of leucocythsemia. According to
Gowers, it occurs in a third of the cases. In most, however, of the
earlier cases recorded, the characters of the leucocytes in the blood have
not been attended to, and we cannot therefore give statistics of the
occurrence of glandular enlargement in each of the two forms of the
disease as above defined ; though the following general statements may
be made. In the spleno-medullary form enlargement of the lymphatic
glands is not common. In the majority of cases the disease runs its
course without any of' the glands being affected ; sometimes, however,
enlargement occurs, but it usually involves only small groups of glands
here and there, and to a small extent. In the lymphatic form, on the
other hand, that is when the leucocytes in the blood are of the small uni-
nucleated variety, enlargement of the glands is very common, though by
no means invariable. The enlargement may occur early or late in the
disease. A single group of glands may show enlargement ; usually
LEUCOCYTH^MIA 643
several groups are affected ; more rarely is there a general enlargement.
The cervical, axillary, inguinal, and mesenteric glands are most frequently
enlarged. The enlarged glands rarely exceed the size of small plums,
and usually remain separate and freely movable. They are somewhat
soft in consistence, and on section appear succulent and of whitish or
slightly pink colour, though there may sometimes be small haemorrhages
into their substance. In the chronic cases some matting of the glands
may occur, but this is not the rule.
In the enlarged glands in the spleno-meduUary form, collections ' of
cells may often be found towards the periphery, similar to those in the
blood and readily distinguishable from the lymphocytes of the adenoid
tissue. Their origin is difficult to determine. They may be the result
of hasmorrhages, and this would sometimes appear to be the case, red
corpuscles being mingled with them ; or they may be carried from the
tissues by the lymphatics.
In the lymphatic form of the disease the enlargement of the glands
is due to an accumulation of lymphocytes, which closely crowd the
various parts of the gland and give a uniform appearance throughout.
The accumulation is sometimes specially dense in the cortical lymph
sinuses. There is usually no trace of thickening of the stroma of the
gland, and caseation does not occur unless some other condition be
superadded.
Thymus. — Occasionally in lymphatic leucocythsemia the thymus
undergoes considerable enlargement and forms a pretty firm mass, some-
what irregular on the surface, in the upper mediastinum. This condition
may sometimes be recognised by percussion during life. It may occur
in the adult as well as in the young subject. In one case observed
by myself, in a woman aged 25, there was great enlargement of the
thymus along with enormous enlargement of the spleen, but with
scarcely any enlargement of the lymphatic glands. Microscopically, the
enlarged thymus shows a well-formed fibrous stroma enclosing pretty
large spaces, which are filled with lymphocytes with a small amount of
delicate reticulum between them.
Liver. — This organ generally shows some degree of enlargement, and
is often 5 or 6 lbs. in weight. In one case at least a weight of over 1 3
lbs. has been recorded. The enlargement is uniform, the surface usually
smooth, and there may be small haemorrhages under the capsule, though
these are not very common. The consistence may be unaltered or may
be diminished, and usually the colour is distinctly paler than normal.
This pallor may be pretty uniform, but often occurs in pale zones round
the portal tracts, thus giving a somewhat nodular marking. Micro-
scopically, in the cases in which the lobules are outlined in this way,
there is found an infiltration of the connective tissue of the portal tracts
with leucocytes, and the infiltration may extend for some distance into
the lobule between the liver-cells and the capillary walls. The infiltra-
tion may be pretty general, or it may occur specially in patches here and
there. The fibrous stroma, as in the leucocytic infiltrations elsewhere,
644 SYSTEM OF MEDICINE
becomes more delicate, and, as the leucocytes are closely packed together,
the appearance is very much as if a growth of lymphoid tissue had taken
place round the portal tract. These infiltrations occur especially, though
not exclusively, in the lymphatic form of the disease. The capillaries
contain large numbers of leucocytes, and some may be plugged by them.
Further, in advanced cases there may be a considerable amount of atrophy
of the liver-cells. As the result of the ansemia, in many cases these show-
fatty degeneration, which is usually most distinct in the centre of the
lobules. There is no evidence that any cirrhotic change ever occurs as
the result of leucocythsemia.
Kidneys. — In the spleno-medullary form the kidneys are usually of
normal size and may show nothing abnormal beyond a slight degree of
pallor. In other cases the pallor is well marked, and there may be
scattered hsemorrhages in their substance or beneath the lining of the
pelvis. Occasionally small irregular whitish areas are present, often
surrounded by red zones ; these are found on microscopic examination to
be due to collections of leucocytes in the connective tissue, with a
varying amount of haemorrhage. More rarely there is a diifuse leucocytic
infiltration of the connective tissue. The tubules may be normal, but
there is very often fatty degeneration of their cells, and occasionally
there may be haemorrhage into their lumen. Sometimes also there are
evidences of catarrh. The glomeruli are usually normal, but hsemorrhage
within the capsule of Bowman is sometimes met vrith.
In the lymphatic form of leucocythaemia the connective tissue of the
kidneys is not infrequently the seat of a diffuse lymphocytic infiltration
which may lead to great enlargement. In the case of a boy aged
eight, reported by Dr. John Thomson and myself, each kidney weighed
16 J ounces, and the left kidney was easily palpable below the spleen
during life. The enlargement usually affects both cortex and medulla
in a uniform manner and in equal proportion. The tissue is pale and the
markings are regular, though there may be small haemorrhages here and
there. The consistence may be nearly normal, or it may be distinctly
soft, so that the kidney substance bulges somewhat when the section is
made. Microscopically there is found in these cases simply an enormous
infiltration of lymphocytes in the connective tissue of the organs, so that
the tubules and other elements become widely separated from one
another. The tubules themselves may remain normal, or any of the con-
ditions mentioned above may be present.
Occasionally infarctions are found in the kidneys as the result of
leucocytic thrombosis, but these are rare.
Other organs, such as the suprarenals, thyroid, ovaries, etc., may
show enlargement of the same nature as that of the kidneys, though they
are less frequently affected. When such affection is present their tissue
becomes softer ; and has usually a diffuse pinkish colour, the normal
markings being somewhat blurred.
In most of the cases in which such diffuse infiltration of the con-
nective tissue of organs occurs, the disease runs a more or less acute course.
LEUCOCVTHMMIA 645
Bizzozero has observed numerous mitotic figures in the leucocytes in-
filtrating the tissues, and Hindenburg found them in the leucocytes in the
spleen pulp, in the capillaries of the liver, and in the sinuses of lymphatic
glands, but not specially in the germ-centres of lymphoid tissue.
Alimentary canal. — The lymphoid follicles in connection with the
various parts of the alimentary canal may undergo enlargement in the
lymphatic form of the disease, and there may be in addition more diffuse
leucocytic infiltration of certain parts. This latter may occur in the
tissues of the gums, leading to swelling which may be followed by
ulceration. The tonsils in some cases may undergo considerable enlarge-
ment, and the lymphoid tissue of the pharynx and neighbouring parts
may be similarly affected. The solitary glands in the stomach have also
been found enlarged in a few cases. In the intestines the changes are
occasionally of a striking character. Swellings of considerable size may
be produced by enlargement of the Peyer's patches or solitary glands, or
by irregular leucocytic infiltration of the mucous membrane. Such
changes may be found both in the large and small intestine, but usually
one part of the intestine is affected in a special degree. The swelling may
be followed by ulceration, which is usually irregular, though the ulcers in
some cases have been described as "typhoid-like." Along with these
intestinal changes there is usually enlargement of the mesenteric glands,
though this latter may occur independently of any affection of the in-
testines. An " intestinal " form of leucocyth»mia was described by Behier
from the condition just described, but it is simply a variety of the lymphatic
form ; different organs being affected very variously in cases of the disease.
Heart. — Fatty degeneration of the muscular fibres of the heart is
often present, and, in cases where there has been marked ansemia, the
inner surface of the organ may show extensive pale yellowish mottling.
The organ often contains yellowish white coagula which, owing to the
large number of leucocytes contained in them, may appear as if pus were
mixed with the fibrin — a condition which attracted the attention of
earlier observers. As a rare condition may be mentioned the occasional
occurrence of patches of myomalacia cordis in the heart wall, the results
of thrombosis of the branches of the coronary arteries. We can find no
evidence that any hypertrophy of the heart takes place as the result of
leucocythsemia, though some writers mention its occurrence. If present,
it is due to some coexisting complication.
Lungs. — In the lymphatic form of the disease the connective tissue of
the lungs may be the seat of leucocytic infiltration. The walls of the
bronchi and the peribronchial tissue are chiefly affected, and the condition
may be diffuse or localised so as to form thickenings. This change,
, which may be found only on microscopical examination, is of the same
nature as that occurring in the connective tissue of other organs. On
microscopic examination also many of the small vessels may be found
plugged with leucocytic thrombi, and hsemorrhages may be seen around
them. The lungs are generally oedematous, and various other conditions
may be present as complications.
646 SYSTEM OF MEDICINE
Soemorrhages. — Small hsemorrliages have already been mentioned as
occurring on the surface or in the substance of various organs ; and they
are also common on serous membranes generally, in the periosteum, and
in the skin. Haemorrhages of larger size may be found in various parts ;
sometimes they are apparently spontaneous, sometimes produced by slight
traumatism ; and often they take place from mucous surfaces. Special
mention must be made of the occurrence of cerebral hsemorrhages on
account of their importance, as they are not infrequently the direct cause
of death. The haemorrhage is sometimes single and of large size, tearing
up the brain substance to a great extent, and may occur in any part. It
is usually progressive and leads to a fatal result, though occasionally
arrest and recovery may take place. Sometimes multiple haemorrhages
are found, as in one case observed by myself, in which there were fully
a dozen haemorrhages of various sizes in the cerebrum and cerebellum,
both in the superficial and in the deep parts. These haemorrhages are
almost certainly the result of leucocytic thrombosis occurring in badly
nourished vessels, the thrombosis probably beginning in the small veins.
Many of the small vessels in the neighbourhood of the hsemorrhage may
be found plugged in this way, and small haemorrhages with large numbers
of leucocytes may be seen in their perivascular sheaths.
Organs of special seme. — The eye and ear may be affected in like
manner; namely, by the occurrence of haemorrhages, and of leucocytic
infiltrations of their tissues. In the retina minute hsemorrhages are
of common occurrence, and are often associated with leucocytic infiltra-
tions along the lines of the vessels and in patches — the condition described
by Liebreich as retinitis leuccemica, though it is not really of inflammatory
nature. Occasionally a more diffuse leucocytic infiltration of the layers
of the retina has been found. Haemorrhage into the Tritreous is of rare
■occurrence. Similar infiltrations have been found in the structures of
the inner ear, and have been associated with subjective symptoms, such
as vertigo ; in one or two cases haemorrhage has been found as the cause
of sudden deafness.
■ Pathological chemistry. — At a comparatively early date chemical
analyses were made of the blood and organs in leucocythaemia, but many
of the results are vitiated to a considerable extent by the fact that the
material used was obtained after death, and therefore at a time when
important changes had been brought about by bacterial action. In some
cases, however, analyses have been made of the blood obtained by vene-
section, and of the spleen excised during life. The statement formerly
made, that the blood has an acid reaction, depended upon examination of
blood in which acidity had been produced by post-mortem change, and is
incorrect ; though the alkalinity is usually diminished. The fibrin has
been found increased in amount, though coagulation takes place slowly
— a circumstance which has been ascribed by some to the presence of
peptone in the blood, though this has not been certainly proved. Matthes
found deutero-albumose in the blood taken fresh, but no peptone.
As the result of many independent analyses, xanthin bases have
LEUCOCYTHySMIA 647
been found in increased amount. Salomon found that hypoxanthin
forms in ordinary blood after it has been allowed to stand; but in
fresh leucocythEemic blood, obtained by venesection, a considerable
quantity is present. Further, more hypoxanthin "has been obtained from
post-mortem specimens of blood in leucocythaemia than under other con-
ditions. According to most authors, uric acid is not found in the
blood, though some have asserted its presence. The presence of certain
organic acids — lactic, formic, and succinic — has also been affirmed,
the first-mentioned being found by Salomon in the proportion of -05
per cent in fresh blood. Lactic acid, again, is formed in normal blood
■when taken from the body, being due, according to Salomon, to a ferment-
ative change in the leucocytes ; and one would expect this post-mortem
formation to be increased in leucocythaemia. By some observers, other
substances — gluten, leucin, nucleo-phosphoric acid, guanin — have been
found as abnormal bodies or increased in amount, but chiefly in specimens
obtained after death.
Though there is probably no chemical substance in the blood peculiar
to the disease, the increase in the xanthin bases, discovered many years
before any definite opinions were formed regarding their origin, is a
well-established fact. According to the view which has recently
obtained pretty general acceptance, these bodies are formed from leucocytes,
and rather from their breaking down than as a product of their meta-
bolism. According to Kossel, their chief source is the nuclei of these
■cells. Horbaczewski has also traced the formation both of the xanthin
bodies and of uric acid to the same source. He found that from portions
of spleen outside the body, by varying the conditions, he could at one
time obtain uric acid, and at another xanthin compounds.
One more point of considerable interest is the occurrence in the blood
and organs after death of the minute crystals known as Charcot's crystals.
They are not present in the fresh blood, but may be found after it has
been kept for some time. They are specially abundant in the spleen and
in the bone-marrow ; and, according to Neumann, they are present specially
in the spleno-meduUary form, being usually absent in the lymphatic form.
They are usually regarded as a post-mortem product, though not
necessarily produced by decomposition; yet Westphal found them in
blood taken from the spleen during life and examined at once on a warm
stage : hence he concludes that, in the spleen at least, they may be
present during hfe. They are not peculiar to leucocythsemia, but may be
found in the marrow in other conditions ; and, as Leyden first discovered
in the case of bronchial asthma, they may be found in the sputum. They
are minute, elongated, symmetrical octahedra, and usually measure 10 /^
in length ; though smaller and larger forms are also found. They are
soluble in warm water and in solutions of alkaline carbonates, very
sparingly soluble in cold water, and insoluble in alcohol, ether, and
chloroform. There is some doubt regarding their exact constitution, but
at any rate they contain phosphorus ; according to Schreiner, they are a
compound of phosphoric acid and a base " spermin " which has the formula
648 SYSTEM OF MEDICINE
CgHjN. They are probably the result of cellular disintegration also, the
conditions under which they are found tending to support this view.
Chemical examination of the organs has given results somewhat
analogous to those described above. Both in the liver and in the
spleen, obtained after death, various observers have found a con-
siderable quantity of peptone, also of xanthin bodies (especially of xanthin
itself, hypoxanthin being less abundant or absent), also of organic acids,
especially lactic, formic, and succinic, and leucin and tyrosin in small and
varying amounts. In most analyses uric acid has not been found. Bocken-
dahl and Landwehr obtained from a leucocythsemic spleen excised during
life — ^peptone, 1 per cent; lactic acid, '012 per cent; succinic acid, '002 per
cent ; xanthin, '038 per cent : leucin was present, but no tyrosin, uric acid,
or glycogen.
The amount of iron in the liver and spleen has been estimated in a
few cases, and has been found somewhat increased ; v. Bemmelen found a
proportion of 0'22 to 0'27 per cent of dried substance in the liver, and
Prof. Stockman 0'337 per cent in the liver and 0'29 per cent in the
spleen. Stockman attributes the increase in his case to the numerous
haemorrhages in the body. Granboom also found more iron in the liver
in leucocythaemia than in a number of other diseases investigated; namely,
0'09 per cent of liver substance (not dried). The liver-cells, however, do
not usually contain pigment granules which give the iron reaction, the
presence of which is such a striking feature in pernicious anaemia.
The general result of chemical investigation in the disease has
then not been to reveal any very striking change in metabolism ;
the various chemical substances found in the blood, organs, and also in
the urine {yicLe infra) being, so far as evidence goes at present, chiefly
the result of excessive disintegration of leucocytes. As the number of
leucocytes in the body is greatly in excess of the normal, and as these
cells have probably a comparatively short life, the amount of leucocytic
destruction must be greatly increased and accordingly the products of
their disintegration also.
Conditions of occurrence and remoter causes. ■ — Leuco-
cythsemia may occur practically at any time of life ; but is most common in
middle adult life — from thirty to iifty years of age. The results of
statistics independently compiled agree in showing that it is twice as
common in man as in woman. Cases are most numerous about the age
of thirty in man and forty in woman, but it appears to affect men at
a greater age than women, being exceedingly rare in the latter after
sixty, while a considerable number of cases have been recorded in men
above seventy. The disease is, however, more common in children than
was formerly supposed ; probably many cases have been overlooked. A
greater proportion of cases of the lymphatic type occurs in the early
years of life than of the spleno-medullary ; but both varieties may aifect
children a few months or even weeks old. It is found in people of
all classes of society, its occurrence being apparently little aflected
by the conditions of life and surroundings; though it is sometimes
LEUCOCYTHMMIA 649
stated to be more common in the poorer classes. It appears to occur
in various countries witt much the same degree of frequency : statistics
of the proportion of cases of leucocythsemia to the total number of cases
in various Continental hospitals for ten years, given by v. Limbeck, show
a considerable difference in different towns ; this difference, however, may
be accidental, as it is met with in the case of towns not far distant from
one another. From this table the average proportion of cases of leuco-
cythaemia to other cases is about 3 to 10,000.
Hereditary influences appear to play little or no part in the proclivity
to the disease. Only a few cases are on record in which more than
one member of the same family have been affected by the disease. Such
cases have been recorded by Chambers, Senator, and Eichorst. Senator,
quoted by Eichorst, observed the disease in twins. Instances in which
one member of a family has suffered from leucocythsemia and another
from splenic or glandular enlargement are also few in number, and
occurrence of leucocythsemia in one of the parents and in one of the
children of the same family is almost unknown. Leucocythsemic women
bear children free from the disease ; on the other hand, the child of a
healthy mother may show the disease when but a few weeks old.
As remoter causes syphilis, rickets, rheumatism, acute febrile diseases,
depressing mental conditions have been mentioned by writers on the
subject, but these would probably be found to be the most common
antecedents of a large number of cases of any chronic disease. With
regard to malaria, however, there does appear to be some connection more
than accidental. Sir W. E. Gowers found a history of previous intermittent
fever in a iifth of a number of cases, and exposure to malarial influence in
a quarter. Though his results have not been entirely confirmed by the
statistics of others, still a malarial history appears to be too common to
be regarded as a mere coincidence. We cannot, however, go beyond
this, that malarial fever probably acts as a disposing condition. It is
also to be remarked that the protozoon, now sufficiently established as
the cause of malaria, has not been found in the blood in cases of leuco-
cythsemia. In many cases of acute leucocythsemia there has been a history
of pre-existing inflammatory or ulcerative conditions about the mouth,
fauces, or intestine ; but it is possible that these were early signs of the
disease itself. A history of a blow over the spleen, or of injury to the
bone, has been noted in one or two cases, but the coincidence must be
regarded as accidental.
In woman sexual processes have been regarded by many as having
an etiological relation to the disease, which has frequently .been observed
to start during pregnancy, after parturition, and, especially, during a
prolonged lactation. Without denying that these processes may have
some relation to the disease, still, in view of the considerable proportion
of the adult life of a woman which on an average is thus occupied, and
of the fact that at such times any abnormal condition is more likely to be
noticed, I think that the connection is only accidental.
We may summarise our knowledge regarding the conditions of
65° SYSTEM OF MEDICINE
occurrence by saying that leucocythsemia may occur at any age ; that no
connection with the surroundings and conditions of life of the patient can
be traced, and that, with the possible exception of malaria as a remote
cause, no relation to any previous disease has been established. In the
great majority of cases the individuals affected had previously . been in
good health.
Further — and this is a fact of importance — the disease is one which
affects the lower animals ; cases have been observed in the dog, cat, ox,
sheep, pig, and others.
Nature and etiolouy. — It is evident that in the case of a disease
such as leucocythsemia, in which there is so marked an alteration in the
corpuscular elements of the blood, any conclusion regarding its nature
must accord with the known facts of the formation and destruction
of the corpuscles. As there are few subjects on which there has been
so great a diversity of opinion, it would be quite out of place here to
discuss the various hypotheses in detail. I shall, therefore, only state
the inferences which appear to be justified from a consideration, on the
■one hand, of the changes in the blood and organs ; and, on the other
hand, of the views now most widely accepted regarding the life-history of
the blood corpuscles.
If we consider first the lymphatic form of leucocythsemia, as being
probably the simpler, we find that the essential change is the presence of
enormous numbers of small uninucleated leucocytes throughout the body ;
both in the blood and in various tissues. Such a condition, in view
of its nature and extent, can only, I think, be due to an excessive and
apparently purposeless proliferation of these cells. And, further, all the
histological changes present can be explained by such a proliferation. In
fact, the condition is closely allied in nature to tumour growth, to sarcoma,
for example ; and the diffuseness of the lesions would be explained by the
characters of the cells involved, these being normally present throughout
the tissues, and constantly in movement. Hence instead of distinct,
tumour-like masses, we find diffuse infiltrations of the tissues, leading to
uniform enlargement of organs. The anaemia may be explained by the
infiltration of the hsemopoietic tissue of the bone-marrow, and by the
gradual diminution of the blood-forming area. As already stated, we
•cannot infer the origin of the disease from the characters of the cells ; we
<;an only judge roughly from the organ or tissue which first shows enlarge-
ment. One of the striking features of the condition is that in different
cases the various organs are affected in a great variety of ways, and this
cannot as yet be explained; though there are analogous facts in the
case both of the infective granulomata and also of malignant tnmours.
In the other, the spleno-medullary form, the character of the cells in
excess suggests an origin in the bone-marrow. The large uninucleated
cells in the blood correspond with the marrow-cells or " myelocytes," the
large eosinophile cells in the blood with the eosinophUe marrow-cells;
whilst the nucleated red corpuscles, which are usually numerous in the
Talood in this condition, are in the normal state only found in the bone-
LEUCOCYTHMMIA 651
marrow of the adult. No doubt, in other abnormal conditions the
nucleated red corpuscles pass into the blood, but never in such numbers
as in this form of leucocythsemia, nor when the degree of anaemia is so
slight as it may be in this disease. It would appear, in fact, as if there
were an extension of the cells of the marrow into the blood.
The evidence of excessive division of these cells as shown by mitotic
figures in the bone-marrow and also in the blood, is not quite conclusive ;
but it must be remembered that the disease is usually a chronic one,
lasting sometimes for several years, and that there also appear to be
remissions, if we may judge by the number of leucocytes in the blood.
We may therefore regard the hypothesis of excessive proliferation of the
cells in the marrow, with an extension of these cells into the blood, as
being that which is most in accordance with facts.
I cannot see sufiicient evidence in support of the view held by many
authors that leucocythsemia is primarily a disease of the spleen. This
organ shows merely a distension of the pulp with leucocytes, and the
result of that distension when chronic, namely, thickening of the stroma ;
and the reason that it is almost invariably enlarged is probably to be found
in the relation of the circulating blood to the spleen pulp. Besides, the
spleen undergoes enlargement (though usually to a less degree, owing
probably to the shorter duration of the disease) in the lymphatic form as
well as in the spleno-medullary. Unless, therefore, we are to assume
that in all cases where the spleen undergoes great enlargement it is the
primary seat of the disease, it must be admitted that great enlargement
may occur secondarily. There is, besides, evidence that in normal con-
ditions leucocytes break down in the spleen, and the enlargement may
really be the result of an attempt to deal with the abnormal supply of
leucocytes. In malaria we have a striking example of the degree which
splenic enlargement may reach as a secondary affection. We cannot infer
a primary affection of the organ from great enlargement.
The view that the disease essentially consists in an excessive prolifera-
tion, in the one variety, of the small uninucleated leucocytes, in which
case the proliferation may start in various organs, and, in the other
variety, of. the cells of the marrow, is the one most in accordance with
the inicroscopical changes in the blood and various organs. It is also in
accordance with the views generally accepted by recent authorities on
the relations of the leucocytes to the red corpuscles. According to these
views, with which, from my own observations, I fully agree, none of the
leucocytes of the blood becomes transformed into red corpuscles, these
being formed from special cells — " erythroblasts " — in the bone-marrow.
The leucocyte is a distinct kind of cell which has a life-history of its own,
and special functions. The so-called " marrow-cells " are merely a variety
of large leucocytes which by their division produce smaller leucocytes,
which afterwards appear in the blood. I accordingly consider that the
view, still held by many pathologists, that in leucocythsemia there is an
interference with the transformation of leucocytes into red corpuscles, has
ho real basis. It is also to be noted that in normal conditions the
652 SYSTEM OF MEDICINE
youngest form of leucocyte and that which shows most active proliferation
is the lymphocyte, whilst the marrow-cells form an older series of cells in
which division is less active. In the form of leucocythsemia in which
those lymphocytes are in excess, the disease usually runs a more rapid
course.
With regard to the chemical changes in the blood, various organs, and
urine (vide infra), I have already stated that probably all can be explained
by the excessive disintegration of leucocytes which must occur in the
disease.
When we come to inquire into the immediate cause of this prolifera-
tion of leucocytes, we find that there is as yet little ground to go upon.
Naturally two hypotheses present themselves ; namely, that it is due to
some microparasite, or that it is of the same nature as tumour growth,
whatever that may prove to be. There are facts to support each, but
neither is more than a hypothesis. No parasite of the nature of the
malarial organism has been observed in leucoeythaemia, and there is no
adequate evidence that any bacterium is concerned in the disease.
Attempts have been made to transmit the disease to lower animals by
injecting either the fresh blood or the juice of a recently excised
leucocythsemic spleen ; but they have been without positive result.
It has recently been suggested that the excess of leucocytes may
be due to the continued presence in the blood of some chemical
substance, such as in normal conditions produces an increase of leucocytes.
Vehsemeyer, for example, has attempted to produce the disease by often-
repeated injection of peptone, and has found a very considerable increase
of the leucocytes, lasting for several weeks. This, however, is only a
continued leucocytosis, not leucocythsemia ; the leucocytes differ in the two
conditions (vide p. 661), and in the former there is no affection of organs
such as occurs in the latter. Leucocythsemia has never been produced
experimentally.
In the absence of knowledge regarding the agent producing the
excessive proliferation of leucocytes, we cannot definitely assign the place
of leucocythsemia in the category of disease. On the whole it presents
most points of analogy to the growth of tumours, the analogy being
specially striking in the lymphatic variety ; but, on the other hand, it is
not absurd to suppose that it may yet prove to be due to a microparasite.
Symptoms. — In describing the symptoms of leucocythsemia, we may
distinguish an acute and a chronic form ; ^ these are fairly well defined,
though cases of intermediate character occur. I shall give an outline of
the course of the disease in the two forms, taking first the chronic form,
which is the commoner.
The onset of the disease is generally gradual and insidious. In many
cases the earliest symptoms are produced by the splenic tumour ; a
dragging sensation or pain in the left hypochondriac region or a general
swelling of the abdomen may first be complained of. In others, weakness,
' These two forms only approximately correspond with the lymphatic and spleno-
medullary forms {vide infra).
LEUCOCYTHMMIA 653
breathlessness on exertion, giddiness, or gastric symptoms are the first
indications. Sometimes haemorrhage from the nose, more rarely from the
bowels, first leads the patient to seek advice. At this stage the patient
usually looks in pretty good health, and has not lost flesh, though a
certain degree of pallor may be present. Examination of the blood may
show a moderate or great increase of the leucocytes (for characters,
vide p. 637), and the red corpuscles may be only slightly diminished.
The spleen, even at this early period, may show enormous enlargement,
and its lower margin may be at the iliac crest. The changes in the
blood and the condition of the spleen usually render the diagnosis easy.
If the temperature be taken regularly, slight irregular pyrexia may often
be detected. This generally occurs at night, the temperature rising a
degree or more on some days, with intervals of a normal condition ; it
may be accompanied by sweatings; though, independent of rise of tempera-
ture, such a tendency to sweating is not an uncommon symptom. Dis-
turbances of the alimentary system often appear, vomiting or diarrhoea
from time to time being not infrequent.
Such are the common symptoms in the early stages of the disease ; and
in distinctly chronic cases patients may remain in pretty much the same
condition for months, or even for one or two years. In some cases, in fact,
they may enjoy tolerably good health with the leucocythaemic condition
of the blood well marked and the spleen of great size. More frequently
the general health is considerably impaired, more prominent symptoms
occurring at intervals and tending to become aggravated. In this stage,
under suitable treatment, considerable improvement in the general health
may take place, and the number of leucocytes may even diminish con-
siderably. Periods of relapse, however, follow, and in the course of time
a greater or less degree of cachexia usually supervenes. Pallor and
breathlessness become more marked, the pulse is often feeble and rapid,
the temperature is more frequently elevated and still shows the same
irregular character. The abdomen may show considerable tumidity,
owing partly to the splenic enlargement, partly to chronic flatulent disteh-
sion, and partly to ascites, which is no uncommon condition. The patient
loses flesh, becomes more and more asthenic, and is confined to bed.
Even in this stage a certain amount of improvement may occur, but too
often the course is steadily downhill. A tendency to hemorrhage, if not
present before, often appears now, and in this way the prostration is
increased.
A fatal termination may be brought about in various ways. In many
cases advancing cachexia and anaemia are followed by the occurrence of
general dropsy, which gradually increases, and the patient dies from heart
failure with pulmonary oedema. This, indeed, is the usual sequence of
events unless some fatal complication occur. In other cases severe
hssmorrhage from the nose, bowels, or elsewhere may be the immediate
cause of death ; and in a certain proportion of cases death is produced
suddenly by the occurrence of single or multiple hsemorrhages in the
brain. Occasionally severe diarrhoea contributes largely to the fatal
654 SYSTEM OF MEDICINE
termination ; in other cases intercurrent affections, such as pneumonia or
peritonitis.
Such, in outline, is the course of the disease in its chronic form, and
most cases of spleno-meduUary leucocythsemia in adults conform to this
description. The disease in this form usually lasts for from one to two
years after the first symptoms, though a longer duration is not uncommon.
After distinct cachexia sets in, the fatal result generally follows in a
few months, though it may occur at any time.
In another group of cases the disease runs a much more rapid course,,
and to these the name aeute leueoeythsemia has been given, though it
has only a relative significance. Leucocythsemia is more apt to have
this character in the earlier years of life, especially when the disease
is of the lymphatic variety. Of 17 acute cases collected by Ebstein, in
only 7 were the patients over thirty years of age ; and in 4 cases observed
by myself the greatest age was twenty-six. In some such cases a fatal
result may follow as early as four or five weeks after the first noticeable
symptoms, or even earlier ; how long after the beginning of the disease we
cannot, of course, say. The characters of the disease are of the same nature
as in the chronic form, but are exaggerated in degree and in rapidity of
course. Rapidly advancing pallor and weakness, or severe haemorrhage,,
may be the first indications of the disease. Irregular pyrexia, often with
great perspiration, thirst and anorexia, vomiting, diarrhoea, repeated bleed-
ings from the nose, gums, or bowels, and subcutaneous extravasations, are
amongst the most usual symptoms during its course. Enlargement of the
lymphatic glands is sometimes well marked, and may be one of the earliest
changes to be noted by the patient. Death may be preceded by a typhoid-
like condition ; sometimes it results from general oedema and heart failure,,
sometimes directly from haemorrhage. In such acute cases the splenic-
enlargement is usually only moderate in degree, or may even be slight;
though the increase of leucocytes is generally great and the anEemia.
sometimes extreme.
■ After this outline of the main features of the disease the more
important clinical conditions may be described in greater detail.
The condition of the hlooi is always of importance, and when examined
from time to time gives valuable indications as to the course of the
disease. In the chronic cases the number of leucocytes often remains
about the same for a considerable period of time, though sHght fluctuations-
occur. Their number, however, varies much in different cases. In one
case, for example, the leucocytes may number 200,000 per c.mm., in
another 600,000 per c.mm.; and when an examination is made som&
months later the numbers in the two cases may be little altered. It is
not the rule to find a gradual increase in the number in proportion to the
duration of the disease, although when the condition of the patient grows
worse the number of the leucocytes often increases. Occasionally, under
treatment, the leucocytes may become considerably diminished, and may
even fall to normal. It is not possible, however, to say that the patient
is cured, though the diminution is usually accompanied by an improve-
LEUCOCYTHMMIA 655
ment in the general health ; the abnormal elements remain in the blood,
and the splenic enlargement is sometimes little altered ; though sometimes
it is considerably diminished. In the more acute cases a considerable
augmentation in the number of leucocytes may be observed in the course
of the disease, and, as there is usually much diminution of the red corpuscles
at the same time, the proportionate increase is more marked still. In a
rapid case observed by myself, the numbers changed from leucocytes
209,000, red corpuscles 2,085,000, to leucocytes 379,000, red corpuscles
902,500, in less than four weeks. Throughout the greater period of the
disease in the chronic type, the red corpuscles usually number about
3,000,000 per c.mm., their number remaining almost stationary for a
considerable time, though falling considerably towards the close of the
disease. It is always a grave sign when the number of the red corpuscles
steadily diminishes in spite of treatment. Moreover, it should be borne
in mind that when the condition of the blood is stationary, or even
improving, a rapid aggravation leading to a fatal result may set in at
any time.
The splenic mlargermni corresponds in general characters with that met
with in other conditions. It is greatest in long-standing cases, and may
exceed that met with in any other disease. The enlargement, for ana-
tomical reasons, extends mostly forwards and downwards ; but sometimes,
when the downward extension is interfered with by adhesions or by a
powerful costo -colic ligament, the extension upwards is very marked.
The lower margin may be as low as the anterior superior iliac spine, or
even lower; whilst the anterior border may reach beyond the middle line,
occasionally even as far as the anterior superior iliac spine on the right
side. The form of the organ is maintained, and, as its consistence is
usually firm, its rounded margin can be readily palpated, the notches
in the anterior margin being often well marked. The enlarged spleen
often gives rise to a sense of dragging or heaviness, the uneasiness being
increased after food ; and sometimes, owing to the occurrence of peri-
splenitis, actual pain of a dull or sharp character may be present, especially
on movement. It may also interfere to a varying extent with the move-
ments of the diaphragm, and complicate respiratory troubles. When such
great enlargement has been reached, the size remains as a rule fairly
constant, showing only slight variations from time to time. Sometimes,
however, considerable diminution takes place, which may or may not be
accompanied by an improved condition of the blood. In the more rapid
cases of leucocythsemia the spleen may extend but little beyond the costal
margin ; and, as its consistence is less firm, palpation of its border is not
so readily effected. Between the size of the spleen and the number of
leucocytes in the blood there is no fixed relation. I have seen in the
more acute cases an enormous excess of leucocytes with but moderate
splenic enlargement ; and, on the other hand, I have seen the number of
leucocytes in chronic cases fall to a little above normal while the spleen
remained of very great size.
The lymphatic glands, when enlarged, may give rise to considerable
656 SYSTEM OF MEDICINE
swellings which are readily visible ; in other cases the condition is dis-
covered by palpation. The anatomical changes have already been described
(vide p. 642), and the clinical characters correspond. The enlarged glands
are usually free from matting or induration around, are neither painful
nor tender, and may show considerable fluctuations in size from time to
time. Occasionally an area of dulness can be determined during life
over the upper part of the sternum, which is due, not to enlarged
lymphatic glands, but to a diffuse lymphoid infiltration of the thymus or
its remains. Pressure symptoms are rarely produced. I repeat that
the lymphocytes may be in great excess in the blood whilst glandular
enlargement is slight or even absent. In one case of this nature recently
observed by myself there was extensive leucocytic infiltration of the
liver, kidneys, and suprarenals, with considerable enlargement of the
spleen ; the lymphatic glands being almost unaffected.
The changes in the bone-marrow are usually unaccompanied by any
symptoms. Hosier was the first to describe tenderness over the sternum
as a symptpm in the disease : this he found to be due to an overgrowth ■
of the marrow, with absorption of the bone ; and a like condition has
been noted in other cases. Occasionally there is a dull pain in addition
to tenderness, and these symptoms may be present in other bones besides
the sternum. Such symptoms are, however, the exception rather than
the rule, and it may be definitely stated that an extensive hyperplasia of
the marrow may be present without any subjective indication whatever.
In a few acute cases of the lymphatic type similar tenderness over the
bones has been noted, so that its presence does not necessarily indicate a
primary change in the marrow.
The thyroid, when it is the seat of leucocytic infiltration, may be
obviously enlarged during life. I have only once observed this, a
symmetrical enlargement of moderate degree and painless, occurring in a
case of acute lymphatic leucocythsemia. So far as I can ascertain, no
symptoms referable to the suprarenals occur when these are the seat of
leucocytic infiltration.
Disturbances of the alimentary system are common, especially in the
more acute cases, and may give rise to most troublesome symptoms.
The tonsils and lymphoid tissue of the pharynx may be enlarged and
interfere somewhat with deglutition, especially when an inflammatory
condition is superadded, as is sometimes the case. The enlargement, as
in the case of the lymphatic glands, may show fluctuations from time to
time. In such cases the condition first described by Hosier as leucsemic
stomatitis is apt to occur also — a condition in which the gums and other
parts of the mouth become swollen, inflamed, spongy, and sometimes
ulcerated; it is often attended with bleeding. The change somewhat
resembles that found in scurvy, and there is often decomposition of the
secretions and blood, with marked fcetor. In a few cases gangrenous
processes have supervened.
The appetite varies considerably. In the earlier stages in chronic
cases it is usually little if at all impaired ; in a few cases it has been
LEUCOCYTH^MIA 657
described as unusually great. Discomfort after a full meal is a common
symptom, and is to be ascribed in part to the pressure of the enlarged
spleen on the stomach. In the later stages of the disease, when there is
cachexia, and especially in the acute cases, gastric symptoms may be very
prominent. There is complete loss of appetite, very feeble digestive
' power, vomiting, and occasionally haematemesis ; though bleeding from
the stomach is not so common as from the nose or bowels, and usually
occurs only late in the disease.
Intestinal symptoms are comparatively common. There may be
flatulent distension and constipation alternating with diarrhoea; a tendency
to the latter is often well marked throughout chronic cases. But diarrhoea
is sometimes severe in degree, especially in the stage of cachexia ; and it
may largely contribute to a fatal result. It is sometimes accompanied by
tenesmus and by bleeding from the bowels, the bleeding varying greatly in
amount, but being sometimes profuse and occasionally the cause of death.
In such cases often no lesion of the intestinal mucous membrane can be
found after death, there being apparently a general oozing of blood from
its surface ; occasionally with the lymphatic variety of the disease the lesions
above described are found associated.
Acute peritonitis may supervene and determine a fatal issue. The
cause of the condition is doubtful, but in the cachexia towards the end of
life micrococci may gain entrance to the blood and lodge in the spleen,
as was found by myself in one case ; and it is possible that thence they
may pass to the surface of the organ and infect the peritoneum. In other
cases peritonitis may be set up by the process of tapping.
Enlargement of the liver can often be ascertained by percussion,
and its lower margin is sometimes palpable; but usually no symptoms
are produced by the affection of this organ. Jaundice is not met
with, unless as the result of some superadded condition. Great
leucocytic infiltration of the portal tracts may, however, possibly aid in
the production of ascites, which is often present towards the close of the
disease. The ascites may occur as part of a general dropsy, but some-
times the effusion into the peritoneum is well marked when there is little
or no dropsy elsewhere, and may require repeated paracentesis. Spon-
taneous hsemorrhage into the peritoneum has been described, but is a very
rare occurrence.
The symptoms in connection with the circulatory and respiratory systems
are mostly referable to the general condition, and especially to the
anaemia. Palpitation, breathlessness on exertion, giddiness, and the like
tend to become worse as the disease advances. The pulse becomes softer
and more rapid, but is usually regular, even in the later stages of the disease,
when, owing to the fatty change which is often present, the heart's action
may be very feeble. Systolic haemic murmurs may be heard over the
heart, and a bruit over the veins at the root of the neck. The heart is
sometimes displaced upward and slightly to the right side by the splenic
enlargement and the abdominal distension. Dyspnoea is often a distress-
ing feature in the late stages of the disease, even to the full extent of
VOT,. V 2 U
6s8 SYSTEM OF MEDICINE
orthopnoea. Several factors are concerned in the production of this
symptom. In addition to the anaemia present and the feeble action of
the heart, effusion into the pleural cavities may largely contribute to it,
and the condition is aggravated by the abdominal distension which
displaces the diaphragm upwards and restricts its movements.. CEdema
of the lungs usually precedes death, which may come about very
gradually. In one case, observed by myself, in which death took
place somewhat suddenly, there was extensive leucocytic thrombosis in
the small pulmonary vessels, along with large pale coagula in the large
trunks. Bronchial catEjjrrh is not uncommon throughout the disease,
and the cough, in some cases very troublesome, is attributed to reflex
causation. Pleurisy and pneumonia may be mentioned as complica-
tions.
Dropsy is common in cases in which there is advancing cachexia ; it
results from the anaemic condition, general malnutrition, and gradual
heart failure. Anasarca may be of extreme degree, the epidermis may be
raised in blebs, and an erysipelatous condition sometimes supervenes.
Effusions into the various serous cavities are common, and, as I have said,
ascites is often considerable.
Hmmorrhage into the tissues, or from mucous surfaces, occurs,
at some period of the disease, in the majority of cases. Of all the
varieties of haemorrhage epistaxis is the commonest. It may occur at
any period, and is not uncommonly an early symptom. It may recur
frequently throughout the disease and be moderate in degree ; sometimes
it is very severe and may be the cause of death. Haemorrhages from the
stomach or from the bowels, though less frequent than epistaxis, are by
no means uncommon, those from the bowels being the commoner. The
amount and frequency of the haemorrhages vary much in different cases.
In the case of intestinal bleeding, for example, there may be only a small
amount of altered blood in the stools; the faeces may be pulpy and contain
a considerable admixture of blood, or almost pure blood may be passed
from the bowel. Haemorrhages from the lungs and kidneys and from
the female genital tract are rarer events. Petechias in the skin
may occur, but usually only in the advanced stages of the disease;
sometimes in the more rapid cases, often of the lymphatic variety, the
skin haemorrhages may be much larger and of more diffuse character, as
in purpura haemorrhagica. Haemorrhage into the joints has also been
recorded. Haemorrhage into the deeper tissues, or muscles, is another
comjjlication, sometimes resulting from slight traumatism, sometimes
apparently spontaneous. I have seen more than a pint of blood effused
into the abdominal muscles, as the result of paracentesis when the
puncture was made a little to one side of the middle line. Haemorrhage
into the brain has been mentioned above as a not infrequent cause of
death. Fatal cerebral haemorrhage may occur suddenly, or may bo
preceded by symptoms, as in the case of smaller initial haemorrhages.
As the haemorrhage is in some cases multiple and in other cases very
extensive, localisation during life is usually very difficult. In giving a
LEUCOCYTHMMIA 659
prognosis in cases of leucocythsemia, the possibility of the occurrence of
cerebral haBmorrhage should be kept in view.
Elevation of the temperature at some period of the disease is almost
invariable. In the early stages in chronic cases slight irregular elevations,
more marked at night, may occur from time to time, with periods of
normal temperature between. In the later stage, and especially in cases
running an acute course, the pyrexia is more marked, though still show-
ing an irregular character. The temperature sometimes reaches 102° or
103° at night, and falls a degree or two in the morning; though some-
times it shows a more continuous rise. Occasionally slight rigors occur
with the rise of temperature, the causation of which is obscure.
The wine is generally normal in quantity, though towards the end of
the disease it may be diminished. Its specific gravity varies, ' but is
usually pretty high; an acid reaction is usually well marked. The
amount of urea has been found to vary in difierent cases, though it is
often little altered ; but increase in the quantity of uric acid, observed
by Virchow at an early date, is an almost invariable occurrence. The
amount of the latter has been recorded as reaching over 3 grms. a
day, but more recent analyses show that it rarely exceeds 1 '5 grm. A
deposit of urates often appears in the urine after standing, and uric acid
crystals may also be found. The xanthin bases, of which traces are
found in normal urine, are also increased in amount, and some of the rarer
members of the series — heteroxanthin, guanin, etc. — have been found by
different observers. Bondsynski and Gottlieb, in a case of spleno-meduUary
leucocyth»mia, found that the xanthin bodies exceeded three to four
times the normal amount. These changes in the urine are to be associ-
ated with those in the blood and organs described above, and probably
all are due to the excessive breaking down of leucocytes, as it is now
well established that xanthin and the lower members of the series are
chiefly excreted in the more highly oxidised form of uric acid. Formic,
lactic, and other organic acids in small quantities have been found in the
urine in some cases ; and peptone and albumoses have been observed
occasionally. Albumin may be present towards the close of the disease,
but, as a rule, the urine is free from it ; haematuria, though occurring
occasionally, is rare. There may be great enlargement of the kidneys
due to leucocytic infiltration, without a trace of blood or albumin.
Sulphates and phosphates have in some cases been found increased in
amount, but this is not a well-recognised alteration. The occurrence of
renal calculi from the increased excretion of uric acid and urates is not
common, though a few cases have been recorded.
In the skin multiple tumour-like nodules, often reaching a hazel-
nut in size, have been recorded in a few cases. This condition was
first described by Biesiadecki, and has been called by Kaposi " lympho-
dermia perniciosa." It has usually been associated with glandular en-
largement, and the structure of the nodules has been described as
resembling that of lymphoid tissue. Further observation appears neces-
sary, however, to determine the exact relation of this change to leuco-
66o SYSTEM OF MEDICINE
cytliaemia. A tendency to boils has been noted in some cases of leuco-
cythsemia. Other changes in the skin have already been mentioned.
Symptoms in connection with the nervous system, apart from those
produced by haemorrhages, are on the whole rare. Mental affection,
especially of a melancholic type, has been observed in some cases, chiefly
towards the close of the disease ; but it is not sufficiently frequent to
indicate any special proclivity. In some of the acute cases delirium and
coma have occurred before death, sometimes apart from marked pyrexia.
In addition to the symptoms produced by cerebral haemorrhage, which
has been referred to above, paralyses of certain of the cranial nerves,
due to haemorrhage or leucocytic infiltration in their sheaths, have been
recorded, and several observers have noted the occurrence of sudden
deafness : in one or two cases this has been found to be due to haemor-
rhage into the inner ear. In some other cases impairment of hearing,
subjective aural sensations, giddiness, and the Hke, have been observed ;
and in one such case Politzer found a leucocytic infiltration of the
structures of the labyrinth.
The retina on ophthalmoscopical examination very often shows distinct
changes, which depend chiefly on the altered condition of the blood
with the occurrence of haemorrhages. When the anaemia is well marked
the fundus is pale and sometimes of yellowish tint ; the veins are usually
dilated, tortuous, and paler than normal, whilst the arteries are narrow.
There is sometimes swelling of the optic disc. Haemorrhages in the
retina are common, and are most frequently situated at the periphery,
though they may also occur in the region of the macula. They vary in
size, though they are usually small ; in shape they are irregular and
have sometimes a striated appearance. Pale spots, usually close to the
vessels and often surrounded by traces of haemorrhage, are also seen some-
times ; occasionally they may reach a considerable size. They are composed
chiefly of collections of leucocytes and degenerated nervous elements. In
some other cases a uniform opacity of the retina has been observed,
which has been found to be due to leucocytic infiltration of the layers of
the retina. Interference with sight may be present or absent, according
to the position of the lesions. As these are most common at the peri-
phery, usually nothing abnormal is noticed by the patient, but in some
cases, where the more central region is involved, defect of the field of
vision may result. In a few cases such symptoms have first led the
patient to seek advice, and in this way have led to the discovery of the
disease. Haemorrhage into the vitreous has already been mentioned as a
rare occurrence.
Reproductive system.— In women there is often irregularity of the
menstrual function. There is sometimes menorrhagia, occasionally met-
rorrhagia, but as the disease advances amenorrhcea is not infrequent.
Women suffering from the disease have been known to pass through
more than one pregnancy and to bear healthy children. In man the
occurrence of persistent priapism, lasting sometimes as long as eight
v,'ceks, is a curious symptom which has been noted in a considerable
LEUCOCYTHMMIA 661
number of cases. It has been attributed to thrombosis in the veins
or in the sinuses of the corpora, cavernosa, and in a case recorded
by Kast evidence of such thrombosis was found after death, the priapism
having occurred a year and a half before.
Diagnosis. — In most cases of spleno-medullary leucocythsemia the
diagnosis is very easy. Frequently attention is first drawn to the great
enlargement of the spleen, and thereafter an examination of the blood
reveals the nature of the disorder. The number of leucocytes may
be so great as to leave no doubt possible ; but it must be borne in
mind that occasionally their number may not be much above normal,
and also that in a number of other diseases the leucocytes may be
increased in number. Here the characters of the leucocytes are of great
importance. Such increase, known as leucocytosis, occurs in certain wasting
diseases, in ansemia resulting from haemorrhage, in acute suppurations, in
various infective fevers, and so forth ; and is no doubt produced by the
circulation of certain abnormal products in the blood. Leucocytosis can
be experimentally produced by the injection of many bacterial products,
of peptone, nuclein, and other substances. The attempt to distinguish
leucocythsemia from leucocytosis by the number of leucocytes is quite
unscientific — the difference being one not merely of degree but of nature.
In leucocytosis theincrease is almost exclusively on the part of the leucocytes
with multipartite nucleus, so that the proportion of these to the other
leucocytes may be increased three- or fourfold, and no abnormal elements
are present. In leucocythsemia, on the other hand, the leucocytes have
the characters already described. As already stated, their number may
fall in some cases nearly to normal, whilst the abnormal elements remain
in the blood. Accordingly, when such a condition is found the case
should be closely watched and the blood examined from time to time.
Examination of the blood will also distinguish spleno-medullary leuco-
cythsemia from other diseases with great splenic enlargement, such as ague
or splenic ansemia. In the latter disease the number of leucocytes may
be slightly increased, normal, or even diminished ; but they never show
the alterations in character met with in leucocythsmia.
In the lymphatic variety, that is, where the lymphocytes are in
excess, the diagnosis is usually made easily in the same way. Such
cases, with enlargement of glands, are sometimes mistaken for lymph-
adenoma, a disease of an essentially different nature. In the latter
the glands are usually of firmer consistence, and often show matting ;
though this is not invariably the case. Of more importance is it
that when the leucocytes are increased in lymphadenoma — their
numbers sometimes reaching 25,000 per c.mm. or even more — ^the con-
dition is a leucocytosis, and the cells have the character just described.
Difficulty, however, sometimes arises in the case of children with
enlarged lymphatic glands, in whose blood there may be a certain excess
of lymphocytes, so that an early stage of lymphatic leucocythsemia may
be suspected. In these cases examination of the blood from time to
time will determine the matter.
662 SYSTEM OF MEDICINE
Some cases of acute leucocytha;mia with extensive hfemcrrhages may
be mistaken for severe purpura and like conditions ; and this is the more
liable to occur as the enlargement of the spleen may not be sufficiently
great to attract special attention. In other acute cases, with high
temperature and without special enlargement of lymphatic glands, the
condition, as Ebstein points out, may even be mistaken for typhoid or
other fevers. In such obscure cases the examination of the blood
should always be undertaken, and will usually reveal the condition at
once, if it be one of acute leucocythsemia. Here again the importance of
distinguishing it from a mere leucocytosis may be noted.
Cases of disease sometimes occur in which diifuse leucocytic infiltra-
tions of certain tissues — for example, of the intestinal mucous membrane
— are present, which changes can scarcely be distinguished histologically
from those met with in the lymphatic form of leucocythsemia, but are
unattended by the characteristic change in the blood. It is quite probable
that when the cause of such changes becomes fully known, it will be found
to be the same in the two series, and some general term may include
them both. In other words, there may be cases of the same disease, in
some of which the lymphocytes of tlie blood are increased, in others not;
just as in some cases of the lymphatic form of leucocythsemia the
kidneys are sometimes affected, sometimes not. But so far as our present
knowledge carries us, it is advisable to consider the blood changes as
constituting the distinctive feature of leucocythsemia, and as forming the
means of diagnosis.
Prognosis. — Though we cannot affirm that leucocythsemia always
ends fatally, yet, so far as prognosis is concerned, it must be regarded as
a condition of the gravest nature. A few cases are recorded in which
a cure is said to have taken place ; but in most of these one cannot but
regard the evidence as inconclusive, as the diagnosis in some of the cases was
uncertain, and in others the subsequent history was insufficient. Cases,
however, certainly occur in which great improvement in the general health
takes place, the number of leucocytes also diminishing greatly ; and this
improvement may last for a year or two. Accordingly, while the disease
practically always ends in death, the duration of life after the recognition
of it is very variable. In some chronic cases the disease has lasted as
long as seven years ; in other cases it has run an acute course in a few
weeks or less. In relation to the probable duration in different cases a
few general facts may be given.
In the first place, as regards age, the disease is usually of shorter
duration in young subjects, especially when it is of the lymphatic variety.
The spleno-medullary form in adults, when there are no bad symptoms,
is usually chronic, and often lasts one or two years. Some writers con-
sider that it is rather more rapid in women, but there is probably little
or no difference between the sexes in this respect.
The number of leucocytes in itself does not. give much indication,
though a progressive increase is an unfavourable sign. The degree of
anaemia present is of more importance, and a steady decrease in the
LEUCOCYTHMMIA 663
number of red corpuscles is especially grave. The size of the spleen
affords little assistance, except, perhaps, that a very great enlargement
points to a comparatively slow course so far, a circumstance which may
sometimes affect the prognosis.
Enlargement of the lymphatic glands, when at all marked, is, as a
rule, a bad sign, since it usually occurs either late in the disease or in
cases which run a rapid course.
Heemorrhages have a varying significance according to their position
and extent. Haemorrhage from the nose is not infrequent in the early
stages of the disease, and, though it may lead to a fatal result, may occur
from time to time in cases which run a very chronic course. Haemor-
rhages from the stomach or bowels are much more serious symptoms, and
usually indicate a condition of special gravity. So also haemorrhages in
the skin are generally the omen of rapidly advancing cachexia. The
presence of dropsy, well-marked or continuous pyrexia, or persistent
diarrhoea naturally makes the prognosis specially grave.
A judgment as to the course of the disease will be materially aided
by observation for a time of the case under treatment. But it must not
be overlooked that a patient suffering from leucocythaemia is in such a
state that a comiplication or sudden aggravation may occur at any time,
and prove fatal. Special attention has already been drawn to the
incidence of cerebral haemorrhage.
Treatment. — Leucocythaemia is a disease for which there is no specific
remedy, and it is one which too often runs a steady course towards a
fatal termination. But while this is so, under careful and judicious
treatment life may be considerably prolonged in many cases, and great
improvement may be effected in some. It ought to be regarded as a dis-
ease in which death may be much hastened by indiscretion on the part of
the patient ; but an intelligent knowledge of the features of the disease
and the complications which are likely to arise will sufficiently guide the
physician in this matter.
It is rather the rule than otherwise for patients in the earlier
stages of chronic leucocythaemia to improve when under treatment in
hospital. The regulation of the condition of the alimentary canal is
of great importance. The diet ought to be arranged so as to exclude
anything likely to lead to gastric disturbance, but otherwise should be as
full and nourishing as the condition of the patient will allow. If a
tendency to constipation be present, the bowels ought to be kept regular
by mild laxatives or intestinal stimulants ; constipation is apt sometimes
to be followed by diarrhoea. Powerful purgatives, however, are contra-
indicated in all conditions which may arise in the course of the disease.
Excess in eating and drinking, exposure to cold, over-exertion, and such
like must be carefully avoided. Such general measures as these, along with
good hygienic conditions, have a distinct effect on the general condition
of health apart from treatment with drugs. The tendency to haemorrhage
should be kept in mind in connection with any surgical interference which
may lio incidentally called for in n, patient suffering from leucocvtheemia.
664 SYSTEM OF MEDICINE
A large number of drugs have been employed in the treatment of the
disease, and with regard to each it may be stated that whilst in some
cases improvement or even cure is recorded, in the majority it has
been found ultimately to fail. Of all the drugs employed I believe
that arsenic is of the greatest value, and in many cases great improve-
ment results from its use. It ought to be given at first in ordinary
doses, to be gradually increased, and pushed as far as possible. Under
its use the number of leucocytes may diminish greatly and may even fall
to normal ; the size of the spleen also may become considerably less,
though sometimes it is little ati'ected. Arsenic has also been administered
subcutaneously and by direct injection into the spleen, but there are
manifest objections to these methods, especially when the hsemorrhagic
tendency is well marked. Some observers consider quinine in large
doses to be of considerable ser\'ice, but I look upon it as distinctly in-
ferior to arsenic. Good results have been reported from the use of
phosphorus in one or two cases, but the general experience is that it is of
no value. In other cases improvement has followed the use of tonic
medicines — cod-liver oil, iron, with or without quinine in small doses,
and chalybeate waters such as those of Pyrmont or Schwalbach. In my
experience, however, arsenic is the only drug which seems to have a dis-
tinct effect on the leucocythsemic condition.
On the view that the spleen is the primary seat of disease, a number
of measures have been adopted to produce diminution of this organ.
Such is the use of certain drugs — eucalyptus, quinine, and piperine
(Hosier), the faradic or galvanic current applied over the organ, electro-
puncture, the cold douche to the splenic region, and so forth. AU these
measures, I believe, are without effect.
Excision of the spleen has been performed in a considerable number
of cases, but almost invariably with a fatal result ; it must be regarded
as absolutely unjustifiable, and it is also, I believe, useless. Transfusion
of blood has also been tried without any satisfactory result. Inhalations
of oxygen have been administered in a considerable number of cases,
sometimes alone, sometimes along with other remedies, especially arsenic.
In the hands of some observers benefit has followed, chiefly in the
early stages of the disease ; but in many cases this treatment has
entirely failed. The amount of oxygen employed has usually been about
30 litres daily, though sometimes as much as 100 litres have been used.
Bone-marrow has been administered recently in this disease, but we can-
not as yet speak definitely of its effects. There seems to be no scientific
basis for this treatment, yet in a disease in which all known remedies
may be without avail the method is worth a fair trial. The marrow may
be administered either in the fresh condition or in the form of prepared
tabloids.
The complications occurring in the course of the disease and most
frequently calling for treatment are the haemorrhages from various
sources, the gastric and alimentary disturbances, and, in the later stages,
the heart-weakness, dyspnoea, and dropsy. All these are to be met by
LEUCOCYTHALMIA 665
the usual metliods. In the more acute form of leucocythaemia arsenic
should also be tried, but usually all remedies entirely fail, and the aid of
the physician is. limited to relief of the more distressing symptoms.
Robert Muir.
REFERENCES
The literature on Leuoocythaemia is so extensive that only a selection of papers is
here attempted. A fall account of the earlier literature will be found in the article
"Splenic LeucooythEemia, " by Gowers, in the System of Medicine edited by Russell
Reynolds.
General Symptomatology and Pathological Anatomy. — 1. Bkhibe. Union mM.
1869, pp. 267, 279.-2. Bennett. Hdin. Med. Journ. Oct. 1845 ; Zeucocythcemia,
or White Cell Blood, Edin. 1852. — 3. Bibsiadecki. Strieker's Med. Jahrluch, 1876,
p. 230. — 4. Cavafy. Lancet, 1880, ii. p. 769. — 5. Dunn. Amer. Journ. Med.
Hei. 1894, p. 285.-6. Ebstein. (Relation to Traumatism), Deutsch. med. Woch. 1894,
p. 589. —7. Fleischee, and Pbnzoldt. Deutsch. Arch. J. Tclin. Med. vol. xxvi.
p. 368. — 8. Kast. Zeitsch. f. hlin. Med. vol. xxviii. p. 79. — 9. KovAOS. Wien.
klin. Woch. 1893, No. 39. — 10. Lauenstein. Deutsch. Arch. f. klin. Med. vol. xviii.
p. 125.^11. Leube and Eleischek. Virchow's Arch. vol. Ixxxiii. p. 125. — 12.
MiDDLBTON. Glasg. Med. Journ. 1893, p. 357.-13. MosLBE. Berlin, klin. Woch.
1864, p. 170 ; 1876, p. 703 ; Deutsch. med. Woch. 1880, p. 617 ; 1886, p. 213 ; Die
Pathologic und Therapie der Leukamie, Berlin, 1872. — 14. Neumann. Arch. d. Seilk.
1870, vol. X. p. 1 ; Berlin, klin. Woch. 1876, p. 465 ; 1878, p. 118.-15. Oekastzow.
Deutsch. med. Woch. 1890, p. 1150. — 16. Pawlowsky. (Organtsms), Deutsch. med.
Woch. 1892, p. 141.-17. Peipbe. Deutsch. Arch. f. klin. Med. vol. xxxiv. p. 352.
— 18. PONFIOK. Virchow's Arch. vol. Ivi. p. 534. — 19. Thomson and Muir. Amsr.
Journ. Med. Sci. 1891, vol. x. p. 329.-20. Vehsembybe. Milnch. med. Woch. 1893, No.
30.-21. ViEOHOW. Froriep's Notizen, Nov. 1845 ; Med. Zeit. 1846, Nos. 34 to 36 ;
Virchow's Arch. vol. i. p. 563 ; vol. v. p. 43 ; Die krankhaften Gcschwillste, vol.
ii. p. 567. — 22. VoGBL. Virchow's Arch. vol. iii. p. 570.-23. Waldeyee. Vir-
chow's Arch. vol. Iii. p. 305.— 24. Wagbnhauser. (Occurrence of Deafness), Arch.
f. Ohrenheilk. vol. xxxiv. p. 219. The articles on Leukaemia by Moslee in v.
Ziemssen's Handhuch d. spec. Path. u. Therapie, by Biech-Hieschfei.d in Gerhardt's
Eandhuch d. Kimderkramkh., and by RiEsa in Eulenburg's Rcal-Encyclopddie d. ges.
Seilk. 3rd edit. 1897, may also be consulted.
On the Acuter Forms of Leuoocythsamia.— 25. Askanazy. Virchow's Arch. vol.
cxxxvii. p. 1. — 26. Oabot. Boston Med. and Surg. Jowrn. 1894, p. 507. — 27. Ebstein.
Deutsch. Arch. f. klin. Med. vol. xliv. p. 343.-28. Eiohoest. Virchow's Arch. vol.
cxxx. p. 365. — 29. Frabnkel. Deutsch. med. Woch. 1895, Nos. 39, 43. — 30. Gutt-
mann. Berlin, klin. Woch. 1891, No. 46.— 31. Litten. Gentralb. f. allg. Path.
1892, p. 369.-32. Mullee. Deutsch. Arch. f. klin. Med. vol. 1. p. 47.-33. Sena-
toe. Berlin, klin. Woeh. 1890, No. 4.-34. Westphal. Miinch. 'med. Woch. 1890,
No. 1. '
On the Characters of the Leucocytes in the Blood and Organs.— 35. Biondi.
Archiv. per le soienz. med. 1889, p. 291.-36. BizzozEiio. Virchow's Arch. vol. xcix.
p. 378.-37. Buchanan. Journ. of Path. vol. iv. p. 242.-38. Ehelich. Arch. f.
Anat. u. Phys. 1879, Phys. Abtheil, pp. 166, 571 ; Zeitsch. f. klin. Med. vol. i. p. 553 ;
Deutsch. med. Woch. 1883, p. 670 ; Farienanalytische Untersuchungen zur Histologic
und Klinik des Blutes. Berlin, 1891.-39. Hayem. Du sang, Paris, 1890, p. 864.
—40. Hindbnbueg. • Deutsch. Arch. f. klin. Med. vol. liv. p. 209. — 41. Kanthaok.
Med. Chron. 1894, vol. ii. p. 25.-42. L6wiT. Sitz. d. kais. Akad. d. Wis. zu Wien.
Abtheil 3, vol. xcii. p. 22 ; vol. xcv. p. 227.-43. Muir. Journ. Anat. and Phys.
1891-2 ; .Journ. of Path. Oct. 1892.-44. MiJllbe. Deutsch. Arch. f. klin. Med. vol
xlviii. p. 47 ; Centralb. f. allg. Path. 1894, p. 553 (summary of literature and refer-
ences).—45. Mullee and Ribdeb. Deutsch. Arch. f. klin. Med. vol. xlviii. p. 96.
— 46. Spilling. "Ueber Blutuntersuchungen bei Leukamie." Inaug. Dis. Berlin
1880.-47. Speonok. Ref. in.Forfs(!a. cJ. il/ed. 1889, p. 740.— 48. Weethbim. ZeUsch
/. Heilk. 1891, p. 281.
Chemical Changes.— 49. v. Bbmmblbn. Zeitsch. f. phys. Cheni. vol. vii. p. 497.—
50. BooKENDAHL and Landwehe. Virchow's Arch. vol. Ixxxiv. p. 561. — 51.' Bond-
666 SYSTEM OF MEDICINE
STNSKi and Gottlieb. "Xanthiu Bodies in Urine," Arch. f. exper. Path. vol. xxxvi.
p. 127. — 52. Fkeund and Obbrmaybk. Zeitsch.f. phys. Chem. vol. xv. p. 310. — 53.
Granboom. Arch. f. exper. Path. vol. xv. p. 299. — 54. Hoiibaczewski. Wien.
Sitzungsber. vol. o. — 65. Jacob. Beutsch. med. Woch. 1894, p. 641. — 56. Kgettnitz.
Berlin, klin. Woch. 1890, No. 35. — 57. Kolisch and BuiilAN. Zeitsch. f. Jclin. Med.
vol. xxix. p. 374. — 58. KossBL. Various papers in Zeitsch. f. phys. Ohem. vol. iii. et
seq. — 59. KrOoeb. Deutsch. med. Woch. 1894, p. 663. — 60. Matthes. Berlin, klin.
Woch. 1894, pp. 531, 556. — 61. Salkowski. Virchow's Arch. vol. Ixxxi. p. 166. —
62. Salomon. Arch. f. Anat. u. Phys. 1876, p. 762 ; Virchow's Arch. vol. cxiii. p. 356.
— 63. Stadthaoen. Virchow's Arch. vol. cix. p. 390. — [On "Charcot's Crystals."] 64.
Charcot. Compt. rend, de la soc. de biolog. 1853, p. 49. — 65. Leydbn. Virchow's
Arch. vol. liv. p. 324. — 66. Neumann. Virchow's Arch. vol. oxvi. p. 324. — 67.
Westphal. Beutsch. Arch. f. klin. Med. vol. xlvii. p. 616. — 68. Zenker. Beutsch.
Arch.f. klin. Med. vol. xviii. p. 125.
Treatment. — 69. Da Costa and Hbkshey. Amer. Joum. Med. Sci. p. 482. — 70.
Cutler and Bradford. Ainer. Joum. Med. Sci. 1878, p. 84. — 71. Fox, Wilson.
Bancet, 1875, ii. p. 45. — 72. Kirnbergeb. Beutsch. med. Woch. 1883, p. 594. — 73.
Lembke. Inaug. Bis. Freiburg, 1890. — 74. Moslbr. Op. cit. No. 13.— 75. MoxoN,
GowERs, and others. Trans. Clin. Soc. Bond. 1876-77.' — 76. Pfletzer. Berlin,
klin. Woch. 1887, p. 701.— 77. Kehn. Wien. med. Woch. 1888, p. 1642.— 78. Sticker.
Miinch. med. Woch. 1886, p. 767. — 79. Taylor, Frederick. Trans. Glin. Soc. Bond.
Nov. 1894. — 80. Thacher. Amer. Journ, Med. Sci. 1889, p. 259. — 81. Vbhsemeyer.
Therap. Monatsheft, April 1893 ; Bie Behamdlung der Beukdmie, Berlin, 1894 (full
feferenoes).
KM.
DEOPSY
General pathology. — Dropsy, like many other morbid conditions, is merely
an exaggeration of a state of health. There is a continual outpouring
of some of the contents of the capillaries into the tissues, which output,
under the name of lymph, is roughly speaking liqv,or sanguinis deprived of
much of its albumin, and other-wise altered by the influence of the vessel
wall through which it has passed. This leakage is disposed of in three ways :
part of it is used in the nutrition of the tissues ; what remains is taken up
partly by the veins and partly by the lymphatics, and so restored to the
circulation. In health the fluid is removed as fast as exuded, so that
there is no accumulation ; if there be any accumulation, it constitutes
dropsy. Hypothetically the dropsical accumulation might be produced
either by an increase of outpour or a diminution of removal, and the
diminution of removal might be hypothetically attributed either to the
veins or lymphatics. How far, and in what manner, these processes or
failures to proceed are connected with dropsy may Appear in what will
follow.
It may be premised that the consideration of dropsy is not held to
include that of serous effusions due to inflammation.
Looking at dropsy from the standpoint of human pathology, we are
at once confronted with the fact that the dropsy liquid in a given
situation is much the same whatever be the disease which has given
rise to it. It varies greatly according to its place in the body, whether
DROPSY 667
the cellular tissue, the peritoneum, the pleura, or the pericardium; but com-
paratively little whether it be dependent on disease of the heart or of the
kidneys, or neither. I have dwelt upon this fact in a paper to which I may
venture to refer (4). From this I reproduce on the following page a
series of estimations concerning dropsy fluids which I made as opportunity
offered, and I append an abstract of the average qualities of these effusions
in various places and with various disorders, including my own observa-
tions and those of others. Many of the figures upon which this abstract
is based are taken from the table here reproduced ; the rest may be
found in the paper to which I have already alluded.
The first fact which strikes us is the uniformity of the mineral salts.
In every place and from every cause the mineral salts of dropsy fluids
present about the same proportion, which is about that in which they
occur in the blood. By whatever process they traverse the vascular
walls this is apparently the same in every place and with every disease.
This looks like some unvarying physical action, like osmosis or dialysis.
It is not so with the albumin, which varies much more with the location
than with the disease. CEdema fluid, whatever the cause may be, contains
only traces of it ; when the cause is cardiac the albumin is greater by about
one-half than when it is renal. Pleural and peritoneal effusions are
always highly albuminous ; sometimes the pleural more so than the
peritoneal, sometimes the reverse. When due to heart disease the
effusions contain more albumin than when due to kidney disease.
Peritoneal effusions due to cirrhosis of the liver occupy an intermediate
position with regard to albumin. The smaller amount of albumin in the
effusions of kidney disease corresponds with the reduced amount of this
substance in the blood under the same condition. With this allowance,
it may be said that the effusions of dropsy in each place are so much the
same in every disease as to suggest that they are produced at least by
similar processes. As to the saline ingredients, these are probably the
results of dialysis from the blood. The albumin as a colloid body cannot
transpire by dialysis, but obtains its passage by pressure, by secretion, or
by both together.
It will be of interest to refer to some of the physiological facts which
bear upon the matter. In virtue of dialysis, crystalloid substances in
solution traverse membranes until the liquid on one side is as fully
charged as that on the other. Colloids, such as albumin, do not so
traverse, if the pressure on each side is equal ; but if the pressure be
unequal, albuminous fluids, serum for example, pass with facility through
a dead membrane or parchment paper until the pressure is equalised on
the two sides. Physical laws, it is needless to insist, are as active within
the living body as outside it, though within it there may be other or
vital laws which modify or counteract. Dialysis and transmission by
pressure are physical ; secretion is vital. In experimenting with mem-
branes and liquids with regard to osmosis, and processes of dropsy so far
as they can be imitated outside the living body, the fact which comes out
with the greatest . prominence is the influence of pressure in moving
668
SYSTEM OF MEDICINE
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CuINSTITUENTS OF DrOPSY FlUIDS IN 100 PAUTS. W. H. I
CASE.
RENAL DISEASE.
E. T. Large white kidney, general dropsy. During life
W. P. Chronic albuminuria, general dropsy. During life .
M. T. Acute albuminuria, general dropsy. During life
A. E. Chronic albuminuria, general dropsy. During li''e .
E. L. Large white congested kidney. During suppre.ision of urine
W. H. Lardaceous disease, phthisis. During life
,, ,, ,, M After death
A. H. „ „ „
E. K. Granular kidneys. P. M
DIABETES.
R. A. During life
,, Four months later. After death ....
I. D. Obtained P.M., after large saline injections into veins
W. E. Diabetes, with fibrotic kidneys ....
DISEASE OF THE HEART.
W. Valvular disease. P. il. .
R. Mitral disease and enlarged liver. During life .
J. P. Mitral regurgitation. P. M. .
D. M. Mitral stenosis. P.M
T. B. During life. From legs, 22 imperial pints
C. D. Mitral regursitation. P.M. (belly tapped 22 times)
B. Mitral disease. P.M
OF PULMONARY ORIGIN.
E. R. Emphysema, broncliitis, cyanosis .....
M. C. Cyanosis, extreme emphysema, bronchitis, slight disease of
mitral valve
HEPATIC.
S., male, aged 7. Hypertropliic cirrhosis, aspiration, ascites
Major D. Ascites, cirrhosis, aspiration, under iodide of potassium
G. C. Cirrhosis, nscites. P.M
J. H. Hypertrophic cirrhosis, a.scites, redema of legs. P.M.
CEREBRAL VENTRICLES.
Appearance.
Sp.
Nearly clear
Higldy
sanguineous
Pule, containeil
web of hbrin
Solids. Alb.
1-467
2-91
Trace
Mineral Salts.
Sol. In.sol. Total,
867
-036
■066
-903
-816
PERICARDIUM
Appearance.
Pale straw
Somewhat
sanguineous
Pale, contained
web of fibrin
Sp.
Solids.
18-5
3-60
5-02
Alb.
.\Iucl
3-086
Mineral Salts.
Sol. Insol. Total.
-03
■O.T
-64
-80
Appearance.
Sp. gr.
Solid
Clear, straw
Clear, colourles
1008-2
1007-3
1-15
Clear, straw
1018-5
2-53
Nearly clear
1010-7
2-05
Slightly turbid
1013-2
Highly
sanguineous
1016-7
4-77
Straw, slightly
1015-5
4-05
sanguineous
Dark slraw
Slightly turbid
1012-2
1012-3
2-84
3-09
Faintly blood-
tinged
Clear, dark straw
1012-8
1014-2
2-98
3-71
Fauts. — W. H. Dickinson.
PLEURX.
PERITONEUM.
CEDBMA.
ance.
8p. g ■Solids.
Alb.
Mineral Salts.
Appearance.
Mineral Salts.
Appearance.
Sp.gr.
Solids.
Alb.
Mineral Salts.
Sol. Insol.
Total.
Sol.
Insol.
Total.
Sol.
Insol.
lotal.
Clear, colourless
1007-1
1-187
-056
■853
•021
-874
straw
ourles
1008-2
1007-3
1-15
-974
■07-^
(opales-
c«nt)
•830
-690
028
-021
-8.58
-716
Clear, straw
1011 1
2-24
-86
•033
-89
'
(opales-
cent)
straw
1018-5
2-536
1-475
-811
•021
-832
Clear, pale
r416
-125
-866
•025
•891
clear
turbiJ
1010-7
1013-2
2-050
-742
-844
-020
-047
891
Slightly turbid
Slightly turbid
1011-6
1013-5
1-921
3-360
-490
-755
-910
•030
•040
-785
-950
Clear, neaily
Colourless (from
scrotum)
Nearly colourless
(froui legs)
Slightly turbid
Slightly blood-
tinged
Clear, straw
1007^3
1009^3
iooy5
1014^3
1 600
1^139
1^33
2-370
-210
-095
-340
-898
-733
-769
-803
-860
-020
■020
-02.-
■034
•913
■753
■794
-837
Light brown
1018 2
4-48
2-416
-861
•047
-908
Pale straw
1010^1
1-615
•385
-870
■023
-893
ll-OUS
1016-7
4-77
2-105
-80
-045
-845
Pale buff, not
bloody
10135
3-49
1-385
-835
...
•036
-871
Pale, nearly
clear
1009 -3
1-765
-230
-830
■031
•861
Clear, straw
Turbid, green-
ish, much fibrin
1016^3
1017^8
5 -295
3-727
3-894
-795
•720
■040
■043
•835
•763
Nearly colourless
1008 ■g
1-62
-33
-758
■030
-788
ightly
leous
traw
turbid
1015-5
1012-2
1012-3
4-05
2-841
3-09
2-909
1 -.140
1-910
-766
-716
•776
-029
•030
-035
■795
•746
-811
Pale straw
Slightly turbid
101 ■•o
10139
2-301
3-676
1-175
1-725
-714
•741
-037
-042
-751
-783
Clear, nearly
colourless
Pale straw, clear
Faintly blood-
tinged
1008 3
1008-2
1008-6
1-49
1-381
1^781
-29
-324
■495
-795
-776
-814
■025
■022
•030
•820
•798
-844
blood-
ed
t straw
1012-8
2-986
1-60
•791
-05
■841
1014-2
3-715
2-230
•780
-032
-812
Clear, straw
1017-9
4-595
3-130
•810
-030
-840
Clear, straw
1008^1
r309
■235
-749
■024
•773
Straw, traces
of fibrin
Straw, clear
Yellow, clear
Pale straw
1008-9
1011-3
1013-5
1017-7
4-776
1-32
1-95
2-12
3-615
•783
•780
•877
■811
-017
■021
■047
-034
■800
■801
■924
-845
Pale, clear
1009-5
3 538
1^39
■774
•03
•804
To face page 668.
DROPSY 669
albuminous fluids through membranes. If an albuminous liquid be
placed at different levels on either side of a membranous septum, the
liquid will quickly traverse in the direction of least pressure until an
equilibrium is attained. It is true that if we put on either side of the
septum liquids having opposite or very different chemical properties, acid
and alkali, alcohol' and water, etc., we may get osmosis which will be
abundant against gravity and pressure ; but such large osmosis has
always been between liquids which have contrasted beyond what is
possible between the inside and the outside of vessels concerned in the
production of dropsy. Osmosis, as an agent in the production of dropsy,
may be put aside as taking little part in it. Pressure and some process
analogous to secretion by the outer wall of the vessel, the one physical,
the other vital, are to be taken into question. The action of the physical
agent is certain and obvious, that of the vital is hypothetical. The over-
ruling influence of pressure in the transmission of fluids needs no insistence;
it is the chief agent in the circulation, and is concerned in all that
depends on the circulation, exudation, nutrition, and cell function.
Theoretically, as has been said, the accumulation of capillary exudation
which constitutes dropsy may be due to excess of production or diminution
of removal. There is only one source of increased exudation, that is the
capillaries. Absorption may take place in theory either by way of the
veins or the lymphatics, and obstruction or arrest in either must be had
regard to in the causation of dropsy. But arrest in the lymphatics may
for the present purpose be put aside. Stoppage in these vessels, as we
know, may give rise to the glandular swellings which constitute ele-
phantiasis, or may occasion chyluria. These are not dropsy, but are
special results of a different kind. The failure of absorption which
produces dropsy has to do only or chiefly with the blood-vessels, to
which channels, therefore, our attention may be limited in considering the
origin of dropsy. The capillaries may either put out too much or draw
off too little, and here lies the whole question. In renal and chlorotic
dropsy we see the results of excessive outpouring ; in cardiac and hepatic
dropsy, and in that of local venous obstruction, we have mainly the
effects of insufiicient withdrawal.
The simplest, or, perhaps, I should say, the least complicated form of
dropsy is that which depends on venous obstruction, and is presumably
due to an exaggeration of the intravascular pressure produced by
mechanical means. Local dropsies in consequence of local obstructions
may be considered first ; they should be easy to understand, and may
help to throw light on less simple conditions. The incidence of local
dropsy must be considered both in the light of experiments on the
inferior animals and in regard to human pathology. Experiments made
by disease on the human subject are entitled, if not to the first, yet to the
greatest consideration where the human body is concerned. It was
observed by Lower 200 years ago that ligature of the ascending cava in
the dog caused oedema of the hind legs. Eanvier on repeating Lower's
experiment failed to obtain the results until the section of the sciatic nerve
670 SYSTEM OF MEDICINE
was superadded, upon ■which oedema appeared on the side of the section,
not on the other. It was shown, however, by Cohnheim that if the veins of
the limb were obstructed by an injection of plaster of Paris, cedema presented
itself though the nerves remained intact. Thus it would seem that venous
obstruction in the dog, unless it be complete and extensive, does nob
suffice to cause exudation unless the blood-pressure is enhanced by vaso-
motor paralysis. In the human subject venous stasis by itself appears to
be generally sufficient to cause this result. The dropsical exudation has
to do only with the blood-vessels ; the lymphatics which are not included
in the obstructing process have no concern in it. The venous obstruction
probably promotes dropsy in two ways : by increasing intracapillary
pressure it increases capillary exudation ; by arresting the venous return
it hinders absorption so far as this process depends on the blood-
vessels.
But there are other factors which complicate even this simplest form
of dropsy. Nature provides many compensations and adjustments. A
vein may be obstructed in a dog, or even in a man, and no dropsy ensue.
Collateral circulation may keep down the pressure below the point
which is necessary to give rise to dropsy. In otherwise good health
dropsy is less likely to be developed than when certain abnormal
conditions, other than mechanical, are superadded. Thus it has been
shown by experiment that local dropsy is encouraged by depletion, or in
other words by hydraemia. Watery blood yields the transudation more
readily than normal blood. Ligature of the femoral vein in a dog may
cause no oedema. But if the animal be repeatedly bled before the
operation then oedema will follow upon it. Certain changes in the
nutrition of the vessel walls, also, may allow of oedema which would not
present itself were these normal. There is reason to believe that
continued venous repletion and lack 'of proper circulation may render the
capillaries leaky or more than normally permeable. Thus after ligature
of a vein in an animal dropsy may not present itself at once, but only
after the lapse of a time wherein the capillary walls have presumably
suffered in their nutrition by reason of want of oxidation, or otherwise.
The clinical aspects of the dropsies of local venous obstruction will
be considered later, it being only necessary here to refer to their varieties
so far as they throw light on their mode of production. (Edema of the
lower extremity is well known to follow upon thrombosis of its veins, as
in phlegmasia dolens, and when coagulation of blood in these vessels is
produced by causes apart from the puerperal state. (Edema in the same
region, but to a less extent, is produced without absolute obstruction by
mere retardation of the venous circulation, such as occurs with varicose
veins. The upper limb and the side of the face and neck become
swollen when an aneurysm or growth presses upon the innominate vein,
sufficiently to obstruct it ; and a similar accident to the vena cava produces
oedema of the upper or the lower part of the body, according to the position
of the obstruction in the upper or lower cava. Hydrops ventriculi may
ensue upon occlusion of the lateral sinus, and further illustrations of the
DROPSY 671
same process are provided by tlie occurrence of ascites as a result of
obstruction of the portal vein, whether in the trunk by way of throm-
bosis, or in its distribution in the liver from contracting fibrous tissue.
Thus in the human body, at least, we see that chronic venous obstruction,
be the mode what may, suffices to cause oedema without the intervention
of any other recognisable or constant agent.' Enhanced pressure in the
capillaries thus produced appears to be the primary and efficient cause,
though certain intermediaries are necessary to its operation. Dr. Lazarus
Barlow has shown by experiment that vessels wherein the blood has been
at a standstill permit of transudation more readily than vessels not thus
circumstanced, so that under increase of venous pressure dropsy does not
ensue at once, but only after a little time has elapsed so as presumably to
allow the vessel walls to undergo changes which make them more
permeable. This, however, does not militate against pressure as con-
cerned with the dropsy process, though it shows that intermediate steps
are necessary before it can be established.
To take now the dropsy of heart disease, as presumably the next in
order of simplicity to that of local venous obstruction, it becomes apparent
that, simple as it may at first seem, it raises many questions and presents
for estimation many factors. It is probable that we do not yet know all
about this form, or about any form of dropsy. We have to consider
vital as well as physical agencies. In the first place, we have to consider
how far cardiac dropsy is due to diminished absorption and how far to
increased transudation. At first sight this form of dropsy would appear to
be due to diminished absorption by way of the veins, for their channels
are undoubtedly abnormally full, and present abnormal pressure ; conditions
which it would seem cannot but interfere with absorption by their means.
But there are other modes and processes which somewhat complicate the
matter. Beyond diminution of absorption dropsy results from increase of
transudation, which may depend on increase of intracapillary pressure,
changes in the capillary wall which render them abnormally pervious,
and changes in the blood, notably hydrsemia, which render it more
apt to transude. Under cardiac failure, produced for example by in-
jections into the pericardium. Dr. Starling has shown that arterial
pressure is diminished and pressure in the systemic veins increased. He
infers that under these circumstances pressure in the systemic capillaries
and small veins is diminished. So far as we may be guided by these
conclusions, we see reason for diminished venous absorption, not for
increased transudation. But the territory of the capillaries is wide, and
it may be that Dr. Starling pushes his conclusion too far. We may
readily believe that under cardiac failure the capillaries in connection
with the arteries are under low pressure and imperfectly filled, but at the
same time the capillaries in connection with the veins may be over-full.
If this be so, transudation may occur in one part of the capillary system, not
in another. Thus we may have increased transudation in heart disease as
well as diminished venous absorption. Wherever continued stagnation of
blood has existed, the vessel walls, if we may judge by experiments
672 SYSTEM OF MEDICINE
acquire abnormal permeability, and probably let out fluid which the
obstructed veins are unable to carry off.
Another factor to be considered in relation to cardiac dropsy is
hydraemia, which is supposed to exist in this condition. But the
hydrsemia of heart disease, so far as it exists, scarcely needs to be con-
sidered in relation to cardiac dropsy. It has been argued (2) that the
capillary pressure is low in this condition, and that therefore absorption
must be promoted from the tissues into the blood to its manifest dilution :
but this is not a dropsy process ; it is, indeed, a process antagonistic to
dropsy. For the present purpose, therefore, the supposed hydrsemia of
heart disease may be neglected. The leading distinctions between cardiac
dropsy and renal, which is the kind to be considered next, are these : in
cardiac dropsy there is fulness and pressure in the veins, the reverse
conditions in the arteries ; in renal dropsy the fulness and pressure are
arterial. Cardiac dropsy is probably due to diminished absorption ;
renal dropsy, so far as it is unassociated with cardiac failure, is entirely
due to increased exudation.
Eenal dropsy now presents itself as a more complicated matter than
cardiac. Not long ago it may have been regarded as comparatively
simple, the efi"usion being vicarious to the renal excretion ; a view
suggested by the general rule, the less urine the more dropsy ; and not
altogether without foundation, though much remained for inquiry as to
the mode in which this inverse relation was brought about. Some who
looked beneath the general result to the modus operandi saw in osmosis
an agent which explained the phenomenon to their satisfaction; the
retention of crystalloids in the blood, which should have escaped by the
kidneys, must undoubtedly give rise to this process, and it was inferred,
before the subject of renal dropsy was looked at in other lights, that
this physical operation was enough to account for it. This was the
opinion of Sir George Johnson, and probably of many others, in the
year 1887, though in the discussion which followed the reading of a
paper which I ventured to lay before the Medical and Chirurgical Society
in 1892 he no longer maintained it. It is obvious that, as regards
albuminous effusions, which those of renal dropsy in^-ariably are, some-
thing more than osmosis is needed to explain them, since albumin is a
colloid body and not amenable like the crystalloids to dialysis.
The dropsy of renal disease must obviously be investigated chiefly
by observation on the human body. A few fundamental facts may be
briefly stated before proceeding to deal with the matter in clinical
detail. There is no constant relation between the occurrence or the
amount of dropsy and the quantity of urine passed, though there is a
general rule, that with disease of the substance of the kidney, like Bright's
disease, the dropsy and the urine vary inversely. It is a remarkable
fact that with obstructive and complete suppression dropsy is usually
totally absent. It is not less worthy of remark, that occasionally, when the
urine is reduced to a minimum by exceptionally acute nephritis, dropsy
may be totally or nearly absent, though much might be expected. In
DROPSY 673
regard to the general question of dropsy, not keeping for the moment to
that of renal origin, it is instructive to contrast these facts with another
which is provided by the course of diabetes mellitus. In this disease
cedema may occur though the urine is superabundant. I have known
the legs to swell, and that without any ostensible cause beyond the
diabetes, though the urine amounted to fifteen pints a day. Thus it
appears that in the production of dropsy, whether albuminuric or dia-
betic, other conditions have to be reckoned with beside the quantity of
the urine.
Any theory of renal dropsy to be satisfying must explain, or not
be inconsistent with, the following facts : — In acute renal inflammation
of the ordinary kind, where the urine is scanty but not suppressed, and
the arterial tension increased but not to the uttermost, cedema is an
early result. When the disease and the consequent increase of tension
have been long continued and given rise to cardiac hypertrophy, then
the dropsy lessens and may be entirely removed, as if the hypertrophy
of the hpart were antagonistic to it. When renal disease is of very slow
and gradual development, as in many cases of the chronic granular
kidney, and the heart allowed time to hypertrophy gradually with
the increase of arterial tension, dropsy may be for long or altogether
absent. We here have absence of dropsy with extreme arterial tension.
Finally, however, if the patient survive to the last stage, comes a time
when the hypertrophy of the heart fails of its purpose, or is deprived of
its effect, by superadded dilatation and mitral insufficiency ; and then
dropsy may present itself for the first time, or reassert itself if it have
been removed under the circumstances indicated. The dropsy now is of
a complicated nature ; mitral regurgitation has much to do with it, and
it may often be regarded as more cardiac than renal.
Pursuing the inquiry from a different starting-point, we find vrith
obstructive suppression, when the urine is totally absent, the tendency to
death is by heart-failure, and the arterial tension, as declared by the pulse
to the touch (for here sphygmometric observations are wanting, though
much to be desired), is abnormally low. Here dropsy does not present
itself, however much the vessels might be expected to relieve themselves
by this discharge. A similar absence of dropsy, nearly or quite complete,
together with extreme diminution of urine, is sometimes observed in
cases of exceptionally intense nephritis. Here we have failure of heart
and pulse, and of dropsy little or none.
So far it would appear for the production of renal dropsy there is
required increase of arterial tension, or, in other words, increase of intra-
capillary pressure. Diminution of urine contributes to cause dropsy, but
does not suffice alone to produce it. Hypertrophy of the heart, so long
as it is not otherwise altered, tends to prevent the development of renal
dropsy, or, if it has occurred, to remove it. This action of cardiac hyper-
trophy must be largely attributed to the expansile force or suction power
of the left ventricle, which must be increased in proportion to the thick-
ness of the walls. The suction thus established or increased must draw
VOL. V 2 X
674 SYSTEM OF MEDICINE
upon the pulmonary veins, clear the lungs, make way for the current in
the systemic veins, and facilitate the drainage of the tissues so far as it
is due to these vessels. With regard to acute renal dropsy, another
factor is to be recognised in the pulmonary inflammation, commonly shown
as broncho-pneumonia, which often, but not always, accompanies it. This,
by impeding the return through the lungs, must assist the dropsy process.
The increase of capillary pressure which has been inferred as attending
acute renal dropsy is not extreme, and probably not unassisted in causing
the result. It has been inferred with much likelihood that there is a
simultaneous change in the capillary walls, in virtue of which they
become abnormally permeable. This has been regarded as inflammatory
(Cohnheim), but since the characteristic products of inflammation are
wanting we may presume that the change does not attain to this con-
dition. It has been already shown that the products of dropsy of every
kind resemble each other enough to indicate that they are the results of
similar processes, and that they all differ essentially from the products of
inflammation.
The starting-point of acute or recent renal dropsy must be the toxic
condition of the blood due to insufiicient elimination by the kidneys.
The capillaries, though not muscular, have been shown to be contractile,
and it must be presumed that they offer abnormal resistance to the
passage of blood which is abnormal in certain respects. Increased
capillary resistance involves increase of arterial tension and of cardiac
effort. With the increase of intracapillary pressure it has been inferred,
and it cannot be doubted, that there is a change in the capillary walls
which makes them unnaturally permeable, since the increase of capillary
pressure, to judge by the arterial tension as revealed to the educated
finger, is not in early cases extreme, and not enough alone to account for
the effusion.
The oedema of chlorosis is evidently nearly allied to that of nephritis.
In chlorosis we have a toxic state of the blood owing to a retention of
what should be excreted, not from renal, but uterine failure ; and with this
there is, as I have elsewhere shown (4), exaggerated arterial tension, and
probably a train of circumstances similar to that which I have indicated
with regard to nephritis.
The various Forms of Dropsy considered severally
I shall divide the subject as appears most natural and convenient,
having regard sometimes to the origin of the dropsy and sometimes to its
location. I shall take local effusions first, which are generally, but not
always, due to venous obstruction, then cardiac dropsy, then renal, and,
lastly, such as depend on changes in the blood other than those due to
disease of the kidneys.
Of LOCAL dropsies the first to be considered is hydrops ventrieuli
or ehronie hydroeephalus.
In dealing with this affection it is necessary explicitly to exclude
DROPSY 67s
effusions which depend upon meningitis or any other form of inflam-
matory action. The complete or almost complete absence of albumin in
the fluid may be taken in assurance of its origin otherwise than by
inflammation. The fluid of true hydrops ventriculi is but a super-
abundance of the natural cerebro- spinal effusion. It must be acknow-
ledged at starting that all the causes of this excess are not understood,
and that some of the causes to which it has been attributed are, to say
the least, extremely doubtful. Venous obstruction, particularly in the
lateral sinuses, appears to be an unquestionable, though not a frequent
cause of intracranial dropsy. This result has been known to come upon
obstruction of the lateral sinus by growths and cysts, though I cannot
learn that it has been traced to thrombosis. This condition commonly
produces acute changes in the brain which do not comprise dropsy j
dropsy is usually a chronic process. As an example, I may mention a
case which I have elsewhere given in detail (5), that of a child whose lateral
ventricles were found to contain %\ ounces of clear fluid, apparently as the
result of the total obstruction of the right lateral sinus by a mass of
tubercle which belonged to the cerebellum. There was no tubercle in
connection with the brain with this exception, nor anything to account
for the efiusion beyond the obstruction of the sinus. Dr. Murray, of
Newcastle, published a case in which a similar result was produced by a
cyst of the cerebellum which compressed the veins returning from the
lateral ventricles.
The frequent association of chronic hydrocephalus with rickets points
to another mode in which it is probable that the intraventricular dropsy
may be produced. The cerebro-spinal fluid, an excess of which con-
stitutes the disease, is controlled in amount by the pressure against
which it is secreted. The purpose, or at least the effect, of the fluid
readily poured out and as readily reabsorbed, is to maintain a slight and
uniform pressure on the nervous centres. The pressure is secured by the
closure and indistensible character of the intracranial and intraspinal
cavities. If the intracranial cavity be laid open so that its contents can
freely escape, the controlling pressure is taken off, and the secretion pro-
ceeds without hindrance and with abnormal profusion. Thus, when the
base of the skull has been fractured so as to make a communication
between the subarachnoid cavity and the external auditory meatus
several pints of the cerebro-spinal fluid have been known to escape from
that exit in twenty-four hours. On the same principle, it may be pre-
sumed that if by rickets or other cause the cohesion of the cranial walls
is impaired, they may yield to the pressure which the cerebro-spinal fluid
normally exerts, and become expanded into the hydrocephalic state.
But, however this process may account for certain cases of intracranial
dropsy, it obviously has its limitations. Hydrocephalus may be intra-
uterine and a cause of difficult labour. For this other causes must be
sought. Within the uterus the skull must always be exposed to con-
siderable external pressure, and the dropsical accumulation cannot be
attributed to the want of it.
b^6 SYSTEM OF MEDICINE
The late Mr. Hilton propounded, in his book on Rest and Pain, a hypo-
thesis of hydrocephalus which must be considered. The fourth ventricle,
■with which the other ventricles communicate, is partitioned from the
subarachnoid cavity by a fold of pia mater which crosses the lower end
of this ventricle. This, however, does not completely divide the ventricular
from the subarachnoid cavity, for it is perforated by a small hole, com-
monly about the size of a pin's head, called the foramen of Majendie,
which makes a communication between the two. In some cases of intra-
cranial dropsy, but by no means all, this opening has been found to have
been closed by inflammatory adhesions. Mr. Hilton supposed that the
accumulation in the ventricles was due to the closure of this opening.^ If
this be so, we must suppose the fluid to be secreted within the ventricles
and absorbed outside them. Thus the functions of the ventricular and
subarachnoid cavities would be opposite ; the ventricular secreting, the
subarachnoid absorbing. In this view the function of the choroid plexuses
would be only to secrete, that of the spinal cavities only to absorb. But
we have no knowledge to warrant this assumption. The probability is
that all the cavities under ordinary conditions both secrete and absorb, so
that cutting off one cavity from another would not necessarily give rise
to dropsical accumulation. Supposing the intraventricular secretion to
be exaggerated by inflammation, or some action akin to it, the arrest of
escape might then lead to accumulation, but the results of inflammation
are not within my present scope.
It is not necessary to include in this bare outline of intracranial
dropsy any clinical description of chronic hydrocephalus or any detailed
consideration of the treatment proper to it, since these will be found in
another part of this work. It may be briefly said that this condition is
not one which yields readily to treatment, while some methods which
have been employed are not free from danger. The disease in some
instances is exceedingly chronic, and indeed may exist for a large propor-
tion of the ordinary term of life. At an early period the treatment for
rickets is often indicated. I have known a limited reduction in the size
of the head to be produced by external pressure by means of a broad
elastic band placed horizontally round the head, with the pressure so
moderated as to cause no injury to the integuments. I have known the
neglect of this moderation to be followed by sloughing and death. Judicious
pressure before the skull is finally ossified may generally be expected to
reduce the circumference of the head by from one to two inches. Evacuants,
mercury, squills, digitalis, and iodide of potassium have been administered,
but mostly with little beneficial result. Tapping has been employed,
repeated, and survived ; but this is not without its dangers, and appears
to be seldom productive of tangible good. Even though no harm result
the fluid usually reaccumulates. It must be borne in mind that the
hydrocephalic head does not always increase in the same ratio as the
body. Thus in the process of growth the head, though becoming abso-
^ I have discussed the nnatomical relations of the intra- and extra-ventricular cavities in
the Lancet for 16th July 1870.
DROPSY 677
lutely larger, will become relatively smaller, and the disproportion
between the head and the trunk may spontaneously lessen.
Other local dpopsies need only brief mention here, since most of
them will find more ample notice elsewhere. Perhaps the most frequent
is that which ensues upon coagulation in the veins of the lower extremities,
and is generally consequent upon changes in the blood, which may be
septic, puerperal (probably generally septic), chlorotic or gouty. It was
formerly supposed that the puerperal thrombosis, known as phlegmasia
dolens, was essentially due to an inflammatory condition of the lining of
the veins of the legs, which travelled after the manner of an erysipelas
from the veins of the uterus to those of the lower limbs by anastomoses,
which the elder pathologists were careful to display by dissection. In
this view the plugging of the veins was the result of phlebitis, not its
cause, as we now believe. The symptoms and treatment of phlegmasia
dolens and other varieties of thrombosis will iind a pLice elsewhere. It
will suffice to say that this disorder, like many others, furnishes an
example of local dropsy, due simply to venous obstruction, as are many
kinds of dropsy which are met with in the course of human pathology,
however this cause presents itself as qualified and complicated in experi-
ments on animals. It is obvious that in the treatment of phlegmasia
dolens the main object must be the safe removal of the coagulum ; in other
words, its solution, rather than, as in old days, the reduction of the
phlebitis by "antiphlogistic" measures. With our present knowledge,
the best means of doing this appears to be the administration of alkalies,
so as to keep the urine alkaline, and thus charge the blood to overflowing
with the alkaline solvent. A mixture of bicarbonate and citrate of potash
answers the purpose, to which ammonia and quinine may be superadded,
in order to obviate any depressing effect which the potash salts might
produce.
Among other local dropsies due to venous obstruction may be men-
tioned those which result from aneurysms and other tumours which press
upon the veins from the outside, whether of the upper or lower extremi-
ties, and thus hinder the return of blood, and give rise to limited oedema.
Such local dropsies are often important diagnostically as indications of
venous obstruction.
The oedema of the legs of pregnancy, generally due to the pressure of
the gravid uterus on the ascending cava, needs but a passing mention.
When uncomplicated with oedema of the face or albuminuria it may be
regarded as purely local and mechanical, and will pass off with the con-
dition in which it has originated. This limited and mechanical oedema
is apt to become complicated with renal disease, which will be indicated
by albumin in the urine, by oedema elsewhere than in the parts drained
by the inferior cava, and possibly by ursemic symptoms ; but I need not
now dilate upon what has been fully dealt with elsewhere (see vol. iv
p. 380).
Ascites may be a limited or local dropsy due to portal obstruction, or
part of a general dropsy of which the causes are manifold. It is to be
678 SYSTEM OF MEDICINE
considered now only as local and isolated. Hepatic ascites furnishes one
of the most striking examples of dropsical effusion from venous obstruc-
tion. This occurs in the portal system, and may be either in the
trunk of the portal vein by thrombosis, or in its minute distribution as
the result of cirrhosis.
Portal thrombosis is a cause of ascites of ideal simplicity, but of
no great constancy. To produce this result the thrombosis must be
extensive, and the survival of the patient must be such as to allow it
to become chronic. I cannot learn that portal thrombosis causes dropsy
in its acute or recent stage, whatever may ensue after lapse of time. I
have known death by syncope or collapse to be due to complete obstruc-
tion of the portal vein by embolism or thrombosis, and no sign of dropsy
to be discoverable after death. It has been shown by experiments on
animals that on ligature of a vein dropsy does not at once show itself,
but only after a time ; an interval being apparently required to allow of
changes in the wall of the vessel whereby transudation is facilitated. So
it would seem, in the human subject, that extensive or even total obstruc-
tion of the portal vein by clot may occur and cause death without any
trace of dropsy. On the other hand, cases present themselves in which
thrombosis is productive of much, even extreme ascites. I call to mind
the case of a gentleman, the subject of cystinuria, who had ascites nearly
to bursting, which was attributed to this cause — a diagnosis which was
confirmed by his ultimate recovery. Many cases have been recorded, and
some have come within my own experience, in which portal thrombosis
has been testified to after death in association with ascites. I published
such an instance in the 14th volume of the Pathological Transactions. In
this the plugging was of old standing, and was such as to occlude the
portal vein completely. The patient was a woman of twenty-one years
of age. The liver was shrunk — ^it weighed only twenty-eight ounces ; it
was not markedly cirrhotic, and it was supposed that the atrophy was the
result of the obstruction, not the cause of it. It is worth noting in con-
nection with serous effusion of this origin that haemorrhage in the portal
territory, into the stomach or bowels, is a not infrequent result of obstruc-
tion of the portal vein by coagulum, as of obstruction of the same vein
by other means.
Apart from thrombi the obstructions of the vein which cause ascites
are several, the chief of which is cirrhosis ; which indeed is by far the
most frequent of all the causes of dropsy limited to the peritoneal cavity.
Before proceeding to this, some other causes of portal obstruction and
consequent dropsy may be briefly dismissed. One of these is malignant
growth which may press upon the portal vein, and even has been known
to intrude into it ; this, like other causes of portal obstruction, may be a
cause of hsematemesis as well as of ascites. Syphiloma is another cause
of hepatic ascites by way of gumma, cicatricial contraction, and iibrotic
change. An infrequent and even a doubtful cause of hepatic ascites is
lardaceous disease. It is a matter of common experience that general
dropsy, including ascites, often ensues upon lardaceous disease which
DBOPSY 679
affects several organs. It is also well known that the liver may suffer
the extremity of lardaceous disease, and yet no peritoneal dropsy super-
vene. It is certain that lardaceous disease of the liver has of itself little
tendency to cause ascites.
With regard to cirrhosis, this is a cause of dropsy of which it is not
easy to exaggerate the importance. In this disease the fibrous tissue of
the liver becomes the seat of hypertrophy, new growth, and subsequent
contraction, to the strangulation of the vessels which it surrounds. The
new fibroid tissue, often highly nuclear, of the embryonic type, collects
chiefly in the portal canals, and involves more particularly the minute
ramifications of the portal vein ; but other vessels of the liver, the hepatic
vein as well as the portal, are affected in the same manner. By
the strangulation, chiefly of the minute portal vessels, the portal circula-
tion is retarded, and the blood caused to accumulate at high pressure in
the venous radicles in which the portal circulation takes its origin. This
leads to congestion of the spleen, often to haemorrhage from the mucous
membrane of the stomach and intestines, and to the exudation of serous
fluid from the visceral peritoneum into the peritoneal cavity. Hence
ascites is one of the common consequences of cirrhosis of the liver.
Whether cirrhosis be attended with increase or diminution of the size of
the liver, ascites may occur, but it is most likely to do so when the atrophic
process prevails over the hypertrophic. The smaller the liver the greater
is the tendency to ascites. But this is by no means a necessary
consequence of cirrhosis of any kind ; this change in all its varieties is
frequently found after death without any such result. Cirrhosis has no
direct tendency to cause oedema, though the lower extremities often swell
under the influence of hepatic ascites as a secondary result of abdominal
pressure. Another result of the pressure on the vena cava due to ascites
is vicarious distension of the abdominal veins. A smaller degree of dis-
tension may be due to cirrhosis independently of ascites brought about by
the various anastomoses which connect the portal with the systemic
veins.
It is not necessary here to recapitulate in detail the symptoms of
hepatic ascites ; no form of peritoneal dropsy attains so great a degree ;
it is not unknown for the abdominal wall to give way at the umbilicus
with discharge of the contained fluid.
The treatment of ascites will be considered in connection with that of
dropsy in general.
Omitting hydrocele, though it might be placed in the category of local
dropsies, I now proceed to the consideration of —
General dropsy, or of dropsy which depends on causes acting on
the system at large. Before proceeding to particulars I will introduce
some details which bear upon the frequency of general dropsy as the
result of the several causes to which it is due.
68o
SYSTEM OF MEDICINE
Causes of General Dropsy, as revealed after Death in 300 Cases taken
consecutively from the Post-mortem Books of St. George's Hospital,
from the Year 1888 to the Year 1897.1
Causes of Dropsy.
Valvular disease of the heart sole or chief cause
Valvular disease and kidney disease not obviously consequent upon it
(Of the foregoing oases mitral stenosis present in .
( ,, ,, ,, pericardial adhesion or pericarditis in
Pericardial adhesions, valves healthy .....
Heart dilated or fatty, valves healthy .....
Aneurysm of arch, with or without valvular disease .
Congenital disease of heart, with or without valvular disease .
Disease of lungs or respiratory organs .....
Thrombosis, pulmonary and scattered .....
Kidney disease sole or chief cause .....
(Including large white, not lardaceous, and nephritis
( , , granular and white contracted ....
( ,, destruction of one by stone or tubercle with consecutive disease
of the other
Lardaceous disease
Diabetes
Anaemia
Leucocythaemia
Sclerema
Tumours central or scattered, lympliadenoma, sarcoma, carcinoma, etc.
Cause uncertain, associated with tuberculous meningitis, tubercular peritonitis,
pyaemia, dysentery, etc. .......
Number
of Cases.
136
12
62)
16)
2
12
11
2
19
1
69
20)
43)
6)
17
2
2
1
1
300
The foregoing table giving the causes, as far as could be ascertained
after death, of general dropsy in 300 cases, was the yield of 3185
necropsies, so that this condition is evident after death in about 1 in 1 0 of
those who die in St. George's Hospital. It must be taken into account
that small amounts of oedema which were apparent before death are
sometimes not observable, or not observed, afterwards, so that the propor-
tion of dropsy in life would be slightly greater than is recorded after
death. It must also be borne in mind that the table indicates only
dropsy, dependent on causes acting generally, to the exclusion of hepatic
dropsy and that dependent on local causes. Had all varieties of dropsy
been included, and this table based on observations made before death
instead of afterwards, it is obvious that the proportion of dropsy to
deaths would have been considerably greater than in the present estimar
tion. (Edema, for which there was no local cause, has been accepted as
an indication of general dropsy ; in most cases there was also eflFusion in
the serous cavities. In a few instances, where multiple serous effusions
occurred without oedema, these were similarly regarded.
' All forms of dropsy which are properly local rather than general are excluded ; such
are all the limited forms of ceiiema which depend upon obstruction of the veins of limbs, and
hepatic dropsy which depends on obstruction of the portal vein. On this ground hepatic
ascites is excluded, even though associated with oedema of the lower extremities.
DROPSY
68i
Of the 300 cases the dropsy was due to affections of the heart or
aorta in 163; to heart disease, together with kidney disease, neither, as
far as could be judged, consequent on the other, in 1 2. Dropsy presents
itself as a cardiac result nearly twice as often as of renal origin, even
though all the lardaceous cases be reckoned as renal, which may properly
be done. Of the cardiac conditions which give rise to dropsy mitral
stenosis is by far the most frequent. Next to the heart in order of
frequency come the kidneys as a cause of dropsy. Of the renal causes,
though the large white kidney is more constantly thus followed than any
other, yet the granular or contracted kidney, from its more numerous
occurrence, more numerously gives rise to this symptom. Disease of the
lungs and bronchial tubes takes the third place as a cause of general
dropsy. Pulmonary dropsy, if not so common an event as might be
expected from the position of the lungs in relation to venous return, is
yet an occurrence of considerable frequency. In 19 of the 300 the
dropsy was due to disease of the organs of respiration.
Conditions of the Organs of Eespiration to which Dropsy was
apparently due in 19 Cases.
Emphysema alone . . ..... 2
,, + bronchitis . . . . . . .4
,, + bronchitis and fibrosis of lung . . . .1
,, + broncho-pneumonia . . . . . .1
Phthisis alone . . . . . . , .3
,, + fibrosis of lung . . . . . . .1
,, + bronchiectasis . . . . . . .2
Bronchiectasis alone . . . . . . . ,2
Fibrosis alone . . , . . . . .1
Extensive pleural adhesions with obstruction of pulmonary artery by clot . 1
Carcinoma, obstructing bronchus . . . . . .1
It may be of interest to look into the particulars. Of the pulmonary
causes of dropsy emphysema takes the first place, being present in 8 of the
number. This was notably associated with bronchitis in 4 cases, and, as
this condition is less conspicuous after death than during life, it is likely
that it existed in all. A fibrotic change in the lung was recognised in 7 cases.
In this enumeration I have assumed, as may safely be done, that fibrosis
was present in every case described as bronchiectasis. Phthisis, mostly
advanced and attended with excavation and often combined with fibrosis
or bronchiectasis, was present in 6. Thus emphysema and fibroid change
are the leading factors of pulmonary dropsy, which may be explained bv
the effect which both these changes have in obliterating or removing the
pulmonary vessels.
It has been shown that heart disease as a cause of dropsy outnumbers
kidney disease by about 2 to 1 ; it may be worth while to ask which
form of dropsy is the more severe, and which tends most to invade the
serous cavities. I find that among the cases under consideration extreme
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qj9{ 9X[^ snqx •uoi:;'B^iSjnS9j jo s^iuiiad qoiqA qo9j9p iuB si 919T{% u9V[m.
90JOJ !}S9^'B9jS gq:} q((iAi 3[0'Bq ^i S9Aup puB 'ifpo9MOO s5[aoA insiu'Bqo9Tn
9q^ u9qA\. spaBAiuo poo^q 9q{^ SaiAup ui j^gq oc> gojoj (jsa^rajS 9q!>
sSuuq siqj^ ■(^unoui'Bj'Bd si 9pIJ(^u9A %pi 9qx ■S99jS9p '}U9j;9_jjip jfppm
UI q§noq^ 'paujaouoo ApAi'iO'e 9jb ■[];u :jnq 'pooS ppq (jqSim siq(> poo^q aq:;
JO uoissiuisuBJ^j gq:} ui pgujgouoo ^pAiss'ed i!^uo qj'eaq aq^f jo s91iia«o aq^
aja^ -aq o^ pa^^ogdxg 9q i^sdoap q.u'eqnsgi 9q!} ^qSini pg^^JBUt aaoui aq^
puB a^'Bipatuiiii ajoxii 9T{% ^pca snouaA uouiuioo aq!) o; si uoisaj aAi:>!)na:jsqo
ue laj'Bau aqjj -apu^uaA :(ja^ aq^ "A ! apian'B qja^ aq^ -ai f uoi^'epoap
ifjBUoaqTid eq:^ •m '. appr^usA ^qSu aq^ -ii '. apuriB %v[3ii aq^ -j — : jfsdojp
ifjijuoxmnd pue ompjceo jo asn^D s%'emixoid aqij si qoiqAV ^13 aou'Bjpuiq
aq:^ '(^apno snouaA aq^ o; ssaui^au jo japjo aq^ ui pao'e^d snq!j di'e raa^s^ls
ij^Buouund a^uipaima^m aq; puB sai^jiATO aqx "paonpojid aq o^ si jfsdojp
pieuaS 10 ■['BSjaAiun ji ip^ :jsniu uoiionjqsqo aq^ ^Bq:} suka oiraa!(Sifs
aq^ o^ uoinuioD aSj^qosip jo eo^id aq; s'b quiod siq; uodn si %i (jnq 'poo^q
snouaA aq:j jo esjnoo aq; ui uo jaq^aBj jfji^nsn si ;i loj 'ajaq si
uoisaj imraud aq; ;'Bq; ;ou '. jfsdojp ouipjeo jo 'eioqi93[ aq; jaq^BJ JO
'i!a5[ aq; si ajajj 'apunB ;qSu aq; .ia;ua spssaA asaq; aaaqAi paoB^d aq
'A\\'en%o'e paapui puB '/n'B0i;9q;odi!q A'em. aou'Bjpuiq ^'Bi;uassa aqj^ -suma
oiuia;sifs aq; jo Suii!;dnia aq; ;onj;sqo o; sb qons si sSun^ puB ;j'Baq
aq; jo a;'B;s aqx 'spssaA-poo^q aq; o; anp si siq; sb jbj os uoi;djosq'B
saqsiuiinip puB 'uoi;epnxa puB ajnssajd ifjBnid'BOBj;ui sas^ajoui qoiqji
'suiBA aq; JO uoi;a^daj asn^o a;'Bipainrai jpq; jmv '^BOiuBqoam i!|^Bi;uass9
^89
ASdOSa
684 SYSTEM OF MEDICINE
referred to in the preceding table mitral stenosis was discovered in 68
cases, mitral dilatation or insufficiency in 38, mitral disease of uncertain
effect in 25. Aortic disease, whether obstructive or regurgitant, presents
itself with much less frequency, while the only lesions affecting the right
valves to any important extent are such as permit of tricuspid regurgita-
tion. Whether obstruction or regurgitation at the mitral orifice be the
more productive of dropsy may permit of question ; both are undoubtedly
effective in this relation, but it is not easy to separate the two. Mitral
stenosis is almost invariably attended, not only with obstruction, but
with regurgitation ; the so-called presystolic murmur which is charac-
teristic of mitral stenosis is, as I maintain, regurgitant. If this be so, of
which I have no doubt, we recognise with mitral stenosis both hindrance
to the normal advancing current and abnormal retrogression. With this
double difficulty dropsy is doubly invited. Both tend to the repletion
of the auricle of the lungs and of the veins. Next in frequency as a
cause of cardiac dropsy comes the aortic valve. Aortic regurgitation, as
the preceding table shows, is more often associated with dropsy than
aortic stenosis. This probably is rather because the regurgitant fault is
the more frequent than because it has the greater tendency to cause the
result. Aortic stenosis interposes a hindrance which must tell upon all
the circulation behind it. So nearly complete sometimes is the closure,
so great the obstruction, that not only is it obvious that the retardation
must reach the sources of the systemic veins, but it is even a wonder
that the circulation was not long ago brought to a standstill. Aortic
regurgitation stands in a very different relation. So long as this is the
only error the course of the blood during systole is clear ; it is only
during diastole that there is any embarrassment, and that not by solid
impediment, but by the intrusion of an abnormal current into the ventricle.
This must compete with the normal flow through the mitral opening,
occasion delay or difficulty at this point, and some of the results which
ensue upon mitral stenosis. But this interference is less effective as a
cause of dropsy than mitral regurgitation, enforced as it is by the systole
of the ventricle. As a matter of experience, aortic regurgitation, so long
as it remains uncomplicated, is but a minor cause of dropsy. The defect
may exist for many years, and in a marked degree, and yet no dropsy
ensue.
To revert to mitral regurgitation. This, as is well known, is by
itself an effective cause of dropsy, but it often occurs in this relation
as a consequence and complication of other disorders. Mitral
insufficiency may result from the dilatation of the ventricle and of
the mitral orifice which ensues upon aortic regurgitation, and thus
may determine dropsy, which the aortic fault alone might fail
to produce. Again, extreme aortic stenosis may, as I have elsewhere
shown (4), occasion mitral regurgitation by increasing the intraventricular
pressure, and thus forcing a healthy mitral valve to leak. By this
process any dropsy due to the aortic constriction could not fail to be
enhanced. And outside the limits of disease primary to the heart, it
DROPSY 685
may be said that mitral regurgitation is one of the causes of renal dropsy.
I may have to touch upon this again, but I may briefly draw attention
to the fact that late renal dropsy is often cardiac and mitral. The
hypertrophy of the heart is succeeded by dilatation. This involves the
mitral orifice and regurgitation ensues, though the valve may be
unaffected except by stretching.
As to the right valves the only defects which present themselves with
any frequency in relation to dropsy are, as the annexed table shows, such
as permit of tricuspid regurgitation. Tricuspid stenosis sometimes occurs
together with mitral stenosis, and from the same causes, but dilatation or
insufficiency of the valve is much more common. This condition occurs
more often in connection with changes in the ventricular wall, such as
are due to mitral disease, than to disease originating in the valve itself.
When present it cannot but be co-operative in the causation of dropsy,
directing as it does a regurgitant current directly upon the venous exit.
Though driven only by the comparatively weak right ventricle, it has
every advantage of situation in its morbid action. Theoretically diseases
of the right side of the heart bearing upon the systemic veins more
immediately than those of the left side should have more to do with the
causation of dropsy, but experience shows that this is far from being the
case, and I have sufiGiciently indicated the reasons. To these may be
added the fact that the left side, as more functionally active than the
right, is more liable to disease.
Besides the valves, the state of the ventricular walls, especially of
the left, has to do with dropsy. Expansion of this ventricle in diastole
is an agent in carrying on the circulation not less real, though less
potent, than its contraction in systole. Its expansion helps to empty
the auricle, and thus indirectly draws upon the venous system by
suction. The thinner the wall the weaker must be this action, while it
must be proportionally increased by its hypertrophy. Thus attenuation
and dilatation of the left ventricle must be placed among the conditions
which contribute to cardiac dropsy, and, to anticipate what I shall have
to revert to in connection with renal disease, hypertrophy of the left
ventricle is the antagonist of dropsy, and may even be called Nature's
remedy for it.
The lungs must not be disregarded as causes of a dropsy, which if not
truly cardiac, is akin to it. I have already shown in detail, which I
need not repeat (see page 681), that general dropsy is due in a certain
minority of cases to causes which obstruct the pulmonary circulation,
notably emphysema and fibrosis.
Renal dropsy. — Proceeding now from cardiac dropsy to renal, we
pass from the more simple to the less. Renal dropsy and dropsy of
other kinds also present an inverse relation to the amount of urine,
which is general but not invariable. The urine may be superabundant,
as in diabetes, and the legs cedematous, or the urine may be absent and
dropsy absent too. With diabetes I have known, as I have said, the legs
to become cedematous with the urine amounting to 1 5 pints a day ; and
686 SYSTEM OF MEDICINE
with obstructive suppression dropsy may be as completely wanting as is
the urine. As a rule with nephritis the urine is diminished and oedema
present, but' sometimes when this disease assumes an exceptionally acute
form the urine may be reduced to almost nothing, and at the same time
there may be almost nothing of serous effusion. Thus it appears that
other factors have to do with dropsy, whether renal or diabetic, besides
the discharge of water by the kidneys. Dropsy fluid, much the same in
every disorder, though not in every place, is the capillary exudation, of
which either too much is poured out or too little removed. In renal
dropsy, to which our attention is now limited, the question narrows
itself for the most part into excess of exudation. It is true, under certain
circumstances which will be presently considered, renal dropsy may be
enhanced by pulmonary embarrassment, which hinders venous return and
probably hinders absorption ; and it is equally manifest that hypertrophy
of the left ventricle bears a part in removing renal dropsy by the increase
of suction which it entails, and the consequent promotion of absorption
by the veins ; but in its most common forms, and while free from com-
plications, renal dropsy may be regarded as the effect of increased
outflow, and our attention may in the first place be directed to see how
this is brought about.
Eenal disease which is productive of dropsy, putting aside the lardaceous
variety, is attended from the first with increase of arterial and cardiac
tension, which increases as the disease goes on, and becomes attended with
hypertrophy of the heart and arterial system. With the increase of
tension dropsy comes, and continues together with it possibly to the end,
or until the process of recovery gives a gradual finish both to the over-
tension and its attendant exudation. But there is a later phase which all
are not permitted to enter upon. Should time be granted and the disease
assume a chronic form, then, with establishment of much arterial thickening,
great ventricular hypertrophy, and further increase of intravascular tension,
the dropsy may diminish, and even in the fulness of time be completely
removed. Thus hypertrophy of the heart presents itself as the antagonist
of dropsy, or at least as concurrent with its removal.
The complicated process which has been sketched in outline, partly
morbid and partly remedial, requires to be considered in further detail.
The hypertrophy is at once the result and the evidence of the over-tension.
The tension must be attributed to the abnormal difficulty in the emptying
of the heart and arteries. Then comes the question where the difiiculty
or obstruction lies. Wherever it is, it is attended with the increased capil-
lary transudation which constitutes renal dropsy. The obstruction must
be either in the arterioles or the capillaries. This question has been long
and perhaps sufiiciently debated. It is certain that the exudation is from
the capillaries, and presumable that there is increase of blood-pressure in
this situation. The arterioles are obviously thickened, with regard to the
capillaries observations are wanting. But it is to be inferred, since the
transudation from them is increased, that their blood-supply is not
diminished, as it would be by any constrictive or stop-cock action on the
DROPSY 687
part of the vessels which feed them. We may, therefore, regard the
capillaries both as furnishing the source of the dropsy-fluid, and also of
the initial resistance to which the subsequent cardio-vascular changes are
due. We must presuppose an alteration in the blood, probably partly
toxic and partly hydrsemic, which causes abnormal resistance in the
channels of these vessels, and occasions their walls to transude abnormally.
It has been supposed that renal dropsy is akin to, or even equivalent to
inflammation ; that the outpouring of fluid is by a process essentially the
same as that which constitutes inflammation. With inflammation there
is certainly obstruction in the capillaries and exudation from them. With
renal dropsy there is exudation from the capillaries, and presumably
obstruction within them. But that the two processes are not the same
is evident from the differences which exist between the products of
inflammation and of dropsy. Inflammatory exudations differ from those
of dropsy in their higher specific gravity, in their containing corpuscular
elements in greater abundance, in their being more albuminous and more
ready to coagulate spontaneously.
The late removal of renal dropsy on the establishment of cardiac
hypertrophy cannot but be associated with, though, perhaps, it is not
wholly to be attributed to, the suction action of the left ventricle, which
must, unless dilatation intervene, be magnified in proportion to the thick-
ness of the wall, so that an abnormal force is brought to bear upon the
emptying of the auricle, and in necessary sequence upon the relief of the
lungs and right side of the heart, and ultimately upon the clearing of the
systemic veins. Another cause which must tend to the diminution of
dropsy in the late stages of inflammatory disease of the kidney is the
usual supervention of fibrotic changes in this organ, together with a
further increase of vascular tension and increase of urine which before
was scanty.
A point which must be adverted to in connection especially with
acute renal dropsy is the state of the respiratory organs. Obstruction
in these by emphysema or fibrosis has been noticed as a sufficient cause
for dropsy in a chronic form, and it is probable that obstruction of other
and more acute kinds may at least be co-operative in causing dropsy of
corresponding, acuteness. I have shown in detail, in the seventy-fifth
volume of the Medico-CUrurgical Transactions, that in about two-thirds of
the cases of acute renal dropsy the respiratory organs are the seat of
some inflammatory process, often bronchitis or broncho -pneumonia.
These conditions, though not the essential cause of the dropsy but prob-
ably only connected with it as the results of a common cause, cannot
but enhance the dropsical tendency. With regard to pleural effusion,
whether early or late, this is at once a result of the dropsical proclivity
and a cause of its increase by the pulmonary obstruction which it
occasions. These complications of renal dropsy are inflammatory and
mostly acute. They are not such as produce any considerable hyper-
trophy of the right ventricle. This ventricle is comparatively little
affected in renal disease. The contrast between the right ventricle and
688 SYSTEM OF MEDICINE
the left is one of the noticeable facts of Bright's disease. Both are
hypertrophied, but the right to a slight and almost insignificant extent.
The hypertrophy of this ventricle in renal disease is much less than
in certain conditions of disease proper to the heart itself ; whereas
hypertrophy of the left ventricle is nearly as great under renal disease as
from any cardiac lesion. In the paper to which I have referred I have
given outlines of the ventricles in section which show among other things
the relatively small hypertrophy of the right ventricle in renal disease.
These outlines may be appealed to as of interest with regard to the
lardaceous disease, the relation of which to dropsy must next be briefly
touched upon. With this disorder there is usually no hypertrophy of the
heart and no increase of intravascular tension. The condition is
obviously different from the dropsy connected with other states of the
kidney. It is associated rather with want of force in the circulation than
with exaggeration of it. The heart after death is often found to be
somewhat dilated and enfeebled rather than strengthened. It is not
improbable that, together with other factors, cardiac failure may have
something to do with this form of dropsy. It is to be observed that the
oedema of lardaceous disease often resembles that of cardiac origin in
affecting the lower extremities in preference to the face.
Next to renal dropsy may be projjerly placed that of chlorosis as
having points of resemblance to it. In making the inquiry to which I
have already referred (4), with the aid of the sphygmograph, I came upon
the fact that with the dropsy of chlorosis the tension of the pulse was
increased, notwithstanding the pallor and general weakness of the
patient. The resemblance which chlorotic bears to renal dropsy is
evident. With both we have a toxic condition of blood due to the failure
of an excreting organ — in one of the kidney, in the other of the uterus.
The chlorotic state requires for its relief, as is well known, not only iron
to obviate the anaemia, but remedies which stimulate the secretions of
the uterus and bowels. The familiar mixture of iron and aloes owes its
efficacy to its double action, at once depurative and restorative. In
idiopathic or pernicious anaemia, extreme as the anaemia may be, we have
no evidence of toxic retention, and as a rule there is no oedema ; though
the rule is not without exception.
Other forms of anaemia, or hydraemia — for the conditions, though not
the same, are commonly associated — tend to produce or assist in the pro-
duction of dropsical effusions. It is a tradition that in the- old days of
depletion patients were sometimes bled into dropsies. Marshall Hall,
in his treatise on the Effects of Loss of Blood, includes a proneness to
oedema and serous effusions, which result, he tells us, has long been
remarked by medical writers. Practice at present is less illustrative in
this respect. Dropsy from blood-letting, perhaps, does not admit of very
exact statement, for we do not know how much to attribute to the
disease for which the patient was bled, or to other disorders which the
patient may have had, but which were not within the knowledge of the
year 1830. Before taking leave of the relationship of anaemia to dropsy,
DROPSY 689
I may revert to the obvious association of this state of blood with renal
dropsy, especially of the acute kinds. Here anaemia is often extreme,
and we cannot but suppose that it is contributory to the efifiision. This
connection is especially worth noting, as it is of practical importance.
Hydrsemia may be a cause of dropsy or of its aggravation. Water
can usually be drunk in large quantities without any effusion, providing
that the glandular exits are free ; the kidneys, bowels, and skin carry ofiF
the excess without any accumulation in the body, and in certain forms of
renal disease, where the kidneys retain their power of response, good may
result from this irrigation of the system ; but when the kidneys are too
far gone to answer to the appeal, enforced water-drinking may cause an
immediate increase of dropsy. I once witnessed this in a case of renal
ascites as the result of the administration of a pint of water every
four hours. The tubular structure of the kidney was found to be exten-
sively atrophied (3). As bearing upon the dropsy of hydrsemia I may
recur to a case of diabetic coma, in which 22 pints of a saline solution
were injected into the veins in the course of 32 hours, with the
result of slight oedema and effusion into the peritoneum, pleurae and
pericardium. Most of the effusions contained blood, whence it was
inferred that intravascular pressure caused by the injection had much
to do with the result.
The dropsy of diabetes is a paradox and a lesson. Great diuresis
with this disease, instead of draining the tissues, may be accompanied
with the accumulation of fluid in them. It may be paradoxically stated
that the more that is taken out the more remains behind ; while it may be
instructive to consider a condition in which the amount of urine and of
dropsy do not display the usual inverse relation. The passage of
saccharine urine is often attended with renal irritation and nephritis,
mostly tubal, but sometimes interstitial This may give rise to dropsy
which is truly renal ; but, apart from secondary kidney disease, diabetic
dropsy has long been recognised. Prout mentions " incurable dropsy " as
one of the results of the disease, and tells us that at a late stage the urine
diminishes, loses much of its saccharine property, and the feet and legs
become oedematous. But this is not the whole story. The dropsy is not
always incurable, nor does it always come on with diminution of urine.
The legs may swell while the urine is still profuse. I have already alluded
to such a case. The pulse was weak, without any trace of albuminuric
tension. The .dropsy disappeared with much promptitude under perchloride
of iron, though it reappeared to some extent before death. I think it may
be inferred that diabetic dropsy has its immediate origin in cardiac weak-
ness and anaemia. It may be observed that the effusion affects the lower
extremities rather than the face. Traces of pitting may often be detected
about the tibiae in this condition, though the patient may be much emaciated
and the dropsy not obvious.
The treatment of dropsy is considered in connection with the
several diseases of which it is a symptom, but a few general remarks
may be here superadded, together with some brief reference to the prin-
VOL. V 2 Y
690 SYSTEM OF MEDICINE
eiples which should guide our attempts to relieve its more important
varieties. First may be placed the regulation of posture in reference to
cardiac disease and to cedema of every kind. The lessening of venous
pressure in the limbs, and the sparing of labour to the heart by the
horizontal posture, are too obvious to need insistence. But with heart
disease there is sometimes the difficulty that in consequence of the state
of respiration the patient cannot endure to lie down, in which case the
vital necessity must be first considered, and the dropsy in the second
place. The disadvantageous posture of orthopnoea may in some sort be
turned to advantage, for this attitude is favourable for the drainage
of the legs after puncture. Not only with heart disease, but also with
renal oedema is the horizontal position beneficial. Under this influence
and the modification of blood-pressure which it entails, oedema of this
origin will often disappear from the legs, and that without reappearing
elsewhere.
Diet in dropsy may be considered before drugs. As dropsy fluid,
whatever else it may contain, mainly consists of water, the question at
once presents itself, What is the effect upon the accumulation of cutting
off the supply ? " If we indulge in harmless fluids we get the dropsy,"
was " a soothing reflection " of Mr. Pecksniff's, and one which, in certain
conditions, as I have shown, is not altogether without warrant. How far
does the converse hold ; to what extent can we diminish the dropsy by
diminishing the drink ?
I have made experiments on the influence of dehydration by diet
upon dropsy of various kinds, — cardiac, renal, hepatic, and ovarian ; and in
cases of large effusion the result of pleurisy. The daily drink has been
reduced, in most cases gradually, to quantities of which the following may
serve as examples. The daily quantities are expressed in fluid ounces —
16, \f>\, 14, 12, 11, 6, 4, 2. The liquids were generally tea or milk,
generally both, sometimes with a small quantity, from three ounces to
half an ounce, of gin or brandy. Earely a lemon was given, which was
reckoned as an ounce and a half of liquid. Acidulated drops were some-
times allowed. The foregoing statements include everything that was
given in a liquid form ; ordinary diet was generally allowed ; the water
contained in the solids is, of course, not included. The privation was
generally well borne, better than I had expected; the tongue usually
remained moist ; if it became dry, the treatment was discontinued. Under
this process of desiccation the appetite diminished, the patient usually
lost weight, and generally, but not always, the dropsy notably diminished
and sometimes disappeared. It was difficult not to suppose that in some
of these cases the patient supplied himself with liquid at the expense of
his accumulations. To mention renal dropsy first, I may say that I
experimented on deprivation of water in this condition with extreme
caution and apprehension, never pushing the restriction far or continuing
it long. CEdema and ascites both lessened under the process, but the
deprivation was ill borne, and I soon came to the conclusion that such
experiments on renal dropsy were unjustifiable. With renal disease, such
DROPSY
as tends to uraemia, an abundant supply of water is indicated to wash out
the toxic products, and irrigation rather than desiccation called for.
With regard to dropsy depending on valvular disease of the heart,
dry diet is generally harmless and sometimes beneficial. Of three cases
in which this was employed without other treatment, in two the effusion,
which was limited to oedema, was much reduced and the patients benefited.
In another in which there was great ascites without oedema, the dry diet
was conjoined with repeated tapping. After five operations in the course
of three months and ten days, the first yielding 1 7 pints 1 2 ounces, the
last 5 pints 18 ounces, the fluid ceased to re-collect, and the patient left
the hospital without any. The dry diet was continued all the time ; the
daily liquid touched a minimum which was represented by 2 ounces of
tea, 2 ounces of brandy, and 1 lemon. It is, of course, possible that the
fluid might have ceased to reaccumulate had no treatment been employed,
but I think this is scarcely likely.
Dropsy from cirrhosis of the liver is under most circumstances
intractable. Of six cases treated by dehydration two only received
decided benefit. One patient unsuccessfully treated lost a stone in weight
in three weeks without any decrease of the ascites. Of the two successful
cases one was that of a man with an enlarged liver presumed to be
cirrhotic and ascites, for which he was tapped twice with reaccumulation.
He then, the belly being distended, but not tightly, was put upon dry diet
without medicine. After fourteen days of this no fluid could be detected.
The regimen was continued for some time longer, and was ultimately dis-
continued without any reappearance of the fluid so long as he was under
observation.
The other case was a somewhat remarkable one ; it was that of a boy
seven years of age, who had extreme ascites with hypertrophic cirrhosis
and suspicion of alcohol. The enormous distension and the dyspnoea
which it occasioned made tapping imperative, and between April 28
and June 21 this was done ten times. The dates and amounts were
as follows : April 28, 80 oz. ; April 29, 72 oz. ; May 5, 89 oz. ; May 10,
95 oz. ; May 15, 117 oz. j May 26, lU oz. ; May 30, 126 oz. ; June 7,
150 oz. ; June 14, 150 oz. ; June 21, 65 oz. The hopelessness of this
continual tapping suggested to me treatment by dehydration. Accord-
ingly, on June 29, when much fluid had again accumulated, and the belly
attained at the umbilicus a circumference of 30 inches, dry diet was
begun. No further tapping was required. The fluid diminished, dis-
appeared, and never reappeared. On July 21 none could be detected,
and the circumference had fallen to 25 inches. At its greatest reduction
the drink was limited to 6 oz. of milk, \\ oz. of brandy, and a few small
pieces of ice. The restriction was well borne, and, so far as the ascites
was concerned, the cure was complete. The restriction was continued in a
modified way for some time after the loss of the ascites. The patient
left the hospital practically well, and so remained for over two years,
when he was brought back with an abscess in the brain, which apparently
had nothing to do with his former ailment. This caused his death,
692 SYSTEM OF MEDICINE
and gave an opportunity for a post-mortem examination. The liver
was contracted and markedly cirrhotic, fibrotic and hob-nailed. The
peritoneal cavity contained no fluid, but was closed by delicate adhesions.
It may be observed in retrospect that the cessation of the morbid secretion
was not the result of the adhesion, but occurred prior to it. The belly
was largely distended when the dropsy began to diminish. The apposed
surfaces adhered after the cavity had been emptied and kept empty by
dehydration ; probably the precedent, dropsy brought about a sub-inflam-
matory state of the membrane which invited adhesion when contact was
established and maintained.
I may mention with brevity that in two instances of large effusion,
the result of pleurisy, the fluid quickly disappeared under dry diet ; this,
of course, is not conclusive as to the effects of the treatment, for the fluid
might have been absorbed had none been employed. A more striking
example of the results of dehydration was afforded by a woman who had
an enormous unilocular ovarian cyst simulating ascites. Under a diet
which at its narrowest limitation comprised no liquid but what was con-
tained in 2 oz. of tea and 1 oz. of brandy in the twenty-foiu: hours, the
patient lost in three weeks 3 inches in girth and 13;^ lbs. in weight.
She ultimately underwent ovariotomy with success.
From the foregoing cases and other experience, I conclude that
dehydration by diet may be used under certain circumstances in the
treatment of dropsy other than renal. With cardiac dropsy, whatever
its seat, this is generally harmless and may sometimes be useful. With
regard to hepatic ascites, considering the safety of tapping and the
immediate relief afforded by it, I think that dry diet may be best
employed, not as a substitute for the operation, but as an adjunct to
it, as in the case of the boy with cirrhosis, of which details have been
given.
The routine remedies for dropsy can be only cursorily dealt with.
The removal of fluid by agents which act on the secretions of the bowels,
kidneys, and skin is familiar practice. Hydragogue purgatives, elaterium,
compound jalap powder, sulphate of magnesia, and bitartrate of potash
must receive acknowledgment, but are too well known to need insistence.
With regard to renal dropsy, useful as such remedies sometimes are, they
must be used with caution lest anaemia be promoted and dropsy thereby
encouraged. It often answers well to mix a little saline purgative with
iron in the periodic mixture. Neither should the diet be too parsi-
monious. But I need not repeat here what I have said in a previous
volume (vol. iv. p. 401). Whether regarded as purgative or as
acting otherwise, small occasional doses of calomel are often of use in
renal as in cardiac dropsy, having regard to the intolerance of mercury in
renal disease. Hot-air baths are often of especial use in renal dropsy, for
they not only draw off the fluid, but relieve the blood of the impurities
upon which the dropsy essentially depends. Of the remedies of the
diuretic class those are most valuable which are also cardiac tonics, such
as digitalis and squill. We know of no remedy which is of equal value
DROPSY 693
in dropsy, whether cardiac or renal, to digitalis. In cardiac dropsy no
combination serves as well as the time-honoured dropsy pill of Matthew
Baillie — digitalis, squill, and mercury. Squill alone, or in other associa-
tions, is often disappointing. The same may be said of most other
so-called diuretics. An exception as regards renal dropsy must be made
in favour of the alkalising salts of potash, tartrate of potash, potassio-
tartrate of soda, and citrate of potash ; these are both purgative and
diuretic, and if pushed to alkalinity of urine may do good by lessening
the coagulation of fibrin in the form of casts. This extreme dosage is,
however, but seldom called for. I must not omit to enforce the necessity of
iron, and the avoidance of a very poor diet, in renal dropsy when this is
associated with anaemia. The inutility of diuretics, and indeed of drugs
generally, is especially apparent in ascites of cirrhotic origin.
The relief of dropsy by puncture may be touched upon. The tapping
of the belly has already been adverted to. Its safety and utility are
well known. It is better done with the aspirator or Southey's tubes
than with the large trocar formerly in vogue. Relieving the abdomen
also relieves the legs by facilitating the return by the vena cava. Where
the pleurae share in general dropsy I have often found it beneficial to the
general condition to tap one or both of these cavities, which relieves the
pulmonary circulation, and by consequence the general dropsical state.
Though relief of the serous cavities indirectly relieves the oedema, the
converse does not hold good. Draining the oedema does not relieve either
pleural or peritoneal accumulation. But with its limited purpose it is
often of use, though attended with more danger than the tapping of the
'serous cavities. Puncture of the legs is, however, a less formidable
operation than it was before the invention of antiseptic surgery. The
dangers which are to be apprehended are erysipelatous inflammation and
cellulitis, which may suppurate and constitute the beginning of the end.
Incisions should be avoided, and acupuncture or Southey's tubes employed ;
I have found the tubes on the whole to answer best. I have known
enormous quantities of fluid to be drained off by these means. Two of
these tubes in each leg in a case of renal dropsy drew off nine pints in
two days, and I knew an instance of cardiac dropsy in which twenty-two
pints were drained off as the result of a similar operation.
W. HowsHip Dickinson.
REFERENCES
1. Arnold. Virchow's Archiv, Bd. Iviii. S. 203. — 2. Cohnhbim. Lectures on
General Pathology, vol. i. p. 502, translated by New Sydenham Society, 1889. — 3.
CoHNHEiM and LiOHTHBiM. Virchow's Archiv, Bd. Ixix. S. 106.— 4. Dickinson, W.
H. "On Renal Dropsy," iJo!/. Med.-Ohir. Sac. Trans, vol. Ixxv. p. 317; 1892.— 5.
Idem. "Lectures on Chronic Hydrocephalus," Lancet, July 16, 1870. — 6. Idem.
Clinical Sac. Trans, vol. xxiii. p. 130, and Soy. Med.-Ohir. Soc. Trans, vol. Ixxv. p.
322. — 7. Idem. Edrveian Oration, Royal Coll. Physicians, 1891.— 8. Hall, Marshall.
Effects of Loss of Blood, 1830, pp. 106, 115.-9. Hallibueton. Text-hook of ClmicaX
Physiology and Pathology. — 10. Hambubgek. Beitr. n. path. Anat. •«,. allge. Path.
694 SYSTEM OF MEDICINE
Zena, Bd. xiv. S. 443 ; 1893. — 11. Heidbnhain. Archivf. d. ges. Physiol. Bd. xlix.
1891. — 12. Hoffmann. Virehow's Archiv, Bd. Ixxviii. S. 250. — 13. Jankowski.
Virchow's Archiv, Bd. xciii. S. 259. — 14.' Johnson, Sir George. Medical Lectures and
Essays, p. 34. — 15. Lassak. Virchow's Archiv, Bd. Ixix. S. 516. — 16. Lazaetjs-
Barlow. Journal of Physiol, vol. xix. pp. 140, 418 ; Phil. Trans. 1894. — 17. Leathbs.
Journal of Physiol, vol. xix. p. 1. — 18. Eanvier. Compt. rend, de acad. des
sciences, vols. Ixix. Ixxiii. — 19. Reed, E. W.' Journ. of Physiol, vol. xi. — 20. Starling.
"Arris and Gale Lectures," Lancet, 1896, vol. i. — 21. Idem. Journal of Physiol, vol.
xvi. p. 224. — 22. Starling and Ttjebt. Journal of Physiol, vol. xvi. p. 140. — 23.
ToHiRKOFF. Rev. de mid. 1896, p. 625. — 24. Thoma. Pathology and Pathological
Anatomy, translated by A. Bruce, vol. i. p. 344.
W. H. D.
HEART DISEASES
CONGENITAL MALFORMATION OF
THE HEART
DISEASES OF THE PERICARDIUM
DISORDERS OF FUNCTION, IN-
CLUDING STRAIN
INJURIES BY ELECTRIC CUR-
RENTS OF HIGH PRESSURE
DISEASES OF THE ENDOCARDIUM
DISEASES OF THE MYOCARDIUM
CHRONIC VALVULAR DISEASES-
DISEASE OF THE AORTIC AREA
OF HEART
DISEASES OF MITRAL VALVE
RIGHT -SIDED VALVULAR DIS-
EASES
ANGINA PECTORIS
CONGElsriTAL MALFOEMATION OF THE HEAET
Synopsis
Seotiou I
Defects in the septa of the heart.
Stenosis and atresia of the pulmonary
artery.
Stenosis and atresia of the aorta.
Transposition of the primary arterial
trunks.
Premature closure or patency of the foetal
Irregularity in the number or form of the
valves.
Anomalous ^epta.
Misplacements of the heart.
Deficiency of the pericardium.
Section II
( Causation}
Fcetal endocarditis.
Mal-development.
Development of normal heart.
Mode of formation of septal defects,
stenosis and transposition.
Section III
Symptoms.
Cardiac signs.
Duration of life.
Causes of death.
Treatment.
The subject of malformation of the tuman teart is one of great
interest, and has attracted the attention of medical observers since the
beginning of the century, but in more recent years these anomalies
have been subjected to a thoroughly scientific investigation. The earliest
observations consist for the most part of descriptions of morbid specimens,
which are scattered through various periodical publications. From time
to time these have been collected together, and have formed the subject
of dissertations or lectures. One of the first of these was a dissertation
by Meckel in 1802, a descriptive account drawing attention to the curious
resemblance presented by some of the monstrosities to the hearts of
reptiles, amphibians, and crustaceans. Chapters on the subject also
appear in various works by Corvisart, Laennec, Hope, and others. A
special essay by Dr. Farre in 1814, and a series of lectures by Dr.
Norman Chevers in 1845 on Morbid Conditions of the Pidmona/ry Artery,
drew particular attention to the very frequent anomalies of this vessel.
In 1855 Dorsch insisted on the importance of foetal endocarditis as a
determining element in the causation of these abnormalities, a hypothesis
which became too one-sided in its application.
Peacock, in 1855, was the first to issue a systematic treatise on the
subject, a work which is stamped throughout with the most accurate observa-
tion. A new edition of the same work appeared in 1 866, and in the preface
SYSTEM OF MEDICINE
Peacock reminds us that it is but recently that attempts have been
made to reduce the different forms of irregulai development to any
scientific arrangement, or to explain their nature and mode of produc-
tion.
In the classification of malformations of the heart he is guided
partly by the period at which the development of the organ becomes
arrested or perverted ; partly by the degree of impediment to the
circulation which such deviation occasions, and the consequent inter-
ference with the functions of the heart after birth.
In 1875, at Vienna, Rokitansky published his most important mono-
graph on the Defects of the Septa of the Heart, in which he differed from
the current views of the development of the septa, and insisted on
the importance of studying the anomalies in connection with the different
stages of development.
In my treatment of the subject I have been guided mainly by the
works of Rokitansky, of Peacock, and of Eauchfuss. '
Section I. is devoted to a descriptive account of the commoner forms
of malformation of the heart. In Section II. the mode of formation of
the anomalies is explained as far as possible by reference to the processes
of normal evolution. Section III. contains some of the more important
phases in the life-history of the subjects of malformation.
Section I
Synopsis. — Defects in the septa of the heart — Complete absence of loth
auricular and ventricular septa — Defects in the auricular septum : Defect
of the primary septum ; Defect of the secondary septum ; Patent foramen
ovale — Defects in the ventricular septum : Complete defect ; Defect of the
posterior septum; Defect of the anterior septum; Defects in other uncommon
Complete absence or very imperfect indication of the auri-
cular AND ventricular SEPTA. — The heart consists of two cavities, an
auricle and a ventricle, with a single vessel which supplies both the
systemic and pulmonic circulations.
Many cases of this kind have been collected by Dr. Peacock, the
specimens showing examples of hearts in very different stages of develop-
ment. One of the earliest records of this malformation was brought
before the Eoyal Society by Mr. Wilson in 1798. The heart was con-
tained in a sac which rested upon the surface of the liver ; the lower part
of the pericardium was absent. There was a single auricle and ventricle,
and one vessel which divided into two branches ; the smaller of these
went to the lungs, and the other passed upwards behind the thymus
gland and gave off the usual aortic vessels. There was no ductus
arteriosus, and the two pulmonary veins entered the descending vena
CONGENITAL MALFORMATION OF THE HEART 699
Other cases are also described, by Dr. FaiTe and by Mr. Forster, in
■which the heart retained its most rudimentary form.
Examples in which there was some dirision between the auricular or
ventricular cavities have been not infrequently recorded; in some the
auricles are more or less divided, but there is only one orifice of com-
munication between these and the ventricle ; in others the arterial trunk
is divided into an aorta and pulmonary artery.
Defects in the auricular septum. — Defects of the primary
septum. — Compute, or almost complete, defect of the interawriculwr septum. —
The auricle remains single and undivided, or there may be a slight indica-
tion of a septum in the form of a sickle-shaped membrane at the upper
•and hinder part. This condition is usually associated with other con-
siderable abnormality.
Partial defect with open or closed foramen ovale. — There may be a large
■defect in the lower part of the septum limited below by the upper and
hinder part of the ventricular septum, while the foramen ovale is closed
and may be seen above the aperture of defect ; in other cases the foramen
•ovale remains open. The pulmonary artery in many of these cases is
wider than the normal, and the aorta may be contracted. The result of
this form of defect is to leave open a free communication between theauricles
a,nd the upper part of both ventricles over the ventricular septum. A
specimen of this form of defect is described by Dr. Norman Moore. The
•auricles were enormously dilated ; the apex was bifid like the heart of a
■dugong. The foramen ovale was completely closed, the septum auriculorum
did not meet the septum ventriculorum, and there was a large opening
below it, but above the flaps of the mitral and tricuspid valves ; one part
•of each of these was attached to the septum ventriculorum just below
this opening ; thus the auricles were in communication with one another,
and each auricle with both ventricles.
Another specimen is described by Peacock in which, in addition to
the septal defect in the auricles, the trunk of the pulmonary artery was
■dilated, and the aortic orifice was very small.
Defect in the secondary septum.— The septum may be deficient either
with or without remains of the primary membranous septum.
The remains of the primary membranous septum may be in the form
•either of a lattice-like membrane, or a pouch-like sacculation which pro-
trudes into the atiricular cavity.
In some instances a defect is found above the foramen ovale, this
latter being closed or open. A few cases of this kind are described by
Rokitansky.
A case is recorded by Professor Greenfield in which there was a
■deficiency of a great part of the upper and anterior portions, and in
addition a perfectly formed but widely patent foramen ovale. The
auricles were enormously enlarged and the appendices elongated, the left
ooming right round to the front of the heart. When opened the auricles
were found separate at the lower part only, and communicated partly
700 SYSTEM OF MEDICINE
with one another by an opening of nearly circular shape, about one
and a half inches in diameter. The upper and a considerable part of the
anterior portion of the opening was formed simply by the wall of the
auricle ; at the lower and more posterior part it was bordered by the
septum. The upper edge of the septum was curved and thick. No ridge
whatever could be discovered indicating where the septum should be
attached on the upper wall of the auricle. At half an inch below the
upper edge of the septum was a patent foramen ovale. On the aspect of
the posterior half of the septum towards the right auricle was an extensive
irregular cribriform membrane, only attached here and there to the
muscular wall. It extended from the entrance of the inferior vena cava
to the aperture of the foramen ovale. The foramen ovale had the normal
oblique direction and the normal funnel shape, but was of unusual length.
In addition to other deviations from the normal, the pulmonary artery
was greatly dilated and its wall thickened, and the aorta had only two
valves, and its orifice was greatly narrowed ; beyond the valves the trunk
was dilated.
Two cases are recorded by Wagstaffe with openings in the auricular
septum above the foramen ovale ; in one the foramen was closed, in the
other open. Cases of this kind are, however, probably rare.
Patent foramen waZ«.— Complete patency of the foramen ovale is due
to failure in the development of the membrane of the fossa ovalis, and is
a very common condition. It may exist without any other cardiac
anomaly, and may give rise to no special symptoms. In the majority of
cases it is associated with pulmonary stenosis, defective ventricular
septum, or other malformation.
Small canals or perforations between the membranes and muscular
partitions are not uncommon, and an oblique valvular opening is fre-
quently to be found at the margin of the fossa ovalis where the membrane
has failed to unite to the ring. In infants who have survived their birth
only by two or three months the opening is normally in the form of a slit ;
but it may persist through life, and is of no clinical significance.
Defects in the ventricular septum. — Complete defect. — The
heart consists of three cavities ; the auricles are divided by a more or
less complete septum, and there are generally two auriculo-ventricular
orifices. The ventricle is either wholly undivided, or there may be a
slight indication of a rudimentary septum at the lowest part of the
cavity. The common arterial trunk is usually divided into an aorta and
a pulmonary artery.
In the cases, described by Peacock, of complete defect of the ventricular
septum, the aorta and pulmonary artery were more or less abnormal,
being either stenosed or transposed ; although in one instance the position
was natural and the orifices somewhat dilated.
Eokitansky states that complete absence of the ventricular septum is
always associated with some form of anomaly of the large arterial
trunks.
CONGENITAL MALFORMATION OF THE HEART 701
A specimen of this malformation was removed by myself from a girl
aged sixteen, who died of pulmonary phthisis. The heart consisted of
two auricles and a single ventricle, and the pulmonary artery and aorta
were transposed. The septum between the two auricles was complete,
but the right was nearly twice as capacious as the left. The coronary
sinus opened into the right auricle, and the right auriculo-ventricular
valve was tricuspid in shape ; the left auriculo-ventricular valve was
somewhat irregular, the aortic cusp being puckered and contracted. The
single ventricle was capacious, and presented only the merest rudiment
of division in the form of a muscular projection at the posterior and
inferior part. The aorta was of large size, but arose from what would
be the normal position of the pulmonary artery ; the aortic valves were
normal, also the openings of the coronary arteries. The pulmonary
artery arose behind and slightly to the left of the aorta, the opening
into the ventricle being situated between one of the segments of the
tricuspid and mitral valves. The pulmonary valves were normal, but
the orifice appeared somewhat smaller than usual. The ductus arteriosus
was closed.
Partial defect of the ventricular septum. — Following the descrip-
tion given by Eokitansky, the ventricular septum may be divided into a
posterior muscular septum, a membranous portion, and an anterior
muscular septum, the latter being again divisible into a front and hind
portion. (See Section II.)
Defects may be seen at one or other of these sites at the base, where
during foetal life the division of the cavities is last effected.
Defect in the posterior septum throws the two ventricles into free
communication. A case of this kind is described by Eokitansky; the
aperture was of considerable size, and, as seen from the right ventricle
anteriorly, opened into the left ventricle, over the free edge of the
rudiment of the ventricular septum; the septum of the auricles was
incomplete. The free upper edge of the rudimentary ventricular septum
was sickle -shaped, and the front portion terminated above in a band
which was inserted between the two arterial trunks. The pars mem-
branacea was also defective.
Other cases of similar defect are recorded, associated with abnormal
size of the right ventricle, persistent ductus arteriosus, or transposition of
the right and left hearts.
Defect in the pars membranacea, or the "undefended space," is
ascribed by Peacock as the cause of almost all the apertures found in the
upper part of the ventricular septum, and in this he has been followed
by many English writers. It is probable that Peacock included in the
'defects of the pars membranacea apertures which extended both in front
of it and behind it. He remarks that if the interventricular septum
be partially defective, the imperfection most generally occurs at the
base. In this situation there exists normally, in the fully developed
organ, a triangular space in which the ventricles are separated only by
the endocardium and fibrous tissue on the left side, and by the lining
702 SYSTEM OF MEDICINE
membrane and a thin layer of muscular substance on the right. Laterally
it is bounded by the attachments of the right and posterior aortic cusps,
and its base is formed by the muscular substance of the septum. The
dimensions of the space vary with the size of the heart, but ordinarily in
the adult the sides may be estimated at about seven Paris lines, and the
base is somewhat wider. When the lower part of the space is perforated,
the left ventricle and origin of the aorta communicate with the sinus of
the right ventricle, but if the defect be situated high up, towards the
angle of attachment of the valves, the communication may be betweea
the left ventricle and the right auricle.
The anterior part of this opening would therefore correspond with an
aperture due to defect in the hinder part of the anterior septum as
described by Eokitansky.
An aperture confined to the " imdef ended space " would be of very
small dimensions, but it may be defective in conjunction with defects of
either the posterior septum or of the hinder portion of the anterior septum.
Complete defect of the anterior septum. — Several instances of this
condition are described and figured by Eokitansky. In these the whole
of the anterior portion is deficient, throwing both the ventricles and the
origin of the arterial trunks into communication.
The majority of these cases showed in addition either transposition or
some anomaly in the position of the large arterial trunks. In others
there was stenosis or atresia of the pulmonary artery. The foramen
ovale was usually open or only partially closed.
Defect of the hinder portion of the anterior septum. — This is a
very common form of deformity, and like the rest is usually accompanied
by malformation of other parts, with abnormality of the origin of the
arterial trunks, or with stenosis or atresia of the pulmonary artery. An
aperture in the hinder part of the anterior septum places the two
ventricles in communication, the left ventricle and origin of the aorta
with the sinus of the right ventricle.
A large number of cases and specimens are described by Eokitansky
and others. The aperture has for its posterior limit the pars membranacea.
Defect of the foremost part of the anterior septum. — ^By this
malformation the origins of the arterial trunks are placed in communica-
tion ; the condition is no doubt rare. Peacock remarks that occasion-
ally, though, so far as his observation serves him, very rarely, the
division between the left ventricle and the infundibular portion of the
right is perforated, so as to form a communication between the left
ventricle and the origin of the pulmonary artery ; he also mentions that
there are two specimens illustrating this condition in the Museum of St.
Thomas's Hospital.
Dr. Sidney Coupland describes an excellent example of this rare form
of defect. The heart was hypertrophied, both ventricles enlarged and
the walls thickened. On laying open the conus arteriosus the upper
part of the ventricular septum was seen to be perforated by a crescentic
aperture, which was of sufficient size to admit a No. 1 2 catheter, and was
CONGENITAL MALFORMATION OF THE HEART 703
seated on the posterior wall of the conus, immediately below and to the
right of the posterior segment of the pulmonary valves. Viewed from
the left ventricle the aperture had the following relations : — Its shape was
more oblong than it appeared on the right side, and it occupied the fleshy
part of the septum about a quarter of an inch from its union with the
anterior wall of the ventricle. The upper margin was formed by the
bulging segment of the anterior, sometimes called right aortic cusp, from
above which issued the right coronary artery.
The orifice was thus placed between the anterior or right and
the left posterior, or left valve cusp, but in closer contiguity to the
former than to the latter. There was no further malformation of the
heart.
Two cases are described by Eokitansky. In one there was a rounded
orifice in the foremost part of the anterior septum on the left side ; it was
situated beneath the right aortic valve 10 mm. in front of the membranous
septum : seen from the right side, it appeared in the conus 1 3 mm. in
front of the membranous portion just below the right pulmonary valve.
The apex of the heart was bifid, the aorta displaced to the right, and
the position of the pulmonary valves was altered. The aorta and
pulmonary artery were of normal calibre.
Defects in uneommon situations. — It is rare to find apertures of com-
munications between the ventricles elsewhere than at or near the base
of the septum.
Rokitansky records a case in which, with other malformation, there
was a perforation near the middle of the septum. Sir Dyce Duckworth
describes a specimen in which there was an aperture in the septum of the
ventricles about the junction of the middle and lower thirds ; the opening
was large enough to admit a crow quill, and was situated somewhat
posteriorly ; the foramen ovale was pervious. Apertures in these unusual
situations do not seem to admit of any general explanation.
Stenosis or atresia of the pulmonary artery. — Stenosis of
the pulmonary artery. — A pronounced example of this the commonest
form of cardiac malformation well merits description. The following
specimen was removed by myself from the body of a child, aged five and
a half years, who died of cerebral abscess.
The heart weighed five and a half ounces ; there was marked
hypertrophy of both ventricles, more especially of the right. On
opening the right auricle it was found to communicate very freely with
the left through the foramen ovale. The pulmonary artery was much
diminished in size, and there was extreme stenosis of its orifice which
admitted the passage of a cylinder only about 8 Paris lines in circum-
ference. The pulmonary valves were only two in number : close to the
ostium there were signs of slight recent endocarditis. The septum of the
ventricles was incomplete at the upper part just in front of the pars
membranacea. The aorta, which was much dilated, was situated more to
the right than normal, it communicated freely with both ventricles.
704 SYSTEM OF MEDICINE
rather more with the right than with the left. The ductus arteriosus
was not found.
Numerous instances are recorded of this condition ; namely, stenosis of
the pulmonary artery, imperfection of the ventricular septum, a dilated
aorta communicating freely with both ventricles. Minor variations depend
on the degree of stenosis, the extent of the septal defect and the degree
of displacement and dilatation of the aorta : the foramen ovale and the
ductus arteriosus may be either patent or closed.
In a large number of these eases there is some deviation of the septum
of the ventricles, so that the origins of the aorta and pulmonary artery
are misplaced ; this deviation of the septum is most frequently to the left,
so that the right ventricle is of large size and the aorta arises wholly or
to a great extent from that cavity.
A case of this kind is described by Dr. Parker. The heart had been
removed from a boy, aged thirteen, who died of pneumonia. The valves
of the pulmonary artery were adherent ; the ascending aorta was much
dilated, and arose from the large hypertrophied right ventricle. The
left ventricle formed only a small supplementary sac with a communication
into the right ventricle. In some instances the septum of the ventricles
is found to be entire while the auricular septum is defective.
Atresia or obliteration of the pulmonary artery is a far rarer condition
than the preceding. Several cases, collected from various sourpes, are
quoted by Peacock ; and he records two cases which came under his own
notice. An important distinction in these two cases is that in the first
the ventricular septum was incomplete, while in the second it was fully
formed. In the first there was obliteration of the orifice and trunk of the
pulmonary artery ; the aorta arising chiefly from the right ventricle and
giving off the pulmonary branches through the ductus arteriosus. The
right auricle was large and its valves thick, and the foramen ovale was
not completely closed by the valve, but would allow the blood to flow
from the distended right auricle into the left. The cavity of the right
ventricle was of very large size, and consisted almost entirely of the
sinus ; the infundibular portion was reduced to a mere chink, and was
entirely closed at the usual point of origin of the pulmonary artery, the
trunk of which formed an impervious cord as far as its union with the
ductus arteriosus ; the septum of the ventricles was imperfect at the base ;
the wall of the right ventricle was extremely thick, and the left auricle
and ventricle were very small in relation to the right. The aorta arose
chiefly from the right ventricle, and was of large capacity so far as the
point at which it gave off the ductus arteriosus, through which the supply
of blood was transmitted to the lungs.
The second specimen was removed from a child which died nine days
after birth. The heart was of unusual form, being broader from side to
side than from above downwards. The left ventricle constituted the
largest part of the organ. The two auricles communicated freely through
the patent foramen ovale. The cavity of the right ventricle was of very
small size. The outlet from the ventricle by the pulmonary artery
CONGENITAL MALFORMATION OF THE HEART 705
was entirely closed by the union of the valves at the origin of this
vessel.
The pulmonary vessel was pervious down to the valves. The ductus
arteriosus was of the usual size, and passed into the aorta, forming a com-
munication between the branches of the pulmonary artery and that vessel.
The septum of the ventricles was entire. The cavity of the left ventricle
was of large size, and was separated from the left auricle by the usual
valves. The ascending aorta was large and the ordinary branches arose
at the arch. After the entrance of the ductus arteriosus the aorta
diminished considerably in capacity. The course of the blood in this
case must have been from the right auricle into the left auricle, thence
into the left ventricle and aorta, and from that vessel to the lungs by the
ductus arteriosus. The right ventricle, being thrown out of use, had
atrophied ; while the left, having to maintain both the systemic and pul-
monary circulations, was unusually capacious and hypertrophied.
A remarkable instance of this condition is recorded by Dr. Hare. It
was removed from a child aged nine months, who died cyanotic. The
right auricle was enlarged, and had only a very small communication
with the left through an opening in the foramen ovale, one-sixteenth of
an inch in breadth and one-tenth of an inch in length. On cutting into
the right ventricle it was found that the columnse carnese were fused almost
into one and the cavity would only hold a moderate -sized pea. The
ventricular septum was perfect. The orifice of the pulmonary artery was
closed, but its trunk was in communication with the ductus arteriosus
and divided into the usual branches. The left ventricle was hyper-
trophied and gave origin to the aorta. The unusually small opening
between the right and left auricles, the only communication between the
two sides of the heart, was remarkable in this case.
In all cases of atresia of the pulmonary artery the possibility of the
circulation being carried on, and life maintained, depends upon the open
condition of either the interventricular septum or the foramen ovale ; or
on the patency of the ductus arteriosus.
There are some important differences in the site of the constriction,
partial or complete, of the pulmonary artery, and the nature of the con-
striction varies also.
The following forms may be recognised : —
Stenosis or atresia of the trunk of the artery.
Stenosis at the conus arteriosus.
Stenosis of the valves with or without narrowing of the trunk of the
vessel, and with dilatation of the pulmonary artery.
Stenosis of the trunk. — The trunk and canal of the artery may be
contracted or obliterated for a greater or less extent in its course, or even
converted into a fibrous cord. The cause of this contraction is no doubt
due, in the majority of instances, to irregularity in, the development or
division of the common arterial trunk, and is usually associated with other
developmental defects. Atresia occurs whenever the deviation of the septum
of the bulb is so considerable that the septum, the convexity of which is
VOL. V 2 z
7o6 SYSTEM OF MEDICINE
directed towards the pulmonary artery, becomes actually applied to the
wall of the vessel and fuses with it as far down as its mouth. The cause
of the incomplete division is probably due to imperfect development of
the fifth branchial arch.
Stenosis at the eonus arteriosus. — The conus or infundibular portion
of the ventricle is usually ill developed, and there is a constriction
between it and the sinus of the ventricle. The degree of stenosk may be
extreme, the orifice being only of sufficient size to admit a small probe.
The condition is usually associated with much thickening of the endocar-
dium and surrounding muscular tissue, with increase of the fibrous tissue ;
these results being in many cases due to the impediment of the passage
of the blood of some duration.
There is often some evidence of recent endocarditis about the
stricture in the form of roughening or small vegetations.
Stenosis at the valves. — When the constriction is at the valves, their
free edges or adjacent parts are adherent, forming a curtain, and leaving
an aperture of varying size and shape for the passage of the blood.
The valves themselves are usually irregular in number, size, or form.
The pulmonary artery is usually found to be more or less diminished
in calibre throughout ; but this is not invariably the case, for in some
specimens dilatation occurs in the calibre of the vessel on the distal side of
the obstruction. A specimen of this latter condition of the pulmonary
artery is described by Peacock. The heart weighed about nine ounces :
the anterior surface was almost entirely composed of the right ventricle,
which was greatly dilated and hypertrophied. The pulmonary orifice
was very much constricted from disease of the valves ; the three curtains
were blended together so as to form a kind of diaphragm which extended
across the orifice, and protruded forwards in the course of the vessel,
and was perforated in the centre by a small rounded aperture. The
trunk of the pulmonary artery was of somewhat large size, and its
coats were thick. The foetal passages were completely impervious.
The case was an uncommon one, for with extensive disease of the valves
of the pulmonary artery the heart was otherwise well formed. It
must be concluded that the degree of obstruction at the pulmonic orifice
must at the time of birth have been only slight. With regard to the
dilatation of the trunk of the pulmonary artery combined with the
stenosis. Peacock remarks that this is generally the case where the septum
of the ventricles is entire, but where the septum is deficient and the
stenosis at or near the orifice, the trunk of the artery is usually small
and its walls thin.
In cases of obliteration of the pulmonary artery the blood is usually
transmitted to- the lungs from the aorta through the ductus arteriosus ;
more rarely from the left subclavian artery or from other branches from
the descending aorta.
Atresia or stenosis of the aorta. — This may occur either alone or
associated with other deformities. A case is recorded by Mr. Shattock of
CONGENITAL MALFORMATION OF THE HEART 707
atresia of the aortic aperture in an Infant from adhesion of the valYes. The
ascending aorta was much diminished in calibre, and arose from the left
ventricle, the cavity of which was almost obliterated and could only hold
a pea. The right side of the heart was large and the ductus arteriosus
was patent.
Dr. Peacock mentions a case of obliteration of the aortic orifice,
reported by Komberg, in a child who lived four days and was cyanosed.
The right ventricle was dilated and hypertrophied, and the pulmonary
artery was large. The left auricle and ventricle were very small, and there
was not a trace of the aortic orifice. The foramen ovale was largely open,
and the supply of blood to the aorta was conveyed from' the pulmonary
artery by the ductus arteriosus.
Similar specimens have been exhibited by Mr. Canton and by Dr.
Hare. In these cases of atresia with complete ventricular septum, the
left ventricle becomes abortive, and is almost entirely thrown out of the
circulation, and they may be well compared with similar cases of atresia
of the pulmonary artery in which the right ventricle becomes abortive.
Rauchfuss has collected twenty-four cases of stenosis and atresia of
the aorta, with perfect ventricular septum ; it appears that atresia of this
orifice is less rare than a similar condition of the pulmonary artery.
Stenosis occasionally affects the left conus arteriosus, but not so
frequently as the right.
Stenosis of the apeh of the aorta at the ductus arteriosus. — A
narrowing of a part of the aorta in this region is sometimes found : a
specimen in the Cambridge Museum shows the arch of the aorta to be
much contracted from the orifice to the ductus arteriosus, which latter
vessel is patent; the aorta then widens to its natural size. It is noteworthy
that in the normal foetus the aorta is considerably reduced in size after
giving oflT the large vessels, that it often presents a marked constriction at
the part corresponding to the attachment of the remains of the ductus
arteriosus, and that this constriction or isthmus is succeeded by a fusiform
dilatation, fhe aortic spindle of His. When the aorta distal to the left sub-
clavian artery is contracted or impervious the descending aorta is usually
wholly or chiefly supplied through the pulmonary artery.
A curious case of aortic stenosis, with other defects, is recorded by
Dr. Greenfield. The heart was greatly enlarged, especially the right
ventricle; the two auricles commimicated freely; the septum of the
ventricles was entire. The left ventricle was somewhat hypertrophied and
dilated : the aortic valve consisted of two cusps, anterior and posterior,
the anterior being formed by the fusion of two. The aortic orifice was
greatly narrowed, and the aorta commencing a little beyond the valve
showed marked dilatation. The ductus arteriosus was closed, and beyond
its point of junction the aorta became narrowed, and then again returned
to its normal size ; the pulmonary artery was dilated.
Hypoplasia of the aorta with smallness of the heart was described by
Virchow in 1856 in connection with chlorosis: more recently Beneke
made elaborate measurements of the vessels at different periods of life
7o8 SYSTEM OF MEDICINE
and found that after puberty the arteries rapidly enlarged and the heart
acquired a great increase of force. Suter, on the other hand, as the
result of careful observations, fails to find any relation between the
" narrow aorta " and anaemia, and concludes that the size of the aorta
varies with age and sex, and that measurements made in the cadaver
cannot accurately represent its size in the living subject.
For other irregularities of the aorta and vessels the reader is referred
to works on Teratological Anatomy.
Transposition or malposition of the aorta and pulmonary
ARTERY. — Many dififerent varieties of malposition present themselves,
from complete transposition to slight aberration from the normal relative
position of these vessels.
The condition of the cardiac cavities associated with complete trans-
position may be perfectly normal, but more constantly shows extensive
derangement. In rare cases the ventricles also are transposed, and the
other vessels more or less irregular. In nearly all cases the foramen
ovale is found pervious to a greater or less extent, and generally the
ductus arteriosus is also open. The ventricular septum may be defective,
absent, or entire.
Two remarkable cases of anomaly in position of the large arterial
trunks have been placed on record by Professor Wardrop Griffith.
In one there was transposition of the thoracic and abdominal viscera
in addition to malformation of the heart and vessels. The child lived
about four and a half months, was cyanosed, and the signs of transposi-
tion were noted during life.
The necropsy revealed essentially two conditions : first, a transposi-
tion of the thoracic and abdominal viscera ; and, secondly, a series of
abnormalities in the vascular arrangements. The latter were as follows : —
The heart was transposed, its apex pointing to the right, and the systemic
auricle was on the left side, while the vestigial fold of Marshall was made
out on the right. The left auricle, which was remarkably displaced,
received above a left superior vena cava, and below another large vessel.
The right auricle was smaller than the left, and received the pulmonary
veins. The auricles opened into a common ventricle which constituted
by far the greater part of the heart, as seen from the front. Passing
from the left side of the base of this ventricle was the aorta ; while just
to the right of this was a very slight flattened elevation exactly in the
position where one would, making allowance for the transposition, have
expected to find the pulmonary artery. The cavity of the ventricle was
large and irregular, and imperfectly divided into two by a septum, which
started below and to the left of the apex, but was incomplete above.
The right ventricle formed the whole of the apex, but was much smaller
than the left. The aorta arose from the upper and left side of the left
ventricle, passed upwards, arched over the root of the right lung, and
then descended to the right of the vertebral column. The aorta was
the only vessel leading out of the ventricles, and the main stem of the
CONGENITAL MALFORMATION OF THE HEART 709
pulmonary artery was represented by a fibrous cord, closely adherent to
the aorta, which could be traced down to the flattened elevation of the
ventricle before mentioned. The two pulmonary arteries received their
blood-supply by a patent ductus arteriosus, and the lungs were further
supplied with blood by the greatly enlarged bronchial arteries. The
position of the left auricle was especially noteworthy in this case, having
been, as it were, dislocated behind the aorta and rudimentary pulmonary
artery. Professor Griffith remarks that it is difiicult to avoid the convic-
tion that it may, by pressure, have prevented the development of the
proximal part of the fifth right branchial arch, and thus led to an almost
total absence of the main stem of the pulmonary artery.
In another specimen, described by the same author, there was lateral
and antero-posterior transposition of the aorta and pulmonary artery.
The heart was somewhat enlarged, the ventricular part being especially
bulky. The two auricles were normal in most respects, but the foramen
ovale was widely patent— the deficiency being above and in front of the
valve, which was also defective at its upper and anterior part. On open-
ing the ventricular cavities they were found to communicate freely with
one another by a large aperture at the upper part of the septum, limited
below by a smooth crescentic-rounded margin. The posterior boimdary
of the opening was continued up as a thin fibrous membrane, and blended
with the upper part of the septal flap of the right auriculo-ventricular
valve, which it separated from the orifice of one of the vessels arising
from the ventricular cavity. There was thus an absence of the anterior
part of the septum which is developed from the aortic bulb septum, while
the posterior part, derived, according to His, from a septum medium, was
normally developed; the ventricles were not transposed. From the
upper and anterior part and from the right ventricle arose a vessel which
arched backwards over the root of the right lung, and was continued
down the back of the chest. It gave off the coronary arteries and vessels
to the head and upper extremities ; from behind this aorta arose another
vessel from' the ventricular cavity, which gave ofi' the branches to the
lungs and then joined the arch of the other large vessel \ a patent ductus
arteriosus also connected the two vessels. The second vessel, therefore,
appeared to have the mixed characters of the aorta and pulmonary
artery. The valves of this vessel formed a bicuspidate cone projecting
into the lumen.
An unusual form of transposition of the primary vessels was found in
a case by Dr. Hess. It was removed from a child eight hours old, who
died with coma and convulsions. The heart was quadrangular in shape,
the auricles were completely separated, and both auricles opened into the
left ventricle. The left ventricle was very large, and at the upper and
posterior part gave origin to the pulmonary artery. The right ventricle
was a small rudimentary cavity from which the aorta arose, and which
communicated with the 1-eft ventricle by a crescentic opening ten lines in
circumference; apparently the sinus and infundibular portion of the
right ventricle were divided by a septum, from the latter the aorta was
710 SYSTEM OF MEDICINE
given off, while the sinus was united with the left ventricle from which
the pulmonary artery arose.
Other forms of malposition are recorded, though far less frequently,
in which the two vessels arise from the left ventricle, while the right
ventricle is merely a rudimentary cavity, and has communication with
the left through an aperture in the septum.
Premature closure, or patency of the foetal passages. —
Premature closure of the foramen ovale. — This condition is extremely
rare ; there are only three cases recorded by Peacock ; in one the child
lived thirty hours, and was cyanosed, the right ventricle and pulmonary
artery were extraordinarily developed, and there was no trace of the
foramen ovale. In the other two cases, which were similar as to the
obliteration of the foran^en ovale, the right cavities were greatly enlarged,
but the left were on the other hand very small.
Patent foramen ovale. See Defects in the auricular septum, p. 699.
Premature closure of the ductus arteriosus. — The duct may be-
come abortive at different periods of foetal life, judging from the fact that
in some malformed hearts no remains of it can be found. In such cases
the pulmonary artery is usually narrow and ill-developed, owing to the
small quantity of blood which circulates to the lungs in foetal life. The
obliteration of the duct is probably due to imperfect development of that
portion of the branchial arch, and may be one of the causes of pulmonary
stenosis. Other deformities usually coexist or supervene as the result of
the premature closure of the duct.
Persistency of the ductus arteriosus is the result of failure of the
normal involution which usually takes place before the fourteenth day.
The vessel may be widely patent or funnel-shaped, and in the majority
•of cases the orifice of the pulmonary artery is stenosed or closed. The
Tight ventricle is hypertrophied, and the trunk of the pulmonary artery
may be dilated. In a few instances the duct has remained patent without
other anomalies.
Irregularities in the number and form of the valves. — Slight
defects in the semilunar valves are of comparative frequency and do not
cause any symptoms ; they may be due to malformation or to foetal endo-
carditis. The number may be reduced or increased.
Bicuspid semilunar valves. — This, the commonest form of anomaly, in
which there are only two segments, affects both the pulmonary artery
and the aorta. One segment is sometimes normal in size, the other,
frequently the larger, appears to be the result of the union of two seg-
ments, showing often an indication of the division between them ; or the
two may be of nearly equal size.
There may be only one curtain, with an indication of its division into
three segments ; it becomes stretched or protrudes in a funnel shape in
the course of the vessel. Rarely there are two large segments with a
small rudimentary one interposed.
CONGENITAL MALFORMATION OF THE HEART 711
The bicuspid form of valve has a great tendency to undergo sclerotic
change, and to result in regurgitation. In the aorta it has been noted
that the segments united are not infrequently those opposite the coronary
orifices. In many the result is due to malformation, but endocarditis
may account for some of those formed in later life, the partition between
the two segments having been destroyed. When the pulmonary valve
is anomalous there is usually found some other malformation, such as
septal defect.
Eedundancy in the number of segments more frequently affects the
pulmonary artery than the aorta. The chief forms are (i.) three of
. nearly equal size, with a smaller one interposed between two others ; (ii.)
four segments of nearly equal size ; and (iii.) three or four segments of
nearly equal size with one or two smaller curtains interposed, and imper-
fectly separated from those adjoining.
The valvular anomalies due to mal-development take place at the
time that the aortic bulb is transformed into aorta and pulmonary
artery. Where the number of segments is deficient there is probably
suppression of one of the endothelial cushions. On the other hand, when
there is redundancy of the segments one rudiment gives rise to two or
more segments. This most commonly happens in the case of the ex-
ternal rudiment, the last to appear.
The awiiculo - ventricular valves. — The segments of the tricuspid or
bicuspid valve are sometimes found united together in the form of a
membranous curtain with a central triangular or circular aperture. In
some the stenosis is no doubt due to fcetal endocarditis or malformation ;
in others it is very difficult to determine whether subsequent endocarditis of
sclerotic origin may not account for the greater part, if not all, of the result-
ing lesion. The two apertures may be affected in the same heart, and with
a history of long-standing cyanosis in a young person, and in the absence
of rheumatic attacks, it is almost certainly of congenital origin. The
united and malformed cusps are very liable to become the seat of
disease, and the stenosis is increased by chronic thickening of the united
valve segments, but vegetations are seldom found.
Anomalous septa. — The majority of cases in which supernumerary
cavities in the heart are described are really due to the existence of an
anomalous septum. This is most commonly found in the interior of the
right ventricle, and at a site where there is normally a strong muscular
band indicating the division between the sinus and the infundibular
portion of the right ventricle. In well-marked cases there is a distinct
resemblance to the right systemic and pulmonic ventricles of the turtle.
There is usually an aperture of communication between the middle
and right ventricles, but the right ventricle has no direct connection with
the auricle. Two cases are recorded, by Dr. Stephen Mackenzie, in which
there were, in addition to many other abnormalities, apparently three
ventricles ; he remarks that the infundibulum of the right ventricle was
shut off from the sinus by means of an imperfect, partly muscular septum,
712 SYSTEM OF MEDICINE
an exaggeration of the division of the muscular columns to ■which the
folds of the tricuspid valve are attached.
Septa or fibrous bands are more rarely found in the auricles. Dr.
EoUeston and Dr. Wardrop Grifiith record such anomalies occurring in
the left auricle. Dr. Fowler describes a similar instance, in which there
was a band attached to the septal wall and continuous with the membrane
forming the fossa ovalis. He regarded this band as an overgrowth of the
valve closing the foramen ovale which had become directed by the blood-
stream towards the outer wall of the auricle, and had become adherent
there.
The so-called moderator bands, which are occasionally found in the ,
interior of the ventricles, consist of muscular fibres surrounded by endo-
cardium. They not infrequently arise from the septum, and are attached
to the wall of the ventricle. In a case recorded by Sir William Turner
the inner surface of the ventricles was almost uniformly smooth.
General anomalies. — Some of these occur in monsters which are
still-born.
External misplacements. — Ectopia cordis. — Clefts of the thoracic wall
and fissure of the sternum may be present, so that the heart is covered
only by membrane and integument, and protrudes ; in other cases there
is no apparent defect of the thoracic wall. There is commonly some other
malformation present, such as protrusion of the abdominal viscera.
Three varieties are usually described : ectopia cervicalis, pectoralis, and
abdominalis. In the first the heart is placed in the neck, in close connec-
tion with the ramus of the jaw. In the second form there may or may
not be a fissure of the parietes of the chest. In the abdominal form the
organ lies below the diaphragm, and is sometimes protruded so as to
form a tumour externally. In one well-noted case the heart was found
to occupy the position of the right kidney, and the vessels arising from
it passed through the opening in the diaphragm into the thorax.
Internal misplacements. — JDextro-cardia. — Transposition of the heart
is generally associated with transposition of the viscera. A few cases
have been observed in which the transposition aifected the heart only.
Two hypotheses have been proposed for the explanation of this
anomaly. Dr. Frazer suggests that the transposition may be due to the
subject having been one of twins which were developed from a single
ovum, and in which dichotomy was complete. Von Baer has found that
in a few instances the embryo lies with its left side directed towards the
yolk, whereas the right side is normally in this position.
Meso-cardia. — The organ occupies a central position in the thorax
similar to that which obtained at the earlier periods of foetal life. It
usually presents anomalies in structure as well.
Bifid apex. — Occasionally there is an indication of a fissure at the
apex of the heart, following the course of the interventricular septum,
and more or less dividing the apex into two, giving a resemblance to the
heart of the dugong.
CONGENITAL MALFORMATION OF THE HEART 713
Defleieney of the pericardium. — Complete absence of the pericardium
is very rare except in association witli ectocardia, or other serious anomaly.
Partial defect is sometimes observed, and the only remnant of the peri-
cardium may be found in the form of a sickle-shaped fold attached to the
diaphragm which forms an incomplete sac for the heart. A specimen
was described by Dr. Bristowe, in which there was a rudiment of the
pericardium at the upper part and right side of the heart. In another
case, recorded by Dr. Boxall, the pericardial sac was incomplete, and
death was caused by dislocation of the heart during a severe attack of
vomiting.
Section II
CAUSATION
Synopsis. — Fcdal end/xarditis — Mal-development — Embryonic heart —
Mode of foTTnatioTh of septal defects — Stenosis and transposition.
The cause of the various forms of cardiac abnormality is an interfer-
ence with the normal processes of development at some particular stage
of embryonic life. Thus, an arrest of development may occur in which
the heart retains in great measure the rudimentary form of the stage at
which its growth is arrested ; or there may be some perversion or
irregularity in development at some part by which distortion is produced,
and which gives rise to secondary changes dependent on the primary
defect.
In some cases in which the malformation has occurred at a very early
date, as for instance where the heart consists of only two cavities, it may
be impossible to detect the primary deviation from the normal. In many,
however, where the heart has been more fully developed, it is often
possible to detect the primary defect, or, at any rate, to trace the
sequence of events by which the secondary changes have been induced.
Foetal endocarditis and mal-development or perversion of the processes of
development are responsible for most abnormalities.
An attack of rheumatic fever in the mother during pregnancy, or a
tendency to rheumatism in the parents, may be a cause of foetal endo-
carditis ; but in most instances no such history can be obtained. The
arrest of development has been attributed by some to maternal impressions
during pregnancy, but in many cases the date of the impression does not
coincide \vith the period of foetal Hfe at which the arrest must have taken
place.
FcBtal endoearditis has by some writers been credited with a large
share in the production of diiferent forms of cardiac malformation, and
probably to a far greater extent than is justified by the evidence.
The chief form of inflammation of the foetal endocardium is of the
sclerotic kind ; the warty form is of far less frequency, although it is
seen occasionally affecting the edges of the adherent and stenosed pul-
714 SYSTEM OF MEDICINE
monary or aortic valves. Minute projections may be found on the
auriculo- ventricular valves of newly-born children ; these have been
mistaken for vegetations. They consist of nodules of translucent or
firm connective tissue which usually disappear in the coui-se of time.
In others the edges of the valves, more often the mitral, are the seat of
hsematomata, caused by small spherical blood extravasations projecting
from the free edge of the valve, and probably due to the rupture of
intravalvular blood-vessels. They seem to arise either before or shortly
after birth, and very soon shrink away ; occasionally they are found in
connection with a stenosed valve. In the sclerotic form the cusps are
thickened and contracted, and the edges often united to those adjoining ;
the chordae tendinese become thickened, and the valvular orifice much
diminished in size. It is often impossible to tell whether the endo-
carditis is of foetal origin, or has at a later period become engrafted
upon an already deformed valve. According to Eauchfuss, foetal endo-
carditis is only more common on the right side of the heart when in
association with malformation, otherwise the left heart is as frequently
affected.
Pepversion of development. — Interruption to the normal course of
development is the cause of the greater number of cardiac malformations.
This is in great measure indicated by the nature of the defect, the early
period of foetal life at which the first deviation must have occurred, and
by other circumstances which tend to show that if any endocarditis is
present it has been engrafted upon an already deformed valve or orifice.
This view is strengthened by the observation that in a considerable num-
ber of instances developmental errors are present in other parts of the
body. Dr. Archibald Garrod has collected a series of eighteen such cases,
the associated abnormalities being of various kinds. In five of the
eighteen cases foetal endocarditis was clearly present, but in three of these
there were other abnormalities which were obviously not secondary to the
inflammation ; in two the associated defects were of a minor kind, and
fcetal endocarditis sufficed to explain aU the appearances. But even if mal-
formation be regarded as the primary cause, we still remain in ignorance
of the nature of the force which disturbs the natural process of evolution.
Before attempting to discuss the mode of formation of the various
specimens of malformation described in Section I., it wiU be necessary to
refer to the development of the embryonic heart. A full account would
be out of the scope of this article, and attention will only be drawn to
those events which help to elucidate the pathology of the malformed
specimens.
Development of heart.— The heart is originally developed out of
two lateral tubes of mesoblast, symmetrical and distinct, which coalesce,
soon after the thirteenth day, to form a single longitudinal tube, which is
slightly twisted upon itself. This single tube has double walls, the inner
endothelial, the outer mesoblastic or muscular ; it is continuous in front
with the two primitive aortae, and posteriorly with the veins. During
the third week slight constrictions become evident which mark off the
CONGENITAL MALFORMATION OF THE HEART 715
several divisions from one another. The anterior of these is the aortic
bulb, the middle thicker part is the ventricular portion, and the posterior
forms the auricular segment.
This tube then becomes bent upon itself in such a way that the
venous or auricular portion comes to lie partly dorsal to, and partly
behind the ventricular portion, the latter being continued forward as the
bulbus arteriosus. Between the primary undivided auricle and ventricle
a constriction occurs which elongates into a short flattened canal, the
auricular canal, which is bounded by two lips, an upper and a lower.
These lips become thickened by the formation of endocardial cushions
which grow across the canal in such a way as to divide it into two
passages, the right and left auriculo-ventrieular orifices.
The internal division of the heart into right and left sides is eifected
by three septa or partitions, which appear within the cavity of the heart,
and which arise perfectly independently of one another ; namely, the
interauricular septum, the interventricular septum, and the septum of the
truncus arteriosus.
The interauricular septum. — The division of the auricle precedes
that of the ventricles and of the bulb. The history of the process as
given by His, Lindes, and Born differs in some important respects.
According to Lindes and Born, when the auricles develop they expand
upwards, and a partition remains between them at the upper part, the
septum primum, or septum superius. This septum increases with the
continued growth of the auricles, and becomes thickened along its lower
edge, and finally separates the two auricles, except under its lower edge,
where the two cavities still communicate. This communication is not, as
has been previously maintained, the foramen ovale, inasmuch as the
septum continues to grow downwards to the auricular canal, and, by
uniting with the partition in the canal, closes permanently the primary
communication. According to Lindes, before the primary septum has
quite reached the roof of the ventricles, certain small apertures may be
noticed in it. These gradually increase in number, converting the
septum into a lattice-like membrane through which the blood streams
from right to left, causing the septum' to bulge to the left.
The parietal portion only of the septum remains imperforate, forming
a muscular frame which is especially well developed anteriorly. Finally,
there is one large aperture left in the septum at its apex and anterior
part, the true foramen ovale. A new septum also appears above the
foramen ovale and to the right of the insertion of the primary septum,
and its edge forms part of the boundary of the foramen ovale. In a
human embryo 25 mm. long, the auricular septum contains numerous
perforations, and in a fcetus of three or four months the septum appears
as a cribriform membrane supported on a muscular frame. During the
fourth month the foramen ovale becomes partially closed by a fold which
acts as a valve and allows the blood to pass from the right to the left
auricle, but prevents its passage in the reverse direction. The final
closure of the foramen ovale does not take place until some time after
7i6 SYSTEM OF MEDICINE
birth, and is one of the last events ; it is at first effected merely by the
close apposition of the valve which projects into the left auricle to the
margin of the aperture by the pressure of the increased quantity of blood
returning by the pulmonary veins ; at a later stage the edge of the valve
gradually coalesces with the margin of the opening, but the union often
remains incomplete for some months.
The ventricular septum and division of the truncus arteriosus. —
The ventricular cavity becomes partially divided towards the close of
the fourth week by a fold, the septum inferius, which rises from its
dorsal and posterior wall, and the position of which is indicated externally
by a slight groove on the surface of the heart.
The formation of the aortic septum is effected by two longitudinal
ridge-like thickenings of the endothelial lining which arise from opposite
sides at the junction of the fifth branchial arch ; these encroach on the
lumen, reducing it to a slit, dumb-bell in section, and then meet so as to
divide the lumen into two completely separate passages.
The septum appears first at the distal end of the truncus, and
gradually extends backwards towards the ventricles. The septum first
appears towards the end of the fourth week, and is well advanced before
the end of the fifth week ; it has a slightly spiral course, so that the two
tubes into which it divide? the truncus arteriosus are respectively dorsal
and ventral at the proximal end next to the ventricles, and right and
left at the distal end of the truncus. Of the two tubes the one which
lies dorsally at its proximal end and on the right side distally is the
systemic trunk, the other which is ventral proximally and on the left
side distally is the pulmonary trunk ; and the same relations are retained
throughout life by the ascending aorta and the root of the pulmonary
artery.
The tnmcvs arteriosus originally arises from the right-hand corner of
the ventricular cavity, and the two trunks into which it splits retain for
a time the same relations. In other words, at a time when the inter-
ventricular septum is already partially formed, both the systemic and
pulmonary trunks arise from the right ventricle, and the left ventricle
has for a time no outlet except through the right ventricle. The com-
pletion of the interventricular septum has to be effected in such a way
that while the pulmonary trunk is left in connection with the right
ventricle, the systemic trunk shall be cut off from this cavity and placed
in communication with the left ventricle. The formation of the inter-
ventricular septum is consequently somewhat complicated. The greater
part of the septum is formed from the septum inferius, but it is completed
above, partly by the endocardial cushion at the lower edge of the inter-
auricular septum, the septum intermedium of His, and partly by the
prolongation of the aortic septum, which divides the truncus arteriosus
into systemic and pulmonary trunks.
The aortic septum grows back beyond the truncus arteriosus, so as to
project a certain distance into the ventricular cavity ; it then fuses With
the free lower edge of the interauricular septum in such a way as to cut
CONGENITAL MALFORMATION OF THE HEART 717
off the systemic trunk from the right ventricle, and to place it in com-
munication with the left ventricle; while iinally the septum inferius
extends so as to meet and fuse with the interauricular septum, and so
completes the separation of the ventricles from each other.
Auricular septal defects. — From the study of the specimens of
defect of the auricular septum in connection with its development it will
be apparent that apertures may exist either at the foramen ovale or in
other parts of the septum. In the latter case, those which exist at the
lowest part of the septum are probably due chiefly to failure of union of
the primary membranous septum with the upper part of the ventricular
septum and with the partition in the auricular canal ; thus leaving a free
communication between the two auricles and between the latter and the
ventricles.
In some cases the septum may be entirely absent, the auricular
cavities remaining undivided. When the growth of the secondary septum
is defective there is frequently to be seen a lattice-like membrane between
the two auricles which imperfectly divides them, and is due to the persist-
ence of a portion of the provisional membranous septum which stretches
across the persistent muscular frame. If absent or largely defective it
may give rise to an aperture at the upper and front part of the auricular
septum ; and the completely formed foramen ovale, either closed or
patent, may be found below. In other cases the persistent membrane
becomes sacculated, and protrudes in a pouch-like form towards the
interior of the auricle.
Defects in the ventricular septum. — Normal arrangement of septa. —
The septum ventriculorum is divided into a posterior muscular septum, a
pars membranacea, and an anterior septum ; the latter being again
separated into a posterior and an anterior portion : the importance of
this division is well insisted upon by Eokitansky in his classification of
septal defects in the ventricle.
In the higher mammalia the normal arrangement of the septa in the
fully developed heart is as follows ; the cross-section of the ventricle is
that of a crescent, the pulmonary artery being at the anterior extremity
of the infundibular portion of the ventricle, while the posterior horn is
occupied by the auriculo-ventricular orifice above the sinus of the
ventricle. The internal wall is composed of two more or less distinct
parts. The anterior is formed of oblique bundles passing from above
downwards and slightly from behind forwards. These bundles arise
superiorly to the left of the pulmonary artery and pass to the superior
half of the anterior margin of the ventricle. They correspond to the false
septum of reptiles. Amongst the larger number of mammals the posterior
border of this septum forms a very evident projection, or else sends
obliquely a fleshy tongue or band to the external wall which accentuates
this distinction. This septum is interposed between the pulmonary
artery and aorta. The radiating fibres of the rest of the ventricle are
placed between the two auriculo-ventricular orifices and the two ventri-
cular cavities. The external wall is covered with fleshy columns arising
7i8 SYSTEM OF M£JJ/CJAE
from the pulmonary orifice, and running obliquely from before backwards
and downwards, which establish a limit between the general ventricular
cavity or sinus and the infundibulum. At the junction of these two
columns with the posterior border of the septum is occasionally seen
a white fibrous line or cicatrix. If this spot is perforated by a needle
the aorta is penetrated below the right sigmoid cusp.
It is supposed by Sabatier that this cicatrix is the vestige of an
orifice from the right ventricle, representing the opening from this
ventricle into the left aorta which is present in reptilia. This anterior
portion of the ventricular septum is muscular in structure, but immediately
posterior to this it will be found thinner and membranous in character ;
this pars membranacea septi or undefended space is more obvious in the
heart of an infant than in an adult. Along the upper line of this thinner
portion is attached the internal flap of the tricuspid valve. It corre-
sponds to the upper border of the middle portion of the interventricular
septum, and behind this again the septum is thicker and muscular in
structure.
Reference to the specimens of defect before described shows that
apertures in the posterior portion of the septum, in the pars membranacea,
or in the posterior part of the anterior septum, wiU place the two ven-
tricles in communication ; while a defect in the front portion of the
anterior septum will cause an aperture of communication between the twO'
arterial trunks. The latter defect is much rarer than the other kinds ;
the aperture is situated below and in front of the right aortic cusp, and
perforates the conus arteriosus just below the mouth of the pulmonary
artery, and involves the fleshy part of the septum. Rokitansky regards
this defect as due to failure in the complete union between the septum of
the bulb and the interventricular septum, which takes place at an early
period before the completion of the hinder part of the anterior septum.
In many cases where there is a defect at the pars membranacea or at
the hinder part of the posterior septum, or an aperture extending intO'
both of these regions, there is a primary defect in the development of the
arterial trunks, and the vessels are either misplaced or one of them is.
stenosed.
Frequently there is evidence of endocarditis surrounding the aperture,,
and the endocardium is roughened or thickened.
Cases are recorded in which the pars membranacea has been found
sacculated and bulging into the cavity of the ventricle, forming the
so-called aneurysms of the undefended space, and due in a few instances-
to congenital weakness at the spot. In some, no doubt, endocarditis has-
an important share in their formation, and they are due to disease in
after-life.
Stenosis or atresia of the pulmonary artery. — This deformity is
primarily due either to irregularity in the division of the common arterial
trunk or to foetal endocarditis.
When stenosis occurs at an early period of foetal life, towards the end
of the second month, or early in the third month, when the ventricular
CONGENITAL MALFORMATION OF THE HEART 719
septum is well developed but not closed, and the auricular septum is
forming, the right ventricle, unable effectually to discharge its contents
through the narrow pulmonary artery, becomes over-filled, but is able to
relieve itself by outilow over the still unclosed base of the interventri-
cular septum, a measure which is sufficient in itself to prevent the com-
plete closure of the septum. The right auricle in the same way, dis-
tended by the backward pressure, finds relief into the left auricle, and
thus the normal course of the circulation is materially impeded. When
the stenosis is considerable and interferes at a still earlier period with the
emptying of the right ventricle, the growing septum becomes pushed
over more and more to the left by the distension of the right side, and
so prevents the proper connection of the aorta with the left ventricle ;
and in addition a constant flow of blood is established from the right
ventricle into the aorta, so drawing the aortic orifice still farther to the
right, and producing a widening of this aperture and also of the ascending
trunk of this vessel. To such an extent may this displacement of the
aorta be carried that this vessel has origin entirely from the sinus of the
right ventricle, the left ventricle being left as a small supplementary sac
with a communication into the right ventricle. This is in the main the
explanation given by Dr. Hunter, and accepted by the late Dr. Peacock.
It is held by some authors that the same series of events might be pro-
duced by an irregularity in the division of the bulb, in which the septum
descended so as to form a wide aorta at the expense of the pulmonary
artery, the aorta being naturally situated farther to the right in the
earlier period of foetal life.
The hypertrophy of the right ventricle in these cases is the obvious
result of the large share it has to take in carrying on the systemic
circulation through the aorta. When the defect in the interventricular
septum is considerable, or the communication of the right ventricle with
the aorta very free, the septum of the auricles is more likely to be com-
plete than where the reverse obtains ; owing to the less degree of dis-
turbance of the circulation through the auricles.
In atresia or complete obliteration of the canal of the pulmonary
artery the obstruction is either due to adhesion of valve segments,
an impervious orifice, or obliteration of the trunk of the vessel as
far as the ductus arteriosus. The primary defect may occur in early
foetal life before the ventricular system is completed ; or later, when the
cavities have been separated. In the former case, as in stenosis, the
right ventricle retains its communication with the aortic orifice, and is
the main agent in carrying on the systemic circulation, while the left
ventricle remains small, and atrophies. When the obliteration of the
pulmonary artery occurs after the completion of the ventricular system,
the right ventricle becomes almost abolished and the right auriculo-
ventricular aperture diminished in size. The left ventricle, on the other
hand, becomes enlarged, and its walls much hypertrophied, as it has
to carry on both the systemic and pulmonary circulations.
In almost all these cases the blood is carried to the lungs by the
720 SYSTEM OF MEDICINE
pervious ductus arteriosus. The foramen ovale is occasionally closed
when the ventricular septum is imperfect, but is necessarily open when
this septum is complete. Of thirty-four cases collected by Dr. Peacock,
in eight only was the ventricular septum completed, and all these latter
died a few months after birth.
In aU cases of atresia of the pulmonary artery the possibility of the
circulation being carried on depends upon the open condition of either
the interventricular or the interauricular septum, and the patency of the
ductus arteriosus.
Atresia, like stenosis, is probably due to an abnormal division of the
bulbus arteriosus. Atresia occurs whenever the deviation of the septum
of the bulb from the normal arrangement is so considerable that the
septum whose convexity is directed towards the pulmonary artery
becomes actually applied to the waU of that vessel and fuses with it as
far down as its mouth.
Stenosis or atresia of the aorta. — When the constriction occurs
before the completion of the ventricular septum, the narrowing of the
aorta must occasion the blood to accumulate in excessive amount in
the right ventricle ; since both aorta and pulmonary artery communi-
cate originally with this cavity. This repletion of the right ventricle
must cause a corresponding repletion of the right auricle, and a dis-
tension and enlargement of the passage of communication between the
two auricles. If, however, development proceeded as far as closure of
the passage through the ventricular septum, and limitation of the aorta
on the side of the right ventricle, the condition of repletion would be
confined to the cavities of the left heart, and would occasion enlargement
in them also.
In atresia of the aorta the left ventricle becomes abortive and is
almost entirely thrown out of the circulation ; as happens in the case of
the right ventricle in atresia of the pulmonary artery.
Transposition or malposition of the aorta and pulmonary artery.
— The condition of the cardiac cavities associated with transposition may
be perfectly normal, but more commonly shows extensive derangement.
The explanation of these deformities must be foimd in connection
with an abnormal division of the bulbus arteriosus, and the development
of the complete septum between the arterial trunks.
The torsion of the axis which takes place during the first seven weeks
has a very important bearing ; for any departure from the normal, or a
failure in bringing the arterial bulb into due relation with the anterior
segment of the interventricular septum, is the direct agent in the causa-
tion of malposition or transposition of the great arterial trunks. It is
probably during the sixth, seventh, or eighth week that these abnormalities
first begin. The union of the forked septum which grows down the
arterial bulb from above with the upper and fore part of the inter-
ventricular septum determines the exact relation of the opening of the
two arterial trunks to one another, and the slightest deviation will
derange the relation. It should be observed also that the bulbus
CONGENITAL MALFORMATION OF THE HEART 721
arteriosus originally communicates with the right ventricle, that it
becomes divided into an anterior pulmonary artery and a posterior
aorta, at which stage both the large arterial vessels belong to the right
ventricle.
The left ventricle would be quite destitute of way of issue, did not
the ventricular septum remain permanently open as the aortic orifice.
At this period the left ventricle pours its blood into the right, whence
mixed blood is driven into both arterial trunks.
Section III
Symptoms and physical signs. — A child suffering from congenital
malformation of the heart is weakly, difficult to rear, and generally
presents at birth, or soon after, signs of derangement of the circulatory
system. Lividity, of a bluish-violet tint, affecting especially the face,
hands, feet, and the visible mucous membrane, is apparent.
The respiration is often laboured, and paroxysms of difficult breathing
may occur from time to time. These are apt to be exaggerated by
screaming, struggling, suckling, or exposure to cold air. The extremities
are cold and the terminal phalanges of the hands and feet may be clubbed.
From observations made by Farre and Peacock the bodily temperature
is not lower than normal, but Henoch and others record considerable
lowering of the surface temperature, although normal in the rectum.
Convulsions and cerebral seizures are frequent and often fatal. In a
case observed by myself the child was liable to attacks of prolonged un-
consciousness. These usually occurred once or twice in the week after a
meal, lasted for several hours, and recovery took place without any ill
effect ; the attack was accompanied by much increase of the cyanosis.
Paroxysms of dyspnoea and palpitation of a dangerous kind are
common, in which the breathing becomes rapid, gasping, and noisy, and
in which the cyanosis is greatly intensified. Convulsive seizures may be
induced, and the attack is often followed by severe exhaustion.
The onset of symptoms is variable ; these may be obvious from the
first, or there may be no evidence of anything wrong with the child until
a year or more after birth, when perhaps the onset of some accidental
affection unmasks the latent defect. The earliest and most definite
symptom is cyanosis.
Cyanosis. — This is present in about 90 per cent of these cases, hence
the origin of the name Morbus Ceeruleus.
The pathology of cyanosis in congenital heart disease has from early
times occasioned much discussion, and divers explanations have been
brought forward to account for it.
The hypotheses ordinarily adduced are those which attribute the con-
dition to intermixture of the arterial and venous blood, or to extensive
venous congestion. The former of these is amply negatived by the
observation that in many cases of single ventricle no cyanosis has been
VOL. V , % \_
722 SYSTEM OF MEDICINE
observed ; and that cyanosis may exist without any admixture of the
blood-currents.
The admixture hypothesis has been attributed to William Hunter by
Peacock and other writers. Reference, however, to Hunter's cases of
congenital malformation does not confirm this interpretation. He does
not even mention the admixture of the blood as the cause of the cyanosis ;
but after remarking on the small quantity of blood which reached the
lungs in two cases of pulmonary stenosis, he says that, as the carnation
tint of complexion depends on the florid colour of the blood, the dark or
gray complexion in these cases corresponds particularly with the observa-
tions of the latest philosophers that the blood takes its bright hue in the
lungs from respi'ration.
The venous congestion hypothesis, advanced by Morgagni, and ably
supported by StilM in America, has been most widely accepted, but
cannot be said to cover the whole field.
It is probable that there are- other factors which combine with venous
stasis to produce the peculiar discoloration. The possibility of suificient
aeration of the blood through the vessels going to the lungs must be taken
into account. Dr. Lees regards this as the essential cause of cyanosis, and
estimates that the amount of cyanosis is a direct measure of the extent to
which aeration of the blood has been hindered. It must also be noted
that it is mainly in cases where obstruction to the circulation has existed
before birth, or long before the full development of the circulatory
system, that the cyanosis occurs. The condition of the integuments will
materially affect the colour ; where the patient is emaciated and the skin
is thin the peculiar purple or black tint is frequently observed ; on the
other hand, when the body is well nourished, or the skin cedematous, the
colour is of a deep rose tint and less intense.
The blood. — More recently attention has been drawn to the condition
of the blood in cyanosis, and Dr. Gibson, in a most interesting paper,
discusses the various explanations of congenital cyanosis and draws atten-
tion to the remarkable concentration of the blood.
He describes the results of his examination of the blood in a case of
this affection : the hsemoglobin was 110 per cent, the red corpuscles were
8,470,000, the white 12,000. He offers in explanation of this concentra^
tion the suggestion that in venous stasis the corpuscles are insufficiently
oxygenated and their functions imperfectly performed, and that there is
less metabolism in the tissues and less waste ; consequently, in cyanosis
the wear and tear is reduced, and the duration of the individual existence
of the red cell is increased. The number must therefore be propor-
tionately augmented, causing a numerical increase and a high percentage
of hsemoglobin.
Toeniessen first observed the condition of the blood in a case of
congenital stenosis of the pulmonary artery ; the red cells were 7,540,000,
and in another case 8,820,000. He also noted this marked increase of
the red cells in all forms of cyanosis from failing circulation.
Baunholtzer, as the result of examination of the blood in a case of
CONGENITAL MALFORMATION OF THE HEART 723
pulmonary stenosis with cyanosis and clubbing, remarks upon the striking
concentration of the blood: the haemoglobin stood at 160 per cent, the
number of red cells at 9,447,000 against 5,000,000, the specific gravity
1071-8 instead of 1035-1068.
Dr. Lloyd Jones observes that in the newly-born child the specific
gravity of the blood is very high (about 1067); and he has made the same
observation in cases in which the foramen ovale had never closed, and in
which the foetal condition of the circulation remains.
The clubbing of the digits consists in a drum-stick enlargement of the
terminal phalanges of the fingers and toes, with often a claw -like
appearance of the nails. It is usually later in its appearance than the
cyanosis, but may be present when cyanosis is absent.
The two symptoms are allied, though possibly not produced under the
same conditions. Dr. Lees considers that clubbing is produced by the
venous congestion, and remarks that in cases where there was no clubbing
there was marked absence of venous congestion.
Cardiac signs. — The detection of cardiac malformation by the physical
examination of the heart is usually not difficult ; but a diagnosis of the
exact form of anomaly must in many cases be impossible.
In some it is possible to arrive at a fairly close decision as to the
existing conditions. On percussion the heart will usually be found
enlarged, with indications of hypertrophy and dilatation of the right
ventricle and auricle ; the impulse is powerful, displaced outwards and
visible over a large area, and there may be some prominence from yielding
of the parietes in the precordial region.
On auscultation there is commonly to be heard a loud, long, systolic
murmur, which can be traced with varying intensity over the whole of
the precordial region, over the back of the chest, and is conducted widely
in all directions. These may constitute all the cardiac physical signs,
and it would be impossible upon these to make an exact diagnosis,
inasmuch as they have been found in the most diverse forms of
anomaly. There are, however, in one class of cases certain signs which
enable us to predict, with a great measure of certainty, the most important
anomaly, namely, stenosis of the pulmonary artery. In many of these
there is to be felt on light palpation, at about the second left interspace, a
fine thrill, systolic in time ; it may be appreciable over a considerable
part of the precordial area, but is most marked at the upper part ; an
impulse can often be felt below the xiphoid cartilage ; on percussion the
dulness extends beyond the right border of the sternum ; on auscultation
a loud blowing murmur, systolic in time, is also present, and is to be
heard louder at the left base than elsewhere. The second sound may be
faint or accentuated, or accompanied by a diastolic murmur. With these
signs pulmonary stenosis is almost certainly present.
The character of the second sound at the pulmonary cartilage is some-
what variable. In many cases it is feeble and faint ; in a few cases which
have come under my observation it has been- loud and ringing. This
ringing sound has attracted the notice of other writers, but its significance
724 SYSTEM OF MEDICINE
has not been ascertained. Garrod reports two cases in which iMe
peculiarity of the second sound was observed, but there was no autopsy.
Peacock regards the accentuated sound at the base as produced by the
aortic valves, this vessel being often unusually large. On the other hand,
it has been suggested that this sign indicates obstruction at the conus
arteriosus. The sign is probably not distinctive of the particular seat of
obstruction, but it may be due to dilatation of the pulmonary artery
immediately distal to the stenosis and a patent ductus arteriosus.
When the pulmonary artery is dilated, with patency of the ductus
arteriosus, there may be great increase of cardiac dulness to the left and
upwards as high as the second rib; a loud rumbling systolic murmur
being audible over the pulmonary cartilage, and an accentuated second
sound. Compensation takes place with great readiness, and the right
ventricle accommodates itself to the lesion ; the possibility of hypertrophy
of this chamber at an early age appears to be very great and materially
influences the prognosis.
A precise diagnosis of imperfections in the septa is not possible. In
these cases a blowing systolic murmur is commonly to be heard over
the precordia, which in defects of the auricular septum may be more
marked at the base than the apex.
Congenital affections of the other valves will create murmurs referable
to the position of their orifices.
The diagnosis of transposition of the main vessels by cardiac physical
signs is impossible. Transposition of the viscera may exist in connection
with this anomaly, and may be recognised.
Differential diagnosis. — There may be difficulty in deciding in
some instances whether a cardiac murmur is of congenital or acquired
ori^n.
No certain rules can be laid down, but the physician will be guided
by the collateral signs, the past history of the patient, and the occurrence
of any illness which would be Hkely to have laid the foundation of any
cardiac disease. In the absence of any guidance from these records it
may be noted that the murmurs of the common forms of malformation
are systolic in time, that the miu'mur is not conducted in the manner
lasual in the acquired forms, and that it may have been observed in early
childhood. In the more severe forms there would be evidence of mudi
enlargement of the right ventricle, with probably some tendency to
clubbing of the fingers. In the slight forms there would be no evidence
of any secondary efiects, or of mechanical interference with the heart's
action.
Duration of life. — There is considerable difference in the age
attained in the various cases of cardiac malformaiion ; the majority of
those in whom there is any very serious defect do not survive birth more
than a few days.
In some the mechanical difficulty of the circulation makes it impossilde
CONGENITAL MALFORMATION OF THE HEART 725
for life to be carried on for any great lengtkof time; while in others with
a considerable degree of malformation the circuit through the heart and
great vessels is sufficiently free for life to be maintained for some years.
Many persons with a slight degree of malformation, such as a patent
foramen ovale, or a small aperture in the ventricular septum, have died at
an advanced age, and have never presented any cardiac symptoms.
The duration of life in pulmonary stenosis depends partly on the
degree of the obstruction, but more particularly on the condition of the
cardiac septa. The prognosis is more favourable when there is some
defect in the septum, as by this means relief is aflforded to the overcharged
right auricle and ventricle. In atresia of the pulmonary orifice life is
much more abbreviated, and wiU also depend mainly upon free communica-
tion between the two sides through imperfect septa. In a few cases the
patients have lived for some time when the lungs derived their supply
from vessels supplied by the aorta.
In transposition of the main vessel's the length of life is usually not
great, but in some instances the patients have survived to adult life or
even longer. An open condition of the septum, or patency of the ductus
arteriosus, is favourable for the prolongation of life. With complete
absence of the ventricular septum the majority die in infancy, but a few
have survived to adult age.
The cause of death in a large number of infants is due to mechanical
interference with the circulation. A considerable number die of convul-
sions, cerebral abscess, bronchitis, or pulmonary complaints. Those who
live to adult age are peculiarly prone to pulmonary tubercle, and probably
the great majority die from this complaint, or from cardiac failure.
Dropsy is comparatively rare. A septic endocarditis is occasionally
engrafted upon the malformed valves or stenosed orifice.
Treatment. — The treatment in congenital heart disease is mainly
hygienic. The surface of the body must be carefully protected against
cold, and a warm climate is desirable. Violent exertion or over-exercise
is apt to produce palpitation and shortness of breath, and should be
avoided.
A carefully regulated diet, especially in childhood and infancy, is of
importance. Special precautions should be taken to prevent the onset of
bronchial aifections and convulsions, which are the commonest causes of
death at an early age. The special liability to tuberculosis of those who
reach adult age must not be forgotten. The treatment of any complica-
tions must be directed to the relief of the more urgent symptoms, and
the remedies employed would be those which are applicable to similar
conditions ensuing in the course of other heart afiections.
The " Schott treatment " for the relief of the dilatation may perhaps
be of benefit in suitable cases.
Laurence Humphry.
726 SYSTEM OF MEDICINE
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Path. Trams, vol. i. ^. 51. — 37. Peacock. Malformation of the Human Heart. Second
edition, 1866. — 38. Idem. Path. Trans, sxxix. p. 43. — 39. Peacock's collection of
specimens of malformation of the heart in the Hunterian Museum. — 40. Rauchfuss.
Gerhardt's Handbuch der Kinderkrankheiten, Band iv. 1. — 41. Rokitanskt. Die
Defecte der Scheidewande des Herzens. Wien, 1875. — 42. Rolleston. Anat. Soe.
Proc. Feb. 1896. — 43. Romberg. Edin. Med. and Surg. Journal, vol. xlv. p. 149. —
44. Sabatier. &vdes sur le cmur. — 45. Shattock. Path. Trans. 1881. — 46. Still^.
"On Cyanosis," American Journal of Medicine, vol. viii. p. 25. — 46a. SuTEE.
Archi/ofur eayperimentelle Pathologic imd Pharmakologie, vol. xxxix. — 47. Tobnibssbn.
Ueber Blutkorperchenzdhlung bei gesunden und kranken Menschen (Erlangen, 1881). — •
48. TuENBE. Anat. Soe. Proc. Feb. 1893. — 49. Viechow. Ueb. die chlorose u. die
da-ndt verbundenen Anomal. am Gefdssapparaie. Berlin, 1872. — 50. Wagstaffb.
Path. Trans, vol. xix. p. 96. — 51. Wilson. Phil. Trans, vol. Ixxxviii. 1798, p. 346.
L. H.
DISEASES OF THE PERICAEDIUM
The normal pericakdium. — Before proceeding to discuss the morbid
changes of the pericardium, a few remarks must be made concerning
this structure in health. The pericardium is a fibro-serous sac, which
surrounds the heart and the origin of the great vessels. It is of a
somewhat conical shape, the base of the sac resting upon the diaphragm,
and being connected with it ; while its narrower portion is directed up-
wards. The external or fibrous layer is dense and unyielding; it is
attached very firmly to the central tendon of the diaphragm, more
loosely to its muscular structure, especially towards the left, by areolar
DISEASES OF THE PERICARDIUM 727
tissue. The fibrous layer is continued for some distance along the large
blood-vessels in the form of tubular prolongations, which become
gradually lost upon and incorporated with their coats. The inferior
vena cava passes through the floor of the pericardium to reach the
heart,' which is tethered to the sac by the attachment of the vessel to the
foramen quadratum in the central tendon of the diaphragm.
The serous membrane lines the fibrous sac, and is reflected over the
surface of the heart, thus constituting its parietal and visceral portions.
These portions are continuous along the great vessels, about an inch to
an inch and a half above the base of the heart ; the aorta and pulmonary
artery being enclosed in a common sheath, and a passage, named the
" transverse sinus of the pericardium," being formed between these vessels
and the auricles. The serous layer is also reflected on the superior vena
cava and pulmonary veins, and forms a deep recess behind, between the
entrance of the right and left veins into the left auricle. The inferior
vena cava has a very scanty covering. A triangular fold — the " vestigial
fold " of Marshall — formed by a duplicature of the serous layer enclosing
areolar tissue and fat, with vessels and nerves, passes between the left
pulmonary artery and the subjacent pulmonary veins. The pericardium
has an abundant supply of vessels, lymphatics, and nerves, the last being
derived from the phrenic, vagi, and sympathetic nerves.
Externally the pericardium is in contact anteriorly and laterally with
the pleurae covering the lungs ; except below and in front where it
approaches the surface in an angular space behind and to the left of the
sternum, a space which varies in extent and shape in different instances.
Under perfectly normal conditions the uncovered portion is somewhat
triangular in outline, with the base below ; it is bounded on the right
by a line along the middle of the sternum from between the fourth
cartilages, on the left by a line from the same point to the apex of
the heart. The pericardium is attached by fibrous bands to the manu-
brium and ensiform cartilage. Behind it is in relation with the contents
of the posterior mediastinum ; and the structures to be more especially
remembered on this aspect are the oesophagus, descending aorta, bifurca^
tion of the trachea and left bronchus, and the other structures which
form the root of the left lung. The phrenic nerves pass down, one on
each side of the pericardium, on their way to the diaplu^agm.
In health the contiguous surfaces of the pericardium are kept moist
by the usual secretion of serous membranes ; this never collects in such
quantity as to be capable of detection by physical examination during
life, though at post-mortem examinations more or less fluid is always
found in the sac, and it may amount to an ounce or two, or even more.
Part of this, however, and in some cases most of it, has certainly exuded
after death. The rubbing together of the surfaces during the cardiac
movements, on account of their smoothness and moistness, does not
give rise to any appreciable external sign.
The pericardium of an adult man with a healthy heart is capable of
holding from fourteen to twenty-two ounces of fluid; that of a boy between
728
SYSTEM OF MEDICINE
six and nine years old, about six ounces ■when the sac is distended to
the full by injecting water into it, by means of a syringe, through an
opening made in the anterior part of the pericardium (Sibson). The late
Dr. Begbie (10) gave the amount that could be injected in an adult as
r<r^rr.
Fig. 33.— Pericardium not distended.
(Sibson.)
FiO. 34. — Pericardium ari^ificially distended with
fifteen ounces of fluid. (Sibson.)
between twelve and eighteen ounces ; but he stated further that the peri-
cardium is distensible. The heart does not completely fill the sac, and is
capable of some degree of movement within it.
Morbid conditions of the pericardium. — The pericardium is
liable to certain very definite morbid changes ; but, before discussing the
more important of these, it will be convenient to refer briefly to
certain conditions of this sac, which, although morbid, are in the lafge
DISEASES OF THE PERICARDIUM 729
majority of instances more of pathological than of clinical interest or
consequence, being indeed usually only revealed when a necropsy is
made.
1. The pericardium in exceptional cases is the seat of more or less
extensive congenital defect. In some instances this is very slight, and of
no importance whatever ; but there may be a fissure or opening in the
sac of sufficient size to allow the heart to protrude through it, constituting
a form of ectopia cordis. Rarely the defect is so considerable that the
organ lies in the left pleural cavity, in contact with the lung, and
covered only with the serous visceral layer of the pericardium ; while the
parietal portion is represented by fringe-like reduplications at the origin
of the great vessels, or by " a kind of loose fold or pocket, which is found
on the right side or upper part of the heart." " The defect seems to
consist in the pericardium, which is apparently reflected from the
external coat of the aorta, not being prolonged so as to cover the front
of the heart and become attached to the diaphragm" (Peacock).
Although under ordinary circumstances this last condition cannot be
detected during life, it might certainly give rise to xmusual and em-
barrassing signs should inflammation and efiusion occur.
2. Diverticula or hernia-like pouches have been met with very rarely
in connection with the pericardium. They are the result of pressure from
within ; usually by chronic pericardial efiusion, exceptionally by blood.
The fibrous layer becomes thinned or yields at a spot, and the serous
lining protrudes as a sac, with a wider or narrower opening ; it is generally
of small size, but has been found sufiiciently large to contain three to four
ounces of fluid.
3. In the case of a greatly enlarged heart, where the pericardium is
otherwise unafi'ected and free from obvious disease, this structure will of
necessity become more or less stretched and distended in proportion to the
size of the organ, and it may become thinned in the process. I am not
aware that such a condition in itself gives rise to any discoverable
signs or injurious consequences, but the condition may be assumed under
such circumstances. An aneurysm of the heart walls, or of the intra-
pericardial portion of the aorta, would also tend to push out the sac
locally, and might even perforate it. Should pericardial efi'usion occur
under such conditions the signs might be unusual.
4. At post-mortem examinations certain white spots or patches (macules
albidce) are frequently observed associated with the pericardium, the
nature and origin of which have given rise to far more controversy than
their importance demands. They are also known as tendinous and milk-
spots {macula v. insulce tendinece v. lactece), and as " corns " or " callosities."
At one time they were thought not to be pathological, but certainly
they cannot be normal. The main discussion has turned on the
question whether these spots or patches are or are not the result of
inflammation. It cannot be doubted that the great majority of them are
not of acute inflammatory origin at any rate ; and the meanings attached
to "chronic inflammation" by different pathologists are so totally at
730 SYSTEM OF MEDICINE
variance, that it really does not matter whether we attribute them to such
a process or not. My strong personal opinion is that these changes are
almost always directly due to the constant mechanical attrition or irrita-
tion to which certain parts of the pericardium are subjected during
the cardiac movements. They are met with in progressive frequency
as age advances ; it has been aflBrmed, indeed, that they do not occur
in children at all ; this statement is incorrect, but they are extremely
rare in such subjects. They are decidedly more common in males than
females, as might be anticipated if this view of their causation be correct ;
and also in persons in whom, from their occupation, much friction between
the pericardial surfaces might be expected. Moreover, the white spots
are by far most frequently observed on the visceral pericardium, over
the portion of the front of the heart which, being uncovered by lung, comes
chiefly into contact with the inner surface of the chest wall, that is to say
the base or middle of the right ventricle ; and they are not uncommon at
the apex of the left ventricle. They do occur, however, on other parts of
the surface ; at the origin of the great vessels, as white stripes on the
auricles, and along the course of the coronary arteries. They are met
with very exceptionally on the parietal pericardium. Some of these
changes are similar to those which affect other serous membranes, and
cannot be very well explained ; others are no doubt the remnants
of a definite past pericarditis, when they present special characters, and
are occasionally accompanied by adhesions or their remains in the
form of filamentous fibrous bands : or there may have been a localised
and trifling "dry" inflammation, which has not been detected during
life.
Milk-spots are most common on large, hypertrophied and strongly
acting hearts, but they are by no means confined to organs of this descrip-
tion. In character and structure they are whitish and more or less
opaque, being in some cases of a dead white or pearly colour ; they are
generally circular in outline ; of varying size, being usually about half an
inch in diameter ; and, as a rule, cannot be detached from the serous
membrane, with which they seem to be intimately incorporated. Indeed
they then consist merely of a local fibroid thickening or sclerosis of this
structure, due to a hyperplasia of the connective tissue ; rather perhaps
to a condensation of fibres previously existing than to a development
and increase of new fibres. Occasionally patches are met with pre-
senting a smooth or granular surface, decidedly opaque, and of some
degree of thickness and firmness, which can be peeled. off from the under-,
lying membrane, with which they are more or less loosely connected.
Such patches are inflammatory in origin.
Clinically these conditions are generally regarded as of no con-
sequence. Certainly they do not give rise to any cardiac symptoms
whatever, and as a rule are not revealed during life by any signs. From
personal observation, however, I feel sure that some white spots or
patches on the pericardium are capable of originating a limited fric-
tion sound which, under certain circumstances, might be mistaken
DISEASES OF THE PERICARDIUM 731
by an inexperienced or careless investigator for an early sign of acute
pericarditis.
5. In rare instances what may be called foreign bodies, lying free in the
pericardial sac, have been found at necropsies. Some of them have been
soft and smooth, varying in size from a pea to a bean ; others firm, fibrous,
occasionally stratified, or calcified, either in a central nucleus or through-
out— the so-called cardiac calculi. These bodies have been regarded as
polypi detached from the inner surface of the pericardium ; or as results
of fibrinous or calcareous deposits about some foreign substance. They
have never been diagnosed during life.
6. It may be mentioned, lastly, that, as a consequence of prolonged
chronic pericarditis in extremely exceptional instances, the pericardium
becomes the seat of extensive calcareous deposit, which may actually con-
vert it into a complete calcified shell surrounding the heart; and the change
may even encroach upon the cardiac walls, constituting the so-called
"bony heart." Calcified spots or patches in connection with this sac
are not uncommon. Although these conditions might be suspected
under certain circumstances, it is very doubtful whether they can be
demonstrated clinically ; yet it has been affirmed that a calcified
pericardium may give rise to a peculiar percussion soimd of an osteal
quality.
Having thus disposed of changes of the pericardium which are almost
exclusively of pathological interest, I now proceed to deal with those
diseases which are clinically important; and, taking a comprehen-
sive survey, they may be indicated as follows : — I. Acute fibrinous and
sero-fibrinous pericarditis. II. Suppurative pericarditis — Pyopericar-
dium. III. Chronic pericarditis — Chronic eiiusion — Pericardial adhesions
and thickening. IV. Hydropericardium — Dropsy of the pericardium.
V. Hsemo- or hsematopericardium — Blood in the pericardium. VI. Pneumo-
pericardium and its effects — Gas in the pericardium. VII. New growths
and parasites.
The diseases just enumerated are attended with pathological effects
which give rise to well-recognised abnormal conditions, often of a
very pronounced character. These conditions not only affect the peri-
cardium and its contents, but also frequently influence neighbouring
structures; while in most cases they are revealed clinically by well-
marked and characteristic physical signs. It is very desirable at the
outset to have a definite general knowledge of their nature, and of the signs
to which they severally give rise. They may be comprehensively summed
up as — (i.) abnormal states of the pericardial surfaces ; (ii.) accumulations
of fluid in the pericardial sac ; (iii.) accumulations of gas, or of gas and
fluid together; (iv.) pericardial adhesions of various kinds; (v.) thickening
of the pericardium, usually associated with adhesions. It must be
remembered that these abnormal physical conditions may be variously
combined in particular cases. I now proceed to discuss the several
diseases of the pericardium enumerated in the previous paragraph, and
in the order there given.
732 SYSTEM OF MEDICINE
I. Acute fibeinous and seko-fibrinotjs pericarditis. Acute
INFLAMMATION OF THE PERICARDIUM.
Acute inflammation and its results constitute by far the most frequent
and important morbid conditions of the pericardium with which we have
to deal in medical practice ; and they often lead to serious consequences,
both immediate and remote. As an acute affection pericarditis varies
considerably in different cases, whether as regards its intensity and extent,
the rapidity of its progress, the nature and amount of its pathological pro-
ducts, or its terminations and ultimate effects ; but the complaint must
always be looked upon with concern. In some instances it may be
described as subacute rather than acute, but there is no line of demarca-
tion between the two classes.
Etiology and Pathologry. — In accordance with modern views of the
relation of micro-organisms to acute inflammatory diseases, it may be
assumed that particular agents of this nature are immediately concerned
in originating acute pericarditis. It will be more convenient and practical,
however, in the first instance, to point out the circumstances under which
this affection occurs, and afterwards to try to ascertain what is reaUy
known of its bacteriology.
It has been customary, from an etiological point of view, to divide
cases of acute pericarditis into primary or idiopathic, and secondary. The
former include those which cannot be referred to any of the recognised
causes of the disease, and in which it attacks an apparently healthy
subject. Under such circumstances the complaint has been usually
attributed to chill of some kind, but cases thus originating are probably
of a rheumatic nature. In some cases called idiopathic the patients were
drunkards, or were suffering from the effects of privation. In my own
experience I have never met with an instance of acute pericarditis which,
when carefully investigated, could not be included as a " secondary "
event in one or other of the etiological groups now to be discussed.
(a) Rheumatic pericarditis. — This is by far the most important variety,
and the number of cases coming under this head is very much larger
than that of all other cases put together. There are several features to
be noticed in this group, and in their discussion I propose to draw atten-
tion to some interesting and practical facts observed by the late Dr.
Sibson, whose article on " Pericarditis," in Reynolds' System of Medicine,
contains the outcome of extensive personal observations, with comments,
many of which are noticed or quoted in the following pages. The definite
connection between acute rheumatism and pericarditis has long been
recognised. The pericardial inflammation is not to be looked upon as a
mere complication, but is an essential part of the disease. The frequency
of the association has been very differently stated by different writers,
and doubtless it varies under different circumstances. In rheumatic cases
pericarditis is not nearly so common as endocarditis ; Sibson found the
DISEASES OF THE PERICARDIUM 733
latter fully three times as frequent in those which he observed. Further,
he noted that, in the large majority of cases of pericarditis, endocarditis
was present also. The late Dr. Sturges drew special attention to this
association in children, and he applied the names peri-endocarditis or carditis
to ' the combination, which he regarded as exclusively rheumatic. He
also laid down the proposition that " the rheumatic heart inflammation
of children when pericardial is always endocardial as well, and when
endocardial is extremely likely, with the recurrence of rheumatism, to
involve the pericardium also." My own experience is fully in accord
with the observations of these eminent physicians, and the eflfects of a
combination of pericarditis and endocarditis come before us in a con-
siderable proportion of the cases of ehronie heart disease which can bo
traced to one or more rheumatic attacks in early life.
It has been stated on high authority that pericarditis of any kind is a
rare disease in children ; and the complaint has been said to prevail most
frequently in middle life. More recent and accurate observations, how-
ever, have shown that such statements are quite contrary to fact. Sturges
pointed out that pericarditis is very common in children. He noted that
" out of 100 fatal cases .of heart disease occurring at the Children's Hospital,
Grreat Ormond Street, between June 1881 and April 1892, of which 54
were of rheumatic origin, and 46 due to other causes, in 6 only was there
no evidence of pericarditis." When introducing the discussion on Acute
Rheumatism at the meeting of the British Medical Association in
1895, Dr. Cheadle also spoke of pericarditis as less and less frequent
with the advent of puberty. Certainly, so far as my own experience
goes, while prepared to meet with rheumatic pericarditis at any age, it is
in children, growing boys and girls, and young adults, that I have found
it necessary to be more particularly on the look-out for the disease, and I
am convinced that this is a point of considerable practical importance.
[Vide art. "The Acute Rheumatism of Childhood," vol. iii. p. 44.]
Rheumatic pericarditis is decidedly more common in males than
females, but the exact difference cannot be stated. Sibsom found the
proportion to be 1 in 4 to 1 in 6 ; and he explained this difference in
part by the infliuence of age and occupation on acute rheumatism and its
complications. He observed that one-half of the males and more than
one-half of the females were below the age of 21 ; while two-fifths of the
male and only one-fifth of the female patients were above the age of
25. Servants formed fully two-thirds of the female patients affected with
pericarditis ; and three-fourths of the servants attacked with pericarditis
and endocarditis were below the age of 21. These facts Sibson explained
by the hard occupation 'Of patients of this class, in view of their time of
life and constitution, which exposes them to the causes of acute
rheumatism and its attendant inflammation of the heart. Those of
tender age who followed no occupation were not attacTsed with inflamma-
tion of the heart with anything like the same frequency as young female
servants. Women who at mature age followed occupations as laborious
as that of the young servants were aff'ected with pericarditis in but
734 SYSTEM OF MEDICINE
a moderate proportion, and in a comparatively mild form. He con-
cludes— " We thus see, in brief, that in acute rheumatism aflfecting the
female sex, youth with labour is nearly always attacked or threatened
with endocarditis or pericarditis, or both ; that youth without labour is
thus attacked with comparative infrequency ; and that mature age with
labour is attacked much less frequently and much less severely with
inflammation of the heart than youth with labour."
With regard to males Sibson observed the following facts : — Of
laborious workers out of doors attacked with pericarditis only I in 10
was below the age of 21 ; while of indoor workers thus affected fully
three-fourths were below that age. The scale was entirely reversed in
those of older age. Of those labouring out of doors four-fifths were
above 25 ; while of those working indoors only one-sixth were above
that age. Sibson writes : " We here, I consider, find the explanation of
the twofold fact, that the male cases of pericarditis usually combined
with endocarditis outnumber the female cases by one-fifth, and that the
number of the men so affected above the age of 25 is three times as large
as that of the women. I think we may infer that excessive labour in
men of mature age is a frequent cause of acute rheumatism having a
strong tendency to pericarditis." He further concludes that "in both
sexes the same causes produce, under like conditions, the same effects ;
and that a very large proportion of the young persons who work on foot
indoors during many hours daily are attacked with inflammation of the
heart when affected with acute rheumatism, while a very small proportion
are thus attacked of the men and women of mature age who are engaged
in the same manner."
The relation between the severity of the rheumatic condition, as
seen in the joints, and acute pericarditis must next be considered.
Sibson noted that in servants attacked with pericarditis the severity
of the joint affection in the great majority of cases bore a strict
relation to the severity of the heart affection. Taking all cases into
account, however, this rule is by no means true in a considerable
proportion of them, and it is highly important to remember that
pericarditis may set in and become very pronounced while the
articular complaint is comparatively or actually mild ; and it may even
occur alone, or come first of the rheumatic series. This statement applies
particularly to children, who are liable even to carditis of rheumatic
origin with little or no joint affection or pyrexia. Another observation
made by Sibson is that in about half the cases, when the pericardial effu-
sion is at its height, the joint affection tends to lessen in severity. The
number of articulations involved, and the implication of particular joints,
bear no relation to the frequency of pericarditis. The disputed question
whether it is more prone to occur during first or subsequent attacks of
acute rheumatism is not of much practical significance, though the general
experience is in favour of first attacks. The appearance of the affection
must be watched for during each attack, whether it has or has not
previously occurred, unless indeed it has left behind universal adhesion.
DISEASES OF THE PERICARDIUM 735
Sibson stated that previous rheumatic attacks favour the occurrence
of endocarditis much more than of pericarditis, and this is in
accordance with my own experience. As to the time at which acute
pericarditis supervenes in the course of a rheumatic attack, it seems to
appear in a certain proportion of cases — according to Sibson, about one-
eighth — at the very beginning, and to be coincident with the joint affection ;
or, as already stated, it may even precede such a manifestation. Not
uncommonly it appears between the third and the sixth day ; and, accord-
ing to Dr. George Balfour, most cases occur within the first week of the
rheumatic onset. In nearly one-half of Sibson's cases signs of pericarditis
were observed on or before the eleventh day of the illness. On the other
hand, the complaint may not be revealed for two or three weeks or more ;
and in seven out of sixty-three of Sibson's cases it showed itself between
the twenty-fifth and sixty-third day. Moreover, it may follow a relapse
of articular rheumatism, the pericardium having been quite free from any
affection during the primary attack. In the case of children pericarditis
may arise at any stage of the rheumatic series, but, according to Oheadle,
most often it comes late, in association with recurrent endocarditis, when
the heart is already hypertrophied and dilated {vide vol. iii. p. 38).
The opinion has been advanced that excessive action of the heart, set
up by the rheumatic condition, may help in the production of acute peri-
carditis. This was evidently Sibson's opinion concerning the relative
severity of the joint affection and that of pericarditis, for he writes :
" When the joint affection is severe, it may call forth excessive labour
or even tumultuous action of the heart. In acute rheumatism inflamma-
tion attacks the fibrous structures, especially if these structures are unduly
strained, and the increased action of the heart may therefore, I consider,
induce inflammation of the fibrous tissues of that organ, such inflamma-
tion being proportioned in severity to the augmented action of the heart."
Cold, damp, and changeable climate and season have necessarily a
marked influence upon the frequency of cases of rheumatic pericarditis.
(b) Renal pericarditis. — The association of acute pericarditis with
different varieties of Bright's disease cannot be doubted, but statistics seem
to show that the frequency of this form depends upon certain circumstances.
Sibson collected a large number of cases, from various sources, of renal
disease thus classified, and found that pericarditis occurred in 8-1 per
cent ; but it differed materially in frequency in different countries, the
proportion in Germany being 10-4, in France only 3, and in England 8-4
per cent. With regard to its relative frequency in the several varieties
of Bright's disease, it appears from Sibson's statistics to be uncommon in
connection with acute scarlatinal nephritis in young subjects, but frequent
in adults who suffer from acute Bright's disease, as well as during the
transitional stage to the large white kidney. When the latter has be-
come established, however, the tendency to general pericarditis disappears
almost entirely; yet it may occJur in a partial or circumscribed form.
In connection with the contracted granular kidney the complaint is far
more common ; and it is of average or moderate frequency in cases of
736 SYSTEM OF MEDICINE
lardaceous disease. It has also been stated to be especially associated
with fatty kidney. Dr. George Balfour regards acute pericarditis as
usually a late phenomenon in renal disease, and states that it is often a
precursor of fatal uraemia. Sibson believed that over-action of the heart
increases the tendency to pericarditis in Bright's disease, as -well as the
enlargement of the organ associated with the granular kidney. He also
affirmed that great enlargement tends to develop partial into general
pericarditis.
(c) Pericarditis from extension or irritation. — The occurrence of peri-
carditis as the result of extension of the inflammatory process from
neighbouring structures is an important fact ; and my observation
of cases in which the disease has thus originated has led me to
believe that they are more frequent than is generally known. In
most instances it follows pneumonia or pleurisy, more particularly when
the inflammation is on the left side. It spreads from the pleura to the
outer surface of the pericardium, and thence penetrates to the interior of
the sac, kindling a more or less pronounced pericarditis. Professor
Shattuck has recently called attention to the frequency of the association
of pericarditis with pneumonia. It must be noted, however, that in
some cases in which these combinations of acute inflammatory diseases
are met with in the chest, the pericardium was involved first, and from
it the inflammation spread to other structures ; or the whole of them may
be implicated so rapidly that it is difficult or impossible to determine
where the inflammation started. In exceptional instances the process
may extend, through the diaphragm, from the peritoneum to the peri-
cardium, without any direct communication between the two cavities. It
will suffice to mention that cases are now and then met with in which
pericardial inflammation is set up by some neighbouring cause of irritar
tion, apart from the inflammatory diseases just considered; such as abscess,
aneurysm, enlarged glands or tumours, or bone disease.
{d) Traumatic and perforative pericarditis. — These two forms may be
considered together. They are of very rare occurrence, and I cannot
speak of them from personal knowledge. The chief injuries from without
which may cause pericarditis are a blow or contusion over the precordial
region; fractured ribs; penetrating wounds by sharp instruments or gun-
shot wounds, and lesions produced by way of the oesophagus, especially by
foreign bodies, purposely or accidentally swallowed, which may actually
perforate the pericardium, or even gain access into its cavity, or, remaining
lodged in the gullet, may injure the adjacent pericardium: examples of
such bodies are false teeth, needles, or fish-bones. Perforative pericarditis
may result from the bursting of any neighbouring abscess into the sac,
whether associated with the bronchial glands, bone disease, or other like
conditions ; or, in very exceptional instances, a communication may be
established from an empyema, from a phthisical cavity, or from the
oesophagus if it be the seat of ulceration or new growth. Still more
rarely the contents of an abdominal abscess find their way through the
diaphragm into the pericardium ; and even a gastric ulcer has perforated
DISEASES OF THE PERICARDIUM 737
its -walls. In all these cases definitely irritating or septic materials of
different kinds gain access to the pericardial sac.
(«) Pericarditis secondary to cardiac or aortic disease. — A separate group
may be recognised of cases in which acute pericarditis is secondary
to some affection of the heart itself, or of the arch of the aorta. As
already pointed out, this affection and endocarditis frequently occur
together in rheumatic cases. It seems probable, moreover, that inflamma-
tion primarily involving the endocardium may traverse the myocardium,
so as ultimately to implicate the pericardium as well ; and this applies
particularly to infectious endocarditis. Myocarditis itself, especially
if ending in suppuration, may likewise originate pericarditis, quite
apart from the bursting of an abscess of the walls of the heart into the
sac. Among very rare causes may be mentioned cardiac aneurysm,
or intra-pericardial aortic aneurysm. With regard to chronic diseases
of the heart, pericarditis has now and then appeared in cases of val-
vular affection, chiefly aortic, especially when associated with cardiac
hypertrophy ; but the connection between these conditions is not very
clear, and it seems to me that on careful investigation of such cases
some more definite cause of the pericardial inflammation would probably
be found.
. (/) Pericarditis associated with neiv growths. — The chief kinds under
this head are malignant and tuberculous pericarditis. The former
class of growths may be situated in the heart, the pericardium, or both ;
and no practical distinction can be drawn between them. Tuberculous
pericarditis is probably more frequent than is usually supposed, and should
not be forgotten. When the inflammation is set up in chronic phthisis,
apart from the bursting of a vomica into the sac, it is essentially a slow
process ; but in acute tuberculosis or very active phthisis it may certainly
be acute. In very exceptional cases pericarditis seems to be the main
tuberculous manifestation, and it is then rather subacute in its onset and
mode of progress.
(g) Septic pericarditis. — This variety deserves separate recognition,
as it -m&j arise in all kinds of general septicaemia and pyaemia ; though
under such circumstances the pericardium is far less frequently affected
than the pleura. Septicaemia associated with puerperal conditions and
acute necrosis -of bone have to be especially remembered in this con-
nection.
(A) Pericarditis associated with miscellaneous general diseases and blood-
-It will suffice under this heading to draw attention to the
fact that in exceptional instances acute pericarditis occurs as a complica-
tion of some of the acute specific diseases, particularly scarlatina (most
commonly during the period of desquamation, when it has been attributed
to rheumatism or renal disease), measles, and small-pox ; rarely of enteric
fever, typhus, diphtheria, erysipelas, cholera, severe malarial fevers,
scurvy, purpura, and hsemophilia ; in these last conditions it is probably
secondary, in some cases at any rate, to pericardial haemorrhage : it may
occur exceptionally in the gouty state ; and in diabetes.
VOL. V ■ 3 b
738 SYSTEM OF MEDICINE
Baeteriology of acute pericarditis. — On a comprehensive survey
of the etiological groups just considered, the relations of micro-organisms
to the inflammatory process can in many instances be clearly recognised
on general grounds. Such organisms have also been frequently demon-
strated in the inflammatory products and in the pericardium itself. At
the same time it c^,nnot be said, so far as present researches go, that
they are in any way specifically related to the disease. The notion seems
to be gaining ground that the rheumatic process is due to a specific
bacillus, to the direct action of which the pericarditis would in this case
be attributable ; but I am informed on the highest authority that up to
the present time no such organism has been demonstrated. The
organisms usually found are those ordinarily associated with the inflam-
matory process, namely, difi'erent kinds of streptococci and staphylococci.
In cases following pneumonia the pneumococcus may be present,
and it has also been found independently. Tubercle bacilli have been
demonstrated in tuberculous pericarditis.
Morbid anatomy. — The changes which occur during the progress of
acute pericarditis are similar in their general nature to those which
characterise inflammation of other serous membranes. It is customary to
describe the disease as following successively the stages of — (i.) In-
creased vascularity ; (ii.) Fibrinous exudation ; (iii.) Fluid effusion ; (iv.)
Absorption ; and (v.) Adhesion. These stages, however, cannot always
be definitely recognised, and in many instances they run more or less con-
currently. Moreover, the pericardium itself is often involved in the
inflammatory process. It will be expedient, in the first place, to describe
individually the changes which take place during the progress of a pro-
nounced case of acute pericarditis ; and afterwards to point out the more
important aspects under which they are presented in practice.
(i.) Hyporsemia, or increased vascularity, no doubt constitutes the
earliest change in acute pericarditis. It involves the serous lining of the
sac and the subserous tissue, and is accompanied with more or less
parenchymatous swelling of the membrane. In its lesser degrees the
hypersemia is revealed by a fine network of vessels ; but in its more pro-
nounced form the surface is extensively and uniformly red, the redness
being either bright or dark. Sibson described the appearance as follows : —
" When the surface of the heart becomes inflamed, a blush of fine vessels,
consisting of a velvety network, appears on the surface of the organ, and
especially over the larger coronary vessels at the base and septum of the
ventricles. The inner surface of the pericardial sac, wherever it rests
upon the inflamed heart, kindles also into a blush of fine vessels. The
surfaces of the heart and sac, instead of being smooth and glistening,
become dull and velvety." Sometimes minute haemorrhages are observed,
especially around newly-formed vessels. The hyperaemic condition is of
short duration, it may last but a few hours, and then either subsides or is
concealed by exudation. As a matter of fact it is seldom seen at
necropsies, and usually only in pericarditis connected with Bright's disease.
It is said to be generally less marked in elderly and cachectic persons.
DISEASES OF THE PERICARDIUM 739
(ii.) The deposit of fibrinous exudation or inflammatory lymph is an
invariable accompaniment of acute pericarditis ; though its quantity,
extent, mode of arrangement, and exact characters vary much in different
cases. As a rule, it is observed both over the surface of the heart and
the interior of the pericardial sac. In some instances there are merely
a few shreds about the roots of the great vessels; in others a thin
film or coating forms at different spots, especially on the visceral surface ;
or a more or less thick and stratified layer covers both surfaces exten-
sively or universally, and is often very abundant. Owing to the in-
cessant movements of the heart the arrangement of the exudation is
often peculiar. It very rarely presents a smooth surface; and in the large
majority of cases it exhibits an alveolar, reticular, or honeycomb pattern.
Sibson thus well describes the appearance : — " Where the two surfaces
touch each other, the soft lymph is drawn into threads and little pointed
ridges and prominences, and wrought into a network, so that when ridges
and prominences are present on the heart, ridges or prominences are
present on the inner surface of the pouch lying upon it, and when a
network of lymph covers the heart, a network of lymph lines the corre-
sponding sac. The constant play of expansion and contraction of the
heart alternately stretches and relaxes its coating of lymph, so that its
surface resembles a honeycomb in structure." Laennec's well-known
and oft -quoted comparison likens the appearance to that presented
on suddenly separating two smooth pieces of wood between which a
small pat of butter has been forcibly compressed. It has also been
called the " bread-and-butter like " appearance ; or it has been likened to
tripe. It must be noted, however, that the lymph does not always
present this kind of arrangement; it may exhibit a shaggy or villous
surface, or peculiar characters, to which such names as cw hirsutwm,
cor tomentomm, etc., have been applied. When abundant, it is said to
accumulate in large masses in the auriculo-ventricular groove and about
the auricles. Should there be much lymph associated with fluid its
surface is covered with floating shaggy processes, which sometimes have
a mammiUated aspect. Occasionally fibrinous papillae or bands pass
across between the opposing surfaces of the pericardium, and these may
even form partitions.
The lymph exuded in pericarditis is usually of a whitish yellow,
yellowish, or reddish colour ; but it may be brownish. In a very short
time a fine network of vessels is developed in its substance, and not un-
commonly spots of haemorrhage are present, or the whole exudation may
be deeply stained. In connection with purpura, scurvy, and allied blood
diseases alternating layers of blood and lymph are now and then observed.
In consistence the material is, as a rule, somewhat firm and elastic, but it
may present different degrees of softness down to that of an almost liquid
jelly. Not infrequently it is mixed with serous fluid. In exceptional
instances of a low type it has been described as granular, crumbling) or
boggy. At first the exudation can be readily separated and peeled' off
from the surface of the membrane, but after a while it becomes more
740
SYSTEM OP MEDICINE
adherent and difficult to detach. In structure it consists of coagulated
fibrin and cell elements, the latter chiefly occupying the deeper layers.
When the material is very soft the cells are in great abundance, and
at the same time molecular disintegration has taken place. Micro-
organisms of different kinds may be found in the exudation.
(iii.) There can be no doubt that in not a few cases of acute peri-
carditis there is little or no fluid effusion ; a form of " dry pericarditis "
being met with, which can be recognised clinically. In such cases very
rapid adhesion may take place between the visceral and parietal surfaces,
even over an extensive area ; the
lymph being thick, sticky, gelatinous;
and specially agglutinative. Sturges
drew particular attention to this course
of events in children. Occasionally a
kind of network of fibrinous strings
passes between the adjacent surfaces,
the meshes of which are filled with
serum. As a rule, however, during
the progress of an attack of acute peri-
carditis, where there are no adhesions,
an effusion of fluid takes place into the
pericardial sac, separating its parietal
and visceral layers. Effusion may in-
deed supervene after the formation of
early soft adhesions, sometimes limited
to one side ; or when the sac is partially
filled with • heavy gelatinous masses of
lymph. The average quantity of fluid
is from 8 to 12 ounces, but it may
range from an ounce or two to two
or three pints or more — Balfour says
"several pints." The amount of fluid
effusion is by no means in proportion
to that of the fibrinous exudation, and
the result of the inflammatory pro-
FiG. 36.-oase of periot^rditis in which sac cess may chiefly be evidenced by either
contained sj lbs. ot flnid. Patient under one or the Other. It is in rheumatic
care of Sir James Anderson. (Sibson.) . t . , • , i , i . .
pericarditis that large accumulations
usually occur, and the effusion then generally collects and increases rapidly,
often reaching its acme in two, three, or four days (Sibson). In opposition
to this statement Dr. John Broadbent affirms that " it is the exception
rather than the rule to find effusion of any extent in cases of pericarditis of
rheumatic origin." Dr. Church seems to be of the same opinion \yide
"Acute Rheumatism," vol. iii. p. 16]; and Dr. Cheadle states that in
children the effusion, though fluctuating in amount, is never very large,
and is usually reabsorbed quickly. In my experience, cases of rheumatic
pericarditis have differed very much in the quantity of effusion. In
DISEASES OF THE I^ERICARDIUM 741
Bright's disease the quantity is often very small. Abundant effusion is
likely to be met with in scorbutic cases, and in these as much as five
pints has been recorded.
The effusion in acute pericarditis is generally of a serous or sero-
fibrinous character, and yellowish or greenish in colour ; it is most
commonly bright, clear, and transparent ; but may present small
fibrinous particles or flakes in suspension, or be opalescent, or even more
or less cloudy and opaque. Occasionally it is brownish or reddish.
The spepific gravity averages about 1018. Under certain circumstances,
as when pericarditis is associated' with purpura or scurvy, the effusion
is obviously mixed with more or less blood or its colouring matter —
" hsemorrhagic pericarditis." The cases in which the inflammation leads
to the formation of pus will be separately discussed ■ and it will suflSce
to state further that in very rare instances — of which there is an obvious
explanation in the presence of some general septicsemic condition, the
effects of neighbouring gangrene or malignant disease, or the entrance
of air containing septic micro-organisms into the" sac — its contents
undergo a putrefactive change, and become " ichorous," foul in appearance
and odour, or actually stinking.
It will be convenient in the present connection to discuss briefly from
a general point of view the immediate effects of pericardial effusion upon
the sac itself and its contents, as well as upon neighbouring structures,
effects which are met with by far most frequently in cases of acute
pericarditis ; and at the same time to point out the changes which the
inflammatory process is apt to set up in the pericardium and heart,
aTid which tend more or less to influence and modify these effects.
Obviously they must vary considerably in nature and degree, according
to the amount of the fluid accumulation, and the rapidity of its collection.
The fact must be acknowledged that a certain quantity of effusion is some-
times found in the pericardium at the autopsy, it may be as much as 6
or 8 ounces, which had not given rise to any evident disturbance, and
was not detected during life. In all such cases, however, which have
come under my personal observation, there has been every reason to
believe that the effusion had taken place shortly before death, from
obvious causes, and usually under circumstances rendering adequate
physical examination impracticable ; and no doubt it is often increased
by transudation of serum from the vessels after death.
Beginning with the pericardium itself, when a collection of fluid
exceeds a certain quantity the sac necessarily becomes more and more
distended, in proportion to its amount, and at the same time stretched
and thinned, so far as the normally tough and firm parietal pericardium
will permit. When acute pericarditis has lasted for some time, however,
and the structures forming the walls of the sac itself are involved in the
inflammatory process, they become more or less swollen, thickened, soft,
and yielding ; so that the pericardium becomes capable of far greater
distension than in its natural state. As the fluid accumulates in in-
creasing quantity the sac undergoes changes in form, which have been
742 SYSTEM OF MEDICINE
well described and figured by Sibson. When artificially distended with
15 ounces of fluid, he noted that the pericardium became pyramidal or
pear-shaped, and in more detailed description he writes : " It is formed,
so to speak, of a larger and a smaller sphere, the smaller one resting on
the top of the larger. The larger and lower sphere contains the heart,
the ascending vena cava, and the pulmonary veins ; and the smaller
sphere holds the great vessels. The distended sac occupies the whole
centre of the chest, filling up the space between the sternum in front and
the spinal column behind, and extending across the chest from a little
within the right nipple to a little beyond the left nipple. The whole sac
is lengthened ; its smaller end reaches upwards almost to the top of the
sternum ; and its floor, being formed by the central tendon of the
diaphragm, presents a large spherical prominence that bulges downwards
into the abdomen, occupies the epigastrium, and reaches as low as the tip
of the ensiform cartilage and the lower edge of the sixth costal cartilage."
This description will apply to the shape which the pericardium usually
assumes when distended with fluid from pathological causes ; but when,
owing to inflammatory changes in the walls previously referred to, they
give way further, the form alters considerably. "As the sac cannot
expand to a material degree either upwards towards the neck, or down-
wards towards the abdomen, it yields sideways and backwards, and widens
to the right and especially to the left " (Sibson). Under these circum-
stances, in short, its width becomes decidedly disproportionate to its
height, and it loses its pyramidal outline, becoming in extreme cases
almost globular.
The secondary changes of the heart and great vessels which may
supervene in acute pericarditis, as well as the efiects of a considerable
effusion of any kind on these structures, must be discussed in some detail ;
and in individual cases they should always be borne in mind, and carefully
studied from a clinical point of view. On these matters there are important
differences of opinion, and they have given rise to much controversy.
There can be no doubt that inflammatory changes beginning in
the pericardium are apt to extend to the muscular tissue of the heart
itself, and this tissue may also undergo an acute degenerative change.
These lesions are, speaking generally, proportionate to the intensity and
duration of the pericarditis ; but they are most frequently met with in
the hsemorrhagic and purulent varieties. They are naturally more
pronounced in the superficial layers, but may grad.ually extend through-
out the entire thickness of the walls. The degenerative changes some-
times attain a high degree, even in wholly acute cases. Whether
the inflammatory process may extend from the pericardium through
the cardiac walls to the endocardium is difficult to determine positively,
but I think it is highly probable. The changes in the heart tissues
have been attributed, not only to extension of the inflammation, but
also to persistent high bodily temperature, and to the circulation of
toxins in the blood. Degeneration has, moreover, been supposed to
result from the inflammatory products pressing upon the coronary
DISEASES OF THE PERICARDIUM 743
arteries, and thus impeding the normal distribution of blood to the
cardiac walls. Pericardial effusion, however abundant, has no direct
influence upon the structure of the muscular tissue of the heart. It
must be noted that the nerves distributed to the surface of the heart
and great vessels may be involved in the inflammatory process.
Dr. John Broadbent maintains that considerable dilatation of the
heart, especially of the right ventricle, occurs during pericarditis ; and he
has brought forward cases to prove that the physical signs usually
attributed to pericardial effusion are really due to this condition. That
such a dilatation does take place in some instances is indisputable,
especially when extensive adhesions have rapidly formed ; but my
experience is certainly opposed to the supposition that it is usually an
immediate result of pericarditis, or that it is apt under these circumstances
to be mistaken for effusion.
What is the mode in which the fluid collects, and what position does
the heart assume within the sac ? These questions have been the subject
of special controversy ; and although , to some writers they present no
difficulty, and are unhesitatingly answered in a particular way, without
reserve, I must confess that in my own clinical experience of individual
instances I have not always found them easy of solution. It wiU
be convenient at the outset to explain Sibson's later views on this subject,
and some of his remarks deserve to be quoted at length. Describing the
mode in which fluid collects in the pericardium, he writes : " At first it
falls into the back part of the sac, but as it increases in quantity it makes a
space for itself between the floor of the pericardium, which it depresses,
and the lower surface of the heart, which it elevates ; . . . and the result
of this is to displace the apex and body of the organ and its great arteries
upwards and forwards." He adds : " The heart, elevated by the fluid
between the under surface of the ventricles and the base of the pericardium
to a degree proportioned to the amount of the fluid, leaves the broader part
of the chest below, and ascends into the narrower part of the chest above."
In another place he writes : " The distension of the pericardium with
fluid produces two other effects on the heart, (a) The heart is heavier
than the fluid in which it plays, and its ventricles consequently tend to
sink backwards so that the left ventricle rests upon the posterior wall of
the pericardium. (J) The other effect of pericardial distension on the
heart is the lifting or tilting upwards of the organ within the sac. The
heart is attached by its great vessels to the posterior and upper part of
the sac, and the whole organ therefore tends to shrink upwards and
gravitate backwards towards its points of attachment." Sibson concluded
that the natural effect of this gravitation, shrinking, and upward displace-
ment of the heart, owing to great accumulation of fluid in the sac, if not
modified by other agencies, would be to cause the interposition of a
layer of fluid between the front of the heart and the anterior waU of the
chest. He affirmed, however, that in practice this is not usually the case
over the mass of the ventricles, though a layer of fluid covers the lower
part of the right ventricle.
744 SYSTEM OF MEDICINE
The displacement of the apex of the heart upwards and outwards in
cases of pericardial effusion was formerly taught as an indisputable fact.
By most authors at the present day, however, though not by all, this
doctrine is regarded as a mistake. The general opinion is that the fluid
collects towards the front, and that the heart, being heavier than the
fluid, falls or sinks backwards, away from the anterior thoracic wall ; the
ventricles, right auricle, and gi'eat vessels being successively covered
from below upwards, and thus separated from the parietal pericardium.
Some writers have maintained that an effusion first collects about the
base, which is turned downwards, the heart lying rather more horizontal
than normal, and the apex turned outwards ; but this part is described as
descending when the diaphragm is pushed down by the effusion.
Another opinion is that the position of the heart is not altered.
This is the opinion of Dr. William Ewart (19), who affirms that the
apex will be found in the usual situation at any necropsy on a case of
uncomplicated pericardial effusion ; and that whilst the heart has pre-
served its normal situation the floor and the sides of the pericardium have
receded from it. Dr. Ewart regards the impossibility of any elevation
of the apex as almost self-evident. He writes : " Slight mechanical dis-
placement might conceivably be brought about by one circumstance only
— the lifting by the distended pericardial sac of the tracheal bifurcation
and of the bronchi, and with them of the pulmonary veins and of the
, heart. Practically this rise is very inconsiderable, and moreover it does
not directly influence the ventricle. On the other hand, we must
remember that the heart is tethered to the bottom of the pericardium by
the attachment of the inferior vena cava to the foramen quadratum in the
€entral tendon, and that the considerable descent of the diaphragm must
depress the level of the right auricle and tend to depress the apex, far
from allowing it to rise. I have in some cases detected a lowering of the
heart's apex in pericardial effusion, and with it a more median position of
the heart, which then tends to hang more vertically from the aortic arch,
the latter becoming slightly straightened."
The late Dr. Sturges, in summing up the opinions just discussed,
expressed his belief that " though apparently conflicting, they are in fact
reconcilable. They all express the truth in various circumstances. The
heart may be moved either forwards, upwards, or backwards in effusion ;
or it may remain where it was ; and of the factors that determine its
conduct, pericardial adhesion, here or there, temporary or permanent, is
the chief." He further stated : " I have repeatedly in fatal cases of
pericardial effusion inserted needles, just before the post-mortem examina-
tion, into the proper apex place, and above the fifth right costal cartilage,
close to the sternum, without being able to detect upon opening the chest
any dislocation of the heart. The validity of such experiments may be
questioned ; but there are clinical facts to show that the early pushing
forward of the heart, . . . although it may be the rule, is not without
exception. The fluid may cover the heart from the first." It appears to
me that Dr. Sturges' observations are rational and practical ; and in
DISEASES OF THE PERICARDIUM MS
dealing with particular cases it is well not to bave too fixed or positive an
opinion as to the position of the heart in pericardial effusion. Should
the sac be quite free, there can be no doubt that in very abundant
effusions the organ is covered by the fluid ; ,and this is evident at
necropsies under such circumstances, the body being in the usual
recumbent position.
The next question is what eifects, if any, are produced by pericardial
effusion upon the walls of the heart and great vessels, when it becomes
so considerable as to interfere directly with these structures ? Sibson
writes on this point : " The muscular walls of the ventricles are so
thick, and their action is so powerful, that the direct effects of the fluid
pressure upon them cannot be very great. But the pressure of the fluid
tells inwards upon the weak and unresisting walls of the auricles, the
vena cava descendens within the pericardium, and the pulmonary veins,
so as to compress and lessen the cubic contents of those vessels and the
auricles, and to resist and impede the currents of blood, on the one hand
from the system along the cava, and on the other from the lungs along
the pulmonary veins. This partial blocking of the double stream from
the system and the lungs to the heart lessens the contents of the organ,
and tends to diminish the size of its cavities. At the same time the
supply of blood to the aorta is lessened, and the ascending aorta is
therefore also compressed by the fluid. The pulmonary artery, however,
owing to the obstacle to the flow of blood through the lungs, tends to
resist the pressure of the fluid in the swollen sac, and to remain dis-
tended." This seems to be a correct description of the case of large
effusions. Sibson, however, was further of opinion that in cases of
pericarditis the compressing influence of pericardial effusion is counteracted
by the protecting and sustaining covering of lymph, which to some extent
shields the weaker parts of the heart, and strengthens the naturally feeble
walls of the auricles and veins.
As regards the effects of pericardial effusion upon the action of
the heart, it is believed that the systole of the auricles and ventricles
is not restrained by such a collection; indeed, according to Traube,
the systolic motion of the organ is greater than normal, the fluid
being less resistant than the pericardium. The compression of the walls
akeady referred to may, however, interfere with the diastolic distension,
and thus diminish the flow of blood into the cavities, especially into the
auricles. The direct interference with the entrance of the blood from
the veins into the auricles, and impairment of the normal elastic traction
of the lungs upon the walls of the heart, add to this difficulty.
It will be obvious that distension of the pericardium with fluid
must interfere with neighbouring structures in proportion to its
amount, and such consequences are chiefly seen in the respiratory
apparatus. Some observers maintain that the portions of the lungs
in front of the sac are pressed at first against the inner surface of the
anterior wall of the chest. The ordinary effects of pericardial effusion
upon these organs are complex. It necessarily embarrasses them more or
746 SYSTEM OF MEDICINE
less, and large collections of fluid also press upon the bifurcation of the
trachea and the bronchi, especially the left bronchus. Hence it is found
in many cases that the upper lobes of the lungs, particularly the right,
are abnormally distended with air, or in a state of inflation, and in time
become the seat of catarrh also ; while other portions are collapsed in
various degrees. As the effusion increases, and attains an excessive
amount, it pushes these structures to either side and backwards, at the
same time compressing them more and more, the left lung especially, which
in extreme cases may become almost or even completely collapsed and air-
less. In some instances rapid and repeated serous effusion has taken place
into one or both pleurae in connection with great pericardial distension.
Ewart states that pleuritic effusion is among the most common complica-
tions of severe pericardial effusion ; that it frequently begins in the right
pleura, but not uncommonly occurs ultimately on both sides ; but that its
occurrence belongs to the later rather than to the earlier stages. This
condition is regarded as of mechanical origin, being attributed to pressure
on the vessels in the roots of the lungs.
A very abundant pericardial effusion may press upon the oesophagus
and descending aorta sufficiently to interfere with their channels.
Whether the phrenic or other nerves within the thorax may be affected
by the mere physical consequences of such an accumulation it is difficult
to say ; but some observers are of opinion that this may be the case, and
it is highly probable, especially if the effusion be rapid.
A considerable pericardial effusion will tend to cause more or less
protrusion of the corresponding portion of the thoracic walls, particularly
in young subjects. When these walls have become rigid no such pro-
trusion can take place. In a downward direction the diaphragm is not
only emba:i'rassed, but often considerably depressed, as well as the con-
tiguous viscera, as chiefly evidenced by the liver.
(iv.) The course of events and the ultimate pathological results in acute
pericarditis differ much in different cases. The natural tendency is for
any serous or sero-fibrinous effusion to become absorbed sooner or later ;
sometimes very rapidly. According to Sibson's observations in rheumatic
pericarditis the fluid after reaching its acme soon begins to lessen, and
in from four to six days usually falls to the normal amount. There is
every reason to believe, moreover, that even fibrinous exudation, up to a
certain amount, can be absorbed completely, after undergoing a molecular
fatty change ; a little pericardial thickening or opacity at the most being
left behind. The probability of such absorption is in inverse ratio to the
extent and thickness of the lymph deposited, and to the duration of
the inflammation. In respect of the " white spots " on the pericardium,
it may be well to note again that fibrous patches resulting from pericarditis
are usually distinguished by greater thickness and extent, irregular dis-
tribution, and special characters ; and as a rule by the coexistence of
adhesions. Very rarely irregular knob-like projections or pedunculated
outgrowths are formed, and the latter may even become detached, and
lie loose in the pericardial sac.
DISEASES OF THE PERICARDIUM 747
(v.) In most cases, after absorption of the fluid, or where only lymph
has been exuded, adhesions of various kinds and degrees are formed. At
first these are soft and easily broken down, and on account of the move-
ments of the heart firm and permanent adhesions are much less easily
established than in other serous membranes. Loose adhesions of con-
nective tissue are probably torn by the repeated pulling and stretching ;
and it is believed that the cardiac action considerably interferes with the
circulation in the newly-formed vessels. On this question Sibson writes :
" In most instances slight threads of adhesion form between the sac and
portions of the right auricle, and often also between the sac and the apex
and interventricular septum, that being the portion of the front of the
heart that presents the least movement during the action of the ventricles.
These soft threads of adhesion are generally drawn out by the oscillating
movements of the heart, until they at length yield and break away, but
sometimes permanent adhesions form which may be partial or universal."
I have a strong impression that there is a general tendency to make
light of the conditions remaining after acute pericarditis, or at any rate
not to regard them as of much consequence ; and I feel it necessary,
therefore, to call special attention to the fact that well-marked pericardial
adhesions not uncommonly persist, particularly in young subjects, and sub-
sequently often become of decided importance. A new growth of con-
nective tissue takes place, originating mainly in the cells present in the
exudation ; the fibrinous portion taking no part in the process, but being
absorbed after undergoing fatty degeneration. In severe cases the tissues
of the pericardium itself contribute to the growth. As the subject of
pericardial adhesions is separately discussed in this article no further
reference need be made to it here. It must be noted that in excep-
tional cases an ordinary inflammatory efi'usion into the pericardium does
not undergo absorption, but remains as a chronic collection, or may become
hsemorrhagic or purulent. These conditions will also be referred to more
fully hereafter.
According to the extent of the disease, cases of pericarditis have been
divided into circumscribed or local, and diffuse, the latter being in many
instances general or practically universal. Local pericarditis may be met
with in any part, but is chiefly observed at the base, about the origin of
the great vessels ; and the inflammation may thence extend to the coats of
the arteries, so far as they are covered by pericardium, and subsequently
give rise to thickenings and callosities.
In the preceding discussion pericarditis has been dealt vrith oijly so
far as it afiects the sac internally. It must be mentioned, however, that
in not a few instances the external surface of the pericardium is acutely
involved at the same time, or alone ; though it is more commonly involved
in a chronic process. The condition has received the names of external
pericarditis, mediastino -pericarditis, or pleuro -pericarditis when the contigu-
ous surfaces of the pleura and pericardium are affected. This form of
disease and its results will be more conveniently dealt with later, and in
other connections.
748 SYSTEM OF MEDICINE
Clinical history. — Acute pericarditis presents considerable differences
in its clinical history, depending upon a variety of circumstances ; and
tkis fact must be clearly recognised at the outset, and always borne in
mind in practice. At the same time the phenomena to be watched for
and studied are definite, and when at all pronounced bear an obvious
relation to the morbid changes which are associated with the disease.
The signs observed by physical examination are of special clinical value,
for the symptoms are not uncommonly anything but characteristic ; while
the more important of these signs can be investigated as a rule without
much difficulty, and it is only by their aid that we can positively
determine the pathological conditions of the pericardium. " Indeed, it
must never be forgotten that, when symptoms are practically absent or
latent, they may reveal the presence of even serious acute pericarditis ;
and this statement applies still more to cases in which the inflammation
is localised. Moreover, physical examination gives the only trustworthy
information as to the progress of the morbid changes.
Taking a comprehensive survey of the circumstances under which
acute pericarditis usually supervenes, it might be anticipated that an
attack is not ushered in, as a rule, by any striking premonitory symptoms,
such as rigors and the like; and experience confirms this conclusion. The
fact must not be overlooked, however, that in certain classes of cases the
illness may begin with phenomena of this nature ; nor must it be for-
gotten that even rheumatic pericarditis may appear as a primary acute
disease, before the joints or any other structures reveal the presence of
the rheumatic condition.
Discussion of symptoms. — ^From what has been just stated, it may be
gathered that it is useless to attempt to give a definite clinical picture of
acute pericarditis, and it will be more practical in the first instance to
consider individually the several symptoms which may be associated with
this disease ; remembering that they differ much in their exact nature,
severity, and combinations in particular cases.
(i.) Subjective sensations. — Pain is a symptom to be looked for in
the early stage of acute pericarditis ; but it is by no means always
present, nor does it bear any necessary proportion to the seriousness of
the attack. I can corroborate, from personal observation, the state-
ment that severe pain may be associated with a limited dry pericarditis
of short duration ; while, on the other hand, it is a familiar fact
that in cases of large efTusion no such sensation may have been com-
plained of from first to last, or it may have been so slight and transient
as not to have attracted any attention. In young children pain seems
to be generally absent. Sibson made numerous careful and interesting
observations on this symptom in rheumatic pericarditis, and some of
his conclusions are incorporated in the following remarks. In the
majority of cases where pain is present it is referred to the precor-
dial region, extending usually from the right of the sternum at its lower
two-thirds to the left nipple. This pain is more or less continuous, but
varies in severity, being in exceptional instances very intense. In char-
DISEASES OF THE PERICARDIUM 749
acter it is described in different cases as dull, aching, shooting, stabbing,
burning, or tearing. Sibson noted that it came on, as a rule, at an early
stage, afterwards diminishing; and usually relief, which was permanent,
came when the effusion was at its height. Pain may, however, either pre-
cede or follow friction sound. Occasionally a return of the pain occurs
with a relapse. The suffering is often increased by deep pressure or per-
cussion ; and now and then there is tenderness without spontaneous pain.
Sibson observed in many cases that the skin over the region of the peri^-
cardium was tender and sensitive ; so much so in some instances as to
forbid the slightest manipulation of the chest, and to make a full
examination of the heart impossible. Sometimes this superficial hyper-
aesthesia is certainly very remarkable. In other cases the structures of
the intercostal spaces seem to be tender.
Another not uncommon seat of pain or tenderness, or both, is the
epigastric region, where, according to some writers, it is even more
frequent than in the precordial. The tenderness is said to be most
marked at one or other of the costal angles, and is particularly brought
out when upward pressure is made. Epigastric pain comes on, as a rule,
later than that over the heart, and in a considerable proportion of Sibson's
cases it appeared when the effusion was at its height. Both varieties are
likely to be increased by the act of respiration and by bodily movements.
Sometimes painful sensations radiate in different directions from the
central points. A deep pain in the chest, between the shoulder-blades,
was noticed in a few cases by Sibson ; it was increased by swallowing or
eructation, and occasionally was only thus brought out. He thought that
in these instances the pain was seated in the back of the inflamed pericar-
dium ; and he also believed that pain and fulness after food might result
from pressure made by the distended stomach over the lower and posterior
part of the sac. In exceptional instances pain of an anginal character,
shooting up the left side of the neck, to the ear, to the shoulder, or down
the arm, is associated with acute pericarditis ; but endocarditis has almost
always been present at the same time, and generally chronic valvular
disease also. The sensations just discussed are believed, to be located
mainly in the sentient nerves distributed to the surface of the heart,
the pericardial sac itself and the portion of diaphragm incorporated with
it, or the pleura covering the pericardium. They are often associated
together in different combinations. Moreover, there may be pain in one
or other side, evidently of pleuritic origin, or referred indefinitely to
the chest. Taking all his cases together, Sibson found that there was
pain of some kind over the heart or pericardium in 70 per cent.
Other subjective sensations besides those actually painful are not
uncommonly complained of in acute pericarditis, as the disease progresses;
and especially if a large accumulation of fluid takes place. They are'
described in different cases as feelings of precordial uneasiness, oppres-
sion or pressure, a weight or load over the heart, tightness, or ill-defined
distress and anxiety. The respiration may be distressed ; and not only
may the patient be conscious of the disturbed heart, but sometimes there
75° SYSTEM OF MEDICINE
is a distinctly painful form of palpitation. Baiimler has noticed painful
sensibility of the left side of the larynx, increased by every movement
of the heart.
(ii.) Disorders of the cardiac action and pulse. — It might naturally be
expected that acute pericarditis would affect the action of the heart in
various ways. In the early stage the heart is excited and irritable, as
evidenced by increased rapidity and force of the beats, the movements
in some instances being more or less tumultuous. Subsequently,
not only as the result of large effusion, but also of the implication of
the myocardium and its nerves, as well as of other influences, the
cardiac action becomes more or less embarrassed and ineffectual, and
this may culminate in marked feebleness or exhaustion, with irregularity
and intermittence, or even faintness or actual syncope which, in ex-
ceptional instances, has come on suddenly or very rapidly, and proved
fatal. With regard to the frequency of the pulse, according to Sibson,
" it rises in number as the disease rises in intensity, is at its greatest
rapidity when the disease is at its acme, and falls in number as the
disease declines." "During the early stage the pulse usually mounts
up to 90, 100, or even 120; but later on it tends to become more
rapid, and in rare cases reached 160." It may, however, not be much
changed from the normal, or from what it was before the pericarditis
supervened ; or after an initial acceleration it may soon subside. In
exceptional instances the pulse is retarded in the course of the disease.
A much quickened pulse-rate, 120 or 130, without adequate rise of
temperature, is said by Dr. Cheadle to be very characteristic of the sub-
acute pericarditis of early life. In the early stage the pulse is generally
full and strong, and may be increased in tension ; as the case pro-
gresses it becomes small, weak, often dicrotic, and of very low tension.
Dr. Ewart, however, draws special attention to the large and slapping
pulse which he has frequently observed in pericardial effusion. He writes :
" The peculiarity of the pulse is its great size and velocity of impact, and
the sudden collapse of the wave. In fact it is Corrigan's pulse, almost of
a typical kind, though never so extreme as in well-marked aortic regurgita-
tion." Irregularity or intermittence may accompany a similar disturb-
ance of the cardiac rhythm ; occasionally this is an early phenomenon,
but usually comes on later. It has been stated that in some cases of
copious pericardial effusion the left carotid and radial arteries are smaller
and pulsate less forcibly than the corresponding arteries on the right side
(Traube). The sphygmograph has been much used to investigate the
pulse in cases of acute pericarditis, but I venture to doubt whether it is
of much practical value. Speaking from personal experience of this dis-
ease, I think it must be acknowledged that no definite description of the
pulse can be given ; but at the same time the study of it in individual in-
stances affords most useful information, and it needs to be watched at
frequent intervals. In grave cases it may become almost imperceptible.
The pulsus paradoxus has been observed occasionally in large pericardial
effusions.
DISEASES OF THE PERICARDIUM 75i
(iii.) Respiratory system. — Some disturbance of breathing is noticed in
the gi-eat majority of cases of acute pericarditis, varying much in its
degree and exact characters, but often well marked or even decidedly
grave. By pain in the early period respiration is rendered quick and
hurried, but restrained and shallow; and this cause may also modify the
movements later, when the physical effects of pericardial effusion, as
well as other influences, especially the cardiac changes, come into play.
If there be much fluid, actual dyspnoea supervenes, the respirations in-
creasing in frequency, with marked activity of upper costal breathing,
but more on the right side than the left. As it accumulates, the breathing
becomes more and more difficult and laboured, the alae nasi work, the
extraordinary muscles are called into play, there is a corresponding
sense of oppression, distress and air-hunger, and the patient may
have to be propped up more or less. In extreme cases the dyspnoea
is very urgent, the respiratory movements are greatly impeded, and
there is persistent orthopnoea, or the patient instinctively bends forwards
to seek relief. As a rule it is more comfortable to lie on the left
than the right side, but dorsal decumbency is usually preferred.
Occasionally the dyspnoea is intensified paroxysmally. As the fluid is
absorbed the respirations fall, and the breathing improves ; but a relapse
may cause fresh disturbance. With regard to the pulse-respiration
ratio, even at the early period it may be altered from the normal to 3:1;
and later the proportion may come to be 2 or 2i- : I. The difiiculty of
breathing interferes with the act of speaking ; and changes in the. voice
have been described in exceptional instances by Sibson and others, and
attributed mainly to pressure upon or implication of one or both re-
current n'erves. A sliort, irritable, spasmodic cough is not uncommon
with a large pericardial effusion, and there may be a little mucous frothy
expectoration. Distressing and painful hiccup is an occasional symptom,
attributed to implication of the phrenic nerve in the inflammatory
process.
(iv.) Dysphagia. — Difficulty or pain in swallowing is occasionally
noticed, mainly the result of the pressure of a large pericardial effusion
upon the oesophagus ; but sometimes it appears to be due to nerve-irrita-
tion. Deglutition is more difficult in the recumbent posture, and is made
easier by raising the shoulders and bending forwards. In exceptional
cases the difficulty is only associated with swallowing solids, or is brought
on by oesophageal spasm induced by an attempt to drink. Earely a
feeling of spasmodic choking in the throat or along the gullet is com-
plained of.
(v.) Genefral symptoms and appearance. — More or less pyrexia may be
expected in cases of acute pericarditis, but it does not present any special
course or characters. Its manifestation in rheumatic cases may not be
attended with any increase of temperature previously raised; it seldom rises
above 102° or 103° at any time, and may soon subside. Sometimes it is
practically normal throughout, or only slightly elevated, from 99° to
100° or 101°, especially in children. It is affirmed that rapid absorption
752 SYSTEM OF MEDICINE
of inflammatory products may occasion some rise of temperature. As a
rule, strengtli is fairly maintained ; but in some instances, especially in
children, there is marked prostration. In severe cases of acute pericarditis,
especially when associated with endocarditis, the expression generally
indicates anxiety, distress, or depression ; and the face is flushed, dusky,
or pallid, or presents alternating hues. Rarely it has a muddy or glazed
appearance. The eyes at the same time are dull, heavy and injected.
Sibson noted a marked change in the appearance of the patient in four-
fifths of his cases, to which he attached much importance : as the com-
plaint subsided he found that the aspect quickly improved, the eyes
becoming bright and clear, the cheeks rosy, and the expression often
quite suddenly cheerful. This observer attributed the flushing and pallor
of the face to the influence of the inflammation on the nerves at the
surface of the heart, inducing reflex dilatation or contraction of the
arteries of the head and face. He stated that the flushing seemed to tint
the face all at once.
The most striking general symptoms in the grave forms of acute
pericarditis are those indicative of interference with the aeration of the
blood, and of general venous obstruction. The patient then presents
a more or less livid or cyanotic appearance ; sweating, often profuse ;
fulness of the veins of the neck, sometimes with pulsation ; and in ex-
treme cases coldness of the extremities. Possibly dropsy of the legs may
occur. A large effusion in children is said to afiect the action of the
heart more rapidly than in adults, and to lead to an earlier interference
with the circulation. In these subjects progressive anaemia and wasting
are in some instances pronounced symptoms. Perspiration was observed
by Sibson to be usually copious when there was flushing. The amount
and characters of the urine will depend very much upon the condition
with which the pericarditis is associated. It tends to be deficient in
quantity, and to present the usual changes associated with the rheumatic
and febrile states. Albuminuria may occur altogether independent of
renal disease.
(vi.) Nervous symptoms. — Patients suffering from pronounced acute
pericarditis are generally very restless, but movements may be checked
by the rheumatism. Headache and sleeplessness are frequent symptoms,
and slight delirium is not uncommon. Vomiting is sometimes a marked
symptom in acute pericarditis, and is regarded as of nervous origin.
In exceptional cases nervous disturbances become very prominent, and
may be grave, sixch as delirium, either active and noisy, or even violent
and maniacal, chiefly nocturnal ; or low and muttering : sometimes a
transition from one to the other variety takes place. The condition
may resemble delirium tremens, the patient being strange in manner,
excited, and incoherent ; or there may be a tendency to stupor, semi-
unconsciousness, temporary insensibility, or actual coma ; or to motor dis-
orders, such as subsultus tendinum and jactitation, "risus sardonicus,"
clonic or tonic spasms, rolling of the head from side to side, chorei-
form movements, general convulsions ending in extreme exhaustion.
DISEASES OF THE PERICARDIUM 7S3
tetanic rigidity ; or to curious emotional attacks in early life, in which the
child is moved to tears or laughter by a word (Cheadle) ; or even to
temporary insanity, usually with taciturn melancholy, and often with
hallucinations ; this derangement may last some time, but is ultimately
recovered from. The particular symptoms of this class and their
combinations differ much in different cases, and delirium may pass
into coma. They cannot, as a rule, be referred directly to the peri-
carditis, but depend rather on the disease to which it is secondary,
its associated complications — hyperpyrexia in some instances, the state of
the nervous system, want of oxygenation of the blood, the previous habits
of the patient, or other circumstances. Some authorities, however, attii-
bute the phenomena to the influence of the pericarditis upon the nervous
system; and Bright believed that such an influence can be communicated
through the phrenic nerve to the spinal cord, and is the cause of choreic
and tetaniform affections. Dr. G-eorge Balfour writes : " The occurrence
of delirium in the course of rheumatic fever ought at once to direct
attention to the heart ; and the sudden occurrence of spasms or coma in
chronic renal disease is only too frequently found to be associated with
pericarditis, both of these phenomena being probably caused by the
saturation of the blood with the products of retrograde metamorphosis,
due to the sudden development of the inflammation." It is important to
note, however, that even in tlie gravest cases of acute pericarditis, ending
fatally, and accompanied with other intrathoracic inflammations, there
may be no marked nervous symptoms throughout, the patient being
perfectly clear to the last.
Sturges described a very fatal form of pericarditis in children, with
little or no effusion, exudation being followed by rapid adhesion ; and he
referred the grave symptoms observed in these cases to the nervous
system. Dr. Cheadle also calls attention to occasional cases in such
subjects which run an acute course with dangerous symptoms ; but he
states that, as a rule, they arise when pericarditis occurs late, when the
heart is already seriously damaged by previous attacks of endo- or peri-
carditis, and when the secondary changes of dilatation and hypertrophy,
and perhaps adherent pericardium, have already advanced to a marked
extent {vide vol. iii. p. 45).
Physical signs. — In discussing the physical signs of acute pericarditis,
it is convenient to recognise certain stages corresponding to the progress
of the morbid changes already described; although it must be clearly
understood that there is no actual line of demarcation between them, the
conditions which give rise to these signs being commonly present at the
same time. It may be remarked that the excited or turbulent action of
the heart which often occurs at the onset of the disease will be evident
on examination, but there is nothing characteristic in this disturbance.
First stage. — During the early period the signs to be looked for are those
indicative of abnormal states of the contiguous pericardial surfaces, which
are pressed and rubbed against each other during the movements of the
heart. They are commonly known as pericardial fridion- fremitus of
VOL. V 3 C
754 SYSTEM OF MEDICINE
thrill, and friction murmwrs or sovmds ; signs which must be considered
in some detail. Many deny that any phenomenon of this kind can be
produced by mere increased vascularity and dryness of the surfaces, but
in my opinion a faint friction murmur may certainly be thus originated.
It is, however, to the fibrinous exudation that the more pronounced and
characteristic signs of the early stage of acute pericarditis are due.
They can, in my opinion, be brought out only when the conditions
producing them exist on the anterior aspect of the heart, although
some writers have made a contrary statement ; and it is highly probable
that when the inflammatory lymph is of a very soft consistence, it may
not give any definite sign perceptible on physical examination.
(i.) Pericardial friction-fremitus or thrill. — The tactile sensation thus
named is practically only recognisable in a comparatively small proportion
of cases of acute pericarditis, and when present it is always accompanied
with a loud friction-sound. For the detection of this sign careful palpa-
tion with the finger-tips may be needed, and I believe that it can thus be
made out more frequently than is generally supposed. It depends more
immediately upon the amount and characters of the exudation, though it
is also influenced materially by the force of the heart's action.
When any abnormal sensation is felt over the precordial region, the
chief point to be determined is whether it is a pericardial fremitus or an
endocardial thrill. It must suffice to summarise here the more character-
istic features of a pericardial fremitus, and to any one practically acquainted
with the usual endocardial thrills the points of difierence between them
will be at once apparent.
(a) A pericardial friction-fremitus has no definite " focus of intensity "
(Sibson), and varies much in its seat and extent. As a rule its area is
circumscribed, and it is felt more towards the base of the heart or over
the middle of the precordium ; sometimes it is limited to the apex. Now
and then, however, the sensation is perceptible over a considerable extent
of surface, or in more than one spot, (b) It always gives the impression
of being peculiarly superficial, as if the condition producing it were
close under the finger. (c) The rhythm is practically systolic, the
fremitus being associated with the cardiac impulse ; it usually begins
and ends rather abruptly, and there is no shock at the close :
sometimes it is irregular in rhythm, differing in exact time in successive
beats, (d) In quality a pericardial friction-fremitus gives more or less
the impression of the rubbing together of rough surfaces, and in different
cases it is described as harsh and grating, rasping, vibrating, or creaking.
Sibson speaks of it as being in many instances a sensation of a thrill, but
in my experience the feeling has certainly never been like that of an
endocardial thrill, (e) As a rule this sign is short-lived and transient
(Sibson), and, should it last any time, often changes from day to day in
its situation, extent, and characters. Pericardial friction-fremitus may be
simulated by one of pleuritic or mediastinal origin, brought out by the
movements of the heart ; and this fact must not be forgotten.
(ii.) Pericardial mwrmur or frictiorirsound. — It is by the adventitious
DISEASES OF THE PERICARDIUM 75S
sounds heard on auscultation that, in the large majority of eases, the early-
stage of acute pericarditis is recognised. Some writers distinguish between
a pericardial murmur and friction-sound, and Sibson made a great point of
this distinction ; but there is no practical line of demarcation between
them. In the following remarks, therefore, I shall employ the term
"pericardial friction-sound" inclusively, merely remarking that the so-
called murmur may be regarded as representing the minor degrees of this
sign, and that now and then an adventitious sound of pericardial origin
may no doubt closely resemble an endocardial murmur in quality.
It is requisite to have a comprehensive and intelligent conception of
the more characteristic features of pericardial friction-sounds, so as to be
able to contrast them with those of endocardial murmurs ; but as a rule
they are easily distinguished. Moreover, by careful attention to the
special qualities of the sounds heard, it is practicable in many cases to
arrive at a tolerably definite notion of the conditions of the pericardium
upon which they depend. It may be observed here that pericardial friction-
sound also may unquestionably be simulated by one of pleuritic origin, or
by a sound originating in the mediastinal cellular tissue over the
pericardium.
{a) While usually more or less circumscribed in extent, pericardial
friction-sound does not correspond in any way, as regards its situation or its
point of maximum intensity, to any of the recognised endocardial murmurs.
In some cases it is audible extensively, though not of the same loudness
throughout its area ; but even then it is generally defined with remarkable
abruptness, and is never conducted in the directions peculiar to the
several intra-cardiac murmurs ; nor, according to my experience, can it
ever be heard over the back of the chest. During the early stage of
acute pericarditis friction-sound never extends beyond the region of the
heart, but in the later it may do so in exceptional instances. When
associated with a fremitus it usually spreads, as from a focus, in all
directions more or less beyond the area where this sensation can be felt.
(b) As a rule pericardial friction-sound has a double or to-and-fro
rhythm, being both systolic and diastolic ; but in some instances, or over
certain parts of the heart, it may be confined to the systole. In pronounced
cases the two parts are of about equal duration, each sound seeming to
fill up its respective space, leaving a short interval of silence between the
two (Sibson). They may, however, occupy the whole time of the cardiac
movement, thus often giving at first a confused impression to the ear;
but intermissions can be made out. As regards the cardiac sounds, the
pericardial murmur seldom corresponds exactly in rhythm with either,
and is prolonged beyond them, while they are often distinctly audible
through it ; though, on the other hand, the friction-sound may be so loud
as to drown them entirely. Moreover, its precise time is frequently
irregular, varying with successive beats of the heart. This is more
especially noticed in connection with the diastolic portion, which is usually
not so loud as the systolic. A double " to-and-fro " adventitious sound
heard in connection with the cardiac movements, of maximum intensity
7S6 SYSTEM OF MEDICINE
at the same spot, is regarded as highly characteristic of pericardial origin.
It has been stated that four murmurs may be audible, the two sides of
the heart each producing a systolic and diastolic murmur of different
duration ; but that most frequently three are heard, one presystolic,
belonging to the systole of the auricles, and two longer sounds, corre-
sponding to the systole and diastole of the ventricles. Earely pericardial
friction is divided into several parts.
(c) While varying much in its intensity, pericardial friction-sound
strikes the ear as being peculiarly superficial ; and this character is more
pronounced in proportion to its loudness. Sibson spoke of it as a
" surface noise."
{d) The precise characters of a pericardial friction-sound vary con-
siderably within well-recognised limits, according to the nature of the
conditions upon which it depends. In the large majority of cases it
conveys to the ear a distinct impression of the rubbing together of con-
tiguous surfaces during the cardiac movements; in short, it is of the
quality of a " friction-sound." In its lesser degrees it is soft or grazing,
whiffing, brushing, or rustling; but its more pronounced varieties are
described by such terms as harsh, rough, grating or vibrating, and creak-
ing, like the bending of new leather. Bouillaud classified pericardial
friction-sounds as grazing, new leather sound, and grating, which are the
common varieties. Sometimes they resemble the rubbing of sand-paper.
Under certain circumstances the sound is more of a crackling (as of paper
or parchment), clicking, churning, or rumbling character, or it may be
scraping, scratching, or sawing. It has also been described as " sticky."
While thus various, pericardial sounds are as a rule entirely different in
quality from endocardial murmurs. Moreover, the double pericardial
friction-sounds never begin with an accent or shock, but begin, con-
tinue, and end, as a rule, with the same tone throughout (Sibson).
When pericardial friction-sounds and endocardial murmurs exist together,
the combinations may be very peculiar and difficult to define.
(fi) Tests. — In certain cases in which a pericardial friction-sound is not
distinctly audible, but its presence is suspected, or where it is doubtful
whether an adventitious sound heard on auscultation be pericardial, endo-
cardial, or pleuritic, the difficulty may be cleared up by the judicious
application of certain recognised tests. These may also help in affording
a more correct knowledge of the conditions of the pericardial surfaces
upon which a friction-sound depends.
(a) Presswre test. — Firm but not too forcible pressure with the stetho-
scope over different parts of the region of the heart has long been
known as an important and useful test of pericardial friction -sound.
It may bring out this sign when not previously audible, especially over
the lower two-thirds of the sternum (Sibson). Its effect upon the sound,
when present, may be to intensify it and make it louder ; to enlarge the
area over which it is heard ; to modify its duration and rhythm, render-
ing it more prolonged and continuous, or making it double — systolic and
diastolic — when previously only systolic ; to alter its character, tone, and
DISEASES OF THE PERICARDIUM 757
pitch, causing it to become more harsh and rough, and especially grating
or creaking, or these qualities come out more propiinently under pressure
(Sibson described a peculiar double sound thus elicited, like the noise
made by sharpening a scythe) ; or to silence the natural cardiac sounds
previously heard, or even mask endocardial murmurs.
ifi) Bespiration test. — The act of respiration may unquestionably
produce a definite influence upon pericardial friction-sound, especially as
regards its extent, less frequently as to its intensity and quality ; and pos-
sibly some help in diagnosis may thus be afforded in doubtful cases. It
is generally stated that inspiration always increases pericardial friction-
sound. Sibson observed that the area of the friction-sound increased
below during inspiration in a large number of cases ; while in a much
smaller number it increased above during expiration. It became more
loud or harsh sometimes during expiration, sometimes during inspiration ;
and in one instance it disappeared at the end of a deep breath. I may
refer here to pleuritic friction simulating pericardial. As a rule it can be
distinguished by its situation at the left border of the pericardium, and by
its cessation when breathing is stopped, but certainly not always.
(7) Effects of exertion and posture. — Should a pericardial friction-sound
not be heard at all or but feebly, in consequence of weak action of the
. heart, it might possibly be brought out or made louder by exciting the
organ by some kind of effort. Moreover, it certainly may be intensified
or increased in area by bending the body forwards ; while occasionally it is
audible in the recumbent but not in the sitting posture. Change of
position may affect the locality and extent of this sign in certain cases.
Personally I doubt whether the tests mentioned under this head are of
much practical value, and at any rate special discretion and caution are
required in carrying them out.
(S) VariaUlUy. — Marked changes in the site, rhythm, intensity, and
characters of pericardial friction-sound from day to day, or within shorter
periods, constitute a series of most important tests in a large number of
instances.
Stage of effusion. — When fluid collects in the pericardial sac in any
quantity, it may be expected to give rise to a very definite group of
physical signs, varying in their degree according to its amount and other
circumstances. It must not be forgotten, however, that rapid adhesion
may take place without any effusion, so that the phenomena of this stage
may be entirely wanting, especially in children. Conversely, it occa-
sionally happens that a large quantity of fluid accumulates very rapidly
and insidiously without forerunning friction signs, or at any rate
without their detection. The possibility of considerable cardiac dilata-
tion, as described by Dr. John Broadbent, must also be borne in mind,
lest a wrong diagnosis of pericardial effusion be made.
We shall first consider how pericardial effusion may modify the
friction phenomena. Sibson made numerous observations on this
problem, and his conclusions were believed by him to support his own
views of the position of the heart in these cases. According to his
7S8 SYSTEM OF MEDICINE
observations the tendency of the effusion is to shift the ■whole region
of actual friction, and with it the friction-sound, upwards ; and steadily
to increase its area in this direction and to the right and left. In
the large majority of cases he found the area of friction-sound greater
at the time of the acme of the efiusion than before ; in a few it
remained the same ; in two only was it less than before. In two
instances the friction-sound disappeared during the acme, but Sibson
attributed this mainly to lowered heart power. He observed that
the tendency is for the sign to increase in intensity also, but in this respect
the exceptions were more frequent. It may be stated with certainty
that even large effusions do not necessarily obliterate the friction-
phenomena ; indeed there may be an abundance of fluid, at least
as much as two pints, in the pericardium, while these signs are pro-
nounced. Dr. George Balfour goes so far as to affirm that if a
friction-sound be once heard over the base of the heart in front, no amount
of subsequent effusion suffices to efface it. I do not think that this
statement will hold good absolutely, and friction-sound over other parts
of the heart is likely to be completely silenced as a rising tide of fluid
separates the two pericardial surfaces.
I proceed now to discuss the more positive signs which are associated
in various degrees with pericardial effusion.
1. The tendency of pericardial effusion, when in sufficient quantity,
is to cause proportionate bulging or prominence of the corresponding
portion of the front of the chest, and occasionally this is a very striking
sign. Some writers have asserted that this condition leads to a uniform
enlargement of the left side ; but although there may be a certain degree
of general distension the prominence is always greater in front. In the
case of a large effusion the margin of the sternum and the left costal
cartilages are pushed forwards, while the ribs are raised bodily upwards,
and the intercostal spaces widened. In extreme instances the fulness
may extend from the second to the sixth or seventh cartilages, but chiefly
from the fourth to the sixth ; the spaces are sometimes felt to be
quite smooth, and an obscure sense of fluctuation may possibly be
detected in them. Sibson stated that in very large effusion the dorsal
portion of the spinal column deepens itself and is curved backwards.
Bulging is naturally more easily produced in children and growing sub-
jects, on account of the yielding condition of the chest walls ; while it
may be entirely prevented by rigidity of these walls, which thus adds
seriously to internal embarrassments by the fluid. The enlargement has
been partly attributed by some writers to inflammatory paralysis of the
intercostal muscles.
Dr. William Ewart (19) regards what he calls the "first rib sign"
as important in the diagnosis of considerable pericardial effusion. This
is an altered relation between the left clavicle and the first rib, so that
the upper edge of the latter can be felt as far as its sternal attachment.
He writes : " This points to a raising of the clavicle not only in its outer
but also in its inner portion, and to a relaxation of the ligament between
DISEASES OF THE PERICARDIUM 759
it and the first rib. The left clavicle is apparently lifted to a higher
level than it is possible for the first rib to reach."
A prominence of the epigastric region may be noticed in eases of
abundant pericardial effusion, due partly to the fluid itself pressing down
the diaphragm, partly to the liver, which is also depressed and congested.
In his case Dr. Samuel West observed the rare phenomenon of a
peculiar elastic semi-fluctuating depression in the epigastrium, which he
regards as additional evidence of effusion having its seat in the peri-
cardium. Dr. Clifford Allbutt has met with a similar phenomenon.
2. Certain signs of pericardial effusion, associated with the cardiac
movements, as revealed by the impulse and apex-beat, demand careful
study : —
(a) There can be no doubt Ihat one of the obvious effects of a free
and uncomplicated accumulation of fluid in the pericardium is a real or
apparent elevation of the apex-beat, which seems at the same time to be
carried somewhat towards the left. Moreover, the movement becomes
unusually extensive in an upward direction, its diffusion being oftec
easy to recognise by inspection and palpation. According to Sibson's
observations there is, as a rule, a relation between the extent of the
effusion and the height of the impulse. This he found raised so that
its lower boundary corresponded to the fourth or even the third
space or cartilage, being also felt at or to the left of the nipple line.
The diffusion varied according to the position of the lower boundary ;
but in the large majority of cases, at the time of the acme, it
extended above this boundary to the extent of one or more of the higher
intercostal spaces. In exceptional cases the impulse was diffused from
the fourth to the second spaces, but generally it was confined to the
fourth and third, or the third and second spaces. Sibson attributed the
raising and diffusion of the impulse to elevation of the heart by the fluid,
and to enlargement of the right ventricle and pulmonary artery from
obstruction of the flow of blood through the lungs. He believed, in
common with other authors, that it is the actual apex-beat which is
felt, displaced upwards and to the left. At the present time, however,
most writers regard this opinion as erroneous, and consider that
the impulse is communicated by a higher portion of the heart. Thus
Dr. George Balfour believes that the true apex is pushed inwards by the
effusion, and removed from the anterior wall ; while the part of the heart
actually in contact with the chest wall is nearer the base of the ventricles.
Dr. William Ewart (19) also writes : " That an impulse can usually be felt
there (at the third space) is not surprising, since the antero- posterior
diameter of the chest at that level (between sternum and spine) is not
much greater than that of the heart itself, whilst the left lung no longer
intervenes between the latter and the chest wall. The impulse is not,
however, that of the apex of the heart, but rather of its base." My
personal observations lead me to agree with these views on the whole
but there may be conditions in certain cases to cause actual uplifting of
the apex-beat.
76o
SYSTEM OF MEDICINE
Series of figures (Nos. 36 to 43), from oases described by Sibson, illustrating the morbid
conditions in pericarditis and the physical signs associated therewith. The black
spaces correspond to the pericardial dulness, the curved lines to the impulses,
and the zigzags to the friction-sounds. In Fig. 41 there is complete adhesion of
the pericardium to the heart.
Fio. 36.
Pio. 37.
DISEASES OF THE PERICARDIUM
761
Occasionally it has been noticed in acute pericarditis with effusion
that the apex-beat is somewhat lower than normal. This may be due to
enlargement of the heart ; but it has also been attributed to the presence
Flo. 42.
Fio. 43.
of a large quantity of fluid pressing down the diaphragm ; or it may be
associated with a more median and vertical position of the heart, the
aortic arch becoming slightly straightened (Ewart).
762 SYSTEM OF MEDICINE
Over the pulmonary artery at the base a double beat is sometimes
felt, the second being the diastolic shock due to the closure of its
valves.
(&) The next change to be noticed in pericardial effusion is a pro-
gressive weakening of the cardiac impulse from below upwards. This
depends mainly upon the amount of the eifusion, but partly upon
feebleness of the heart's action. "When the fluid is in moderate
quantity there is often, as just stated, a strong impulse over the upper
spaces, its lower and outer boundaries being also well defined. As it
accumulates, however, in increasing abundance, and separates the heart
from the chest wall, the cardiac movements become more and more
obscured, until finally they may be wholly lost, and not perceptible
over any portion of the precordial region. This sign is occasionally very
striking in a case of inflammatory pericardial effusion when it first
comes under observation.
(c) It is a disputed question whether pericardial effusion can pro-
duce any definite change in the character of the cardiac movements,
tactile or visible. Certainly the impulse observed over the upper part of
the chest may be more or less undulatory ; and a wave-like motion has
been described, which can be seen but not felt, and is supposed to be
communicated to the fluid by the action of the heart. I must say that
I have never been able to recognise this phenomenon positively. Some
authorities regard an undulatory impulse as a sign, not in favour of
pericardial effusion, but against it.
((Z) In some cases of pericardial effusion the rhythm of the im-
pulse has been described as lagging behind the ventricular systole in a
peculiar way. Irregularity, with or without inequality in the strength
of the beats, may become very marked as the result of embarrass-
ment of the heart by a large collection of fluid, and of changes in its
walls.
3. One of the most frequent and characteristic signs of pericardial
effusion of any extent is an increase in the area of the normal cardiac
dulness, with change in its shape and outline ; and not uncommonly
these alterations are so pronounced as to attract immediate attention
in cases of acute pericarditis. The exact quantity recognisable by
percussion cannot be definitely stated, and no doubt it varies under
different circumstances ; but I believe that methodical and careful
determination of the cardiac dulness may afford valuable information in
cases where the fluid is present in comparatively small quantity. It is
necessary to study systematically and thoroughly both the superficial or
absolute and the deep or relative cardiac dulness. As the patient lies
on his back the increase of dulness is first observed towards the base of
the heart. The limits ultimately reached vary much in different cases.
The extension takes place chiefly in a lateral and upward direction,
the length and breadth of the dulness being thus increased ; the former
usually preponderating. In most instances it reaches the third cartilage
or space, but may extend as high as the second cartilage or first space,-
DISEASES OF THE PERICARDIUM 763
or even above the clavicle. Dr. Sansom maintains that whenever marked
dulness extends above the third rib there is a strong probability of peri-
cardial eifusion. Over the sternum, which is absolutely dull, as the
fluid increases the dulness reaches a higher level than over the costal
cartilages, and in extreme cases it may reach its upper margin. From
side to side at its greatest width the dulness may extend from an
inch or more to the right of the lower part of the sternum, or the right
mammary line, to an inch outside the left nipple, or even to the left
axilla. In a downward direction it seldom passes below the sixth rib,
but in extreme cases it may be made out as low as the seventh or
eighth rib, and be indistinguishable from the • hepatic dulness. A sign
suggested by Dr. Eotch, as valuable in the early diagnosis of efiusion into
the pericardium, is the presence of dulness in the fifth right inter-
cartilaginous space, due to the accumulation of the fluid in the right
corner of the sac ; but this sign is by no means invariably to be
trusted.
A notable feature of the dulness in cases of considerable pericardial
effusion is its shape, which corresponds with that of the sac itself. Thus
it narrows from below upwards, assuming a more or less triangular, pyra-
midal, or, more strictly speaking, pyriform or pear-shaped outline, with
its truncated or "peaked" apex above, and its base below, at the level of
the lowermost limit of the fluid. The left border has been described as
usually, somewhat curved, or indented at its upper part, while the right is
more nearly vertical. Dr. Ewart well describes the outline of a large
efi'usion as "that of a bag of fluid spreading out at the base." In its
diagnosis from cardiac dilatation he lays stress upon the projection of
lower angle of the dulness to the right, as well as to the left ; a prominent
angular outline being made out by careful percussion instead of the normal
outline of the heart. When the pericardium becomes extremely distended,
the characteristic shape is more or less modified, and may ultimately be
altogether lost. Shattuck renounces all faith in the doctrine of a pyrilorm
or pyramidal area of dulness in pericardial effusion, but I differ from him
entirely on this point.
In cases of pronounced pericardial effusion the extreme degree of the
dulness is very striking. Dr. Sansom insists on the importance of the
well-defined transition from the resonance of the lung to such dulness as a
factor in the diagnosis of this condition, and in many cases the contrast is
certainly very remarkable. In other instances, however, it must not be for-
gotten that the distended pericardium is overlapped by the margins of the
lungs, which yield a superficial resonance; and that its full extent can then
be made out only by very careful percussion beyond the limits of abso-
lute dulness. A large effusion imparts an increased sense of resistance to
the fingers.
Another important point is that the dulness of extensive pericardial
effusion can be made out distinctly towards the left, considerably beyond
the position of the apex-beat, which is then only to be recognised by
auscultation. ^
764
SYSTEM OF MEDICINE
Pia. 44.— -Illustrating "Botch's sign " (dulness in the right 5th space, 5 to H); also contrasting the
angles (on either side of H) of the dulness as due respectively to effusion and to dilatation. The
heart's outline is normal in size and position. The outer lines are those of the dulness in moderate
effusions. The " supra-hepatic line " (dotted) and the " hepatic line " limit the normal "modified"
dulness of the liver ; and H is placed on the absolute dulness. (Aftra Ewart.)
Fzo. 45. — Outline of a large effusion, which the pulmonary ftinges overlap, and of its total area of
dulness. The liver is depressed from its normal level H (infrastemal notch) to the tip of the
xiphoid. F shows the position of the finger for the " first rib sign." (After Ewart.)
DISEASES OF THE PERICARDIUM
765
FiQ. 46.— Outlines of the total and of the absolute areas of pericardial dulness. A, position of the
cardiao apex (5th space) in the effusion. The dulness is shown by the arrows to extend tar beyond
and below A. The right auricle (not shown) descends with the diaphragm. T, the infta-mammary
patch of tubular breathing. (Alter Bwart.)
Fw. 4?.-The " posterior pericarfial patch of dulness "(shaded); and the " posterior pericardial natch
of tubular breathing and aegophony. " (After Bwart.) P«n<=arQiai paten
766 SYSTEM OF MEDICINE
The rapid development of increased precordial dulness while a
patient is under observation is strongly in favour of accumulation of
fluid in the pericardium, and under circumstances where acute peri-
carditis might be anticipated this sign must be specially looked for. It
may soon become quite pathognomonic, but the possibility of the occur-
rence of acute dilatation must not be overlooked.
4. The auscultatory signs which may directly result from effusion
into the pericardium demand brief notice. The tendency of the fluid
itself, as it increases in amount and rises higher and higher, is to weaken
the heart -sounds in a progressive manner from apex to base ; or they
may seem deep and distant. These efifects may be due both to imper-
fect transmission of the sounds through the intervening fluid, and to
embarrassment with enfeeblement of the cardiac action. Most commonly
in pronounced pericardial effusion the sounds are weak or perhaps
inaudible over the region of the normal apex-beat, and for some distance
upwards, but become gradually more perceptible towards the base of the
heart, where they may- be well heard ; over the pulmonary artery the
second sound may actually be intensified. In cases of extreme effusion
the sounds may be practically absent over the whole precordial region.
Some observers have described a basic systolic murmur as a sign of peri-
cardial effusion, the result of pressure by the fluid upon the great arteries.
I have never met with such a murmur within my own experience, but it
may possibly occur. On the other hand, pericardial effusion may certainly
obscure or render inaudible endocardial murmurs previously heard.
5. Bigm connected with neighhouring structures. — The effects produced
on the lungs, especially the left, by a large pericardial effusion, are likely
to be indicated by more or less pronounced signs, which, however, will
vary in different cases according to their exact nature and degree. The
respiratory movements over the upper part of the chest are often obvi-
ously excessive, but especially on the right side ; and should the ffuid be
very abundant, a striking contrast will probably be observed between
the activity of the two sides, the movements on the left being very
deficient. Over the region of absolute cardiac dulness there will be
entire absence of breath - sounds, as well as of vocal fremitus and re-
sonance. Beyond its limits there may be hyper-resonance and puerile
breathing ; and towards the left side the percussion sound is occasionally
somewhat tubular, and the breathing bronchial or tubular, with increased
.vocal fremitus and resonance. Ewart (19) calls attention to a sign which,
although not constant, should, he says, be looked for in severe cases ;
namely, tubular breathing below the right mamma. He describes it as
situated usually in the nipple line, a little above the hepatic line, and
he states that it is sometimes restricted to expiration. Dry rhonchi of
various kinds may be audible in severe and protracted cases, the result
of catarrh of the bronchial tubes.
In considerable pericardial effusion the condition of the left lung
may give rise to a definite group of' signs at the back of the chest on
that side ; namely, a limited area of deficient resonance or actual dul-
DISEASES OF THE PERICARDIUM 7^7
ness, about the size of a crown piece, generally referred to the vicinity
of the angle of the scapula, with increased vocal fremitus, bronchial or
tubular breathing, and bronchophony or segophony. Sansom regards
these as valuable signs in children and young subjects. Ewart attaches
special diagnostic importance to the didness, which he describes as
follows : — " Whenever fluid is effused into the pericardium the normal
resonance is modified at the left posterior base in a most definite way.
A patch of marked dulness is found at the left inner base, extending
from the spine for varying distances outwards, usually not quite so far as
the scapular (angle) line, and ceasing abruptly with a vertical outer
boundary. Above, its extension is also variable according to the size of
the effusion ; commonly it does not extend higher than the level of the
ninth or tenth rib, and here again its horizontal boundary is abrupt. Its
shape is that of a square, and it is quite unlike that of any dulness
arising from pleuritic effusion." He attributes this patch of dulness to
the altered dorsal relation of the liver, and states further that partial
dulness also extends for a short distance to the right of the correspond-
ing vertebrae, and that, when the effusion is considerable, the extension
of the patch in the right chest may become almost absolutely dull. With
regard to auscultation signs, this writer afSrms that over the dull patch
to the left of the spine respiratory sounds are found to be absent and the
voice sounds feeble. He locates tubular breathing and aegophony to a
patch about two inches in diameter immediately below or slightly to the
left of the tip of the left scapula. He concludes that this sign, although
not so important as that, of the patch of dulness, is very commonly, if
hot always, present in cases of considerable efi'usion, and gives valuable
confirmation to other signs. The editor of this work tells me that he
once found these signs very definitely in a case of a large . collection of
blood slowly efiused into the pericardium from a ruptured coronary
artery. The patient, a lady of some threescore, lived about sixteen hours
from the onset of the symptoms.
As previously stated, pleural effusion on one or both sides is not
uncommon as a consequence of a large collection of fluid in the peri-
cardium ; in which case the signs will be modified accordingly. When it
begins on the right side the contrast may be helpful in diagnosis. Signs
indicative of downward displacement of the liver are very pronounced in
cases of extensive pericardial effusion, and there may also be some degree
of enlargement due to venous congestion.
6. Effects of change of posture.— The study of the effects produced
by changes of posture upon the chief signs just discussed has generally
been regarded as important in the diagnosis of pericardial effusion. In
a large proportion of cases these signs are so definite that it is quite
unnecessary to test them in this way, and under such circumstances it is
highly dangerous to place the patient in the sitting or erect posture;
such disturbance may even prove immediately fatal.
The following are the chief modifications in the signs produced by
changes of posture, which are regarded as of more or less diagnostic
768 SYSTEM OF MEDICINE
value. It may happen that the impulse is not perceptible in the re-
cumbent position, but becomes evident when the patient is made to sit
up or bend forwards. Increased mobility of the apex-beat with change
of posture has also been looked upon as important, but certainly this is
very untrustworthy, to say the least. The eifects of position upon the dul-
ness have been more particularly insisted upon as evidence of pericardial
effusion, and in doubtful cases may be worth studying. It is increased
in extent, especially at its upper part, in the sitting posture, and still
more if the body is bent forwards. It may also be modified in a lateral
direction, as the patient turns to either side. The relative loudness of
the cardiac sounds or of endocardial murmurs might also possibly be
similarly influenced. Modifications of the signs observed in connection
with the left lung posteriorly are also said to be produced by change of
posture. Sansom writes : " If the patient bend well forward, or assume
the knee-elbow position for a short time, the dulness disappears, and
in its place a tympanitic sound is elicited ; in like manner the former
auscultatory signs of lung-consolidation vanish, or only slight crepitant
rales are heard, which also very soon become inaudible. The former
signs return when the vertical position of the body is resumed."
It must again be insisted upon that the physical signs of pericardial
effusion vary much in different cases, and most of the special signs de-
scribed by Ewart and others apply rather to cases in which it is so
abundant as to raise the question of operative interference, when a posi-
tive diagnosis is obviously of extreme importance. With some of them
I am not familiar, and I hardly think that apy of them are absolutely
trustworthy. Shattuck denies the existence of the dorsal signs of peri-
cardial effusion. It may be mentioned that skiagraphy has been em-
ployed for the diagnosis of pericardial effusion and other conditions of
this sac, but it is too early at present to attempt any definite statements
as to its real and positive value.
Stage of absorption. — During the progress of absorption of inflam-
matory pericardial effusion the signs indicative of this condition pro-
gressively diminish, until the phenomena become practically normal, or
point to the formation of adhesions. The friction signs, if they have
been obscured by the effusion, return for a while ; or they alter in their
situation, intensity, extent, and characters. Friction-sound in most cases
increases in a downward direction as the fluid declines (Sibson). It lasts
a variable time. Friction-fremitus may at this period be noticed for the
first time ; and the sound is often rough and creaking or churning. The
dulness diminishes more or less rapidly from above and laterally ; while at
the same time the sounds become more distinct. It must be remembered
that one or more relapses may take place, with further increase of the
fluid, the signs of which then return, again to subside as the fresh
effusion becomes absorbed. What the ultimate position of the heart and
the apex-beat will be depends on the course of events. As a rule, in
simple and uncomplicated cases of pericarditis it returns to its normal
situation, but this return may be prevented by adhesions, by the effects
DISEASES OF THE PERICARDIUM 769
of endocarditis, or by other causes. The signs indicative of adherent
pericardium will be separately considered, but it may be remarked that
in not a few instances, if carefully watched for, they can be traced in pro-
cess of development during the period of convalescence.
Course and terminations. — As already stated, acute pericarditis pre-
sents much diversity in its clinical history, and it does not follow any
uniform course. When, however, the symptoms and physical signs dis-
cussed in the preceding pages have been adequately and intelligently
mastered, they can be studied with advantage in individual cases on the
lines indicated. Among the chief circumstances which influence the
nature, severity, and combinations of the symptoms, may be mentioned
the causation of the pericardial inflammation, and the character of the
general disease to which it is secondary ; its intensity and rapidity of
progress ; the characters and amount of the inflammatory products, espe-
cially of the effusion ; the presence of previous organic changes affecting
the heart or pericardium, or of other chronic intrathoracic diseases ; and
the association of the pericarditis with endocarditis or myocarditis, or
with pleurisy or pneumonia.
Attempts have been made by Stokes and others to classify cases of
acute pericarditis into groups, according to the intensity of the symp-
toms, and the morbid changes affecting the pericardium and heart associ-
ated therewith; but distinctions of this kind are quite arbitrary, and
have no practical foundation or value. It may be affirmed that as a
rule the clinical phenomena are not so pronounced or so grave as is com-
monly supposed, or as the older writers used to describe. Not un-
commonly the symptoms are not at any time prominent; they may
be practically latent, or they may quickly attain some degree of severity,
and as speedily subside. Shattuck, indeed, specifies "latency " as the most
characteristic clinical phenomenon of pericarditis. In some instances one
or more relapses occur, with corresponding increase of the symptoms after
their subsidence. Acute pericarditis may run a favourable course in a few
days, even when there is considerable effusion, which then undergoes rapid
absorption. The entire duration of the majority of cases is from eight
or ten days to a fortnight, but not uncommonly longer; convales-
cence may not be established for three to six weeks or more, or the
disease, after beginning more or less acutely, may afterwards assume a
subacute or chronic course. As a rule it terminates in recovery, so far
as the immediate result is concerned, and no doubt in a considerable
proportion of cases the restoration is practically cotnplete ; but in not a
few instances definite organic changes are left behind, the effects of
which are sooner or later revealed, it may be within a short period.
Sometimes the patient can hardly be said to recover, a condition of
obvious chronic pericarditis being established, with well-marked symp-
toms and physical signs which will be considered later. It is impossible
to make any definite statement as to the direct fatality of acute peri-
carditis, and the more important points bearing upon this matter will be
more conveniently referred to under prognosis. It may be affirmed how-
VOL.V 3 13
770 SYSTEM OF MEDICINE
ever, that death is selilom due solely to this aifection, though evidences
of pericardial inflammation may not uncommonly be found at post-
mortem examinations, or it may partly contribute to the fatal result.
Occasionally acute pericarditis assumes a very grave aspect from the
first, advancing with great rapidity, exhibiting extremely severe symptoms,
and ending in death within a short time, it may be even in less than
twenty-four hours ; but such a course of events only occurs under special
circumstances, and mainly in heemorrhagic cases.
Tlie course of rheumatic pericarditis in children is described by Dr.
Cheadle as usually subacute, chronic, recurrent. It frequently merges
into the condition of pericardial adhesion and its consequences, with
their attendant phenomena. [For fuller details the reader is referred
to the article, "The Acute Eheumatism of Childhood," vol. iii. p. 44
et seq.]
Diagnosis. — Several important matters bearing upon the diagnosis
of acute pericarditis have been sufficiently dealt with under its clinical
history, especially in the discussion of its physical signs ; and in further
consideration of this part of the subject, I propose merely to draw atten-
tion to its more prominent and important aspects.
An ordinary case of acute pericarditis arising in the course of definite
rheumatic fever ought to present little or no difficulty in diagnosis, if
due attention be paid to the symptoms and physical signs. Eemember-
ing, however, that the inflammation may supervene very insidiously in
this complaint, and when the joint-symptoms are not pronounced, it is
necessary, whenever any rheumatic condition is suspected, to be constantly
on the watch for its appfearauce. Nor must we forget that pericarditis
may be the first indication of such a condition. From these points of
view it is a disease to be particularly watched for in children, though in
such subjects its symptoms and signs, as well as its mode of progress,
may be very anomalous, even where there is well-marked or perhaps
a large pericardial effusion, a state of things, however, which ought not
to occasion any difficulty to an intelligent and practised clinical observer.
The occurrence of acute pericarditis in other than rheumatic cases may
easily be overlooked by an incautious observer, but it should be thought of
at any rate as a possible complication of Bright's disease, or of pneumonia
or pleurisy.
Assuming that the diagnosis of pericarditis has been made, it is
obviously very important to determine, within due limits, and without
endangering or needlessly distressing the patient, the actual morbid con-
ditions present, and more especially the amount and characters of the
fluid effusion, as well as the changes which take place during the pro-
gress of the case. Most of these points can be positively made out by
physical examination only, conducted on the lines already explained. It
must not be forgotten that extensive friction-sound is not incompatible
with a very abundant effusion. The rapid extension of general peri-
cardial adhesion in some cases is also worthy of note, especially in
children. The probability of the fluid being hsemorrhagic, suppurative,
DISEASES OF THE PERICARDIUM 771
or ichorous is mainly founded on the conditions with which the peri-
carditis is associated, and on the general symptoms ; yet these may be in
no way characteristic.
What other conditions of the pericardium, or of the heart itself, are
apt to be confounded with pericarditis ? A dropsical accumulation —
hydropericardiwm — may certainly be mistaken for an inflammatory effusion,
especially if it be abundant. However, the circumstances under which
it occurs, the fact that it usually follows hydrothorax, the absence of
symptoms of pericarditis and of any friction phenomena, and, as a rule,
the comparatively small amount of the effusion, will usually enable a
diagnosis to be arrived at readily. A morbid growth involving the peri-
cardium has more than once been mistaken for pericarditis with effusion.
The distinction of pericarditis from endocarditis at an early stage is
mainly founded on the differences between the tactile and ausculta-
tory signs already discussed, but the symptoms may also help. When
marked effusion occurs, any previous difficulty is cleared up. Of course
the frequency with which the two diseases are associated together, espe-
cially in children and young subjects, must always be borne in mind.
Implication of the heart substance is indicated by evidences of serious
embarrassment and feebleness of its action, and when grave symptoms
arise in the course of pericarditis, changes in the muscular tissue of the
heart may be regarded as highly probable. Much has been written
about the difficulties of distinguishing between pericardial effusion and
cardiac enlargements, especially dilatation, but in my opinion they have
been greatly exaggerated, when we remember that due consideration is
to be given to all the facts of an individual case. It is possible, indeed,
that a much dilated heart, especially if associated with extensive ad-
hesions, might be mistaken for effusion ; and such a mistake has actually
happened several times, the heart having been punctured in an operation
for the removal of a supposed pericardial collection of fluid. Difficulty
might also arise when acute dilatation with rapid adhesion occurs in
pericarditis, instead of effusion. Should inflammatory effusion supervene
where the heart is enlarged, and the pericardial sac distended, the dia-
gnosis might likewise be obscure ; as well as when acute inflammation
involves a narrow area of the pericardium, the rest of the sac being
obliterated by previous adhesions.
The diagnosis of acute pericarditis from neighbouring conditions is,
as a rule, quite easy. Occasionally the distinction between this com-
plaint and pleurisy might be difficult, and certainly this applies to the
friction-sound. A superficial exo-pericardial sound, or even a fremitus
produced in the mediastinal cellular tissue, might also simulate peri-
cardial phenomena. The only circumstance in which a pleural effusion
is at all likely to resemble one in the pericardium is when it happens to
be peculiarly limited by previous adhesions. It has been stated that
such conditions as pneumonia, phthisis, aneurysm, accumulation of fat, or
intrathoracic tumour might be mistaken for acute pericarditis, but I have
certainly never met with any difficulty of this kind. It must not be
772 SYSTEM OF MEDICINE
forgotten that this disease may be associated with other inflammatory
affections within the chest, or be secondary to certain adjacent morbid
conditions.
Prognosis. — ^Acute pericarditis must be regarded as a serious disease,
thoagh in uncomplicated cases the immediate prognosis is usually favour-
able. The mortality is comparatively small, but it is not practicable
to give any definite percentage of deaths. Much depends upon the
conditions .with which the disease is associated, rheumatic cases being
seldom immediately fatal. It is far more dangerous when it supervenes
in connection with Bright's disease or other such grave chronic maladies,
and is then likely to end fatally. Septic cases of all kinds are also very
grave. Seeing that pericarditis and endocarditis so often go together,
the prognosis under such circumstances must be guided by a due con-
sideration of the effects of the combination in each particular case ; but
obviously it must always be more serious, especially if the myocardium
is involved also. When there are other acute inflammatory affections
within the chest, in addition to those implicating the heart and its cover-
ing, the danger is very imminent.
Among the factors influencing the immediate prognosis in individual
cases the following are worthy of note : — Pericarditis is very serious in
infants and young children ; and the very fatal form described by Sturges,
attended with grave nervous symptoms, and ending in rapid adhesion,
must again be specially mentioned. In old people also the danger is
decidedly greater. Previously impaired health, or a weak condition of
the patient, and particularly the presence of old heart trouble or other
chronic diseases, especially intrathoracic, may further complicate matters.
The character and amount of the morbid products in acute pericarditis
greatly affect the prognosis. The danger is obviously more serious in
proportion to the quantity of fluid effusion ; as well as if there be reason
to believe this to be of a hsfemorrhagic, purulent, or ichorous nature.
Due observation and study of the symptoms may afford important indica-
tions. Among those of more or less grave import are serious dyspnoea,
especially if amounting to orthopnoea, with signs of cyanosis or asphyxia ;
greatly embarrassed or very feeble or irregular cardiac action, with corre-
sponding pulse, and tendency to faintness or syncope ; hyperpyrexia ;
dysphagia ; severe vomiting ; marked prostration ; and pronounced cere-
bral or other nervous disturbances. The general appearance and the
expression of the face and eyes are often useful guides to the immediate
prognosis. It must never be forgotten that sudden death from syncope
may happen in cases of large effusion into the pericardium, especially if
the patient is made to sit up, or to change his posture for the purpose of
physical examination. Finally, the mode of treatment materially influences
the immediate prognosis in acute pericarditis. Undue activity may cer-
tainly do much mischief ; but, on the other hand, a dread of energetic
measures, when circumstances demand them, may as certainly lead to
a fatal result.
The remote prognosis in a case of acute pericarditis always demands
DISEASES OF THE PERICARDIUM 773
special attention, though it is often impossible to give a positive opinion
on this point until the course of events has been watched for some time.
I believe that the general tendency is to take too favourable a view of
the ultimate prognosis, and not adequately to recognise the importance of
the after-effects of the inflammatory changes. Such after-effects are met
with in a considerable number of cases, and may be very serious, as will
be pointed out in relation to pericardial adhesions. They are more likely
to give trouble in proportion to the amount of lymph effused ; to its
presence over the exterior as well as the interior of the pericardium ;
to the slow or subacute progress of the disease ; and to the formation
of pus.
Treatment. — The treatment of each individual case of acute peri-
carditis demands careful and intelligent consideration, and it is decidedly
a mistake to follow any regular routine plan, or to adopt needlessly
active measures. When it occurs in connection with rheumatism it may
not be requisite or desirable to change the previous treatment in any
way, but much will depend upon the nature and degree of the morbid
changes which the pericardial inflammation produces. The administra-
tion of salicylates is not contra^indicated, and many believe that they
help in averting the complaint, but certainly their use requires caution.
Dr. Gee has recently stated that large pericardial effusions are much less
commonly met with now than formerly, and suggests that this may be
due to the use of salicylates. Whether it be possible to prevent the
development of pericarditis in rheumatic cases is a doubtful question, but
at any rate complete rest, avoidance of chill, and due protection of the
precordial region may help in this direction. Should there be a tendency
to much cardiac excitement, I believe it is a good plan to administer
opium or morphine as a preventive measure in suitable cases, the effects
being of course duly watched.
When acute pericarditis has actually arisen, the treatment must be
guided by circumstances. In every case the patient must be kept as
much as possible at rest, and must not be unduly disturbed or moved for
the purpose of physical examination. Posture must be intelligently studied
in relation to the pericardial conditions, the symptoms, and the feelings
of the patient. As fluid accumulates it is often necessary to have the
head and shoulders raised ; but, if so, the patient should be propped up
comfortably and effectually supported ; this arrangement requires special
attention. The judicious administration of nourishment constitutes an im-
portant part of the treatment in many instances ; and alcoholic stimulants,
especially brandy and champagne, are often needed ; the quantity must
be determined by the requirements of each individual case, as judged
chiefly by the degree of general weakness or depression, and the cardiac
action and pulse. In bad cases a considerable amount may be
required.
The treatment of acute pericarditis in the early stage has for its objects
the relief of pain and restlessness, the calming of the heart's action, and
the arrest or control of the inflammatory process. The practice of
774 SYSTEM OF MEDICINE
bleeding and giving calomel, formerly adopted by many as a matter of
routine, need only be mentioned to be absolutely condemned ; nor in my
opinion can anything favourable be said for the use of cardiac depress-
ants, such as antimony, aconite, or green hellebore. In suitable cases
advantage may certainly be derived sometimes from the application of
a few leeches. As a rule, however, efficient poulticing over the front of
the chest gives most relief at first, and answers best in the majority of
cases, cotton-wool being afterwards applied. Fomentations or spongio-
piline are also convenient applications. I have thought that the applica-
tion of a blister over this region at an early period has in a few instances
checked the progress of the inflammation, but it is easy to be deceived
in this matter. The application of cold, by means of ice-bags over the
precordium, is strongly advocated by Dr. Lees and others, but this
treatment certainly requires caution. Should the pain be severe, opium
may be given, Dover's powder being a useful preparation ; or morphine
may be administered subcutaneously, and repeated as occasion demands.
There is no harm in judiciously applying anodynes, such as belladonna,
over the precordial region ; but I doubt whether they are really bene-
ficial.
The treatment of pericardial efiusion must be guided by its quantity
and mode of progress. If it is not abundant, and shows the natural
tendency to become absorbed quickly, no special measures are needed.
Otherwise it may be desirable to apply a blister, or even two or more
in succession. Some prefer applications of tincture or liniment of iodine
as counter-irritants ; others advocate the inunction of mercurial ointment
or oleate of meroiu'y. The internal administration of iodide of potassium
or sodium may be of service, combined with tincture of digitalis. Iron
preparations may also be helpful, especially the tincture of perchloride ;
and a combination of tartrate of iron with the iodide has been recom-
mended. Very active measures to promote absorption are certainly to
be deprecated ; and, when the efiusion is large, special care must be taken
not to make the patient sit up suddenly lest fatal syncope should occur.
In all cases of acute pericarditis it is necessary to watch carefully the
action of the heart and the pulse from the point of view of treatment. I
have already expressed my opinion that at no time is it desirable to give
cardiac depressants. Some authorities recommend the administration of
tincture of digitalis from the outset, but I do not think that a routine
use even of this drug is desirable. However, should there be any indication
of cardiac weakness, or a marked want of tone in the arteries, with
dicrotism of the pulse, the tincture should be given every three or four
hours in ten-minim doses, its effects being duly watched. Strychnine
afibrds valuable help in bad cases, and may be combined with digitalis ;
or it may even be thought desirable to employ subcutaneous injections of
strychnine and digitalin. Of the use of strophanthus or other cardiac
tonics in pericarditis I have no experience. As temporary stimulants,
ammonia and ether might be of decided service in some cases; or possibly
subcutaneous injection of ether. Of course alcoholic stimulants are often
DISEASES OF THE PERICARDIUM 77S
of the greatest assistance, and large quantities of champagne or brandy
may be demanded. The administration of the agents mentioned in the
preceding remarks needs the most careful supervision, and they must
not be employed indiscriminately or rashly, for it may be desirable at
any time to diminish the dose, or to stop them. Special care must be
taken in the treatment of children.
Pericarditis not of rheumatic origin must always be treated as a part
of the general condition with which it may be associated, such as septi-
caemia, tuberculosis, or renal disease; and in its association with
endocarditis, or with other intrathoracic inflammatory affections, the
knowledge, experience, and judgment of the practitioner will often he
severely taxed, though not uncommonly but little can be done. Much
difficulty may also be experienced in the treatment of symptoms,
which must be conducted on ordinary principles, though considerable
discretion and caution are demanded in carrying them out. Among the
most important symptoms which may need attention are dyspnoea,
especially if accompanied with a tendency to cyanosis or apnoea, dysphagia,
severe vomiting, restlessness and sleeplessness, delirium or other cerebral
disturbances, and high fever. Dr. George Balfour recommends chloral
hydrate as a sedative and antiphlogistic along with digitalis ; it is, how-
ever, a depressant of the heart, and must at any rate be cautiously
used. Want of sleep is a very trying symptom, but such remedies as
sulphonal, trional, or paraldehyde in suitable cases may help us better.
Subcutaneous injection of morphine may be imperatively demanded, even
if risky. Dr. Cheadle speaks highly of nepenthe for children. Inhalation
of oxygen may help the breathing in some cases. The measures to be
adopted to bring down temperature, especially hyperpyrexia, must be
determined by circumstances. Difficulty in swallowing may, perhaps, be
relieved by making the patient bend forwards, so as to relieve the oeso-
phagus from the pressure of the distended pericardium ; but special care
must be exercised in doing this. The bowels need due regulation ; and
in bad cases it is important to see that the bladder is properly emptied.
The quantity of a serous effusion, and the imminent danger to life
resulting therefrom in exceptional cases, may raise the question of sur-
gical interference, but I cannot agree with those who are too ready to
resort to paracentesis for pericardial effusion. It is rarely required at
any rate in rheumatic pericarditis. Dr. Clifford AUbutt (1) was the first
to introduce as a practice the operation of paracentesis pericardii into
this country in 1866, when it was successfully performed on a patient of
his by Mr. Wheelhouse ; the patient, who was moribund at the time of
the operation, made a good recovery. In another case it was performed
for him by Mr. Teale in 1869. For a full description of the operation
reference must be made to surgical works (see especially Surgery of the
Chest, by Mr. Stephen Paget), and it will only be necessary to refer here
to two or three practical points. To determine that fluid is really present
an exploratory puncture may be made, in the first instance, with a hypo-
dermic syringe ; and, as a dilated heart has even within a recent period
776 SYSTEM OF MEDICINE
been actually perforated for a supposed pericardial effusion, this precau-
tion is certainly advisable in any obscure case. Some prefer even to
make an incision 'down to the pericardium. The fluid is best removed
by means of an aspirator with antiseptic precautions, but the instrument
must not be too powerful, as the effusion needs to be taken away very
gradually. Some operators prefer a small trochar and canula. Either
the fourth or fifth left interspace' is usually selected, at a distance of an
inch (Dieulafoy) to 2 or 2 1 inches from the margin of the sternum ; but
the exact spot may vary with circumstances. The puncture has even been
made on the right of the sternum. Eotch recommended the fifth right
interspace. The late Marcus Beck recommended the use of a No. 2
needle, which he passed obliquely upwards and inwards, taking care to
turn on the vacuum as soon as the eye is covered. The moment the
fluid gets into the syringe the needle must be held steadily until the flow
ceases. The patient must be in the recumbent posture during the opera-
tion, and its effects carefully watched. When pericardial is associated
with pleural effusion, the removal of the latter may sufficiently relieve all
urgent symptoms, but if it tend to return it may then become necessary
to relieve the pericardium also. The subject of paracentesis pericardii
has been very ably dealt with in a paper by Dr. Samuel West, who gives
a tabular summary of eighty cases thus treated up to 1883. Subse-
quently it has been discussed by Sir T. Grainger Stewart and others,
and many scattered cases have been recorded.
The management of cases of pericarditis during convalescence is a
matter requiring due consideration, especially in relation to the formation
of adhesions. Personally I have been disposed as a rule to enforce pro-
longed rest, but some years ago Dr. Cantlie drew attention to the
desirability of encouraging exercise after an attack of acute pericarditis
in young subjects, with the view of exciting the cardiac action, and thus
helping to make the adhesions loose and filamentous. This question has
usually to be considered in relation to the presence or alisence of endo-
carditis and its consequences, as well as the state of the cardiac walls ; so
no general rule can be laid down, and every case must be studied on its
own merits.
II. Suppurative pericarditis; Pyopericardium
The formation of pus within the pericardium has already been men-
iioned under acute pericarditis, but it will be expedient briefly to consider
this condition separately, including also those cases in which the fluid is
of an ichorous kind.
Etiology and Pathologry. — Pyopericardium is occasionally acute in
its manifestation, but is much more commonly the result of a subacute or
chronic process. It is very rarely the outcome of an ordinary acute
pericarditis, either primary or rheumatic, being then a late or secondary
phenomenon, a serous or sero-fibrinous effusion gradually changing into a
DISEASES OF THE PERICARDIUM 777
more or less purulent collection. In the large majority of cases, however,
the circumstances under which such a collection is met with are peculiar,
and it may not only be formed within the pericardium, but in some in-
stances is partly due to the bursting of a neighbouring accumulation of
pus into the sac. Pathologically it is associated, of course, with
pyogenetic organisms. It has been stated that the production of pus
within the pericardium is favoured by abundant exudation, and the
extensive formation of new blood-vessels in its substance. The longer a
])ericardial effusion remains unabsorbed the more likely it is to become
purulent.
Pyopericardium occurs most frequently in cases of pyaemia or septi-
csemia of all kinds ; thus it may appear as a complication of certain
of the eruptive fevers. It has been said to be associated particularly
with injuries and diseases of bones, such as osteomyelitis and acute
necrosis. Purulent pericarditis is more likely to occur if an abscess
has previously formed in the myocardium, but this is by no means neces-
sary. Very rarely it appears to have been secondary to malignant
endocarditis. In another class of cases pyopericardium is due to the
rupture of a neighbouring collection of pus into the sac, especially of an
empyema ; or it may even be set up by contaminated air, which has
entered through a perforation. Exceptionally it results from the exten-
sion of empyema, low forms of pleuro-pneumonia, neighbouring ulcerative
or gangrenous diseases or abscesses, or possibly peritonitis. The peri-
carditis associated with Bright's disease is believed to have a special
tendency to the formation of pus ; and a similar tendency has been
attributed to the tuberculous variety. Among the cases of operation
collected by Dr. Samuel West (53), however, in no instance of tuberculous
pericarditis was the effusion purulent. Such a condition may be associated
with pulmonary phthisis, owing to the rupture of a cavity into the sac.
Pyopericardium is far more common in young subjects, and in males.
Anatomical ehapaeters. — As the name indicates, the essential change
in pyopericardium is the presence of pus in the sac. It may be in small
amount, or the accumulation may be very large ; in the latter case it will
produce the same mechanical effects upon the heart and neighbouring
structures as other forms of effusion. In Dr. Dickinson's most interesting
case ( 1 7) as much as 1 9 ^ oz. were drawn off at one time ; and in Dr. Samuel
West's case 14 oz. and 16 oz. were successively removed. It may collect
entirely in the posterior portion of the pericardium, the anterior surfaces
being adherent as in a case of Sears. The pus is usually laudable and
inodorous, but may often be shreddy, flocculent, curdy, or even mem-
branous ; and it may be mixed with lymph. Exceptionally and under
particular circumstances it is offensive, and may be of an "ichorous"
nature, very foul or even stinking. It may also become foetid after
operation. Occasionally there is an admixture of blood. In most cases
the surface of the membrane becomes like that of the granulating surface
of a wound. Earely part of the parietal pericardium becomes destroyed,
and perforation takes place, which has even ended in a superficial fistula ;
778 SYSTEM OF MEDICINE
but at the present day such a termination could hardly be permitted to
occur. There seems to be good reason to believe that a purulent collection
in the pericardium may in exceptional instances be absorbed, leaving
dense and thick adhesions ; or some of it may remain in an inspissated
condition as a yellowish white paste, limited and encapsuled by adhesions,
consisting of caseous material, in which calcareous particles may after-
wards form ; thus it may ultimately be converted into a chalky pulp, or
even into a hard calcified mass.
Clinical history, Diagnosis, and Prognosis. — Speaking generally,
the symptoms and physical signs of pyopericardium will be more or less
like those of serous effusion, modified not • only by the quantity of the
pus, but also by the circumstances under which it has formed. It will
only be necessary, therefore, to draw attention to certain special points
in the cKnical history of this condition. When it supervenes in an ordi-
nary case of acute pericarditis, there are no trustworthy indications of a
change from a serous or sero-fibrinous effusion to one of a purulent
nature ; but if the course of the case happens to be prolonged, such a
deterioration would be suggested if fever, perhaps of a septic type, per-
sist. Pyrexia may, however, be entirely absent. Considering the circum-
stances under which pyopericardium occurs, it is easy to understand
how insidiously it may set in ; its symptoms, if any, being entirely over-
shadowed by those of septicaemia : thus it often remains undiscovered
until the necropsy, especially if the amount of pus be small. In cases
of this kind symptoms of serious interference with the respiratory and
circulatory functions may show themselves suddenly ; and on examination
be found to be due to a large but previously latent purulent collection
in the pericardium. General symptoms are of little or no value in the
diagnosis of pyopericardium. In some of the most pronounced cases
neither rigors, pyrexia, nor sweating have been present. CEdema of the
legs seems not to be uncommon, but probably is not more frequent than
in connection with other large pericardial effusions and their consequences.
It may be noted here that oedema over the precordial region may suggest
the purulent nature of such an effusion.
With regard to the physical signs, the absence of friction-sound
throughout cases of purulent pericarditis has been noted by careful
observers ; or it may be very indefinite and transient. Whether this
sign be usually absent, as has been affirmed, it is difficult to say ;
at any rate it cannot be relied upon in diagnosis. The ordinary signs
indicative of pericardial efi'usion will be evident on examination, in
proportion to the amount of the pus. Should gas be present at the
same time, the phenomena associated with this combination will probably
be noted, but these will be considered separately.
From the foregoing remarks it will be gathered that the diagnosis of
pyopericardium is extremely uncertain, and often impossible. Should
there be evidence of effusion into the sac, its purulent nature can only be
determined positively by the aid of the exploring needle or other
apparatus, by which a specimen can be obtained for examination. Some
DISEASES OF THE PERICARDIUM 779
such instrument should be used at once if there be any reason to suspect
the presence of pus.
The prognosis of pyopericardium is necessarily grave, especially on
account of the conditions with which it is associated. In suitable cases,
however, efficient operative interference gives reasonable hope of recovery ;
and some remarkable results have been thus achieved by modern
surgery.
Treatment. — The treatment of pyopericardium is entirely surgical,
and it would be quite beyond the province of this article to attempt to
discuss the important questions involved. Suffice it to say that mere
paracentesis is of uo use ; the operative procedures adopted must be
thorough and bold, and should be carried out as promptly as possible.
Free incision, with drainage and due antiseptic precautions, is the method
of treatment usually practised.
III. Chronic pericarditis ; Chronic effusion ; Pericarbial
ADHESIONS AND THICKENING
The cases which come within the category of chronic pericarditis may
be arranged for practical purposes under two groups ; namely, those
of — (1) Chronic effusion; (2) Pericardial adhesions and thickening. These
conditions are in exceptional instances more or less combined, but it is
needless to make an independent group of such complex cases. It will be
sufficient to discuss separately the two main divisions just indicated.
1. Chrome pericardial effusion. — This morbid condition requires
but brief comment. It occasionally happens that acute or subacute in-
flammatory effusion into the pericardium remains chronic, though fluc-
tuating in amount ; or it may return again and again after paracentesis.
In rare instances even a simple pericarditis is chronic from the outset ;
but this course of events is observed chiefly in elderly persons, and there is
reason to believe that in some of these cases the effusion is originally a
mere hydropericardium. Chronic pericarditis is more likely to be of a
hsemorrhagic or purulent nature ; or it may be associated with new
growths, especially tubercle or malignant disease. Dr. Samuel West
mentions a remarkable case of supposed mediastinal cyst, which was
tapped several times during a period of four years; the fluid removed
on the first occasion deposited a large amount of cholesterine ; on post-
mortem examination it proved to be a chronic pericardial effusion. In
very exceptional instances an accumulation of this nature originates a
diverticulum of the pericardium.
Clinically, chronic pericardial effusion does not, as a rule, give rise to
any prominent symptoms ; practically it is only recognisable by the
physical signs already described. In prolonged cases, owing to the
changes produced in the pericardium and the walls of the heart, the cir-
culation becomes more or less seriously obstructed, with the usual
symptoms, including dropsy. The treatment of this condition must be
conducted on the general principles applicable to different kinds of pert
78o SYSTEM OF MEDICINE
cardial eflfusion, some operative procedure being generally required ; but
each case must be dealt with on its own merits.
2. Pericardial adhesions arid thickening. — The conditions coming under
this head are of much pathological and clinical importance, and are
worthy of far more attention than they generally receive. It is a familiar
fact that they are frequently met with at necropsies in various degrees,
when they have not been diagnosed during life. It may be acknowledged
at once that their diagnosis is often, for obvious reasons, impracticable,
or may be a matter of great difficulty or mere surmise ; not un-
commonly, indeed, there is no reason whatever even to suspect their
presence. On the other hand, to teach that the diagnosis of adherent
pericardium is impossible is absolutely wrong and misleading. If peri-
cardial changes of this nature were always borne in mind and syste-
matically looked for, they would be recognised much more frequently
than they have been hitherto ; as a matter of fact they are seldom
even suspected in the ordinary routine of practice, and are therefore
necessarily overlooked. Not uncommonly they can be positively demon-
strated by physical examination ; while in other cases their presence
may be reasonably inferred. Dr. John Broadbent, in his valuable mono-
graph on " Adherent Pericardium," duly recognises this truth, and writes :
"The comparative rarity with which the existence of adherent pericardium
is diagnosed may be accounted for in many instances by the fact that it
is not thought of. Especially is this the case when it is associated with
valvular disease, for the valvular lesion is judged to be sufficient to account
for the symptoms that arise."
Etiology. — The various conditions of the pericardium now under
discussion are always of inflammatory origin, and in the large majority of
cases they are the remains of one or more acute or subacute attacks of
pericarditis, of which there is often, but not necessarily, a definite history.
As was mentioned in relation to this disease, extensive adhesions may
rapidly form in the stage of fibrinous exudation, especially in children ;
and if the termination be not fatal, they become organised and permanent.
Most commonly, however, they are formed after the absorption or re-
moval of fluid effusion. As might be anticipated, pericardial adhesions
are likely to be more firm and extensive in proportion to the number of
attacks of inflammation, and to their duration. After a first attack partial
adhesions may form, which in subsequent attacks become extensive or
general. When a pericarditis beginning acutely assumes a prolonged
and chronic course, they are usually well marked, and again when the
effusion becomes purulent. The occurrence of acute inflammation over
the external surface of the pericardium leads to the formation of adhesions
between this structure and the chest wall, the pleurae and, sometimes, the
posterior mediastinal structures or the spinal column.
An important group of cases in which pericardial adhesions and
thickening occur are those which are chronic from the outset, and in these
cases they are particularly liable to be overlooked. They may naturally
be expected when an inflammatory effusion runs a chronic course through,
DISEASES OF THE PERICARDIUM 781
out ; but the cases which must be more especially borne in mind are those
in which there has been no such effusion, but the morbid changes leading
to the pericardial conditions have taken place slowly and imperceptibly.
Some of the " white patches " are of this nature, but the most striking
cases are those in which a chronic inflammatory process extends from
neighbouring structures, particularly in connection with pleurisy or
])ulmonary phthisis. Adhesions are also usually associated with new
growths involving the pericardium, which are practically either of a
tuberculous or malignant nature. When the changes leading to these
conditions have once started, it seems highly probable that they may
extend and increase considerably, as the result of a continued chronic
process, which may be regarded as inflammatory, and leads to a pro-
gressive hyperplasia of fibrous tissue. In this way it may possibly happen
that an adhesion may, as it were, grow through the parietal portion
of the pericardium from within outwards or from without inwards, and
thus ultimately fix it more or less extensively on both aspects.
Pericardial adhesions may be met with at all ages. They have been
observed in very young infants, and even in new-born children, when
they are attributed to pericarditis occurring during foetal life.
Anatomical eharaeters and effects. — It would not serve any useful
purpose to describe in detail the numerous and varied aspects under
which pericardial adhesions present themselves, but a comprehensive
knowledge of the more important groups of cases in which changes of
this kind are met with is of decided practical advantage. Before
attempting any such classification it will be well to point out that the
adhesions are either partial or general ; internal or external, or both ; that
they differ much in length, toughness, and firmness, and are often ac-
companied by more or less pericardial thickening, which may reach an
extreme degree. In exceptional instances there is much thickening,
with little or no adhesion between the surfaces. Structurally the morbid
formations now under consideration consist either of cellular or fibrous
tis&Me^-peneardial fibrosis. Sometimes they are associated with the en-
capsuled remains of fluid, thickened pus, soft caseous or chalky pulp, or
dry brittle calcareous concretions, which may attain a considerable size.
As already stated, an adherent pericardium may itself undergo calcifica-
tion. The effects which the morbid changes may produce upon the
heart and vessels must be considered separately.
The groups under which I propose to arrange the cases, as they have
come under my personal observation, are as follows : —
(a) In a large proportion of instances there are merely partial and
small adhesions between the contiguous surfaces of the pericardium, it
may be in different portions of the sac at the same time. Usually such
adhesions assume the form of filaments or threads, or of bands, often of
considerable length, stretching between the two surfaces. They may be
delicate and cellular, or firm and fibrous, sometimes attaining the thick-
ness of a finger or more. Occasionally adhesions occur in circumscribed
closely adherent spots or patches. Ultimately the bands often give way
782 SYSTEM OF MEDICINE
by stretching and attenuation, their remains hanging loosely within the
sac, especially near the apex of the heart. The situation, extent, and
characters of localised pericardial adhesions are affected by the degree
and range of the movements of different parts of the heart and arteries ;
the relation of the heart to the pericardium ; and the effects of gravitation
of the organ within the sac in cases of effusion. According to Sibson,
they are more frequent a little above and to the left of the apex, and
along the line of the ventricular septum ; at the outer border of the left
ventricle, and the outer side of the right auricle ; along the posterior
surface of the left auricle and of the ventricles which rest upon the sac ;
and over the great arteries at their higher part. In several instances he
noticed that a patch of the right ventricle, to the right of the septum and
midway between the pulmonary artery and the lower border of the
veptricle, was adherent, when the rest of the ventricle was free ; this
being the part of least extensive movement.
(h) A second group of cases may be made to include those in which
an extensive or general internal adhesion exists between the pericardial
surfaces, the external surface being quite free ; and this group may be
subdivided into cases without and with thickening. Here again many
varieties are observed in individual instances, and in the same case the
adhesions often differ in their characters over different parts of the
pericardium. They may be in the form of fibrous threads or bands, more
or less loose and long, and interfering but little with the free play of the
heart ; or of short, close, firm, and strong attachments. Again quoting
Sibson's observations, the adhesions are generally longer at the apex than
elsewhere ; those over the left are longer than over the right ventricle ;
those over the auricular portion of the right ventricle are longer than
those over its body and near the septum, and the same holds good in the
case of the left ventricle. Over the right auricle they are much shorter
than over the right ventricle. The attachments of the left auricle, the
aorta, and the pulinonary artery are generally closer than those of the
right auricle. In some cases the contiguous surfaces of the pericardium
are agglutinated together, the sac being entirely obliterated ; and when
this condition is of old standing, separation of the two surfaces is impossible
without tearing the heart substance. Occasionally, when comparatively
recent, they may with care be drawn asunder ; or firm adhesions of old
standing may exist side by side with those of recent origin, the result of a
fatal intercurrent acute pericarditis, which can be easily broken down.
The degree of thickening differs a good deal, but it may be very remark-
able, as much as a quarter to half an inch or more ; it chiefly affects
the visceral layer. The heart is then enclosed in a dense, strong, tight
envelope or casing, which compresses and strangles the organ in its grip.
(c) There is a distinct class of cases in which the adhesions are
entirely external or exo-perkardial, the outer surface of the pericardium
being more or less extensively fixed to the front of the chest, and often
to the pleurse, while the internal surfaces are quite free. They are usually
chronic in their course, and secondary to neighbouring morbid con-
DISEASES OF THE PERICARDIUM 783
ditions ; they are especially met with in association with very chronic
phthisis. These exo-pericardial adhesions may, however, extend from
similar pleuritic changes, or may possibly result from a mediastinitis
occurring at the same time as the attack of pleurisy which led to the
pleural lesions. I have comparatively recently had under my care a case
in which pericardial and pleuritic adhesions were diagnosed, associated
with extreme double mitral disease and much enlarged heart ; and except
that the pericardial adhesion was entirely external, the diagnosis proved
to be correct. The condition now under consideration is really mediastinal,
and has been named chronic mediastimtis {vide " Diseases of the Media-
stinum," vol. vi.)
(d) The most serious group of cases of pericardial adhesion are those
which are both internal and external, there being a general matting
of the sac to the heart, as well as to the chest wall in front, to the
adjacent pleurae, especially the left, to the diaphragm more extensively
than in health, and occasionally to the structures in the posterior
mediastinum and the spinal column. As a rule these conditions are
accompanied with much thickening. When there is little or no general
mediastinitis the term pericarditis externa et interna is applied; when
there is a considerable increase of fibrous tissue in the mediastinum the
condition is known as indurative mediastino-pericarditis. [These changes
are more fully dealt with under " Diseases of the Mediastinum,"
vol. vi.] The external adhesions vary considerably in area, but in
extreme cases may extend from the second cartilage to the sixth ; from
the manubrium to the upper half of the ensiform cartilage ; and from the
right border of the sternum to the apex of the heart to the left o£ the
nipple line (Sibson).
(«) Exceptional instances are met with in which the prominent
change is marked thickening of the pericardium, especially of its visceral
portion, with little or no adhesion of the surfaces ; and there may even be
more or less fluid incarcerated between them. It is important to bear
this variety in mind, for it may produce very serious eifects upon the
heart, with the consequent symptoms, without giving rise to any of the
physical signs of pericardial adhesion. A very striking illustrative
example was under my care not long ago in University Hospital.
affects upon the heart and great vessels. — There has been much con-
troversy as to the effects of pericardial adhesions upon the heart ; they
may vary much, of course, under different circumstances. In a consider-
able proportion of cases the organ is unaffected, either functionally or
structurally, and, provided it be free from valvular disease, remains of its
normal size. The obvious tendency is to embarrass its action more or
less; the embarrassment is greater in proportion to the extent and
firmness of the adhesions, and greatest when they are both internal and
external.
One of the most frequent and important structural changes affecting
the heart which may result from adherent pericardium is enlargement of
the organ. Hope maintained that this morbid condition always gave rise
784 SYSTEM OF MEDICINE
to compensatory cardiac hypertrophy ; but systematic and accurate
observations have amply shown that such a statement is not correct :
even complete obliteration of the sac is not necessarily followea by
enlargement. No trustworthy statistics of the frequency of this cflange
can be given ; but it is certainly not uncommon. There is a distinct
class of cases in which this lesion is the sole cause of considerable
enlargement of the heart, which probably occurs in more than half ot
such cases (Sibson affirmed in about two-thirds) ; while in other instances
the increase in size may be due mainly to associated valvular disease.
Indeed it has been questioned whether in the latter group of casea
the pericardial changes have anything to do with the enlargement,
Sibson compared a double series of cases of valvular disease side by side,
in the one series with, in the other without, adherent pericardium. He
found that the cases with adhesions were on an average 5J ounces
heavier than those in which there were no adhesions; but, in many
instances, the increase was to a considerable extent accounted for by the
augmented thickness and weight of the pericardial sac. He concluded
that in these cases the valvular disease is the essential cause of the
enlargement of the heart, yet that the adhesions, by an additional demand
upon the strength of the organ, add to the enlarging causes. From
personal observations I am decidedly of opinion that a generally adherent
pericardium, when associated with valvular disease, does often materially
contribute to the cardiac increase ; at any rate it promotes and hastens
its development.
With regard to the mode in which adherent pericardium may
promote cardiac enlargement, the explanation usually given and accepted
is that it is mainly by the additional work imposed upon the heart, by
the hampering of its movements and the increased resistance, aided
by the changes in the myocardium which accompany the process.
It has also been suggested that the eccentric contraction of cicatricial
tissue may in some instances bring about dilatation of the ventricles,
especially when the structures are fastened to the spinal column or anterior
chest wall. It seems highly probable that inability on the part of these
cavities to empty themselves, on account of the adhesions and muscular
changes, may lead to dilatation, followed by compensating hypertrophy.
Dr. John Broadbent gives the following explanation of the cardiac
enlargement, when it occurs : — " When the heart is found to be dilated and
hypertrophied as a result of adherent pericardium, there being no valvular
disease to account for it, it is due to the fact that it has been left in a
condition of dilatation after the original attack of pericarditis, and that
.while in this condition of dilatation the pericardium has become adherent;
then the adhesions becoming organised, the heart is effectually pre-
vented from again recovering its normal size. Subsequently it under-
goes some hypertrophy." He further believes that, when the heart
is of normal size, it either had not dilated during the original attack of
pericarditis, or else had recovered from its dilatation before adhesions
were formed. I have no doubt that this explanation is applicable to
DISEASES OF THE PERICARDIUM
78s
some cases, but I cannot think that it represents the usual course of
events.
Fig. 49.
Figures sho^ring position of internal organs in cases of adherent pericardium. (Sibson.)
As regards the nature, extent, and degree of the cardiac enlargement,
Bonsiderable differences are observed in different cases of simple peri-
VOL. V ■ 3 J,
786 SYSTEM OF MEDICINE
cardial adhesion. As a rule there is a combination of hypertrophy and
dilatation, the latter commonly preponderating ; and it may exist practi-
cally alone. Both sides of the organ are usually involved more or less ;
but I fully accept Dr. John Broadbent's statement that pericardial
adhesions in themselves are much more likely to aflfect seriously the right
ventricle than the left, for reasons which he has pointed out in his mono-
graph. The auricles are much less affected; indeed it may happen
that, ■while the right ventricle is much enlarged, the auricle is compressed
and may even be practically obliterated. When the enlargement of the
heart is associated with valvular disease, it will necessarily be influenced
chiefly by the nature of such disease, but in particular instances it may
certainly be modified by the adhesions. In some of these combined con-
ditions, with firm adhesions, Sibson described the ventricles as undergoing
a change in form, becoming flattened out, the right in front of the left,
and the septum flattened instead of bulging forwards into the right cavity.
As a result of dilatation produced by adherent pericardium, and involving
the orifices, valvular incompetence is prone to follow, especially at the
tricuspid opening, which may become greatly enlarged.
In a small proportion of cases the effects of pericardial adhesions upon
the heart are quite the opposite to those just considered. In children the
natural growth and development of the organ may be prevented ; or it
becomes small and atrophied, its walls being grasped and compressed, and
its cavities forcibly contracted in size by the dense, thick, tight envelope
surrounding them. This may happen also from mere thickening of the
visceral pericardium, without any adhesion. Other cardiac changes apt
to occur in these conditions are degenerations — either fatty, pigmentary,
or fibroid. They may result from direct pressure, or pressure on the
coronary vessels ; or the last may be due to a chronic interstitial
myocarditis spreading from the pericardium. In some instances, no
doubt, these cardiac changes are the outcome of myocarditis associated
with an acute attack of pericarditis. They are often of considerable
importance, and contribute largely to the symptoms of pericardial adhe-
sions and thickening.
When the pericardium is fixed externally, the great vessels at the
base of the heart are often abnormally exposed. Sibson observed
that with enlargement of the heart " the great arteries are lifted up on
the top of the ventricles into an unusually high position, and are crowded
into the narrow space at the tojs of the chest, almost as high as the root
of the neck." Occasionally one or both are compressed or constricted by
pericardial adhesions ; or their walls undergo degenerative or fibroid
changes. As the result of obstruction to the general venous circula-
tion, produced indirectly by adherent or thickened pericardium, the large
veins become more or less dilated, and such dilatation may ultimately be
extreme.
Clinical history. — It is obviously impossible to give any definite
clinical description that will apply even to the majority of cases of
adherent pericardium ; all I can do will be to point out the symptoms
DISEASES OF THE PERICARI>IUM 7S7
and physical signs whicli may be associated with, this condition, as
well as the relations of these phenomena to each other, upon which a
diagnosis may reasonably be founded. They vary considerably in individual
instances, not only in respect of the actual nature and degree of the
changes affecting the pericardium, but also of their effects upon the
heart, and their association with endocardial lesions, with vascular diseases,
or with neighbouring morbid conditions.
As was stated in the introduction to this subject, a large number of
cases of pericardial adhesion do not exhibit any symptoms or physical
signs whatever ; and, unless there happen to be a well-known history of
acute pericarditis, the condition cannot even be suspected during life.
This applies not only to partial and loose adhesions, which often do not
disturb the heart in any way, but even to cases in which there is general
agglutination of the internal surfaces ; provided the organ itself be not
materially damaged. It is well to bear in mind the possibility of this
condition, if with acute pulmonary inflammatory affections the heart
should exhibit signs of embarrassment quite out of proportion to their
severity. My observations have led me to the conclusion that it may add
seriously to the danger under these circumstances, and even account for
an unexpected death. The more pronounced the pericardial changes, the
more prominent and definite are the clinical phenomena likely to be ; and
they are especially well marked when there is much thickening, and when
the adhesions are both external and internal.
The symptoms and physical signs which may be met with will now be
considered separately.
That pericardial adhesions may be the cause of 'paAn — of painful,
dragging, or other unpleasant sensations over the precordial region, I
have not the slightest doubt, and when in cases of obvious chronic
cardiac disease such sensations are much complained of, their existence
may be reasonably suspected, and they should be carefully looked
for. I have met with not a few instances in which they were associated
with adhesions easily demonstrable on physical examination. Moreover,
the pain occasionally comes on in attacks of an anginal character, when the
case, if accompanied by other symptoms characteristic of such attacks, may
present a perilous aspect. A feeling of precordial oppression, and inability
to take a deep breath, are sometimes prominent symptoms, especially when
the external adhesions are extensive. The patient is usually conscious of
the disturbances of cardiac action associated with adherent pericardium
and is then likely to complain of palpitation, even at rest, but especially
after exertion; and this symptom is sometimes very prominent.
Adherent pericardium ought always to be thought of as a possible cause
of palpitation. The heart's action is in some instances irregular or unequal
and it may be so embarrassed as to lead to faintness or actually to
syncope. The persistence of rapid cardiac action, in spite of treatment
may be important evidence of thfe formation of pericardial adhesions in
children and young persons.
Pericardial adhesions may themselves unquestionably cause dyspnoea
788 SYSTEM OF MEDICINE
on exertion, sometimes well marked ; and thus also they often add to
the difficulties of other cardiac affections. No other respiratory symptoms
can be definitely attributed to these conditions alone ; but when there is
much thickening, with compression of the heart and changes in its walls,
the pulmonary circulation is likely to be embarrassed, and cough,
expectoration, or even haemoptysis to set in.
A very important and prominent group of symptoms in certain
cases of pericardial adhesion are those indicating serious hampering,
or actual failure of the right ventricle, and consequent interference
vnth the general venous circulation. These either come on gradually,
becoming more and more pronounced ; or, occasionally, they supervene
with great rapidity, the ventricle appearing to break down and give
way very speedily, or even suddenly. They occur not only in cases where
this cavity is obviously dilated, but also where the heart is strangled
and compressed by dense fibrous thickening ; and in such cases they may
be extreme. No doubt they depend in great part upon the associated
changes in the cardiac structure. These symptoms are similar to those
which arise in other forms of heart disease affecting the right side; namely,
general dropsy, involving the serous cavities as well as the subcutaneous
tissue more or less extensively, congestion of the hepatic and portal
system and its consequences, and also of the kidneys, nervous system,
and other structures. The dropsy usually begins in the legs, but it may
ultimately involve the trunk, and even the arms. In exceptional instances
ascites is noticed before anasarca. Eemarkable cases occasionally occur,
entirely due to pericardial adhesions and their consequences, in which the
peritoneal cavity and pleurse become repeatedly full of fluid, and have to be
tapped again and again in order to afford temporary relief. Under these
circumstances the breathing is likely to be much distressed, even to
the degree of orthopnoea. The appearance of the patient differs in
different cases. Cyanosis with distended veins may be evident; or,
on the other hand, there is sometimes marked pallor, with puffiness of
the face. The liver becomes enlarged so that it can readily be felt
below the ribs, and may be painful and tender. Occasionally it reaches
even below the umbilicus, appearing to be very large ; but then it is
usually displaced downwards as well : after a time the organ yields an
a,bnormally firm sensation on palpation, and may become irregular ; in
prolonged cases it may even pulsate. Symptoms connected with the ali-
mentary canal are often prominent, and sickness may be troublesome. The
spleen is sometimes perceptibly enlarged. The urine is more or less
diminished in quantity, concentrated, and often albuminous. I have known
the amount of albumin to be so large that the urine became almost solid on
boiling, simulating serious renal disease. In bad cases the patient is very
Testless and sleepless.
Dr. John Broadbent, speaking of the symptoms which have just been
•discussed, deduces from his observations the following corollary : — " That
when symptoms of right ventricle failure supervene in cases in which
there is no evidence of left ventricle failure due to valvular disease or
DISEASES OF THE PERICARDIUM 789
kidney mischief, constant high tension, or other obvious causes, or of
lung disease such as chronic bronchitis, etc., to account for their appear-
ance, the presence of adherent pericardium should be suspected as the
cause, and other indications of it carefully sought for. So, too, in
valvular disease of the left ventricle, in which the lesion is judged to be
slight, and compensation breaks down unaccountably, adherent pericardium
should be thought of." Further, speaking of the difference in the symp-
toms of right ventricle failure when due to pericardial adhesions, and
when secondary to valvular disease of the left ventricle, he writes : "In
cases of right ventricle failure attributable to adherent pericardium, there
is no cyanosis, though the respirations may be hurried, and there may be
some dyspnoea ; there may be an entire absence of dyspnoea, though the
other symptoms are severe ; there is usually no congestion or oedema of
the lungs. The dyspnoea, when present, is probably due to deficient
supply of blood to the lungs and a feeble pulmonary circulation owing to
the failing powers of the right ventricle." While fully recognising
the correctness of these conclusions in their application to a certain class
of cases, I must point out that they by no means always hold good in
relation to adherent pericardium ; for the effects of the difficulties in the
right side of the heart may themselves lead to cyanosis and dyspnoea,
while the limgs may be also implicated when the entire heart is gripped
by strong adhesions. Moreover, pericardial adhesions may help in pro-
ducing this class of symptoms in cases where there is pronounced valvular
disease on the left side.
Physical signs. — The existence of pericardial adhesion can often
be recognised positively and demonstrated by careful and systematic
physical examination ; and it is most desirable to have a clear and
definite knowledge of the signs which, in different combinations, have
to be looked for and studied in respect of this condition. At the same
time it must be understood that they are frequently absent, or at any rate
not at all characteristic ; and this may happen even when there are very
pronounced symptoms directly due to an adherent pericardiiun ; for
example, if the heart is compressed and atrophied, though the symptoms
may be extreme, the signs will be wholly indefinite. They are likely to
be better marked as the adhesions are more extensive and dense, and
especially when these are external as well as internal. They result not
only from these lesions themselves, but also from their effects upon the
heart and vessels, and upon the circulation. They may be considered in
the following order : —
(i.) Change in shape. — In exceptional instances a distinct and permanent
depression of .more or less of the precordial region, with narrowing of
the intercostal spaces, is observed ; the structures being drawn in by thick
external adhesions. Far more commonly, however, there is abnormal
fulness or bulging, due to enlargement of the heart ; but as this usually
depends mainly on other causes, it can hardly be regarded as an indication
of adherent pericardium, except under particular circumstances.
(ii.) Signs associated mth cardiac movements. — Certain visible and tactile
790 SYSTEM OF MEDICINE
signs coming under this head are of the utmost importance, and demand
somewhat detailed consideration. Sometimes there are peculiarities in the
cardiac movements which cannot well be described, but which are very-
suggestive of these changes, when prominent cardiac symptoms are present,
and are not obviously due to any other organic affection of the heart.
The following are the more definite signs to be studied : —
(a) Apex-beat. — In cases of adherent pericardium, the ordinary apex-
beat presents many differences as regards its position, force, and characters;
but these depend mainly upon the effects of the particular valvular
disease or diseases with which the condition happens to be associated.
Thus it has been noticed far to the left, and presenting all the
indications of a greatly hypertrophied left ventricle. One of the signs
to be looked for is a displacement of the apex-beat, which is fixed
in its abnormal position, and cannot be modified by any change of
posture. As a rule it is carried somewhat outwards ; but the most
suggestive displacement is elevation, it may be to the fourth space or even
higher, while perhaps at the same time there may be marked evidence of
hypertrophy. In many instances the apex-beat is very feeble, or even
imperceptible when other phenomena, to be presently described, are well
marked; and even when it extends 1 to \\ inch outside the left
nipple. This is attributed to small size and weak action of the heart ;
to restraint of the organ by adhesions ; or to much thickening of the
pericardium. When it is wholly due to feeble cardiac action, the beat
may at times be perceptible, at other times not. There may, however, be
a distinct impulse over the ensiform cartilage or in the epigastrium.
(6) Impulse. — Taking into account the entire impulse, it must be
admitted that in cases of adherent pericardium great variation of its
situation, extent, force, and characters is observed ; but there are certain
points deserving of attention. A remarkable extension of its area is
often noticed, especially upwards over the precordial region ; and it may
reach the second space or cartilage. This may be associated with obvious
elevation and fixation of the apex ; or it may be impossible to localise
any definite apex-beat. At the same time the impulse is often strong and
superficial, the heart pulsating in close contact with the chest walls. In
some instances the movement presents to the eye a decidedly undulatory
or wave-like character, from the base towards the apex. In others it is
peculiarly jarring, or has an abrupt jogging quality. The rhythm of the
cardiac action is sometimes markedly disturbed, and pericardial adhesions
may undoubtedly give rise to irregularity. When the heart is at the same
time enlarged, the extent of the impulse is correspondingly increased,
often passing considerably beyond its normal limits, and probably tending
more towards the right, in consequence of the greater enlargement of
the right ventricle.
(c) Systolic recession or retraction. — A visible recession or retraction
of certain parts of the chest wall, associated with the ventricular systole,
has attracted much attention in respect of adherent pericardium. There
can be no doubt that the signs coming under this head are of great im-
DISEASES OF THE PERICARDIUM 791
portance in the diagnosis of this condition, and they deserve particular
study in any suspected case. They come practically under three cate-
gories, namely : —
(a) Kecession over the spot corresponding to the apex of the heart,
occurring with or immediately after the systole. This phenomenon, when
present, is usually associated with a definite apex-beat, but is sometimes
noticed when there is no perceptible impulse at this point.
(/8) Systolic depression of more or less of the precordial region,
generally involving one or more of the intercostal spaces to the left of
the sternum, especially the third, fourth, and fifth, along a variable extent
of their length. The movement is sometimes distinctly wavy. In
certain cases, where the adhesions are extensive and strong, and the
heart is acting powerfully, the cartilages are also involved, or indeed
even the lower half of the sternum, the ensif orm cartilage, and the
epigastrium. When the recession occurs simultaneously with an obvious
and strong apex-beat, the combination is very striking, but it may be
indefinite or absent. Should the right ventricle be greatly enlarged, a
similar movement may possibly be visible in the intercostal spaces to the
right of and close to the sternum ; of this I believe I have seen examples.
According to Friedreich, the pitting is more marked at the height of in-
spiration.
(y) Eetraction of the posterior or lateral portions of the thoracic
walls. — I cannot say that I am personally familiar with this sign, which,
when present, is regarded by Dr. John Broadbent as a most important
diagnostic sign of adherent pericardium ; he describes it in the following
words : — " In cases of adherent pericardium, marked systolic retraction
of some of the lower ribs on the lateral or posterior aspect of the thorax
may sometimes be seen. This phenomenon is best seen when the patient
is sitting up in a good light, and the movements of the chest are care-
fully observed from a short distance off, first from the front and then
from the lateral aspect. When a pulsatile movement is seen over the
lowest part of the left side posteriorly, it may at first sight appear to be
expansile. On a more careful scrutiny it will be found that there is a
tug on the false ribs during the cardiac systole, and a sharp rebound
during diastole, which can be felt as well as seen when the hand is laid
flat upon the chest wall at the spot ; it is more marked when a deep
inspiration is made ; it may be seen occasionally not only on the left side
but also on the right, especially if the patient leans over to the left."
Space will not permit of any long discussion of the associations of
the phenomena just indicated with conditions other than pericardial
adhesions, or of their precise significance in any individual case of
such adhesions. A few general observations on these points must
suffice. Apical recession very rarely occurs except as Nthe result of
adherent pericardium, but it was observed by Friedreich in a case of
aortic stenosis where there were no adhesions; and has also been
noticed under other circumstances. When it is associated with a definite
beat it probably indicates that the apex of the heart is fixed to the
792 SYSTEM OF MEDICINE
chest wall, and drags on it during the systole. The adhesion need not,
however, be extensive, for a narrow band may cause the depression,
provided the pericardium be fixed externally. When there is no palpable
apex-beat, it is supposed that the heart is prevented by adhesion to the
diaphragm or vertebral column from performing its normal forward and
rotatory movement during systole ; or that the cardiac impulse is too
feeble to be felt through the adhesion.
Skoda was of opinion that systolic recession of the intercostal spaces
is pathognomonic of adherent pericardium, but numerpus observations
have shown that this is not the case, as the phenomenon may occur in
cases of considerably enlarged heart, as the result of atmospheric
pressure, especially when associated with aortic regurgitation. Still
it is an important sign of adhesion, and its presence should always
have due weight in diagnosis. As a rule it indicates that the con-
tiguous surfaces of the pericardium are adherent, and also that the
sac is fixed in front to the chest wall, and to some structures
posteriorly, so that when the heart contracts, being firmly attached
behind, it pulls in more or less of the yielding anterior thoracic
wall. "When there is no posterior adhesion, and yet systolic depression
occurs, it is supposed that the firm attachment of the pericardium to
the central tendon of the diaphragm forms the fixed point from which
the heart acts in drawing in the front of the chest, or possibly that the
effect may be produced by the contraction of the organ itself. Friedreich
is of opinion that the lower surface of the heart must be firmly adherent
to the diaphragm. I have met with this phenomenon in a pronounced
form in cases of external pericardial adhesion with enlarged heart, where
the internal surfaces of the sac were quite free. As a result of diminution
in the force of the cardiac action, a marked systolic retraction may in
course of time become less and less evident, and finally disappear.
The systolic retraction of the posterior or lateral portions of the
thoracic walls, which, as we have seen, is regarded as a positive sign of
adherent pericardium by Dr. John Broadbent, who states that it is quite
distinct from recession of the lower ribs in inspiration, is explained by
him in the following way : — " The heart is, by means of the pericardium,
adherent not only to the central tendon of the diaphragm, but probably
also to a large area of the fleshy or muscular portion of the diaphragm,
and, it may be, to the anterior thoracic wall as well ; as it contracts it
drags upwards and inwards the less resistant fleshy part of the diaphragm
towards the central tendon or anterior chest wall ; hence the points of
attachment of the digitations of the diaphragm to the lower ribs and
costal cartilages are dragged inwards and downwards. It will always be
found in such cases that the retracted portions of the chest wall corre-
spond to the floating ribs or costal cartilages of the lower ribs at the
points of attachment of the diaphragm."
{d) Diastolic shock or concussion, -r- This is a very exceptional sign,
only occurring where the pericardium is firmly adherent to the anterior
chest wall, and when the lieait is actin'r powerfully. It follows imme-
DISEASES OF THE PERICARDIUM . 793
diately after the systolic recession, and is in proportion to its force. The
diastolic shock is felt by the hand as a "back stroke." It may be per-
ceptible only at the apex-beat, over one or more intercostal spaces, over a
more extensive surface — possibly over the entire precordial area ; or even
round the left side to the back. The phenomenon is attributed to the
elastic recoil or rebound of the chest wall, at the beginning of diastole as
soon as the systolic dragging force has ceased. In well-marked cases it
may be felt as a distinct jerk or blow, which is occasionally so strong as
to be like the impulse of the heart. When present it is regarded as a
pathognomonic sign of adherent pericardium.
Apart from the sign just considered, I feel sure that in some cases of
adherent pericardium, with exposure of the heart and great vessels, a
diastolic impulse is felt, due to the closure of the aortic and pulmonary
valves. It is noticed over the base, and is quite independent of systolic
retraction.
(e) Posterior systolic impulse. — I believe that this sign is sometimes
of value in the diagnosis of adhesion of the pericardium to the structures
posteriorly ; especially when there are indications of probable agglutina-
tion of its two surfaces, and of anterior adhesions. It is best recognised,
not by the hand, but by the head, when this is placed over the back of
the left side of the chest in the practice of direct auscultation. The move-
ment is directly due to the hypertrophied heart, and is often associated
with more or less compression of the lung, which therefore conducts the
sensation more readily ; but I think that it is likely to be more pro-
nounced when the structures are matted together by adhesions.
(iii.) Owrdiac dulness. — Pericardial adhesions or thickening do not in
themselves appreciably affect the cardiac dulness, as a rule ; but a mass of
fibrous tissue about the vessels may certainly cause some increased dulness
towards the base. When, as a consequence of adhesions to the chest
wall, the heart and great vessels are abnormally exposed and superficial,
the area of cardiac dulness will be proportionately enlarged, and may be
of considerable extent, being often markedly increased in an upward
direction, sometimes reaching the second rib. Part of this altered per-
cussion sound may be due to adhesion and collapse of overlapping lung.
When enlargement of the heart is associated with the pericardial condi-
tion the dulness will be modified accordingly, and is not uncommonly
very extensive. Dr. John Broadbent writes : " When, during an attack
of pericarditip, the area of cardiac dulness has been noted to increase con-
siderably in extent, and after the subsidence of the attack remains
permanently increased, it is extremely probable that adhesions have
taken place, fixing the heart in a condition of dilatation." In well-
marked cases the dulness resulting directly or indirectly from pericardial
adhesions and thickening is very pronounced or even absolute. As
already stated, when extensive calcification has taken place, the percussion
sound in rare instances has been described as presenting a peculiar osteal
quality.
(iv.) Auscultatory signs. — It cannot be said that there are any actually
794 SYSTEM OF MEDICINE
pathognomonic or trustworthy auscultatory signs of adherent pericardium;
but one or other of the following points may be worthy of attention in
particular cases : —
(a) Should the pericardium be fixed to the chest wall the heart
sounds are likely to be remarkably superficial. The first sound is
certainly often abnormal in character. In some cases it is peculiarly
sharp and valvular in quality ; in others it is markedly dull or mufiled at
the apex or over the mid-cardiac region ; or again it may be prolonged
and reduplicated. The second sound is frequently reduplicated, but
Friedreich maintains that this may be due to the rebound of the chest
wall which causes the diastolic shock, and produces a dull sound heard
after the second sound of the heart. Dr. John Broadbent regards a
weak pulmonary second sound, when there is evidence of hypertrophy
of the right ventricle, as a very important indication that the cause of
the hypertrophy was probably not back pressure through the lungs
due to left ventricle trouble, but some intrinsic cause, perhaps adherent
pericardium. Marked conduction of the heart sounds towards the back
of the left side of the chest, especially when associated with the feeling
of pulsation already referred to, is suggestive of posterior pericardial
adhesion.
(6) A rough pericardial friction -sound may remain over different
points of the precordial region, especially towards the base, for some
time after an attack of pericarditis ; and, should it be associated with
suspicious signs of adhesion, might be useful as corroborative evidence.
Its eventual disappearance would probably indicate that adhesions had
formed at the spots where it was previously audible, and have since
become more or less general.
(c) With regard to endocardial murmurs, a kind of rumbling pre-
systolic murmur is sometimes heard at the apex, which does not, however,
indicate the presence of mitral stenosis ; this kind of presystolic murmur
is specially common in children (J. Broadbent). It is possible that a
basic systolic murmur may result from the pressure of pericardial thicken-
ing upon one or both of the great ai-teries. The several valvular diseases,
when present, will give rise to their corresponding murmurs, but I believe
that these may be modified in their character by adherent pericardium,
and a tricuspid regurgitant murmur may ultimately result from enlarge-
ment of the right ventricle owing its origin to this condition.
(v.) Signs connected with respirator^/ movements. — When searching for
pericardial adhesions, it is often highly advantageous to study the effects
of deep inspiration and expiration. In the first place, the fact that the
position of the apex-beat and the area of extended cardiac impulse are
not thus affected may be of much importance ; as well as that the area
of precordial dulness is not altered. It implies the presence of adhesions
between the external surface of the pericardium and the thoracic wall,
and the want of any modification in the dulness is particularly marked
when the sac is adherent to the margins of the lungs also. As a result
of extensive external pericardial adhesions, inspiratory expansion may be
DISEASES OF THE PERICARDIUM 795
decidedly less on the left than on the right side. Another sign some-
times observed, coming under this head, is impeded descent of the
left half of the diaphragm in inspiration, as indicated by diminished
movement of the upper part of the abdominal -vrall on that side. This
may occur either with or without adhesion to the anterior chest wall ; in
the latter case it has been attributed to abnormal attachment of the peri-
cardium to the muscular portion of the diaphragm, which hinders its
descent. Tracheal tugging might possibly result from adhesion of the
pericardial sac to the bifurcation of the trachea, but I have never found
this to be the case.
(vi.) Arterial signs. — In some cases in which pericardial adhesions
were proved after death to exist, I have observed a peculiar visible
movement, in connection with the large arteries at the root of the neck,
which I believe may be of more or less significance. It gives the impres-
sion that the heart is making an effort to drive the blood into these vessels,
but is prevented from doing so effectually on account of the embarrassed
action due to the adhesions. The movement may be modified by the
coexistence of aortic or mitral disease. Irregular pulse may be associated
with adherent pericardium, but commonly this is not the case until
cardiac failure sets in ; and in diagnosis no positive reliance can be placed
on this disturbance. I think that in cases of mitral disease the condition
tends to increase the irregularity. The arterial sign to which Kussmaul
attached special importance is the presence of a marked pulsus paradoxus,
the pulse intermitting with inspiration, which has been chiefly noticed in
cases of indurative mediastino-peri carditis, but occurs under other cir-
cumstances, and is by no means trustworthy. Kussmaul attributes it
to the presence of fibrous cords encircling the aorta, which, by dragging
on it during inspiration, constrict its lumen.
(vii.) Verwus signs. — Sudden collapse of the veins of the neck during
tlie ventricular diastole has been specially studied by Friedreich, who
regards it, when associated with systolic retraction of the intercostal spaces,
as a most valuable sign of adherent pericardium ; it is never present
in any striking degree without such retraction. The veins, often tensely
filled during systole, disappear from view during diastole, the subsidence
being synchronous with the diastolic shock felt in connection with the
chest wall. Sometimes the supraclavicular fosses are deepened at the
same time. The explanation of this phenomenon given by Friedreich is
that, owing to the diminution of the thoracic space, the return of blood
through the cervical veins is hindered during systole ; and that the
subsequent sudden diastolic enlargement has an aspiratory effect, drawing
in the blood from the veins : it is supposed also that the diastole takes
place with unusual force and rapidity, owing to traction by the adhesions
from without, and the descent of the raised diaphragm. He further
assumes that in consequence of the diastolic descent of the heart, especially
as caused by the action of the diaphragm, the large vascular trunks,
including the superior vena cava, become elongated, and thus the down-
ward current of blood from the cervical veins is hastened.
796 SYSTEM OF MEDICINE
Dr. John Broadbent quotes a case of adherent pericardium, observed
by Fran9ois Franck, in which systolic emptying of the veins of the neck
occurred, and was ascribed to an aspiratory periventricular effect caused
by the adhesions. He also describes another case — where the pericardium
was universally adherent to a greatly hypertrophied heart, and also to
the chest wall over a large area — in which systolic emptying of an
enlarged vein on the front of the chest, to the right of the sternum,
was followed by filling during diastole. "The explanation suggested
was that the pericardium adherent to the heart and chest wall dragged
apart the walls of the internal mammary vein during systole, causing
a suction action, so that the blood was drawn into its lumen from the
afferent veins during systole." I think I have recently met with a similar
case.
Diagnosis. — It must be repeated that in a large proportion of cases
where pericardial adhesions exist, there are no trustworthy data upon
which a definite diagnosis can be based; though nevertheless the possibility
of their existence may suggest itself in explanation of cardiac disturbance
of obscure origin. The rule is not to forget these lesions in any case,
and to take some trouble in their clinical investigation. In not a few
instances the diagnosis of adherent pericardium is evident enough, and
yet the condition is entirely overlooked. It is not enough to say that
pericardial adhesions exist ; an endeavour must be made to determine
their extent and nature ; whether they are external, internal, or both ;
and their effects upon the heart. Moreover, their association with
valvular diseases of this organ must not be lost sight of, as they are often
important factors in such combinations.
If the patient have had one or more attacks of acute or subacute
pericarditis, or of rheumatic fever, we may suspect adhesions ; especially
if they have formed under the observation of the practitioner who has
subsequent charge of the case, and who can give definite information at
first hand. I have not uncommonly watched their formation during
the period of convalescence, and had the opportunity of studying their
after-effects. In other instances an indefinite history merely points
to cardiac inflammation of some kind. The frequent association of peri-
carditis and endocarditis in childhood has an important bearing on
diagnosis ; and, when the origin of valvular disease can be traced to
early life, pericardial adhesions should be particularly looked for. Un-
fortunately, in a large proportion of cases no history pointing to
pericarditis can be obtained; and it must not be forgotten that the
formation of adhesions may be a chronic process throughout.
The positive diagnosis of adherent pericardium is founded upon
careful and systematic investigation and study of the sympLoms and
physical signs already discussed, not only in themselves, but also in
relation to each other. Individual cases differ much in their exact
characters. Sometimes the diagnosis has to be made on physical signs
alone, there being no prominent symptoms. On the other hand,
progressive signs of general venous obstruction following an attack of
DISEASES OF THE PERICARDIUM 797
pericarditis, inducing extreme dropsy of the subcutaneous and serous
cavities, only to be relieved by repeated operations, may iilune indicate
the presence of a thick, dense, adherent pericardium, compressing the
heart, there being no obvious physical signs of the condition. In other
instances, again, enlargement of the heart, especially of the right ventricle,
occurring without other adequate cause, or perhaps developing with
unusual and inexplicable rapidity in connection with valvular disease,
suggests adherent pericardium as a possible cause. With regard to the
relation of symptoms to physical signs. Dr. John Broadbent writes:
"When symptoms of cardiac failure, more especially of right ventricle
failure, occur of greater severity than the physical signs preseiit seem to
warrant, or where compensation breaks down unaccountably, adherent
pericardium must be suspected. When rest and suitable treatment fail
to give relief, provided the patient is not of advanced age or thoroughly
broken down, this affords further evidence in favour of adherent peri-
cardium, and other confirmatory signs of it should be carefully looked
for." With these remarks I cordially agree. Sir Samuel Wilks has
expressed the opinion that severe heart symptoms in young persons,
without valvular murmurs, point to pericardial adhesions; while in persons
of mature age they indicate cardiac degeneration. There is a good
deal of truth in this statement, though not a few exceptions will be
met with in both directions.
Ppognosis. — No general rules of practical value can be stated under
this head; every case in which pericardial adhesions exist must be studied
individually as regards prognosis. Often they are of no consequence
whatever; in other instances they are merely a source of discomfort,
and do not endanger life. Sometimes, however, they are extremely grave
in themselves, and then the outlook is very serious, while they make
life exceedingly miserable. It may be impossible to give any relief
to the symptoms; or a dropsical condition may be kept at bay only
by repeated operations. That pericardial adhesions add seriously to the
effects and dangers of valvular diseases cannot be doubted, and they
often hasten their progress and fatal termination.
Treatment. — Pericardial adhesions once formed cannot be got rid of.
Eest, good nourishment, and other suitable measures are of value in
preventing or delaying their ill-effects, and in maintaining the nutrition
of the myocardium. Whether the various exercises now in vogue in the
treatment of cardiac disease are likely to be of any service in this kind I
do not know, but in cases where extensive and firm adhesions exist they
certainly may do much mischief, if carried out thoughtlessly. Cardiac
tonics may be useful in some cases ; but it must be remembered that
pericardial adhesions may materially interfere with the action of digitalis
and allied agents upon the heart, and then such agents may do much
more harm than good. Symptoms must be dealt with on ordinary
principles ; and dropsy often requires repeated removal by operation.
7g8 SYSTEM OF MEDICINE
IV. Hydropbricardhtm J Dropsy of the pericardium
Pathology and Etiology. — Hydropericardium, or hydrops pericardii,
signifies a serous effusion into the pericardial sac, occurring during life, of
a dropsical nature, as distinguished from one of infiammatory origin. As
has been previously stated, a certain quantity of fluid, varying under
diflferent circumstances, is found in this sac at most necropsies ; this is
merely due to transudation from the vessels and heart occurring during
the act of dying, and for a time after death. It usually amounts to from
half an ounce to an ounce, but under favourable conditions may reach three
ounces or more. Definite hydropericardium may occur under the follow-
ing circumstances : — (i.) As an acute or active effusion in connection
with certain cases of Bright's disease, thus it may follow scarlatina,
(ii.) As a part of chronic dropsy, more or less general, usually in cases of
cardiac or renal disease ; but occasionally associated with scurvy and
allied states, grave forms of anaemia, tuberculosis, cancer, and other
cachexise affecting the blood. In this group the pericardial dropsy
almost always follows effusion into the pleurae, and the pericardium is
much less frequently involved than other serous membranes. (iii.)
Exceptionally from some mechanical difficulty interfering with the local
circulation. It may thus occur in connection with certain affections of
the lungs, or even of the heart itself, impeding the return of blood from
the cardiac and pericardial veins ; and with disease or thrombosis of these
veins, atheroma of the coronary arteries, aneurysm, chronic mediastinitis,
or a mediastinal tumour causing pressure upon the veins. Hydroperi-
cardium has been known to follow sudden extreme pneumothorax.
Dr. W. Ewart (20) has drawn special attention to cases of latent and
transient pericardial effusions, which may occur, independently of acute
pericarditis, under the influence of rheumatism, of cardiac affections, of
Bright's disease, and so forth. He considers that they may be dependent
upon a subacute inflammatory process, but that probably they are more
often passive or mechanically induced. No doubt such cases are met with,
and if the fluid be rapidly reabsorbed they may run their course entirely
unobserved.
Anatomical ehaFaeters. — The essential morbid condition in hydro-
pericardium is the presence of a quantity of serous fluid in the sac, which
has collected during life, but which is not accompanied by any indications
of inflammation. The amount varies considerably in different cases. In
the large majority of instances it is moderate, from six or eight to twelve
ounces ; but it certainly may reach a pint to a pint and a half ; as
much as four pints have been reported, though it is very doubtful whether
such large effusions are not really of inflammatory origin. The fluid
is, as a rule, clear, and either colourless or of a yellowish or greenish tint.
It is sometimes turbid from admixture of degenerated epithelium, or may
be tinged with blood pigment or bile. Hseranglobin may, however, have
escaped after death. The effusion is alkaline ; and in composition re-
DISEASES OF THE PERICARDIUM 199
sembles more or less the serum of the blood, with differences in the
relative proportion of the albumin and other constituents. Even a
dropsical accumulation in the pericardium may be spontaneously coagulable.
In renal cases it may contain urea. When the fluid is abundant it tends
to produce, in proportion to its amount, the physical effects upon the sac
itself, the heart, and neighbouring structures already discussed under
inflammatory effusion. In prolonged cases the pericardium may become
sodden, its epithelium being also changed ; and it is said that the subserous
tissue about the heart loses its fat and becomes cedematous. Possibly,
moreover, the pressure of the fluid in course of time may impair the
nutrition of the myocardiunL In the majority of cases of hydroperi-
cardium, however, there is but little to be noticed beyond the presence of
the fluid.
Clinical history. — The circumstances under which it occurs make it
unlikely that there will be any definite symptoms of hydropericardium,
especially if the fluid be but in small or moderate quantity. There is
never any pain or other acute subjective sensation such as is met with
in pericarditis. Should the effusion attain a large amount, it may
certainly cause a feeling of weight and oppression across the chest, with
precordial anxiety; and it will either induce or aggravate previous
dyspnoea, obstruction of the venous circulation, and low arterial pressure,
with the usual symptoms arising therefrom. In the large majority of
cases it merely intensifies pre-existing symptoms, and it is often very
difiicult to determine the share of pericardial dropsy in their manifestation,
though sometimes its effects are obvious enough, especially if it come on
rapidly. It does not give rise to any febrile symptoms j and, as a rule,
there is no particular disturbance of the heart's action.
It will thus be evident that by physical examination only can
hydropericardium be positively recognised. The absence of friction
phenomena, such as are associated with acute pericarditis, is a most
important point of distinction between the two conditions. The signs
of the effusion are similar to those fully described under pericarditis, to
which the reader is referred. As a rule they only indicate the presence
of a moderate amount of fluid, and there may be so little that it cannot
be detected at all. It is aflarmed that the dulness is more readily altered
by changes of posture than in cases of inflammatory effusion. Hydro-
pericardium generally follows effusion into both pleurse ; and the physical
signs of this latter condition will probably be well marked before those of
pericardial dropsy are revealed. The combination may also cause a
difficulty in diagnosis. I have never met with a case in which acute
pericarditis and hydropericardium could not be distinguished by due
attention to the circumstances under which they severally occur, and to
the points of distinction already indicated. Possibly in connection with
Bright's disease an effusion might collect which it would be difficult to
classify definitely as inflammatory or dropsical. As regards diagnosis,
the chief danger is that hydropericardium is not thought of, and is con-
sequently overlooked when physical examination would clearly have
Soo SYSTEM OF MEDICINE
revealed it. The cases of latent and transient pericardial effusion referred
to by Ewart must also be borne in mind, for it is probable that even when
considerable it is likely to be overlooked, unless accurate and searching
physical examination is made. Should the condition be associated with,
and secondary to certain local affections within the chest, the diagnosis
may be very obscure and difficult. The prognosis in cases of pronounced
dropsy of the pericardium is, for obvious reasons, usually very grave, and
it generally indicates a speedily fatal termination. Temporary improve-
ment or even recovery may, however, take place in some instances under
favourable conditions.
Treatment. — As a rule treatment has to be directed to the cause of
the hydropericardium, and the measures persisted in which have been
previously carried out for the relief of the general dropsy which it usually
complicates. It might be desirable in some instances to relieve the
venous circulation by venesection or local removal of blood. Cardiac
tonics are to be used when required. The application of blisters has been
found advantageous occasionally in promoting the absorption of pericardial
dropsy. Whether tapping is permissible or desirable can only be deter-
mined by a careful consideration of the circumstances of each individual
case.
V. H^MO- OR HiEMATO-PERICAKDIUM ; BlOOD IN THE PERICARDIUM
Etiology. — It is not uncommon to find a certain amount of blood
mixed with inflammatory products in the pericardium; but the circum-
stances under which pericardial hsemorrhage may occur as an independent
condition are as follows : — (i.) As a consequence of traumatic injury from
without, or by foreign bodies penetrating from the oesophagus, (ii.)
Associated with scurvy, purpura, or, extremely rarely, leucocythaemia and
allied conditions, (iii.) From rupture of the heart or of a cardiac aneurysm,
(iv.) From lesions of the aorta. An aneurysm of the first part of the
arch is very apt to open into the pericardium, not uncommonly by
a pin-hole rupture. Rarely this event happens in the case of aneurysm
of the descending aorta ; and in one reported by Dr. Herbert Habershon
the aneurysm was situated at the junction of the transverse and
descending portions of the arch of the aorta. A case is reported by
Dr. Charlewood Turner in which rupture of the inner coats of the
aorta was followed by a dissecting aneurysm, which perforated into
the pericardial sac. Dr. Eolleston has described a very interesting
condition (39) where the inner and middle coats of the commencement of
the aorta ruptured transversely, and the blood leaked into the pericardium
through a small hole the size of a pin's head in the external coat ; but
there was no dissecting aneurysm, (v.) From rupture of smaller vessels,
namely, one of the coronary arteries, especially if it be the seat of
aneurysm ; or of vessels in a new growth.
Anatomical characters. — The quantity of blood which collects in the
pericardial sac varies under different circumstances. When there is a
DISEASES OF THE PERICARDIUM 8oi
large opening and rapid extravasation takes place, it is much less than
when it escapes gradually through a small aperture. When an aneurysm
bursts freely into the pericardium, the quantity usually found is said to
be about 7 ounces, whereas in the case recorded by Dr. Eolleston already
referred to it amounted to over 24 ounces. A traumatic case has recently
been reported by Dr. Mansell Moullin in which over 6 pints of thin dark
fluid blood were removed from the pericardium in the course of three
hours. The patient recovered. The blood may appear as a soft red
clot, jelly-like, or more or less decolorised ; while a variable and sometimes
considerable amount of serum will probably have separated from it. In
Dr. Habershon's case the pericardium contained about a pint and a half of
dark fluid blood. Haemorrhage in the pericardium may set up pericar-
ditis. The sac is distended in a proportionate degree when there is a
large collection of blood in its interior.
Clinical history. — There may be previous symptoms or physical signs
of the morbid condition which causes the pericardial haemorrhage, but
not uncommonly such is not the case, and the lesion is quite unexpected
and sudden. Immediate or very rapid death usually occurs, but the
event may be preceded by grave cardiac symptoms or collapse. In those
cases where the accumulation takes place gradually, the patient may live
some time, and may complain of pain, associated with serious cardiac
disturbance, faintness or syncope, dyspnoea, and signs of loss of blood.
The physical signs, if noted, will be those of an accumulation of fluid in
the pericardial sac. (ViAe Dr. Allbutt's case, p. 767.) The prognosis
is hopeless as a rule.
Treatment, as a rule, can only be symptomatic. Stimulants and
cardiac remedies may be of temporary service in the more prolonged cases.
No operative interference is practicable in the great majority of cases,
but Mansel Moullins' case, above referred to, is very suggestive as to
what may be possible in some instances.
VI. Pneumopericardium and its effects ; Gas in the
PERICARDIUM
Pneumopericardium is extremely rare, and it needs but brief con-
sideration in this article.
Etiology. — Gas in the pericardium has been referred to the decomposi-
tion of fluid in the sac, especially if the fluid be of an ichorous nature ;
and it has even been said that this is its most frequent source. The proba-
bility is that such decomposition, in the large majority of cases if not
always, is a post-mortem change. Its presence has also been attributed to
secretion by the membrane, but on no adequate grounds. The two classes
of cases in which it is clinically important are — (i.) Traumatic, from
penetrating wounds, including paracentesis for effusion ; fractured ribs ;
contusion or crushing of the chest, or injury from the side of the oesophagus,
(ii.) Perforative, in which a communication is formed externally, or between
the pericardium and a cavity or tube containing air. This kind of lesion
VOL. V 3 F
8o2 SYSTEM OF MEDICINE
has been alreadj' sufficiently described in relation to acute and suppurative
pericarditis, and it will suffice to mention, as illustrations, perforation from
the oesophagus, especially in connection with cancer; rupture into the
pericardium of a phthisical cavity or pyopneumothorax ; and perforation
of a gastric ulcer. A remarkable case is on record in which a hepatic
abscess communicated with the stomach and the pericardium, and thus
air gained access to the latter. The entrance of gas into the sac may be
aided by pressure, by the elastic traction of the lungs upon the peri-
cardium, or by diminution of the size of the heart during systole.
Anatomical eharaeters. — The gas in cases of pneumopericardium
varies in its amount and composition, but it is generally ofTensive. It
may so distend the sac, that when this is punctured the gas escapes with
a hissing noise. Blood or other materials often gain an entrance at the
same time as the gas ; or at any rate inflammation is so speedily set up
that pneumopericardium has never been clinically observed alone, fluid
being always present, rarely serum — hydropneumopericardium — usually pus
— pyopneumopericardiwn ; or the fluid may be ichorous. In a case
described by the late Dr. Begbie (9), yellow lymph was present on the
surface, and a quantity of dark brown foetid fluid in the sac. Whatever
the position of the patient the gas will always be uppermost and the
fluid below. The lungs will be pushed aside and compressed, and the
diaphragm depressed, in proportion to the degree of distension of the
pericardial sac.
Clinical history. — As might be anticipated, the symptoms of pneumo-
pericardium and its consequences vary much in different cases, and are
by no means characteristic. Sometimes there are none ; or the patient is
merely weak and apathetic. Should gas collect rapidly, there will
probably be much precordial distress and sense of distension. The chief
objective symptoms which have been observed in different cases are severe
dyspnoea, cyanosis, fits of syncope, collapse, a feeble and irregular pulse,
and rarely dysphagia. Sleep is necessarily disturbed, and delirium some-
times occurs. Occasionally pneumopericardium is accompanied with rigors,
high fever, profuse sweats, and diarrhoea ; but such symptoms are probably
due to other and more general causes.
Physical signs. — It is upon the physical signs that the diagnosis of
pneumopericardium and its consequences is practically founded ; these
being due to the presence of gas and fluid within the sac : most of them
are very striking and peculiar. They may be briefly described as
follows : —
(i.) The precordial region is likely to present abnormal fulness or
bulging, which may be very pronounced.
(ii,) The apex-beat is weak or absent, but is better felt when the
patient bends forwards. Sometimes an impulse is observed over several
intercostal spaces.
(iii.) The cardiac movements occasionally bring out a very peculiar
crackling sensation, due to the bursting of air-bubbles. Possibly a
succussion-splash might be felt on shaking the patient.
DISEASES OF THE PERICARDIUM 803
(iv.) Percussion signs axe usually very remarkable. Over the region
corresponding to the distended pericardium there will be a tympanitic
percussion sound, often with a pronounced metallic quality. It is said
that a variation in its height, owing to alterations of the shape of the
body of gas in the pericardium by the rhythm of the heart, may be
detected by rapidly-repeated percussion. It has also been affirmed that
the note differs in its degree of resonance during the systole and diastole
respectively, the ' organ being situated farther forward and downward
during the former period, and thus pressing back the air. A distinct
cracked-pot sound has been described in several cases, but only when
there was an opening in the pericardium. In the recumbent posture the
extent of tympanitic resonance is greatest in front. When fluid is present,
if the patient be slowly raised to the sitting posture and made to lean
forwards, this area diminishes progressively, and the clear sound is replaced
below by the dulness of fluid. Lateral changes of position will modify
the relations of gas and fluid in a similar way, and thus very rapid and
striking changes in the situation and relative Hmits of the respective per-
cussion sounds are produced. Metallic instruments have been used to
bring out the peculiar characters of the percussion sound.
(v.) Auscultation signs are also very peculiar, and often remarkable
for their loudness. They vary according to the relative amount of gas
and fluid in the sac, and the consistence of the latter ; but as a rule
difi^erent sounds are audible. If there be but little fluid the heart-sounds
are abnormally loud, and are accompanied with a clear metallic ring, com-
pared to a chime. Should there happen to be an endocardial murmur or
friction-sound, it will probably assume a similar quality. The agitation
of fluid and air within the pericardial sac by the action of the heart, and
also by deep inspiration, produces adventitious sounds of the most extra-
ordinary kind. They are all of metallic ringing quality, and have been
described in different cases as splashing, spluttering, guggling, gurgling,
rattling, large crepitating, and churning. They have been likened to the
sound of a water-wheel or mill-wheel (bridt de roue hydraulique, bruit de
moulin); and in one case to the "shaking of shot in a shot-pouch."
Occasionally metallic tinkling has been noticed, due to the dropping of
fluid in the pericardial sac. From a case observed by Dr. Flint, in which
recovery took place, it would appear that sounds of the character just
described might be produced by the presence of air and blood in this sac.
In some instances the cardiac and adventitious sounds are so intense as
to be heard, not only by the patient, interfering with sleep, but by those
about him, or, it may be, even at a considerable distance off. Sometimes
a splashing sound is brought out on succussion; or a bell-sound can
be elicited by percussion with coins. It is affirmed that the signs of
pneumopericardium have followed those of pericarditis, namely, friction-
sound and evidences of effusion, when it is supposed to have resulted
from decomposition of fluid.
Diagnosis. — If the physical signs just indicated were always pro-
nounced, the diagnosis of pneumopericardium and its accompaniments
8o4 SYSTEM OP MEDICINE
would be quite easy. Otherwise it would present much difficulty, or might
be impossible. No reliance can be placed on symptoms. The only condi-
tions with which it could possibly be confounded are a large cavity in the
lung, in the vicinity of the pericardium ; a localised pneumothorax ; or
a greatly distended stomach. Due consideration of the general circum-
stances of each case, and of the clinical history and phenomena, should
obviate any such mistake.
Prognosis. — This is obviously very grave, and the termination is
almost always fatal, especially as the pneumopericardium is usually a
complication of some grave disease. A few cases of supposed recovery
have been reported, but these have been chiefly of traumatic origin.
Treatment. — But little can be said under this head. The patient
must be kept as quiet as possible, and in the position most comfortable
to him. Stimulants, sedatives, or cardiac agents should be administered
as- circumstances require, but each case will dictate its own methods. The
question of operation naturally presents itself, and in suitable cases it
might be desirable to let out some of the gas by means of a fine trochar,
the patient being in the recumbent posture ; or to open up the pericardium
freely, especially if it contain inflammatory or other products of a low
type. This matter must be regarded and dealt with entirely from a
surgical point of view.
VII. New growths and pakasites
In order to complete the account of diseases of the pericardium some
reference must be made to the morbid growths which may affect it. At
the same time it is difficult to say anything of clinical importance, and
a few general remarks must suffice. The reader may also be referred to
the article " Diseases of the Mediastinum," in the sixth volume.
Tubercle is by far the most frequent morbid growth met with in the
pericardium, and perhaps in its minor degrees it is more common than is
usually supposed. It is only in exceptional cases, however, that the
membrane presents gray granulations in general acute miliary tuberculosis.
In the large majority of instances tubercle of the pericardium is chronic,
and secondary to tuberculous disease elsewhere, especially of the lungs,
from which it spreads directly. It may, however, follow disease of the
bronchial or mesenteric glands. A simple pericarditis appears to be
more common than tuberculous, even in cases of pronounced phthisis ; and
chronic inflammatory products in the pericardium may possibly become
infected with tubercle. Dr. Habershon records an interesting case of
general tuberculosis affecting unusual structures, where there was exten-
sive tuberculous pericarditis. In a case of phthisis wliich came under
my observation, changes due to chronic pericarditis were well marked,
but careful examination failed to detect any tubercles or tubercle bacilli.
In some instances gray and caseating tubercles are scattered over the
serous coat, or in the midst of inflammatory products or bands of
adhesion.
DISEASES OF THE PERICARDIUM 805
Carcinoma of the pericardium is extremely rare, and always secondary.
The sac is nearly always involved by extension from neighbouring
structures. A growth in the heart walls may project into the peri-
cardium ; but most frequently this structure is implicated during the
progress of a mediastinal tumour, or one starting from the oesophagus.
Exceptional cases are those in which cancerous nodulqs appear on the
serous surface, associated with a similar condition of other serous mem-
branes, these being secondary to cancer elsewhere. When the growth
results from extension, the parietal portion of the pericardium usually
presents a diffuse infiltration, but occasionally a nodular mass projects
into the sac.
A case of malignant sarcoma of the pericardium, believed to be
primary and independent, has been described by Sir W. Broadbent
(144
Hydatids of the pericardium are so rare that out of 1897 cases col-
lected by the late Dr. Davies Thomas of Adelaide, in only two was this
structure affected. Moreover, in no instance had a hydatid cyst in the
cardiac walls ruptured into the pericardial sac, probably because of adhe-
sions between the two surfaces. This writer mentions one case, however,
in which a cyst situated between the liver and the diaphragm ruptured
into the pericardium.
The effect of any new growth in connection with the pericardium would
probably be to set up inflammatory changes. These have already been
fully discussed, and it will suffice to state here that they are very seldom
acute ; they may be subacute, but by far most commonly are chronic in
their development and 'results, constituting the ordinary forms of tuber-
eulous and carcinomatous pericarditis. The combinations in these chronic
cases of adhesions, pericardial thickening, and localised collections
of fluid, along with the morbid growths, may be very complicated.
The effusion is commonly haemorrhagic ; but in malignant cases it may
be purulent or ichorous, and possibly also in those of a tuberculous
nature.
Clinically new growths in the pericardium could only be suspected
or recognised by the appearance of symptoms and physical signs of peri-
carditis, especially chronic, in such cases as tuberculosis or old phthisis,
or an intrathoracic tumour. It certainly is desirable to watch the
pericardium in cases of chronic phthisis, though, as already stated, the
changes which may then arise are by no means always tuberculous. It
is very likely that tubercle or cancer may produce a friction-sound, and
this has been definitely asserted ; but no definite diagnosis could
be founded on this sign. The implication of the pericardium in these
growths, in cases where the primary seat of mischief is away from the
chest, could only be made out by the occurrence of pericarditis and its
consequences, which would draw attention to this part.
Treatment is entirely symptomatic and constitutional, and no
definite rules can be laid down. Operative interference mit;ht be indi-
cated for the removal of fluid to give temporary relief, but nothing can
8o6 SYSTEM OF MEDICINE
be done for the growths themselves. Obviously when the pericardium
becomes involved in malignant disease the end cannot be far off.
Fkedbeick T. Egberts.
REFERENCES
1. Allbutt, T. Clifford. "On Paracentesis Pericardii," Lancet, 1869, vol. i. p.
807. — 2. Idem. Brit. Med. Journal, 1870, vol. ii. p. 31. — 3. Aran. Archives gin. de
mid. tome iv. p. 476. — i. Balfoue, 6. W. "Diseases of the Pericardium " in Quain's
Dictionary of Medicine, 2nd edition, vol. ii. p. 334. — 5. Bambbegbr. Allg. Wien. Zeit.
1883, xxviii. 5. — 6. Batjbr, J. "Diseases of Pericardium," v. Ziemssen's Cyclopcedia
of Practice of Medicine, vol. vi. — 7. Baumlee. Trans. Olin. Sac. London, 1872, vol.
V. pp. 8-10. — 8. Beck, Makous. "Paracentesis Pericardii," Quain's Dictionary of
Medicine, 11th edition, vol. i. p. 126. — 9. Begbib, J. Warbueton. " Pnevimoperi-
cardium," Reynolds' System, vol. iv. p. 182. — 10. Idem. " Hydropericardium,"
Reynolds' System, vol. iv. p. 532. — 11. Bouillaed. Traiti de nosographie midicale,
1846. — 12. Beamwell, Btrom. Diseases of the Heart and Aorta, IWi^. — 13. Beoad-
BBNT, J. F. H. Adherent Pericardium,, 1895. — 14. Beoadeent, W. H. and J. F. H.
Heart Disease, 1897. — 14a. Beoadbbnt, W. H. Trans. Path. Soc. London, vol.
xxxiii. p. 78. —145. Cantlib, J. Brit. Med. Journ. 1889, vol. i. p. 333. — 15.
Chbadle, W. B. Brit. Med. Journ. 1896, vol. i. p. 65. — 16. Coevisabt. Maladies
du ccBwr, 1818. — 17. Dickinson, W. H. Trans. Clin. Soc. London, vol. xxii. p. 48. —
18. DuEOZiEZ. Traiti clinique des maladies du cosur. Paris, 1891. — 19. EwAET,
"William. " Diagnosis of Pericardial Effusion," Brit. Med. Journ. 1896, vol. i. p. 717.
— 20. Idem. Lancet, 1896, vol. ii. p. 1446. — 21. Flint, Austin. Diseases of the
Heart, p. 357. — 22. Feanok, Franqois. Traiti de midecine, edited by Charcot,
Bouchard, and Brissau, 1893, vol. y. p. 66. — 23. Feiedrbioh, N. "Zur Diagnose der
Hertzbeutel Verwachsung, " Virchow's Archiv, 1864, Bd. xxix. — 24. Gaiedneb.
Edinburgh Monthly Journal of Medicine, 1851. — 25. Idem. Edinburgh Med. Journ.
1858. — 25a. Gee. St. Barts. Hospital Reports, 1S97 . — 26. Graves. Clinical Lectv/res.
New Sydenham Society. — 27. Habeeshon, S. H. Trans. Path. Soc. London, vol. xl.
— 28. Haeeis, T. Indurative Mediastino - Pericarditis, 1895. — 29. Hope, James.
Diseases of the Heart, 1839. — 30. Kennedy, H. "Adherent Pericardium and its
Results," Edin. Med. Journ. 1858, p. 986. — 31. Kiekes. "Pericarditis consequent on
Pyaemia," Med. Times amd Gazette, 1862. — 32. Kussmaul, A. Berl. Tclin. Woch. Jahr.
X. 1872, S. 433. — 32a. Idem. Von Ziemssen's Cyclopcedia of Practice of Medicine, voL
vi. p. 649 et seq. — 33. Labnnbc. Traiti de V auscultation des maladies du cceur, chap,
xxii. — 34. Lees, D. B. "Treatment of Pericarditis," Lancet, 1893, vol. ii. p. 188. —
34a. MouLLiN, Mansbll. Clin. Soc. Trans, vol. xxx. p. 217. — 35. Paget, S.
Surgery of the Chest, 1896, p. 384 et seq. — 36. Paeker, R. "W. Trans. Clin. Soc.
London, vol. xxii. p. 60. — 37. Peacock. "Congenital Displacement of the Heart,"
Quain's Dictionary of Medicine, 2nd edition, vol. i. p. 793. — 38. Idem. "Adventitious
Products in the Heart," Reynolds' System, vol. iv. p. 165. — 39. Rolleston, H. D.
Trans. Path. Soc. London, vol. xl. — 40. Rosenbach. "Pericarditis," Eulenburg's
Beal-Encyalopaedia. — 41. Rotch, T. M. "Absence of Resonance in the Fifth Right
Intercostal Space diagnostic of Pericardial Effusion," Boston Medical and Surgical
Journal, 1878, vol. xoix. p. 427. — 42. Sansom, A. E. The Diagnosis of Diseases of
the Heart and Thoracic Aorta, 1892. — 42a. Sears. Boston Hospital Reports, 1897. —
426. Shattuck. Paper on Pericarditis, read at Twelfth Annual Meeting of Associa-
tion of American Physicians. — 43. Sibson, Francis. "Pericarditis, adherent Peri-
cardium," Reynolds' System, vol. iv. ; see also Sibson's Works, edited by Dr. W. M.
Ord. — 44. Skoda. Zeitsch. der Gesellschaft der Aerzte zu Wien, 1852, 1. 306. — 45.
Stewart, Sir T. G. Trans. Med.-Chirurg. Soc. Edin. 1884-85.— 46. Stokes, W.
Diseases of the Heart and Aorta. — 47. Sturges, 0. Lumleian Lectures on Heart
Inflamination in Children, 1894. — 48. Thomas, J. Davies. Hydatid Disease. Adelaide,
1894.— 49. Traube. Gesell. Beitr. zur Path, und Physiol. Berlin, 1878, iii. 135-141.
— 50. Trousseau. Lectures on Clinical Medicine, New Sydenham Society, vol. iii.
p. 364 et seq. —51. Turner, F. C. Trans. Path. Soc. London, vol. xxxvi. — 52.
Walshe, W. H. Diseases of the Heart, 3rd edition, 1862.-53. West, S. Trans.
Roy. Med. and Chirurg. Soc. London, vol. Ixvi. p. 235. — 54. Wheelhouse. Brit.
FUNCTIONAL DISORDERS OF THE HEART 807
Med. Journal, 1868, vol. ii. p. 385.-55. WhittAkek, J. T. "Diseases of Heart and
Perioardiuin," in Twentieth Century Practice of Medicine, vol. iv.— 56. Wilks, S.
" Adherent Pericardium as a Cause of Cardiac Disease," Guy's Hospital Meports, 1871
(third series), vol. xvi. p. 196. — 57. Williams, C. J. B. Diseases of Chest, 1840. —
58. Idem. " The Prognosis and Treatment of Organic Disease of the Heart," London
Journal of Medicine, 1850, vol. ii. p. 464.
r . T. It.
FUNCTIONAL DISOEDEES OF THE HEART
To the purist the vulgar distinction between functional and structural dis-
ease is a false one. We are assured that in every change of function a
change of structure is implied ; indeed, that structure and function are
one, and to use them severally is to see the same thing in different
aspects. It is not so much that the materialist and the idealist have
lain down together, as that the idealist has swallowed the materialist.
Yet, granting all this, we remember that as it is convenient to detach
the study of physiology more or less from that of anatomy, so it is
with nosology when we analyse symptoms apart from morbid anatomy ;
although we shall not forget that knowledge thus obtained must be inte-
grated by bringing the two studies together from time to time.
Furthermore, we shall not be discouraged from using the term
functional disease in a still narrower and more artificial sense, — in the
sense of a perturbation of a more or less contingent kind, of a contingency
sufficient to rock but not to upset the moving equilibrium (11). Every
beat of the normal heart is a disturbance of equilibrium, and we do not
forget that, in any system, cessation of all disturbance is the peace of death ;
on the other hand, disturbance beyond the resistance of the equilibrium
is disease or death also. Between the death of apathy, as of the old
man who falls asleep, and the death of defeat, as of the man who succumbs
in his prime to a clot in the pulmonary artery, there may be two
periods, — the period of health and the period of transitory discord. In
health the disturbances are rhythmic, harmonious, controlled ; in func-
tional disease they are arrhythmic, uncontrolled. In functional disease the
going system halts or staggers, but not beyond recovery ; the humnling-
top swerves under a pufi' of wind, or reels as it travels over a grain of
mustard seed ; but the deflection is counteracted, and is presently re-
solved. Such temporary eccentricities are common to the heart with
.other organs, but are more conspicuous in the heart, because its workings
are nearer to our consciousness, and lie, moreover, in the track of
emotional gales and typhoons. Is there a man so stoutly knit, whose
inhibitory nerves are so powerful and alert, that in passion or " twixt
doubtful fear and feeble hope " he has never felt his heart climb into
his throat 1 Thus it is that functional disorders of the heart are familiar
to us all, and occupy our thoughts the more, as the heart teUs us where
8o8 SYSTEM OF MEDICINE
the centre of life is, and where we cannot afford to have things go wrong.
But it may be objected, and in a very important sense truly objected, that
these are but matters of degree — that persistent functional disease ends in
structural disease. With this inquiry we shall deal at length ; meanwhile
I would say that this is not necessarily so. While, on the one hand, we
warn the student not to overlook the stealthy inroads of structural
disease, of " functional " disorders, which are the first signs of the
invasion of structural disease — ^such as retardation of the heart, for
example, on the other hand, we shall not put them in the same reckoning
with the functional disorders which are not of this kind — such, for example,
as acceleration of the heart. Whether a purely functional disorder by
damnable iteration can hammer disease, as it were, into a harassed organ is
hard to say ; as yet we can only say that in many cases a lifetime of func-
tional disorder of no little persistency is not long enough to bring this
event about, and perhaps that such is the usual issue : on the other
hand, it seems no less certain that perennial depressing causes, exile or
bondage in an invisible Babylon, may induce degenerative changes in
the heart and blood-vessels, or in the kidneys, as I alleged in 1877,
and have had yet more reason since to believe. That tachycardia,
usually perhaps when severe, may wear out the heart is true ; yet I
scarcely think we can regard this truth in the light of our present argu-
ment, as such gradual inroads are rather of the nature of dilapidation
than of mere disorder : moreover, in a particular case it may be hard
to distinguish between a perturbation, such as a variation in rate, which is
an indication of incipient heart failure, and a perturbation of central or
eccentric nervous origin. Anxiety long continued seems to pervert
nutrition at its sources ; perhaps to prevent healthy metabolism, and to
favour auto-intoxication with its damaging effects on kidney and heart.
Such influences, however, come rather under the head of the remoter causes
of diseases of the myocardium than under that of functional disease of the
heart ; as, again, many of the conditions of functional heart disorders will
be dealt with in the chapter on Neurasthenia. For our present purpose
functional disease may be taken to include temporary irregularities of rate,
rhythm and tone, and even of force and volume ; though these last rather
pertain and are subordinate to other diseases — that is, to other symptom
groups. While rate, rhythm, and tone make important parts of many
maladies, yet their errors are often themselves the leading morbid features,
and appear to the patient, and often indeed to his medical adviser like-
wise, to stand almost alone. For instance, if in the irritative stage of
meningitis we mark a slow pulse, we do not group this phenomenon with
functional disease of the heart, however logically we might do so ; thus
to class it would be to darken our conceptions, to introduce false conno-
tations. So again the quick pulse of a later stage of meningitis, or that
of pneumonia, will in like manner be classed, not with functional diseases
of the heart, but with the phenomena of fever. For our present concern
is with clinical medicine, not with the broader views of general
pathology.
FUNCTIONAL DISORDERS OF THE HEAR! 809
A more diflScult problem of nosology is to decide where we are to
place the quick pulse, say, of larval Graves' disease ; if both goitre and
exophthalmos be absent, as often they are, are we in the presence of an
obstinate case of functional disease of the heart 1 Again, I think that to
speak thus would be an abuse of terms ; if we suppose that on due
analysis this pulse has affinities with the symptom group which we call
Graves' disease, we must not put the pulse characters in an independent
category ; we shall regard them as a part of that other group. Let
it not be said that this discussion is otiose ; for if the argument be well
founded we shall no longer allow ourselves to call any quick pulse
"tachycardia," nor any slow one "bradycardia." Tachycardia, for
instance, appears to be a definite and primary functional disease of the
heart ; the affection has characters of its own : whether bradycardia is
such a substantive malady is less certain ; this question we shall discuss pre-
sently. If it is not, the specific name should be given up, as one without
a consistent signification.
We cannot consider the heart apart from its nervous connections ;
like a well-handled pair of horses, its good going depends as much on
the man on the box as on the muscles in action. Although the heart
muscle has an independent and inherent rhythm of its own, this rhythm
goes astray if the organ be severed from its nervous governance. The
inherent rhythm may suffice for less complex organisations, but it will
not do for a mammal. In the higher animals, for instance, the contrac-
tion of the left ventricle, although it is always a maximum effort, does
not at every beat supply the whole arterial tree. That at a very low
pressure, all the arteries being expanded, it might do so is possible ; some
of the strange perturbations of women attended with heat and flushing
may thus come about ; but probably even in them the distribution is
more or less partial. In health, at any rate, the output is tinned now
here, now there, as — if I may be permitted so unsavoury a simile — in a
sewage farm the fertilising streams are diverted by locks in this way or
that. The lock-keepers belong to the nervous parts of the cardiac
machinery. In study the active brain, after a meal the stomach, demand
their alternative streams ; by means of the nervous system an anaemic
area calls for more blood, satiated areas for less ; and by means of the
vagus nerves the heart itself is protected from too great an importunity.
If in an anaemic girl the heart beat too fast, we shall not call that a
functional disease, which is an attempt on the part of the heart to respond
to the cries from ansemic areas all over the body ; though in many such
cases as this we do for the moment, and provisionally, apply such a name
to mark a region of our own ignorance.
As we carry our explanations into such regions we gradually
diminish our group of functional diseases of the heart. Let us consider
the eflFect of certain poisons on the heart. In so far as these and
their effects are known — as, for example, in the cases of coffee, tea,
and tobacco, — we shall scarcely call their ill effects on the heart func-
tional disease of this organ ; we shall turn rather to the chapters on these
8io SYSTEM OF MEDICINE
drugs, and regard the cardiac perturbations subordinately as features of
the symptom group or series of groups associated with the agent concerned.^
Now the heart is often set on edge by obscure causes which seem to us
to be of the nature of poisons, of poisons generated, perhaps, in the
body and circulating in the blood which irritate or depress the heart
directly ; or, perhaps, disturb it indirectly by some obscure interference
with the blood-pressure : such a state of things is surmised to exist in
the malady popularly known as " suppressed gout." But when we know
all about " suppressed gout " and wherein it consists, we shall remove the
cardiac phenomena from the chapter of functional diseases of the heart,
and put them in their own place as subordinate phenomena of the gouty
group. All we know about " suppressed gout " at present is that it is not
a mere dilution of articular gout ; that, however related to the latter, it
ie a different disease rarely occurring in the same persons ; or, if in the
same, at different times of the life of the individual. Cardiac disturb-
ances often appear, it is true, in articular gout also, and are described in
treatises on this disease as "gouty"; but of "suppressed gout" high arterial
pressure is characteristic, from articular gout high blood - pressure is
commonly absent. How terrific and how various may be the effect
of the poisons of certain of the iiifectious diseases upon the cardiac
mechanism is familiar to us all. In diphtheria the heart's action may be
reduced " almost to extinction " (Powell), and of the effects of influenza in
the same direction an excellent account is given by Dr. Sansom (11).
Syphilis, again, is said to cause irregular heart, as a functional disorder
apart from arterio-sclerosis. Of this I have no personal knowledge.
Such considerations as these seem to threaten the very existence of
Functional Diseases of the Heart, save in the sense of a survey of the
general behaviour of this organ under all sorts of maladies, not excluding
its own structural diseases. Meanwhile, however, we must deal with the
unrelated cardia.c disorders in a somewhat miscellaneous way ; and certain
of them seem to have an individuality of their own. Before studying
functional diseases of the heart as groups of symptoms, we may profitably
consider the elements of the groups separately — such as tone, tension,
rate, rhythm, volume, and so forth.
Tone. — The old-fashioned word " tone '' has fallen into disuse ; the
more is the pity. When I was a student we were asked how the pulse
might be for tone \ now if a student be asked such a question he talks
about " tension," although he does not clearly know what he means. To
measure or even to estimate roughly the degrees of stretching of the
coats of an artery is a very complex and usually an insoluble problem;
yet to these coats only can the word " tension " apply. The blood itself
canjiot be tense in any but an abstruse mathematical sense, which no
student of this subject has in his mind. If the radial artery contract
tightly on the blood within it, the pressure on each superficial unit of
' A pair of interesting tracings is published by Dr. Waller on page 32 of his Physiology
(ed. 1897) ; the first of irregular and low pressure pulse under tobacco, the second a correc-
tion of the same pulse under digitalis.
FUNCTIONAL DISORDERS OF THE HEART 8ii
internal surface is increased no doubt ; but this is not tension, or at any
rate not in any simple sense. Tension is that stress which tends to
split the artery either longitudinally or transversely ; and such stress
is at more advantage when the vessel is relaxed. Tension and tone
have, indeed, something like an inverse relation one to the other, as we
see more readily, perhaps, in the ventricles of the heart. We may say,
indeed, that one of the chief functions of tone is to resist the tension
which calls it forth. How tension acts upon an artery is best seen in
aortic regurgitation, in which malady the effects of tension seem at their
highest. We have but to look at any long artery in an advanced case
of this kind to see what tension, in the longitudinal direction, really is ;
the artery is not actually split transversely, perhaps, but it is lengthened
enormously and thrown into curves. No doubt, under all circum-
stances, whether the radial artery be tight or slack, there is more or less
tension of its coats ; but it is most difficult to ascertain the degree of
this, even roughly : yet such is the love of obscure diction, that, instead
of endeavouring to express the facts in terms as comprehensible as
possible, that factor which is at once the least appreciable and the least
immediately important is chosen for description.
Without saying that any factors in this application of hydro-
statics are easily estimated, we may assert that tone and blood-pressure
are easier to measure approximately than the tension of the arterial coats.
The finger can tell with some approach to accuracy whether the pressure
be low, moderate, or excessive, though it is only by such instruments as
the sphygmometers of Eoy, Leonard Hill, or Oliver that the degree of
it can be recorded. Tone, again, is easy to make some guess at, or
even to formulate with sufficient accuracy for clinical purposes. Tone
in a vessel is that which preserves its mean diameter, which pre-
serves a certain proportion between the extremes of dilatation and
recoil, and which has furthermore the somewhat different virtue of
keeping the vessel well home upon its contents. Therefore when we
speak of a pulse of good or ill tone we are not talking altogether of what
we do not understand. We mean that the difference of pressures between
the base of the pulse-wave and the apex is somewhere about 35 mm. Hg.
And again, when we speak of high arterial blood-pressure we are talking
of that which we can estimate with some correctness — namely, a mean
pressure of about one-eighth of an atmosphere. These two conditions the
skilled finger is able approximately to ascertain. But when we speak of
the tensile stress on the walls of a vessel we are talking in the dark ;
other things being equal, the higher the blood-pressure the more the
tensile stress, but until we have allowed for tone the net tensile stress,
however considerable it may be, is inappreciable. Now, in functional dis-
orders of the heart and arteries tone is often signally deficient. The aorta,
structurally healthy, may nevertheless be seen beating diffusely in the
epistemal notch and in the epigastrium ; the wall of the chest may thrill
as the hand is laid over the heart; the sounds of the heart are
carried far along the vibrating walls of the carotid ; the abdominal aorta
8i2 SYSTEM OF MEDICINE
leaps like an aneurysm; nay, even the patient himself may complain
of the bounding of slack arteries all over his body. In some such
cases even a capillary pulse may be seen. To the finger the radial or
other artery is ill-filled, and the sphygmographic curve shows that the
due proportion between the expansion and the recoil of the vessel is
no longer preserved ; the lever falls almost to the abscissa before the
dicrotic wave is formed. I have often seen a temporary extension of
the area of cardiac dulness in such cases. This state of the circulation
is perhaps never so primary and eminent as to amount to a functional
disease of the arterial circulation, and as a derivative condition its
importance is discussed under Chlorosis, Neurasthenia, and elsewhere.
The mechanics of the subject will be dealt with hereafter by Dr. Leonard
Hill.
Tone, Dr. Gaskell tells us, is innate in muscle, but it may be excited,
raised, or reduced by nerves. Tone may vary under nervous govern-
ance, but it persists beyond all nerves. Some of Dr. Waller's experi-
ments suggest that nerves like muscle may have their refractory periods,
and the same character has been indicated by certain observers, for
example by Eichet at the Toronto meeting of the British Association
in 1891.
Rate. — How widely the rate of the heart-beats may vary between its
extremes is too familiar to need description. In one bed may lie a
patient with a pulse of 30, in the next one whose pulse is 180 ; and even
these are not the utmost extremes. Under bradycardia and tachycardia
we shall discuss those phenomena more intimately. The most general
factor in acceleration of the heart is loss of vagus control, for the vagus
may be regarded as the escapement of the arterial train. Loss of vagus
control may be relative or positive ; the .accelerator nerves may be
abnormally stimulated, and thus may overbear even a normal vagus
control ; or the vagus may itself be more or less in abeyance, as after a
dose of atropine which palsies its ends in the heart. Again, agents acting
directly on the heart itself may either stimulate the vagus, and so slow
the pulse, or may overbear its control and the pulse-rate may rise ;
variations in blood-pressure have these eflfects, an increase of pressure
tending, as a rule, to the retardation of the heart, aijd a fall to accelera-
tion of it. In functional heart disorders we are frequently met by
problems of this kind, and sometimes they are very difficult to analyse ;
we may remember, however, that controls are a later development than the
functions below them, and therefore tire sooner. Vaso-constrictor action
never tires so long as the nutrition of these nerves goes on, and the
vagi tire before the accelerators. Thus the accelerating nerves often
fatigue the vagi and run away with the heart. This may be the explana-
tion of rapid pulse in certain poisonings, infections, and the like ; but we
have also to remember that in fever blood -pressure often falls also,
probably from some change in the viscosity of the fluid ; and again that
quasi-normal catabolic products may act directly on the heart, as we
believe that fatigue products do. That states of the cardiac muscle itself
FUNCTIONAL DISORDERS OF THE HEART 813
are often directly concerned in its rate seems also probable from the
clinical phenomena of "irritable heart," which can scarcely be due to
fatigue products only. Conversely fatty degeneration of the heart is often
betrayed by retardation of the pulse.
Once more ; we have to deal not only with the nerves, but also with
the cardiac centre in the bulb, a nervous factor which may conveniently
be considered apart, as through its efferent fibres it is chiefly concerned
in regulating response to the demands of the system. Not in the case of
circulating poisons only, but also under the fluctuations of ordinary blood
changes, the cardiac centre is constantly in exercise. In haemorrhage or
chlorosis, for instance, the call of extensive anaemic areas throughout the
body, — the afflux, in this case, of impoverished blood to the cardiac centre,
— excites the centre to quicken the heart. On the other hand, a rise of
arterial blood-pressure stimulates the vagus roots in the bulb, and the
pulse is slowed. The name tachycardia, as we shall see, is improperly
applied in the sense of mere rate ; it is the name of a particular disease.
The name " embryocardia," which is creeping into clinical language, is
pedantic if it means merely a very rapid heart, misleading if it suggests
that the heart has undergone some reversion to a foetal quality, or even
that the organ is primarily failing. The heart goes " tic-tac " whenever
its rate reaches a certain degree, and I may repeat that a quick heart is
not in itself a sign of enfeeblement, but of extreme reflex excitation of
the accelerantes, due probably in typhoid and the like to a diminution of
the total volume of the blood, or to alterations of its density, though,
no doubt, the effects of morbid or catabolic poisons often intensify the
state. It must be remembered that a rapid rate does not necessarily
mean an increase of total work done : on the contrary, although dilatation
is no uncommon result, hypertrophy, in the absence of valvular disease,
is rare.
Abnormal rates of the heart depend then on many factors, and the
variation of any one of these will modify the action of the organ under
observation.
Rhythm is not synonymous with rate, as is too often assumed. A few
weeks ago I read a valuable physiological essay in which rhythm was
used almost throughout in the sense of rate ; such abuse of language
leads to confusion of thought. Ehythm is not the rate but the proportion
of motion. Strictly, force and volume are contained in the conception of
rhythm ; but custom and convenience have ordered that by rhythm we
shall mean the numerical proportion of motion ; that is, a true cardiac
rhythm shall consist of the same number of beats in every unit of time.
Here again, although we find that the vagus is chiefly concerned in the
variations of rhythm, such variations being due for the most part to
vagus interference, yet, as in the case of rate, we learn that the rhythm at
a given moment is due to a composition of causes which are not always
easy to analyse. For instance, clinical experience suggests to me that
intermittence of the heart is often duje to a direct effect on the cardiac
muscle itself, or is a compound effect of direct influence on the heart and
Si4 SYSTEM OF MEDICINE
vagus together. Digitalis may be an instance of an agent acting in such
a double fashion, and some morbid poisons, such as .that of influenza, seem
to have a like compound property. Intermittence, transient as it usually
is, is no uncommon feature in the degenerate heart.
We divide disturbances of rhythm into "irregularity" and "inter-
mittence," terms which speak for themselves. That these two abnormalities
may be and often are present together is familiar to every student. Irre-
gularity of rhythm is for the most part graver as a sign of disease than
intermittence. Its signification in muscular and valvular disease of the
organ in chorea, in cerebral disease, and so forth, will be discussed in
the several parts of this work which deal with such subjects. I need
scarcely say that there is an irregularity of the radial pulse and another of
the heart, and herein we see that irregularity is not only an alteration of
rate, but also of volume and force ; the ventricle not only acts irregularly in
time, but also delivers variable quantities of blood with variable impulse ;
the output is unequal. There may be, as in cerebral disease, for instance,
an irregularity of time only, the volume and force remaining constant ; but
such a condition is rare, for if equal quantities of blood are not delivered
from the several chambers in equal times, inequalities of distribution in
the chambers and of systolic output must accumulate. Strictly speaking,
no pulse is regular, as a time line at the foot of a sphygmographic tracing
will prove ; if not otherwise influenced, the respiration at any rate disturbs
the order, as does muscular effort, even the slightest, especially in nervous
or otherwise unstable systems. To ascertain how far the effort and
position of the upright attitude, or a slight muscular exertion, quicken the
rate is a good test of vascular resistance ; for Dr. Waller's electrotonic
work brings out into more prominence the truth that increased capacity
is associated with diminished susceptibility to contingent impressions, such
as relatively slight changes of blood-pressure. At the same time, it seems
that in some persons the pulse is habitually irregular in the clinical sense.
Sir Thomas Watson mentions such a case in a brother of his own ; whether
the brother was a tobacco-smoker his distinguished kinsman does not
record. In my own experience I have often met with an irregular
pulse in smokers — never, I think, in the normal state. In acute disease
irregularity generally means irregularity of output, and warns us of evil;
probably of dilatation of one or both ventricles.
Intermittence is often of grave augury, no doubt : in suspected cerebral
disease it is an alarming sign ; it is a grave sign in any acute disease,
especially in the pulmonary attacks of the elderly ; but in cardiac disease-
it is of less gravity than irregularity. It is common enough also in
dyspepsia, in suppressed gout, in smokers, and even in persons in whom
no flaw is to be found. I once found intermittence in two brothers who
came together to me for life insurance ; both of them were very angry
with me for refusing them, or rather for stating the facts which led to
their refusal by the company. Neither were smokers, or very moderately
so, nor were they large tea or coffee drinkers. They were vigorous young
men, their digestions were good and their teeth sound. The intermissions
FUNCTIONAL DISORDERS OF THE HEART 815
were occasional, on an average about one in thirty or forty. Perhaps
no one passes through life without an occasional sense of cardiac inter-
mission ; and therewith is often found, though at much longer and more
uncertain intervals, a flutter, felt rather in the epigastrium than about
the heart. This flutter seems not always to be cardiac ; ther^ may
be some alternative machinery for its production : sometimes it is
certainly due to a series of rapid and irregular beats, but the disturbance
is so quickly over, so hard to catch, that its precise causation is unde-
termined. This flutter, like the intermittence which is often associated
with it, is of dyspeptic origin ; and the best remedy for these discomforts,
for they are little more, is to insist on slow mastication. They are very
apt to arise in persons who bolt their food. It is incorrect to say
that if such intermittence arise in advanced life it necessarily signifies
incipient cardiac degeneration, for even in cases when the symptom has
endured for two or three years in persons of sixty years and upwards,
careful attention to the diet and a vigilant supervision of the use of
coffee, tobacco, and the like, will spare them to die at a riper age of some
other symptoms ; on the other hand, even in much younger persons,
intermittence may accompany vascular deterioration, cardiac strain, or
valvular disease. Sometimes the intermittence is radial only ; the heart
beats regularly, but not always effectually. Sometimes the intermittence is
rhythmic ; it will occur every two, three, or four beats for a while ; such
an intermittence is often found in persons under the use of digitalis. As
a functional disorder the form is insignificant, or no more significant than
ordinary sporadic intermittence. To say that the " pulsus bigeminus,"
the " pulsus trigeminus," or the " pulsus alternans " is a sign of cardio-
arterial degeneration, to assert that it is necessarily significant of grave
cardio-arterial involution, is to ignore daily experience. If indeed it be
associated with an abiding or persistently recurrent retardation of the
pulse the prognosis is less hopeful, as it may be also when such coupled
intermittences obstinately return in spite of treatment. I had written
these lines when a pamphlet by von Noorden came into my hands, giving
descriptions and sphygmograms of such pulses in hysterical cases (9).
It is said that an intermitting action which does not reach the con-
sciousness of the patient is of worse omen than that which attracts his
attention. Many persons are alarmed by a perceptible intermittence,
especially by the bounce which often follows it ; perhaps it is this bounce
or thump, rather than the intermittence, which gives rise to the well-
known sensation. Certainly that the comparatively harmless inter-
mittence is perceptible enough common experience teUs us ; and I have
noticed that intermittences occurring in failing hearts are less obtrusive
or indeed unfelt ; whether the absence of the sensible bounce indicates a
feeble heart in all instances is more than I can say myself or find in
the records of other observers. Certainly in the intermittences of
acute disease, as of senile broncho-pneumonia, the missing beat is not
perceived by the patient. The mechanism of intermittence is not quite
understood ; it is probable that a beat occurs, but is abortive, and that
8i5 SYSTEM OF. MEDICINE
the bounce is a leap of the heart against the low pressure of the unfilled
arteries. The sign is more ominous when associated with irregularity.
Palpitation. — This disorder is even more common than intermittence ;
m greater or less degree it lies within the experience of every one. It is
more common in women than in men ; and in the former is often
a very distressing and persisting torment. Under the alarm of a
severe attack of palpitation, with its no less painful sense of choking,
even long and trying experience is scarcely enough to steel the patient
against the dread of its return. Indeed, as the gale in which the heart
is caught often arises from the quarter of the nervous system the
apprehensions are disordered as soon as the heart itself, or even before
it. A sensitive woman, physically courageous perhaps, yet one who
starts at every sudden sound, may well be appalled by the fear of heart
disease and of sudden death. Attacks of palpitation often pounce upon
the sufferer in a moment — even in a quiet moment — and, it may be,
without apparent cause. It is no unusual thing for an attack to set in
with nightmare during sleep. Either thus, or more gradually, the heart
begins to throb tumultuously, and its function is often beset in all the
directions in which we have been regarding it; it becomes irregular,
intermittent, variable in force, volume, and rate, though always rapid,
until the vagus control is regained either by the lapse of time or by some
reflex stimulant such as smelling-salts, or a cordial; or again by some
pain or conflicting impression. The attack may subside gradually, or it
may cease suddenly with a shock, as if rending the patient before
quitting her body. Such a finish is usually seen also in tachycardia, and
may be due to the same causes as the throb of an intermittence. The
patient instinctively presses her hand upon the region of the heart
during palpitation ; a kindly pressure seems to sootTie the tumult. Under
the hand the heart's beating, like the arterial pulse, is vibrating,
diffused, turbulent, and disorderly ; now striving and violent, now
tremulous and faint. The attack is followed by the calm of exhaustion.
The history and circumstances of such seizures are generally enough to
serve us for interpretation ; indeed, such storms are unusual in organic
cardiac disease. Still, the static conditions of the heart are not often to
be appraised during the discordant and confused dynamics of such
seizures. It is well, in the case of a new patient at any rate, to postpone ii
final diagnosis till the ship is in calmer waters.
Murmurs are often present in the palpitation of functional disease ;
they may be heard at apex or base, and at any part of the cardiac
revolution. A systolic murmur at the apex is the most frequent of these.
The causation of these transient murmurs is unknown ; some may be
" ansemic " ; some may be due to inordinate action of the papillary
muscles ; some again may be " pulmonary " (Potain). Until the patient
is tranquil, and ther physician at liberty to map out the heart and to
listen to its sounds without embarrassment, no final opinion should be
given. In a functional case the murmur will probably then have ceased,
and dilatation, if any, will be reduced ; although resonance of the second
FUNCTIONAL DISORDERS OF THE HEART 817
sound at tlie apex and the sharp knocking quality of the systole wiU
probably mark the case as neurotic.
Of these murmurs Dr. Sansom says (13) that a systolic murmur,
arising independently of structural disease, seldom attains its maximum
audibility at the exact apex, but slightly to the right and left of it.
It is usually soft, and does not replace the first named. Again, it does
not occupy the whole, but the middle of the systole (" it is meso-systolic ").
It is much influenced by respiration ; it is intensified both during expira-
tion and inspiration (especially the latter), but it often becomes inaudible
at the end of an expiration. I may add that to me the quality is often that
of the apex first sound in those cases of systolic murmur generated at the
base in which the murmur is scarcely audible, as such, at the apex, yet where
the first sound is blurred by it. For Potain's elaborate and almost too
ingenious doctrines concerning the pulmonary origin of such murmurs —
anaemic and the rest — the reader is referred to his well-known article in
the Clinique de la Chariti, 1894.
The immediate prognosis can rarely need much direction. Generally
speaking, the diagnosis in such cases is too dark ; a woman is told that
she has got a "weak heart," and thus the confidence in herself which is
essential to her cure is shaken. The palpitation of chlorosis I am
accustomed to regard as the result of the combination of poverty of the
blood in oxygen value with persistent mass, with no less a demand upon
the heart, that is, in respect of output. The treatment during the
attack consists in recumbency, warmth to the legs and feet, and such
stimulants to the abated vagus nerves as ether, ammonia, valerian, smelling-
salts, and hot applications to the cardiac region ; remedies which are
rather to be recommended than alcohol. Belladonna also is better avoided,
and digitalis, if an occasional ally, is not to be trusted. In acute attacks
these measures will suffice; but in some cases the palpitation does
not take the form of isolated attacks, but, though less violent, is
either persistent or chronically recurrent. In these cases treatment, if
addressed still to the vagi, may well be addressed also to the accelerators,
especially if the pupils be dilated and the face flushed, and thereby
excitement subdued. As palpitation, if consisting partly in defect of
central control, is nearly always set up by some eccentric cause, rules for
general management, such as regulation of the bowels and other secretions,
attention to piles, uterine disorders, overwork ; temperance in food and
avoidance of alcohol ; moderate exercise, cold baths, and regular hours of
sleep, will be found in the articles on hysteria and other neuroses. At
times such sedatives as aconite and the bromide of soda, ammonia, or
camphor may be needed. Aconite has served me well in many such, cases,
and its use, cautious as it must be, may yet be more than occasional!
With palpitation run other symptoms, such as precordial pain, panting,
globus, vertigo, and perhaps even syncope — though I have never seen it
under ordinary circumstances. During the attack the urine is scanty,
but it is generally profuse after it, as in megrim and other neuroses
accompanied by fluctuations of blood-pressure. Such symptoms receive
VOL. V 3 (J
8i8 SYSTEM OF MEDICINE
full attention in other parts of this work. The causes of palpitation,
also, are dealt with elsewhere. I will but remark that sudden vaso-motor
changes, either in the direction of constriction or relaxation, are common
incidents in palpitation, and perhaps common causes of it. When we
remember that, in the bulb, the cardio-inhibitory, the vaso-motor, the
respiratory and the gastric centres abut upon each other we shall feel no
surprise that the functions related to all these centres should often
influence each other or be influenced: together. The expulsion of a worm
has sometimes proved to be the cure of troublesome palpitation. Palpita-
tion coming on for the first time in later life is a matter for anxiety, but
may be gouty or dyspeptic (bad teeth).
False palpitation. — It is not uncommon for patients, especially for
highly neurotic or neurasthenic patients, to complain of palpitation
although on examination little or nothing of it is perceptible, or the
heart may be accelerated by some five or ten beats at most ; yet to judge
by the bearing of the patient the distress is acute. Such patients
will probably complain of other hyperaesthesias, and of pains in other
regions, such as the head and back. In the cardiac region the patient
complains of tightness and oppression — " precordial anxiety " — of urgent
heaving, or bursting of the heart, or of cramp in the part, in which they
fear to die. Or the pains may be boring or cutting : the husband of such
a sufferer, in writing to me, tore out from his Bradshaw the advertisement
of a corset-maker, and drawing a dagger with its point entering the left
submammary region, enclosed the picture as a graphic representation of
his wife's agony. As many of these patients suffer from air hunger and
pains in the chest and arms the cases melt into the class of " pseudo-angina
pectoris." The attacks may recur many times a day, and are not difficult
to appraise in the broad sense as neurotic : the story of the case rarely
leaves much doubt of this interpretation. The blood-pressure rises
during the attacks and rapidly falls as it passes off. But in my opinion
the vaso-motor phenomena are not causes, but consequences — are of reflex
origin and secondary to the neuralgia or distress. As auscultation and
other means of investigation reveal no change or but little, the intimate
nature of these phenomena is not easy to a,scertain. In ordinary palpi-
tation, as the pulse rises, perhaps to 1 20, the pressure falls and the face
flushes ; or the patient turns pale and the pressure rises ; but neither of
these events is seen in the false palpitation. Until a better hypothesis
is suggested, we may suppose that there is some morbid susceptibility to
the impact of ordinary stroke of the heart. There would seem also to be a
like hypereesthesia in the vessels, as rushings in the arteries, whizzings in
the head, and other " determinations of blood " are complained of, sensa-
tions perhaps due to slackness of the arterial walls.
Weak heapt is used in two senses ; as a heart of lax or even failing
fibre, and as a heart subject to certain kinds of transient disturbance.
Of the former we have not here to speak ; the second is as follows : —
The patient usually, but not always, a neurotic woman, tells us the
heart ceases to beat ; in the severer cases the patient is convinced of this.
FUNCTIONAL DISORDERS OF THE HEART 819
and fears that each attack in turn may be fatal. Sometimes as the
attack comes on the face turns gray, and the lips blench ; in other cases
illness is betrayed rather by the expression of apprehension and distress
in the face than by any signs of organic disease. The hand is pressed to
the region of the heart where pain may be felt ; but often it is not so
much a pain or a throb as a sinking, and the sinking is not at the heart
only, but a general " lypothymia." She may also complain of pins and
needles, of turning cold, and other evidences of irregular blood distribution.
After a time the distress passes off and the patient recovers with that
sense of extraordinary exhaustion which is so well marked in functional
affections of the heart. The pulse during the attack is not very
characteristic ; it is certainly weaker, it falls more or less in pressure ;
and therewith it increases in rate a little — say 100 to 110 ; but it is not
the pulse of syncope, nor indeed do these patients faint away; they gasp
and return to life with a sigh or two of relief. Speaking generally, there
is no danger in the attacks except that which lies in the habit of taking
drams to cure or prevent them. Mrs. Gamp's prescription of two drops
of brandy on a lump of sugar is too well known to these patients and
their friends ; the medicine is at hand and is assiduously administered,,
with the rubbings of the extremities, the hot bottles, and the like, which
are grateful to these patients. And no doubt for the moment the alcohol
is helpful ; it pulls the heart together, or imparts something or other which
may be mere Dutch courage, or something more mechanical ; probably
its chief effect is to dilate the arteries of the surface, and thus perhaps to
divert the blood from the splanchnic areas into the arteries of the skin
and limbs which were certainly for the time ansemic. It is not apparent,
however, that constriction of the arteries is primarily at fault — a
dilatation of the splanchnic areas may be. Almost as I write these lines
I saw with Dr. Henry Head a very curious case of functional cardiac
instability. A gentleman, aged thirty-three, apparently healthy in all
other respects, but of nervous temperament, complained to us of breath-
lessness on ascents. No anginal or other pain. At nights he awakes
with a sense of faintness or impending death. His pulse, while he is
standing, is 130, and but little less on sitting down; but as he lies down
flat the radial pulse instantly undergoes striking oscillations for two or
three seconds, and then falls to a steady rate of 80. He has some reason
to suspect that his nocturnal discomforts are due to a still slower rate of
the circulation. Aspect healthy; no cyanosis. Does not smoke nor
drink tea or coffee. The heart on examination proves to be free from any
abnormal sign, unless it be that the apex beat is obscurely seen, and the
impulse rather diffused. He has had attacks of the kind before, if not
quite so severe, and has always been cured by going to sea. I thouo-ht
that the effect of a well-adjusted abdominal pad might be tried. I have
seen at least one other such case. As bearing on the conclusions
of Dr. Leonard Hill and Dr. George Oliver, I may say that in one patient,
who suffered much from heart sinking, as above described, to raise the
arms was almost a certain means of producing an attack or a threatening
820 SYSTEM OF MEDICINE
of it : hence she assured me that she dared not raise her arms to knock
at the outer door of a house. Until I read Hill's papers I thought this
was all moonshine ; now I think it was not. Whatever be the underlying
conditions, the repeated taking of drams is very mischievous ; it encourages
the very oscillations in blood distribution which we ought to control by
the wet sheet, douche, regular exercise, massage, and such means ;
and after a few months or more of the dram-drinking the doctor is told
that an unaccountable nausea and retching in the morning, and loose
motions, either before breakfast or during the forenoon, are added to the
tale of her symptoms. The next stage is that of pains and palsy in the
legs and feet. Such is a common enough story. Some cordial these
patients will have, perhaps ought to have ; they are frightened out of their
wits, and a stimulant seems their only help. Well, then, let us prescribe
ether, valerian, ammonia, or peppermint for the moment; and as the
immediate anxiety passes away, attention to the general therapeutic needs
of the case will, in a broader and more wholesome sense, ere long remove
the need for dramming at all. It cannot be too strongly urged upon these
patients that temperance, even to the point of total abstinence from
alcohol, is paramount in the treatment of neurotic cases : it is even a
more important condition in them than in the gouty. Cardiac neuroses
are nearly always part of general neurosis ; in all its phases neurosis
means lack of inhibition, relative or positive ; generally relative. Dr.
George Oliver's comparisons of the range of radial volume in the healthy
and in the unstable respectively are full of instruction in this respect.
It is possible that in some of such cases there may be a lack of suprarenal
incretion and a corresponding loss of arterio-vascular tone. But this is a
dark matter ; I have even found the radial blood-pressure rise at the
outset of an attack and fall again as it passed off. In these phases of
high initial pressure the patient is flustered at first and sinks afterwards.
An increase of the muscular reflexes is often seen in these patients, as in
the following disorder : —
Passing by gradations into, or even confused with the above derange-
ment, is that of eardiae asthenia, which, in a recent pamphlet. Da Costa
has distinguished from irritable heart (4). The author says that for
long periods the action of the heart in these sufferers is feeble ; a feeble-
ness to be distinguished from the weakness due to organic causes, and
again from that of lithsemia, gout, tobacco, and the like.
The affection generally manifests itself in those persons whose nervous
system has been strained by worry or overwork ; whatever the warning
signs, the full brunt of the disease is often sudden in its incidence. The
patient is prostrate in bed ; all attempts at sitting up cause swooning and
vanishing pulse. The heart's action is feeble ; the pulse is small and soft
and generally increased in frequency. Although vidthout pain there is a
sense of uneasiness in the cardiac region. The bodily temperature, as
well as the warmth of the extremities, is lowered. The breathing is un-
affected— a point of distinction from organic disease. " I am out of heart
rather than out of breath," was the reply of one of Da Costa's patients.
FUNCTIONAL DISORDERS OF THE HEART 821
Insomnia is not infrequent. The patient rallies but slowly ; two months
in bed may be his portion, and months more of ailment before he recovers ;
for the issue is as tedious as the onset may be brusque. In some few cases
the rhythm of the heart is irregular. The disorder may occur in either sex,
and at any time of life between childhood and old age. There is no
percussion dulness, the impulse is feeble. The first sound is short, lacking
in volume ; the second sound is not accentuated. Hysterical symptoms
are conspicuously absent. In " irritable heart " the patient can get about,
the heart's action is more obviously disordered, the impulse is jerky and
diffuse, the second sound is sharp and distinct. Tobacco heart might
resemble that under discussion, but in my experience the tobacco heart is
more prominently irregular, and is often " irritable." In distinction from
organic disease are the disproportionate prostration, the absence of
dyspnoea, and the freedom from any oedema of the shins or feet. An
apex murmur may appear in the functional disease as in almost any kind
of cardiac functional diseases. The prognosis is good.
The treatment recommended by Da Costa is as follows : At first rest
in bed ; then, as some ground is gained, carefully regulated shower-baths
are to be given. The next stage may be massage, but often some time
elapses before this means can be borne. Then Swedish exercises and
gentle riding on horseback can be arranged by degrees. Nutritious
feeding is of course essential, and, in Da Costa's opinion, a generous allow-
ance of alcoholic stimulants is necessary also. Among drugs strychnine
" stands pre-eminent." The dose need not exceed ^ gr., but it must be
given continuously. Arsenic is the next best drug ; iron is not usually
indicated, and the need of digitalis, if any, is but occasional. Nitro-
glycerine does no good. Bromides, valerian, or even opium may be
required under special circumstances. If I may venture to guess at the
pathology of these cases, it would seem that a dilatation of the vessels in
the splanchnic area is the most probable explanation of them, and an artful
compression of the abdomen might be found useful. The observed useless-
ness of the nitrites may support this view of the pathology. My patient,
who could not knock at the door (p. 820), was perhaps one of this
class, and I think I have seen many cases of the kind described. The
state of the pupils might give us some useful indications in such cases ;
my impression is that they are either dilated, or at any rate contract slowly
and imperfectly. Diminution of the mass of the blood, with correspond-
ingly small output, may, as for example in the acute fevers, be a cause
of such cardiac symptoms, however sound the organ itself. In cases such
as these we have a truly "functional" disorder; the heart may be
healthy, but its work is upset by circumstances.
Irritable heart.— Since the publication of Da Costa's and Myers' well-
known papers this derangement has been too exclusively attributed to
muscular over-exertion. It seems, however, that we must divide the subject
of irritable heart into two classes : the irritable heart of young persons
now to be described, a very curable disease, and the " Soldier's Heart,"
to be described under "Mechanical Strain," p. 851, which is too often
822 SYSTEM OF MEDICINE
incurable. The irritable heart of young persons is a product of many-
conditions. The irritable heart of older persons — the irregular fretful
heart which goes on too often to dilatation and static disease — ^is more
definitely the result of over-exertion than that of young adults. In the
irritable heart of young adults the upstroke in the sphygmogram is brisk
and high ; in that of dilating heart it is low and less brisk, and the
rhythm is often irregular. The irritable heart of the former kind is
much as follows : — A young man, for a man it is oftener than a woman,
comes to tell us that he is bothered by his heart; he has a pain in
it, always tiresome, often sharp ; and the organ throbs and jumps ; it
never lies outside his consciousness. If he exert himself it beats violently ;
if he lie still in bed it also makes itself a nuisance, banging away
when he ought to be asleep. When he is stripped he is generally a
spare, long-chested fellow with wide intercostal spaces ; and in the fifth
space the apex is seen as it were kicking, rather than heaving, against
the thin web of the interspace, although the blood-pressure is low and the
dicrotic wave high. The heart may be a little out of place, displaced
somewhat outward, but more downwards ; still this is difficult to ascertain
in lanky young men so built that the flat chest and the ill-developed lung
leave more of the heart uncovered. A few years later such a man
thickens, his lungs become more expanded, the heart relatively recedes.
It may have been rather dilated before, possibly a little hjrpertrophied ;
but it was probably no more than too palpable and visible. Now
in many of these men there is no doubt a story of considerable if not
of excessive exertion. On the other hand there often is not ; the youth,
indeed, has been warned not to play football, not to row, and so forth —
advice which has its good side, but which may be too rigidly enjoined.
To the stethoscope the beat simulates hypertrophy : it is possible that
in some cases there is a true hypertrophy (vide p. 916). In some cases
of physical strain a little hypertrophy may exist, but even then dilata-
tion is the main change. That in the intervals of rest the mean arterial
blood-pressure is nearly always low is witness against persistent hyper-
trophy : when pressure falls, the heart cannot long remain above its
strength. The peripheral arteries are lax, the pulse is dicrotic, and its
slackness is in remarkable contrast with the excitement of the heart
itself : the action seems laboured and perhaps heavy under the hand ;
the rhythm is often a little uneven, and the second sound at the
apex too loud. The first sound is rarely muffled, however, as in un-
questionable hypertrophy ; it may even be shorter than normal, or at any
rate smart enough. Sometimes there is a murmur, more often there is an
"impurity" of the first sound, as if dimmed by some distant murmur
overheard. These murmurs are often " pulmonary " in origin.
To account fully for this state of things in the circulation of such
patients is to know all the ins and outs of the habits of youth. This
comes to us best by reflection on our own young days. Is it with
laughter or with tears that one looks back on the reckless forenoon break-
fasts washed down with those detestable compounds called " cups " ; the
FUNCTIONAL DISORDERS OF THE HEART 823
sherry and half a box of mixed biscuits at luncheon ; the manly absorption
of grown-up and more than grown-up doses of tobacco ; the black coffee
and cognac of an evening after a large gobbled -up dinner; the hot
arguments on the framework of the universe and the destiny of man pro-
tracted till two o'clock in the morning ; the spasmodic bouts of study ;
the examination bogie ; the conflict with untamed and rebellious passions,
some wholesome, some not so wholesome ; the violent games and the
bear-fights ; the ardent hopes and the bitter griefs— what elder is there
who recalls all these things, and does not long to dash pell-meU into it all
again and accept irritable heart into the bargain ? There is but one step
between the wise young man and the prig, and this a narrow one ; still
that is no priggish advice which would cut out of this gay, ardent and
careless life some of its idler and less lovely follies, and complete the cure
of irritable heart by better-regulated exercises, — not violent stress one day,
and idleness not unmixed with dissipation on the next, but regular training
which shall promote a uniform development, not only of lungs and heart,
but also of all the parts of body and mind. Muscular exertion, then, is a
cause of irritable heart when it is pursued in an irrational and unsystematic
manner by a more or less nervous and dyspeptic young person whose
lungs are not big enough to carry off the blood as quickly from the
right heart as it is delivered there ; and whose ethical and intellectual
life is lived after the same fitful fashion.
The irritable heart described in recruits, especially those suddenly
removed from civil into military life — clerks turned into soldiers (Da Costa,
Herz, etc.), is a' difierent disease ; and Mr. Simson Snell of Shefiield, in a
private letter to me, says that colliers are very liable to an acute irritability
of the heart, due probably to severe bodily efforts in awkward positions
and in bad air. In these persons transient dilatation not infrequently
becomes permanent (wd^ p. 851).
The treatment of the slighter and common forms of the malady is then
one of regulated habits, and the avoidance of such poisons as alcohol,
tobacco, tea, and coffee, except in doses which prove to be harmless to
the individual. Muscular exertion must be systematic or indeed pro-
hibited for a while or severely restricted. Of specific means none is
required ; it is better to avoid digitalis and the like, unless the symptoms
be unusually vexatious, when small doses with a little bromide may be
used economically. These patients are often a little shy and sombre in
spirit; change of scene, pleasant society of both sexes, and frank and
kindly advice on sexual matters, are a part of the services which a
sympathetic physician may render to young men; for while we may
have a kindly smile for their heroics, we must remember, nevertheless, that
they are often acutely miserable. Some excellent remarks on this subject
by Sir William Broadbent are reported in the Larvoet.
The neurotic element In organic disease of the heart. — We are too
much disposed to think that death from organic disease of the heart is the
direct result of its utter demolition; that the crippled organ stumbles
along until it can do more, and staggering under an intolerable burden
824 SYSTEM OF MEDICINE
sinks to its rest. We are too ready to assume that the diseased heart
fails by means of its sheer mechanical inability. This may perhaps
be the case here and there. Dr. Solomon Smith has on more than one
occasion reminded us, however, that in many instances, at any rate, this
is not the course of events. To put Dr. Smith's view of the matter
summarily, he would have us see that the heart in advanced disease may
fall, or stagger, under the intrusion of some neurotic accident, of some
nervous perturbation, whether of reflex or inherent origin. The harmony
between the reflex stimuli from the difierent segments of the heart
may and frequently does become deranged ; and it is not surprising that
irregularity should result. Again, derangements of the stomach or
bowels, torpor of the liver, pulmonary spasm, cerebral or bulbar inter-
ference, the absorption of toxic products, and so forth, are potent to
depress or disturb the heart's action far beyond its mere mechanical dis-
advantage. Thus it is that in most cases great oscillations occur : at one
time the patient is pretty well, at another he is at death's door ; yet again
he comes round, and this not necessarily as a result of treatment, or if of
treatment, of such a remedy as an injection of morphine, which may re-
adjust or permit the readjustment of the harmony of internal cardiac
stimuli; or may block some reflex arc with its superadded neurosis. Again,
the vomit of a little sour mucus or the discharge of an offensive stool may
set matters right, even in a few minutes. It was with this conception
in my mind that in 1869 I recommended the subcutaneous injection of
morphia in heart disease ; not only does it, in appropriate cases, cut short
a neurosal paroxysm of dyspncsa or restlessness, or restore the order of
rhythm, and thus pacify the organ rocking under the tumult of its un-
balanced parts, but it may prevent the heart from being " tripped up by
the intrusion of a neurosis," as Dr. Smith puts it. The complex rhythm
of the several parts of the heart and its allied vessels is but too easily broken
in upon at one or more points. The importance of these considerations in
respect of treatment is obvious. " Our choice of remedies lies no longer
only among cardiac stimulants or depressants, arteriole constrictor* or
dilators ; a whole range of remedies is opened to us which, although with-
out direct action on the heart, relieve heart trouble all the same by remov-
ing the starting-points of nerve derangements." I may add that not only
are new remedial means thus opened out, but in these words we have the
explanation of the value of many remedies which, in a more or less em-
pirical fashion, have long been familiar to us.
Tachycardia. — The . names tachycardia and bradycardia are often
used merely to signify rapid heart and slow heart respectively ; such uses
have not even the accuracy of pedantry. Dr. Herringham, indeed, thinks
that tachycardia is a " symptom rather than a disease," but in thus writing
he scarcely does his own monograph 'justice. If any rapid pulse, ranging,
let us say, over 130, is to be decorated with this fine name there is an
end to clinical nomenclature. Dr. Watson Williams implies that tachy-
cardia is a disease, but he prefixes the qualifying epithet " paroxysmal,"
FUNCTIONAL DISORDERS OF THE HEART 825
which from his point of view is superfluous. Dr. Herringham, in refusing
to go beyond the bare etymology — the " prairie value " — of the name,
argues, truly enough, that " no real distinction can be drawn between
the cases with and those without . . . organic lesions." But is not
this to deny also the validity of the names asthma, epilepsy, chorea ?
The author is right in warning us against the danger of " erecting a
separate tjrpe " in such a case as this, a truth which I have endeavoured
to emphasise in the introduction to this work ; but, as I have there said,
I do not think that the existence of mixed or transition cases for-
bids us the precise use of types. For what do we mean by " a disease " %
Surely no more than the recurrence of symptoms in fairly uniform groups.
A disease has no more " real " existence than has a constellation ; stars,
like symptoms, have a way of grouping themselves about centres of relative
density ; to such groups we give names, and no one should pretend that
any disease has more than this relative or, if the reader please, this
" subjective " existence. A type is an abstraction, an ideal pattern con-
structed from an infinite number of cases; and the moment we contemplate
a particular case we leave type for embodiment : no two cases are identical,
and no case corresponds in all respects with the type. Like Dr. Herring-
ham, I am not fond of teaching by types, but they have their use in
summarising and classifying our observations ; and if we remember that
they have no more claim to "reality" than this, we may use these
conceptions without much harm. If, whenever we talk of " tachycardia,"
for example, the mind is to range over an indefinite scattering of cases in
which the pulse is excessively quick, we shall waste a great deal of time
in discussion and a great deal of space in books.
To what symptom group, then, do we apply the name tachycardia ?
Not to any case of quick heart, but to an enormous quickening of the
pulses of a heart not necessarily the seat of static disease ; a quickening
which attacks the patient suddenly ; which does not persist indefinitely,
but for a variable space, rounded oif by an equally sudden reversion to the
normal state less certain phenomena of exhaustion. Heart disease, in the
static sense, may coincide with tachycardia, it is true ; mitral stenosis may
coexist with chorea, nay, may even favour the occurrence or intensify the
peculiar symptoms of chorea ; but that surely ought not to deprive us of
the name chorea, nor justify us in including under this name, as too often
we do, any twitchings or gestures whatever which look at all like chorea.
Careful clinical observation and no less careful verification after death
(so far as this has gone) indicate, at present, that attacks of rapid heart
coming on suddenly, departing suddenly, and attended with certain other
symptoms, objective and subjective, are consistent if not always coincident
with a heart apparently sound ; that coarse heart lesion is therefore not a
necessary antecedent, or, in other words, is not a cause of this malady.
Hypertrophy is not usual in rapid pulse, of any origin, as such ; for increase
of rate generally means diminution of output per beat, and probably per
second also. If output per beat and per second is increased the rise in
rate can be but moderate '(Stewart). The recoids of necropsy in tachy-
826 SYSTEM OF MEDICINE
cardia are few, no doubt, but we can only go upon such evidence as we
have ; and the sudden subsidence of these attacks without leaving behind
them any evidence of disease of the heart supports the interpretation of
the scanty pathological material. The interpretation is that tachycardia
is a fairly uniform symptom group ; and, as one of its eminent characters
is its paroxysmal occurrence, the addition of this qualification to the
name is superfluous.
The attack is as follows : — As I describe it I have in my eye two
cases now under my care. The first is in a woman, passing (at the time I
now write) through the menopause without any peculiar derangement, who
since her adolescence has been liable to seizures of tachycardia. She is a
well-nourished person, and is now getting stout. Her anxious and fidgety
temperament may indicate the neurotic bent, or may be the consequence
of her distressing malady ; but the family history is without apparent
bearing on the case. Her own life, though broken into more than once by
calamity, has, on the whole, been one of prosperity ; moreover, her ailment
dates from adolescence, years before these heavier trials had afilicted her.
She is happily married, but has had no children. The attacks, which have
preserved the same characters from her adolescence, are as follows : — She
turns a little shivery and pale, at times even ashy ; and a peculiar lassitude
and restlessness possess her ; the extremities are cold, and these and other
parts are " numb." She soon becomes aware of a tightness, tremor, and
oppression rather than of a beating about the heart ; the tightness may
amount to actual pain, and may dart here or there. The pulse is now
beating at the rate of 160 to 200 a minute (the reckonings of the pulse
have not been systematic ; and often the only record is that the pulse
could only be counted at the heart). After the attack has continued for
a day or two I find that the area of cardiac dulness has extended
towards mid-sternum, or even beyond it ; the sounds are tick-tack, but no
added sounds are to be detected. As the attack goes on she becomes very
fretful and wretched, but the oppression and tightness and other signs
suggestive of peripheral arterial contraction pass off. The urine in most
cases is scanty ; at first, perhaps, from contraction of the renal arterioles,
later from low arterial pressure ; but in her and in another of my cases
nervous polyuria attends the attacks throughout. It seems certain,
from the change in the volume of the heart, that the residual blood
in the ventricle is large and the output correspondingly small. The
relief of oppression does not signify that the tension of the ventricular
walls and aorta is diminished, but that the sensibility of the heart is
blunted. In severe attacks she is more or less aphasic, with the aphasia
of exhaustion — a phenomenon not uncommon, in megrim and in persons
spent by fatigue. Such an interval of aphasia is described by Tyndall
in his own person after a dangerous and exhausting scramble among the
rocks above the G-rimsel. The most complex of muscular co-ordinations
give out early, as we might expect ; but, as in many cases of nervous pros-
tration, she has often a special sense of weakness or palsy in the left arm.
The duration of the attacks is very variable. In some patients an attack
FUNCTIONAL DISORDERS OF THE HEART 827
may cease after a few hours or a few minutes ; or again it may continue for
three, four, or five days. It is said to have lasted in some cases as long
as ten or eleven days ; or indeed for weeks at a time, but suspicions of
a wrong diagnosis present themselves on the consideration of such records.
Perhaps the longest attacks of those carefully recorded were in a case
recorded by Bouveret, in which they endured for thirteen days. In my
second patient the attacks would return in groups, giving thus an impres-
sion of a longer paroxysm than was strictly the case. He might have a
series of four or five attacks, and then none for a year or more. During
the one or more nights of an attack the patient may be almost sleepless ;
but during sleep the tachycardia pursues the same course. Sometimes
•during these nights the female patient described above is a little delirious.
The beating of the heart is regular in all cases unless the ventricle be
■dilated, when every piilse may not reach the wrist. In a case recorded by
Dr. Bristowe the pulse number reached 308 a minute.
The cessation of the attack is always brusque, generally sudden;
it may end in a few slow hard beats, or in one violent rebound,
followed, says my second patient, by " a sort of swim." The trial is now
over ; exhausted as the sufferer may be, there is freedom — till next time.
The urine in these two cases has never contained sugar, albumin, or any
substantial excess of urates or phosphates. Attacks cannot be traced as
a rule to any cause or to any season ; they may come on at a moment of
rest ; often they begin or end during sleep. My second patient is an
epileptic tailor, with a good family history. In him over-exertion often
brings on an attack ; but an attack thus produced can always be arrested by
holding his breath in inspiration and then stooping tightly down with
his belly on his thighs. Spontaneous attacks cannot be thus cut short,
though once (the third of four attempts) he stopped one in my presence
for a few seconds ; the pulse fell suddenly from 166 to 80. As he rose
nip the rate as quickly returned.
Such is the ordinary course of a well-marked case of tachycardia, though
•cases of greater and of less severity occur. In one of my present patients
there is no abnormality of the heart save the usual short, sharp action of
neurosis ; in the other there is a permanent apex systolic murmur, but no
dilatation ; in worse cases irremediable dilatation of the heart is brought on.
During the severer attacks oedema of the lungs may accentuate the signs
of dilatation, and later the feet may become cedematous, and albumin may
appear in the urine. A repetition of such incidents renders the heart less
and less able to recover its normal tone, and the symptoms of dilapidation
set in which need no description in this place. Death may be by asystole,
or by syncope ; probably nearly always by syncope.
I may add to the story of my lady patient, that her first attack cut
short a prolonged and severe sMpping effort, when she had reached a
high tale of skips. Ever since she has been subject to attacks, but they
are not so severe as formerly. They seem to come on capriciously, she
thinks more in spring and autumn than at other seasons. Sometimes
they have been determined by a shock, physical or emotional, as once
828 SYSTEM OF MEDICINE
when she made a false step in the street and " jarred " her foot ; and
once again when a drunken man seemed disposed to accost her.
Dyspepsia may seem to call forth an attack, but, in both these cases, by far
the majority "come on of themselves." Her pulse generally runs about
200 ; the highest that has been noted accurately was 280. The attacks
go off somewhat variously : either " hardly," that is, more gradually with
a peculiar sense of agony, when she used to think she must die ; or
suddenly with a thump or two. The attacks may last for a few seconds,
a few minutes, or a few days ; some attacks have lasted as much as
ten days, but this duration has been unusual. She feels conscious
enough of the beating ; it is like a rapid tapping or vibration : when she
was younger it would shake the bed and even the room. In latter years
she can bear them better, no doubt they are milder ; she can even read
during the attack. Formerly she was prostrate throughout the course of
them, and long after them ; indeed, they are all most exhausting. Her
family history is very good ; her parents are hale octogenarians. No
notable nervous disease has been heard of in the family. I described her
as a nervous and fidgety person, but she assures me that the tachycardiac
attacks have been the cause of this disposition by the injury they have'
wrought upon her nervous system. This is probably true, as she is
of sturdy build and well nourished. She has no permanent signs of
cardiac failure. In the epileptic case the fits came on at aet. 42, the heart
attack at 14. The two maladies move quite independently of each other.
Morbid anatomy. — I have said that the evidence of necropsies is as
yet scanty, though the two or three careful examinations on record agree
in indicating that, these evidences of cardiac decadence apart, no constant
changes are found. Examination of the vagi, of the sympathetic nerves,
and of the intra-cardiac ganglia have been negative, except for secondary
changes such as the degeneration of muscle and ganglia in common. As
then the evidence of the stethoscope is . also negative, and as for many
years the patients recover their ordinary health between the attacks, we
must regard tachycardia for the present as a functional disease. If the
ultimate prognosis be doubtful, if in a certain number of cases the event
be death, the immediate prognosis, in the earlier years at any rate, is
hopeful. Indeed, Dr. Watson WiUiams records a well-marked case in a
patient aged — at the time of his writing — eighty years. The patient I
have referred to is about forty-eight. In cases which, after the lapse of
years, have proved fatal the necropsy may reveal, as in a case of Fraentzel's,
fibroid degeneration of the walls of the heart and dilatation of its cavities
in all directions. Broadly speaking, then, in tachycardia no primary or
constant morbid lesion has been discovered. Ultimately the disease often
wears out the heart ; but where or how it is engendered we know not.
Pathogeny. — With the best will in the world I cannot follow the
example of recent writers in discussing the " theory '' or " theories " of
tachycardia. No theory exists. Certain surmises, such as no competent
physiologist would fail to suggest at first sight, are offered to us ; but it
would be an abuse of language to call them even hypotheses. I will take
FUNCTIONAL DISORDERS OF THE HEART 829
them in order : (i.) That the vagi are spent, or thrown out of gear. The
suddenness of the attacks, both in onset and issue, seems against the
opinion that these nerves are spent ; thrown out of gear they may he.
We know of many cases in which the vagi are thrown out of gear ;
as for example in bulbar disease-, or under the pressure of growths
or glands (of. Probsting's well-known case), or in experiments upon
animals ; but in such cases the rapidity of the heart has not been by any
means so great. It does not seem probable that abeyance of the vagi in
man gives the heart play beyond 120 beats in the minute, or thereabouts,
(ii.) That the vagi may be in abeyance, and at the same time the
accelerators may be excited or vaso-motor centre affected. This suggestion
sins against the economy of causes, and, as we must assume a close
synchronism of disorder in each, we should be thrown back upon some
cause, behind them both. Some temporary change in the bulb might
at once throw out of gear both vagi and vaso-motor governance ; never-
theless such may be the case, (iii.) That the accelerators may be so
stimulated as to overbear the normal vagi. It must be admitted that
the onset and issue of the attacks seem in favour of some such supposition.
In no experiment, however, has such a rate been obtained by accelerator
stimulation; and reflex irritations of eccentric origin do not push the
heart beyond 150 as an extreme limit, (iv.) That the cardiac ganglia are
the seat of the disorder. But we find no changes in them which are
inconsistent with a secondary origin ; moreover, the latest researches
on these ganglia by Dr. Gaskell and others seem to prove them to
be remnants of the innervation of the arteries, and thus to have but a
secondary importance in the cardiac functions, (v.) Some sudden change in
arterial blood-pressures; this will not serve us, as the arterial blood-pressures
are by no means constant, they are always rising and falling ; any constant
change of pressure would soon be compensated in the normal way :
furthermore, while no ordinary tides of blood-pressure, as Mosso's experi-
ments (Junot's boot, etc.) show, are competent to bring about so extreme
a change of rate, there is no evidence of extensive areas of ansemia, as
on dilatation of splanchnic veins, which might be adequate to call forth
such phenomena. Were the heart abandoned to its own inherent rhythm
its action would be irregular, which in tachycardia it is not, unless con-
siderable dilatation has taken place. I confess that I leave my suggestion
of extensive areas of anaemia somewhat wistfully, as a sudden expansion
in the areas of the abdominal venous system would produce such results,
as we see by the results of experiment and in exhausting diseases ; still
on this supposition the heart should not be distended, unless simultaneously
the peripheral arteries are constringed. I think, however, the pulse is
small in tachycardia, because by virtue of their tone the arteries fit them-
selves to diminished contents. We cannot, then, do more than guess
whether the immediate causes of tachycardia lie in the cerebral cortex
in the mesocephalon, in the bulb, in the vagi, in the accelerators, in the
cardiac ganglia or muscle, in anaemic areas, or in eccentric irritation, such
as floating kidney (Balfour). Neuritis has been alleged as a cause'; but
830 SYSTEM OF MEDICINE
there is no evidence of its presence, nor would it consist with the long
intervals of health. As the phenomena are remarkably uniform, the
causation is probably not complex.
Of the immediate causes there is little to say. Over-exertion, dyspepsia,
mental shock or emotion, uterine disorders, auto-intoxication, loaded bowels,
any or all of these have been alleged with more or less hesitation. All that
we can say, then, with any approach to certainty is that the victims of this
disease are of the neurotic habit, and that in a few cases it has seemed to
be hereditary (Williams). It is alleged that Graves' disease, in which a
rapid heart is the chief feature, may be the instant result of an acute
mental shock.
Sex. — The records of cases indicate that this factor has little or no
influence in the causation of tachycardia, the disease falls almost impartially
on the two sexes.
Age. — In forty cases of Dr. Herringham's collection the age was
recorded. In seven the malady dated from childhood ; of these seven, five
were women. In twelve the first attack appeared beween the ages of
twenty and thirty ; of these, six were men and six were women. In
thirteen cases the onset fell between the ages of forty and fifty ; in three
the patients were over fifty when it occurred. Dr. Watson Williams
reports a case in a man of eighty-one, in these attacks the pulse would leap
suddenly from 60 to 130. H. C. Wood reports a case as still recurrent in a
physician of eighty-seven years of age ; the attacks began in his thirty-
seventh year ; the onset is abrupt, and the pulse rises quickly to 200.
Diagnosis. — Tachycardia is an intermittent disease ; if we remember
this we shall avoid confusion with other diseases in which a rapid action
of the heart is a more persistent feature. The larval form of Graves'
disease — a by no means uncommon form in which the th3rroid is not
enlarged nor the eyes prominent — ^may be distinguished from tachycardia,
in cases which have been watched for a sufficient time, by the long per-
sistence of the rapidity. Moreover, in Graves' disease the action of the
heart is more thumping. Fine tremor may be seen in many cardio-neurotic
cases, as may exalted reflexes also. Tachycardia is not a mere incident
of neurasthenia. The pressure of a tumour on the vagi may be attended
with a persistent rapidity of pulse. In eases of idiosyncrasy, cases in
which the pulse runs in the individual at accelerated rates, the persistence
of the peculiarity will again decide the judgment against tachycardia ;
and it may be added that in these cases, and in others of more or
less persistently quick pulse, the patient suffers less instant distress.
Cases are recorded on good authority in which the pulse of a person
presumably healthy habitually ran at 150 a minute. Binswanger has
recorded such a case in a woman ; in her the peculiarity had endured all
her life. I remember one day, when I was driving with a medical friend,
a man passed us on horseback — a fine-looking country squire in whom
there seemed no flaw ; my friend told me to note him as he passed,
because his pulse ran habitually at 1 20. The owner of the pulse, patient
I cannot call him, enjoyed fair health, but in the doctor's opinion would
FUNCTIONAL DISORDERS OF THE HEART 831
be a " bad subject " for acute disease ; this opinion he founded not only on
a mistrust of the pulse, but also on a certain lack in him of resistance to
fatigue and trivial ailments. Dr. G. Balfour, again (Senile Heart), refers
to the case of a lady, then over seventy, who had had a large family and
enjoyed good health, though of nervous temperament ; her pulse had never
been under 150. Of heart diseases the two to be excluded are dilatation
and mitral stenosis. The tobacco pulse, if rapid (at first it is slow),
is irregular. Alcohol, if it accelerate the heart's action, does so by inducing
degeneration of the organ, and this lesion may be betrayed by its own
phenomena. The accelerated pulse of cardiac dilatation is irregular. Old
men who give themselves up to sexual indulgence have a pulse of
increased rapidity, but tachycardia is not very likely to attack a man for
the first time in old age. Fevers, diarrhoea, and other toxic or exhausting
causes may be attended by a quick pulse, but such causes are not likely
to be overlooked. In bulbar palsy the pulse is persistently changed ; and
if accelerated, is irregular and intermittent ; in tachycardia the rhythm
is even : moreover, bulbar disease has its own characters, such as faintness
attended with a fear of death, a kind of " angina sine dolore." Finally,
in none of these is the disease paroxysmal.
Prognosis. — ^Dr. Herringham thinks that after thirty years of age no
patient of tachycardia is safe, and that few pass fifty. This, I think, is
rather a darker forecast than I should be disposed to make. Much
depends, as Herringham says, on the duration of the particular attacks
and on the frequency of their return ; if these last longer than five days the
stress on the dilating heart leads to strain, especially in the elder patients.
Two patients of mine are well past their climacteric, and to Dr. Watson
Williams' patient of eighty-one I have already referred. In him, as in
most patients as they advance in years, the return of the attacks is
generally postponed ; the intervals are longer, and there is more time for
recovery.
Treatment. — Unfortunately this paragraph is but a short one — not
because we have a prompt remedy, but because little or nothing seems to
be of much service either in cutting short the attacks or in the prevention
of them. As I have said, the attacks may get less both in number and
severity with advancing years; and, perhaps, something can be done
on general principles to make the system less susceptible to the causes of
them, whatever these may be. That they lie in the nervous sphere
the result of tonic treatment seems to indicate. During the attack
tincture of digitalis in a little brandy is sometimes serviceable. The
brandy I find is necessary, as in tachycardia the foxglove is especially
apt to set up nausea. However, brandy or no brandy, it is often of little
use, and patients soon give it up. If digitalis does not modify the rate of
the heart it often causes diuresis ; now in a heart quickened by the failure
of intrinsic disease the drug often fails to prodiice diuresis, a result of bad
prognostic meaning. One of my "patients still clings with faith to a
prescription of salicylate of soda and sodium bromide which I gave her
ten years ago; she assures me that it is of much service to her in
832 SYSTEM OF MEDICINE
mitigating and shortening the seizures. I gave it on a strong hint of
goutiness in her family. This patient has had a fibroid tumour for many
years, but the attacks are certainly of still older date ; there is no evidence
that the fibroid has affected her tachycardia in any way for good or evil.
I recommend compression of the abdomen with a binder, but I think
this method has not been well applied ; a trained midwife should be
engaged to instruct the patient in the proper use of the bandage. Wood's
patient was relieved by drinking iced water and strong coffee, as if to
arouse reflex inhibition by the vagi. The application of electric currents,
of this kind or that, to the vagi in the neck, however promising at first
sight, has disappointed those who have well tried it. Finally, it is said
that a compression of the chest by the patient himself sometimes succeeds
in stopping an attack. I have not had a good opportunity of putting this
method to trial. It is to be essayed as follows : — The patient will thrust his
feet as hard as he can against the foot of the bed ; then, pressing his arms
closely into his sides, he will take a long inspiration ; in the next place,
closing the glottis, he will make a strong expiratory effort, thrusting hard
the while against the walls of the chest with the upper arms, and clasping
them with the forearms. In this way it is said that the rate of the heart
may be directly controlled. After this fashion an old friend of mine used
to cause his heart to intermit. During the intervals of quiescence per-
severing efforts must be made to nourish and invigorate the system. The
digestion and the excretory organs are to be vigilantly watched and
corrected, and all means are to be adopted to secure serenity of life and a
wholesome and regular occupation. One of my tachycardiacs began to
ride a bicycle two years ago, and with much advantage. Oertel's " heart
massage " seems to me to be no more than ordinary massage plus sugges-
tion ; but massage is very useful in emaciated or podgy people, and, in
the more vigorous, Swedish gymnastics may be cautiously used with
advantage. It will be remembered that any over-exertion or stress may
bring on an attack ; the treatment must therefore be trimmed between
the extremes of indolence and fatigue or sudden effort. A patient who
rides the bicycle tells me that in this respect the bicycle is better than horse
exercise ; a horse may, and often does make a sudden demand on the rider's
nerve. The use of the graduated douche or of the wet sheet proves
very useful in some cases; but for further particulars of this kind the reader
is referred to other chapters.
Bradycardia. — The reasons which justify us in retaining the name
" tachycardia " make for the banishment of " bradycardia." Bradycardia
is a superfine name to denote slow pulse ; it connotes nothing. In
literature a little pedantry may be harmless, nay, as a protest against
slovenliness may have occasionally its welcome side; in science it is a
pest. The name "bradycardia" is as pestilent as the rest because it
hoodwinks the student, who does not rid himself of the false preposses-
sion that in so large a word must lie a specific meaning ; he does not
realise its emptiness. By neurasthenia we do not mean mere nervous
FUNCTIONAL DISORDERS OF THE HEART 833
debility, but a particular and definite group of symptoms of which
nervous debility is but one feature. "With the word "tachycardia" we
introduce a new conception — that which I have endeavoured to set
forth ; with bradycardia we introduce nothing ; the word is but wind.
We know of no symptom group to be thus designated ; bradycardia is
slow pulse and nothing more.
Relatively to the heart slow pulse is a "functional" disorder when it
is found independently of intrinsic and static lesion of the heart ; thus
slow heart in meningitis, terrible as is the disease itself, is yet a functional
disease in respect of the heart. Slow pulse in fatty degeneration of the
heart is not, in clinical language, a functional but an organic change.
But, slow pulse connected with organic disease, whether in the heart
itself or elsewhere, will not be discussed here.
The proposition that in all cases slowing of the pulse is due to the
control of the vagus is not perhaps invariably true, though it is of very
general application. I have said already that in a few cases slowing
seems to be attributable, at any rate in part, to the muscle itself ; but
even then it is hard to say how far pulse retardation may be due to the
vigilant nursing of the vagi. But in the case of certain poisons the
muscular contractions seem to be slowed down directly, though even in
them, as in fatty heart, it is difficult to share between the vagus and the
muscle the function of each; whatever be the inherent failure of the
muscle the vagus may and generally does intervene to spare it. In such
states as senile broncho-pneumonia, where the tendency is to dilatation,
the action of the vagus, whatever its immediate protection may be worth,
turns to evil ere long even in the heart itself ; as vagus action not only
reduces the rate of the heart, which in itself might not lessen its work,
but reduces the work also ; and the organ cannot overtake its arrears.
Therein lies dilatation, excessive internal stress and imminent strain.
However, to leave these questions we have to turn rather to the slow
pulse which depends not upon organic disease of the heart, nor indeed
upon organic disease of eccentric position acting by reflection on the heart
through the vagus, but to those functions, all perhaps following some
reflex paths, which slow down a relatively healthy heart. Of these the
following classes may be made : — (i.) Rise of blood-pressure, as seen, for
instanee, in its simplest form in the " expiratory diminution of rate " ; or,
conversely, in the temporary suspension of vagus action by continual sipping
of a fluid : thus the heart's frequency may be raised twenty or thirty beats
a minute (Waller), (ii.) Blood containing intrinsic poisons, such as carbonic
acid or that of uraemia ; or extrinsic poisons such as lead, tobacco, digitalis ;
or bacterial products, as in diphtheria, most of which act directly on the
vagus or its centre, but some of which seem to affect the heart itself,
(iii.) Reflexes from the irritation of eccentric derangements, such as
those arising in the gastro-intestinal canal (dyspepsia, etc.), in the pelvic
organs, in the throat or ear, and so forth. (iv.) The slow pulse of
children, (v.) The slow pulse of hysteria, melancholia, and other
psychical disorders, (vi.) The slow pulse of exhaustion, as after fevers
VOL. V 3 H
834 SYSTEM OF MEDICINE
or great fatigue (probably not reflex?), (vii.) The slow pulse of pain.
The slow pulse of cerebral, bulbar, and cervico- spinal disease. (The
slow pulse of heart disease, disease rather of its walls than of its
valves, we have deliberately excluded from the section of functional
disorders.) Epileptiform attacks (Stokes-Adams disease) seem, like
syncope, rather to be an occasional consequence of slow pulse than a
cause of it ; in uraemia the two events may spring from a common cause.
Vertigo and syncope are more frequent consequences of the kind ; they
are in my experience grave symptoms when associated with slow pulse,
and suggestive if not conclusive indications of cardiac degeneration.
Again, in some persons an infrequent pulse may pertain to their
normal state. I have never had my finger on the pulse of an epileptic
at the earliest moment of an attack, but scores of times, as for instance
in the wards of lunatic asylums, I have felt the pulse at the instant of
the seizure becoming manifest; I have never, however, found any
characteristic change in the rate. I find that Sir E. Gowers makes the
same remark. In the cases in which the association of slow pulse with
epileptiform convulsion has been noticed it seems probable that the pulse
retardation comes first, and that the intermediate factor is cerebral
ansemia ; that, indeed, the phenomena are those of convulsion on extreme
phlebotomy, the stage beyond deliquium. Of " normal slow pulse " we see
many examples; the most remarkable I have recently seen was in a vigorous,
cheerful man who was in the Radclifie Infirmary during the Michaelmas
examination for the M.B. degree in 1897. In this man a pulse of 28 could
be raised on excitement to 32 or 33. Being a weather-beaten person well
over 60 years of age his arteries were not, of course, free from signs of
degeneration; but it was difficult to say that they were older than his years.
Of the rate of his pulse in former years he knew nothing ; he was unaware
of it until we told him. I suspect that it had gradually come on as he
grew older. He felt quite well, and was vastly amused by our determina-
tion to find some grave mischief within him. He was admitted for
some trivial ailment, in order that be might be hunted well over by the
candidates, who, however, found nothing more to report ; and Dr. S. West,
Dr. Mallam, and myself found him free from any other malady than
that of eld. A pulse of 60 is no very uncommon i-ate in healthy persons,
rather in men, perhaps, than in women ; in a friend of my own a pulse of
58, sometimes slowing down on fatigue to 54 or 55, has proved consistent
with great nervous and. muscular activity up to years which are now more
than mature. For him a pulse of 80 is fever; it never rises over 100 or
thereabouts, except of course under severe muscular exertion. Corvisart's
record of Napoleon's pulse as habitually 40 is well known ; Sir William
Broadbent has, I believe, recorded somewhere the case of an athlete
with a pulse of 36. Osier, who within the limits of his Practice of
Medicine rarely misses a point, tells us that physiological slow pulse is
seen in parturition, whether premature or at term. The rate may decline
from 60 to 44, and has sometimes fallen as low as 34. It is needless to
say that in all cases of alleged slow radial pulse the number of the cardiac
FUNCTIONAL DISORDERS OF THE HEART 83S
revolutions must be counted at the centre ; as some of the waves may fail
to reach the periphery. Some records of egregiously slow pulse can scarcely,
one would think, have been of cardiac pulses. Eoy used to say that a
healthy heart might drop six beats and recover ; but can a deteriorated
organ cross such an abyss of time % We read of pulses of 20 — nay, of
12 a minute; of stops of 15 seconds' duration — in one instance of an
arrest of 30 seconds. An absolute stop of 15 or 20 seconds must
surely mean fatal syncope, or epileptiform convulsion. Very feeble
heart-beats may be inaudible even to the stethoscope. Fibrillary con-
traction is sometimes recovered from in animals, probably not in man.
All I know definitely about " hysterical slow pulse " I have found in
von Noorden and Buchholz. If I have seen it I have made no note of it.
For the variations of the pulse in mental diseases the reader is referred
to the following chapters on these subjects. In respect of poisons we
know that some of them, such as lead, may act indirectly by perverting
the metabolism of the body, and thus generating intermediate poisons ;
uraemia and jaundice are often associated with a slow pulse. Most if not
all these catabolic substances act, no doubt, directly on the vagi, centrally
or peripherally. The poisons generated by bacteria — ^the infections — not
infrequently begin by stimulating the vagi, so that the pulse is slowed ;
then the vagus is exhausted, the pulse quickens, and in the later stages is
much accelerated — the mass of the blood being often much reduced in these
diseases. In convalescence the cardiac centre seems unstable, and the pulse
may bo slowed or quickened by influences which in the normal state would
prove indifferent. That muscarine slows the pulse is a familiar laboratory
demonstration; and the accelerating effect of its antidote atropine is
more familiar still. Tobacco, again, stimulates the vagi at first, and then
paralyses them, or leaves them exhausted so that, in extreme cases, the
heart is rapid and so irregular as to seem to be abandoned to its own
rhythm. Eise of blood - pressure may retard the pulse remarkably;
the fact is familiar to all clinical observers ; but the rule that the rate of
the pulse is inversely as the blood-pressure is open to many contingencies;
it only holds when other things are equal : I think it better to put it
that pressure is that part of the energy of the blood which is not turned
into speed. The sum of the energy may be reduced. In the slow
pulse of exhaustion the blood-pressure is often low ; if vagus control be its
cause the low pressure is due to the effect of this nerve in slackening as
well as of slowing the heart ; the residual blood in the left ventricle is
more. I have seen this retardation fall to 45 in many cases of persons
whose pulse in the normal state is of ordinary frequency. Some fifteen
years ago, when very arduously engaged in practice, I was returning by
night from a consultation in the west of England, when on leaning my
head on my hand I felt my temporal arteries beating too slowly ; the
rate, then about 48, fell gradually to 44. I got a glass of hot brandy
and water at Bristol Station soon after, thinking to mend my condition;
but its immediate effect was to reduce the pulse, which had recovered to
some 50 beats, again to 45. On the basis of this observation I have
836 SYSTEM OF MEDICINE
supposed that the slowing of exhaustion is a protective effort of the vagi,
which, in my case, were further stimulated in their gastric area by the
brandy. After the brandy I fell asleep, and on awaking my malady was
gone. It was attended with a sensation of sinking or depression ; and at
times I have since recognised some abnormality of the kind by the same
warning. During the last eight years, of a less harassing life, the
derangement has altogether disappeared. Now here we had a bold
breach of the rule that rate is inversely as pressure, for in my case the
pressure was, as I have said, low ; and it rose as the normal rate was
regained. The heart's output was probably increased.
Sexual exhaustion is efi&cient to reduce pulse-rate. But the other
day a patient was sent to me by a distant medical friend who had
found in him a slow pulse, about 40, attended with a sense of depres-
sion, almost melancholic, especially of a morning. It was a great effort
for him to get up to breakfast ; although after he had got to work or
play the sensation wore off. At the times of slow pulse the temperature
also would fall to 95°. He was in business, but in an easy one ; he had no
cares, his habits appeared to be correct, and he had had no troubles. He
was fond of physical exertion, and could and did ride, shoot, and so
forth even to the full, without being the worse. His age was forty. On
examination of his heart nothing abnormal was to be found. His own
medical man had cut down his tobacco (usually 2f ounces a week) with
advantage, but without much relief. I ascertained that he gave himself
up to excessive marital intercourse, even to daily indulgence. My pre-
scription was a separate bedroom, which will probably work a cure.
In some cases of temporary slow pulse with "nervous exhaustion"
the voice becomes hollow or even feeble. In one case I remember the
patient, partly in timidity perhaps, intimated that he was too much
exhausted to do more than whisper a brief reply. It is possible that
some of the cases of slow pulse in children are due to self-abuse ; but by
no means all. To find a pulse of 50 or 45 in a little boy or girl used to
frighten me no little ; I regarded them as the barbarians regarded St.
Paul. But as, often enough, nothing happened I gained heart ; and am
now, if still on my guard, not prophetic of evil. In some cases worms
may be the cause of the retardation ; but antidotes for worms do not
always prove the connection. Nevertheless, as some arrhythmia may be
present, and perhaps some heaviness or drooping of manner may be
exaggerated by anxious parents, these cases are not a little embarrassing
for a few days. Gastric catarrh, again, is among the causes ; and prob-
ably in the child the heart centre, like the temperature centre, is more
susceptible than in later years. The ages of such patients run from
four or five to fourteen or fifteen. The child may be languid and out of
spirits, or dyspeptic, when the state of the pulse is found, out, as it were,
accidentally. Irritation of the vagi is again the probable explanation;
indeed, this seems to be the first factor to be thought of in all cases of
slow or intermittent pulse, yet it may not be the invariable cause. Slow
pulse children are usually of neurotic constitution.
FUNCTIONAL DISORDERS OF THE HEART 837
The slow pulse of convalescents from fevers and other exhausting
diseases, is a common event, and is sometimes suggestive of cerebral
complications, especially in children ; it is probably due to vagus irrita-
tion, set up, it may be, by carbonic acid or by some toxin. Or the
cardiac muscle may be poisoned. Thus I have seen it in severe bronchitis
with distended right ventricle, much residual blood, and greatly over-
charged veins. Intermittence is seen in these cases also, which may point
to vagus protection.
The slow pulse of pain is a phenomenon full of interest : it must
be due to reflex stimulation of the vagus ; thus it can readily be
produced by experiment ; and it is not unfamiliar, under the like condi-
tions, to the practising physician. Sir Eichard Powell mentioned an
interesting case of this kind at the meeting of the British Medical As-
sociation in 1894. The patient was subject to neuralgia and to palpita-
tion, but not together. An attack of pain would stop the cardiac
disturbances. Sciatica is perhaps the pain most eificient in producing
this result; but almost any sudden paroxysm of pain of sufficient
severity may be reflected in the pulse. Its chief interest lies in its
bearing on the causation of angina pectoris, whether of the graver or of
the " functional " kind. Whether slow pulse may ever be due to a failure
of the accelerants we cannot tell ; in the cases of " exhaustion " above
described such may be the case entirely or in part. Of the intimate
relations of the intra-cardiac ganglia to the functions of the heart we
know little, or indeed nothing; Dr. Gaskell regards them rather as
survivals of the nervi vasorum than as dominant factors in mammalian
cardiac evolution.
As bradycardia denotes a symptom and not a disease, or as; in
other words, it signifies no more than a phenomenon common to many
definite groups of symptoms, and as there is not, as with tachycardia,
any peculiar group of which it is itself the main or central feature, it can
have no diagnosis or prognosis. All that can be said is that it may
depend upon irritation of the vagus only, the heart being sound. In such
cases it will often, of course, be associated with arrhythmia and inter-
mittence. Such conditions are usually curable by removal of the causes,
and especially by careful mastication of the food. Momentary efforts
often aggravate the condition, but in a soimd heart persistent exercise
removes it for the time. It is usually worse after meals, and is attended
with flatulence. The urine must, of course, be minutely and repeatedly
examined in all its qualities, and signs of cardio-arterial degeneration
duly appraised; remembering however that, if due to degeneration of
the coronary arteries, the most usual organic substratum of slow pulse,
signs of disease may be absent or very indefinite. But we cannot pursue
these parts of the subject ; from what has been incidentally said the
reader will know where to turn for descriptions of the symptom groups
to which slow pulse is subordinate. Under these several heads will also
fall the means of treatment, if slow pulse can be said, any more than
cough or dyspnoea, to have any treatment of its own. Static disease of
838 SYSTEM OF MEDICINE
the heart apart, slow pulse needs not even palliative treatment ; it has
no dangers of its own.
It is impossible to give any list of references in respect of a mere
symptom such as slowness of the pulse. The reader will find two recent
articles on the subject in the Lancet of 30th January 1897 by Dr. John
Ogle, and one by Professor Osier in that of 27th February 1897. In
these articles, however, the symptom is chiefly regarded as significant of
intrinsic cardiac degeneration.
Syncope. — Whether the heart stops altogether in syncope is yet
unknown ; it probably beats with a beat so feeble as to escape our senses.
It may be arrested, but it seems impossible that the heart should be
arrested during all the span of a long faint; I have said elsewhere
that Roy, on the basis of large experimental observation, thought that
the heart certainly may drop six beats, possibly more ; but that beyond
some such number as this there is great danger of death. Yet when we
are discussing the ordinary fainting fit these calculations of more or less
around the margin of the grave seems fanciful : " No one dies of a faint,"
one may say ; or another may say with equal truth that sooner or later
almost every one does. Yet the syncope which cuts the vital thread
at the end of most fatal illnesses is evidently something so different in
degree and contingency from the ordinary faint of the ladies who are
carried out into the vestry, that here we must fix our attention ex-
clusively upon the functional disorder. The church faint is not primarily
a cardiac failure, but an expansion of cutaneous and splanchnic vessels
with fall of arterial pressiu-e.
Yet of this curious disorder no full explanation is forthcoming, surmise
as we may. It is a very common malady ; perhaps no woman passes
through life without experience at least of its premonitory symptoms. To
faint is not the exclusive privilege of woman ; every physician has seen
men fall like oxen — for instance, in the gallery of an operating theatre.
A very sturdy and stout-hearted man once fell suddenly to the floor in
my consulting-room, where a moment before he was complaining to me of
some temporary disorder ; partly dyspepsia, partly fag. I have known
bim for some quarter of a century since that day, and, so far as I am
aware, he has never fainted since. Again, an old friend of mine, then a
young man of some five-and-thirty years, then and since hardy and
sound, on rising suddenly from bed in the middle of the night to empty
his bladder, fell backwards, drenching himself with the contents of the
chamber-pot. His wife told me that he lay unconscious for a " minute or
two." The anxiety in such a case is whether the attack were a faint or
an epilepsy : the circumstances of this attack, chiefly the person's sudden
uprising, pointed rather to syncope, and time seems to have ratified this
opinion, for no such attack has reappeared. On the other hand, syncope is
not usually an isolated event in the life of the patient. People who faint
are, as a rule, " given to fainting " ; such persons dread hot rooms and
congregations where the distribution of the arterial blood may widely
FUNCTIONAL DISORDERS OF THE HEART 839
oscillate. Or, again, they dread certain strong sense impressions — such as
the sight of blood or strong odours, which mSy inhibit the heart ; Italian
women are said to be peculiarly liable to faint on the smell of flowers. On
one occasion I was dining with a charming hostess who had decked her table
with charms like her own : as we sat down, one of her guests, apologising
for his weakness, said that he should faint if he sat with his back to the
fire, and at some sacrifice of harmony he was conveyed to another seat ;
no sooner had he been dealt with than another guest thought he had better
add that he himself was subject to faint in the midst of a strong scent
of flowers, and that he also had better mention his unhappy susceptibility
in time. There was nothing for it but to clear the table of the spoils
of the Eiviera ; after which twofold commotion things fell a little flat.
Both these men were literary men of more sensitiveness, perhaps, than
virility, and had better have stayed at home. In such persons, of
either sex, the pulse varies too widely on quickly rising, sitting, or lying
down. The limits of such variations should be within five beats ; if they
are wider, and they are often as wide as twenty beats or more, the com-
pensatory mechanism is defective.
Syncope without any organic disease may be fatal ; such cases are
not extremely rare ; they are common enough to give a colour, of , caution
to prognosis, and of care to the treatment. In my experience of such
sad events I am disposed to think that the faints due to agonising pain
are more likely to be fatal than those aiising from sudden displacements
of blood-pressure. The inhibitory effect of intense pain may, it would
seem, arrest the heart through the vagus to a degree incompatible with
life. Death in angina pectoris is due to this reflex effect of pain ; the
pain, in my opinion, having its seat in the aorta.
The premonitory symptoms of fainting are known to every one. He
is a fortunate man who, in the weakness of some acute malady, influenza
or the like, has not been conscious of the swimmings and exhaustions
which may usher in a full attack. If some of us have never fainted, we
have all of us felt faint. When the attack is fully established uncon-
sciousness is complete, the .respiration is only to be detected by the use
of a feather or a mirror, or not even thus ; and the pulse, cardiac and
arterial, is likewise imperceptible. If the urine or fseces are voided, it
may be said with some certainty that the attack was worse than a faint.
Whatever the remoter causes, such as general anaimia and debility
and the rest, the immediate cause of fainting is encephalic anaemia. The
same is true, of course, in organic diseases, such as those of the heart.
It is the first duty of the physician, as it is the care of nature herself,
to place the patient in a position to favour the return of blood to the
brain; the head must be dropped even lower than the trunk of the
body. As on the one hand Junot's boot will produce syncope, so on the
other to elevate the legs will aid in its dissipation. The blood-pressure
must also be raised by causing contraction of the superficial blood-vessels ;
cool air, and the admission of it to the skin by unfastening the bodice
is one means of attaining this end ; and it is, no doubt, of some use thus
840 SYSTEM OF MEDICINE
to loosen any bands which may be hampering the respiration ; a deep
gasp, if it can be obtained, stimulates the heart to contract by unloading
the right ventricle. The respiration is called upon by reflex stimulants
also, such as smelling-salts, dashes of cold water, and so forth. In cases
of anaemia compression of the abdominal veins may be useful, or the
application of an Esmarch's bandage to one leg or both legs, and in
extreme cases artificial respiration, or even transfusion of blood, might
be needed ; but such difficult means are fortunately rarely if ever
necessary in the functional cases which alone are under our discussion
in this place. It is desirable, perhaps, to add that after the restoration
of consciousness the physician should not leave the patient without a
strict caution against the resumption of the vertical position until all
tendency to a return of the attack is averted. For a fuller discussion of
the physiology of events of this kind the reader is referred to an article
on the circulation of the brain, which will appear hereafter.
T. Clifford Allbutt.
REFERENCES
For many of the references to tachycardia I am indebted to the bibliography affixed
to Dr. Herringham's article.
1. Balfoue, G. W. The Senile Heart. Londonj 1894. — 2. Binswangek,, 0.
Neurasthetiie. Jena, 1896. — 3. BucHHOLZ. Beitr. ». Kenntniss der Vagusneurosen.
Berlin, 1892. — 4. Da Costa. Amer. Jow. Med. Sci. April 1894. — 5. Farquharson.
Brit. Med. Joum. London, 1875, vol. i. p. 770. Case. — 6. Herz. "On Irritable
Heart," Gentralb. f. innere Med. No. 10, 1894. — 7. Mackenzie, James. "Heart Pain,"
Lancet, Jan. 5, 1895. — 8. Mitchell, John K. " Irritable Heart," Trans. Coll. Pkys.
of Pkilad. 1&92. — 9. voN Nookden, Gael. " Ueber hysterische Vagusneurosen,"
Charitd-AnnaUn, 18. Jahrgang. — 10. Osler. Practice of Medicine, W95. — 11. Sansom,
E. "Heart Disorder due to Nasopharyngeal or Aural Irritation," Trans. Med. Soc. vol.
xvi. p. 107. — 12. Idem. Brit. Med. Jour. Nov. 10, 1894. — 13. Idem. Brit. Med. Jov/r.
Oct. 16, 1897.— 14. Smith, S. 0. Med. Soc. Trans, vol. xvi. p. 114.— 15. Idem. Clinical
Jour. July 4, 1894.-16. Stewart, G. N. Jour, of Phys. Nov. 20, 1897.
Tachycardia. — 17. Bbnsen. Berl. klin. Wochmschr. 1880, S. 248. Case cured by
pressure in the neck. — 18. BouvBRET. Bev. de m4d. Paris, 1889, tomeix. pp. 753-793,
837-855. Cases and digest. — 19. Bowles. Brit. Med. Joum. London, 1867, vol. ii.
p. 53. Brief notes of two cases. — 20. Bribsbe. Chariti-Ann. Berlin, 1888, Bd. xiii.
S. 193. Case, with post-mortem. — 21. Beistowb. Brain, London, vol. x. p. 164.
Cases with criticisms. One post-mortem. — 22. BuoKLAND. Trams. Clin. Soc. London,
vol. XXV. p. 92. Case in a child after measles. — 23. Bunzbl. " Ein Beitrag z.
essentiellen paroxysmale Tachycardie, " Kirch. Arch. Nos. 28, 29 ; 1896. — 24. Bunzl-
Fedeen. Prog, riled. Woch/nsch. 1891, Bd. xvi. S. 496. Case, with ocular palsy. — 25.
Cavafy. Brit. Med. Joum. London, 1875, vol. ii. p. 294. Case. — 26. Cotton. Brit.
Med. Jow. 1867, vol. i. p. 629 ; and 1869, vol. ii. p. 4. Cases. — 27. Debovb and
Boulat. Bull, et mlm. soc. mid. des h6p. de Paris, 1890, 3rd ser. tome vii. p. 953.
Case — 28. Ecoles. Lancet, London, 1891, vol. ii. p. 118. Cases. — 29. Faisans.
Bull, et m4m. soc. mAd. des h6p. de Paris, 1890, 3rd ser. tome vii. p. 964. Cases in a
family with malaria. — 30. Fkankbl. Cha/riU-Anm. Berlin, 1878, Bd. v. S. 273. Case
after compound fracture, with post-mortem. — 31. Feantzbl. Ibid. 1889, Bd. xiv.
S. 357. Case.— 32. Idem. Deutsche med. Wochnschr. Leipzig, 1891, Bd. xvii. S. 321.
Case, with post-mortem. — 33. Feeyhan. Ibid. 1892, Bd. xviii. S. 866. Cases ; argues
that the disease is neurosis. — 34. Gbehardt. Samml. klin. Vortr. Leipzig, 70 (209).
Cases briefly given. — 35. Hampeln. Deutsche med. Wochnschr. 1892, Bd. xviii. S. 787.
Curious case after pericarditis. — 36. Heeeingham, W. P. "Concerning Paroxysmal
Tachycardia," Edinburgh Medical Journal, April 1897. — 37. Hoohhaus. Deutsches Arch.
MECHANICAL STRAIN OF THE HEART
/ hlin. Med. Leipzig, 1893, Bd. H. S. 17. Case, with post-mortem. — 3S. Hubkk. Ibid.
1890, Bd. xlvii. S. 13. Case, with hysteria. — 39. Huppert. Berl. klin. Wochnschr. 1874,
Sa. 223, 237, 247, 261.— 40. Kelly. " Essential Paroxysmal Tachycardia " (4 cases),
Med. and Surg. Eeforter, No. 17, 1896. — 41. KiRSCH. Deutsche med. Wochnschr.
Leipzig, 1892, Bd. xviii. S. 726. Digest, with argument for reflex origin. — 42.
Klempeker. Ihid. 1891, Bd. xvii. S. 334. — 43. EoBSBii. "Ueber paroxysmale
Taoliycardie," FtVcA.^rcA. No. 143 ; 1896. — 44. Nothnagel, H. " Ueber paroxysmale
Tachycardie," Wiener med. Blatter, 1887, Nos. i.-iii. — 45. Nttnnelt. Lancet, London,
1871, voh i. p. 8. Case. — 46. Oettingbr. Jfei. ?F"cefc, Paris, 1894, p. 470. Hereditary
case. — 47. Oliver. Brit. Med. Joum. London, 1891, vol. i. p. 217. Case after injury.
— 48. Pkeissendorfer. Deutsches Arch. f. Min. Med. Leipzig, 1880, Bd. xxvii. S. 387.
Case cured by dieting. — 49. Proebsting. Ibid. 1882, Bd. xxxi. S. 349. Critical digest,
based on Gerhardt's cases. — 50. Rosenfbld. Verhandl. d. Oong. f. innere Med. Wies-
baden, 1893, Bd. xii. S. 327. Treatment by compressing the thorax. — 51. Schott.
Brit. Med. Jour. Oct. 16, 1897. Treatment by baths. — 52. Spehglek. Deutsche ined.
Wochnschr. Leipzig, 1887, Bd. xiii. S. 826. Case. — 53. Talamon. Serimine mid. Paris,
1891, tome xi. 2, p. 13. Case after fall on head ; argues it epileptic. — 54. Taylor,
Seymour. Practitioner, London, 1891, vol. xlvii. p. 18. Critical article, with brief
cases. — 55. Trechsel. Rev. m4d. de la Suisse Rom. Genfeve, 1893, tome xiii. p. 119.
Case and criticism. — 56. TucHZEK. Deutsches Arch. f. klin. Med. Leipzig, 1878, Bd.
xxi. S. 102. Case. — 57. Watson, Sir Thos. Brit. Med. Joum. London, 1867, vol. i.
p. 752. Case, with post-mortem. — 58. West. Trans. Med. Soc. London, vol. xiii.
p. 318. Cases ; argues for myocarditis. — 59. Williams, Watson. 'Bristol Med.-Ohir.
Journal, June 1897.— 60. Wood, H. C. Quoted by Osier, loc. ait. p. 687.
T. C. A.
MECHAlSriOAL STEAIN OF THE HEAET
Strain of the heart, it need scarcely be said, is not a malady, but the
cause of maladies, both of this organ and of the aorta ; possibly, also, of
arterial disease beyond the aorta (Traube) j in respect of this last suggestion,
however, the evidence of an affirmative kind is as yet scanty and uncertain.
We shall see presently that to measure stress as a factor of heart and
aortic disease, with any approximate accuracy, is beset with no small
difficulty, That stress — mechanical stress — is an important factor in
disease of the heart no experienced observer can doubt ; moreover, as we
shall find, in certain acute cases of strain this factor can be indicated with
some precision : in chronic cases, however, stress is so intimately confused
with other factors — such as the abuse of alcohol, the infections of rheu-
matism or syphilis and the like — that it is often exceedingly difficult
to distribute its due weight to each one of such factors. For example,
many most useful observations concerning strain of the heart have
been made upon soldiers ; yet there is perhaps no class of persons in whom
the various factors of cardio-arterial disease, including improper dress,
are more difficult to estimate severally. On the other hand, however, the
part of stress in the causation of heart diseases comes out plainly when
we consider such cases in numbers large enough to eliminate, or rather to
reduce, the risk of error ; — when, for instance, we contrast large numbers
of persons engaged in laborious callings with large numbers of those whose
842 SYSTEM OF MEDICINE
pursuits are mechanically less urgent, — when we compare forgemen, hod-
men, navvies, wharfingers, Cornish miners or Tubingen wood-cutters, who
have no monopoly of vice, with clerks, professional men, or even with
persons whose callings are in the open air, but not to heavy muscular
exertion. The part of stress, mixed as it still is with other factors, is
made evident, again, in the comparison of the cardiac affections of men
with those of women and children. In any case, while we remember
that, relatively speaking, the function of every heart, healthy or diseased,
is concerned in muscular exertion, yet when we enter upon a discussion
of strain of the heart we are understood to refer to the effects of muscular
exertion upon hearts which before the strain were either strictly or
virtually sound. At the same time, we shall not forget that unusual
exertion too often brings out a latent defect in a heart which under
ordinary circumstances, and for some time at any rate, would have passed
as sound. In men beyond middle life a breakdown of the heart is often
thus acutely determined. In most cases of angina pectoris, suddenly
appearing in persons previously regarded as healthy, some unusual
bodily effort determines the first attack.
For clinical purposes strain in its effects upon the heart may con-
veniently be divided into functional disorders, injuries to the cardiac
muscle, and injuries to the orifices and valves of the organ, — chiefly to the
aortic. It is apparent at once that this distinction is a superficial one ;
mechanical disorders tend to become permanent, and aortic diseases,
especially in the long run, are apt to be associated with muscular faults.
Still, the distinction may be admitted for clinical purposes ; and dis-
orders of the first class have been considered in the chapter on " Func-
tional Disorders of the Heart," p. 821 ; those of the myocardium will be
in the chapter devoted to this subject in the next volume ; and those of
the third class among the valvular defects. Withoufc some such divisions
the subject of heart diseases would be almost unmanageable.
When Harvey announced that the circulation of the blood belongs to
the sphere of mechanics he wrought a revolution in physiology. Under
his teaching vague and fanciful apprehensions gave place to more positive
conceptions. From the time of Harvey, although physiologists have not
asserted that mechanical conceptions can cover the whole phenomena of
the circulation, they have learned to see, nevertheless, that these concep-
tions cover so much of the ground that in mastering them they and their
children may find reward enough. If this lesson be not thoroughly
learned it has gained a good hold, and is proving its fruitfulness ; yet
it is not till the days of Marey, Ludwig, Eoy, and Gaskell that we find
a serious endeavour to ascertain the order of the phenomena of the
cardio-vascular apparatus as a machine, and to indicate the limits of its
physics in the direction of those nervous agencies which can only be
called mechanical in a forced acceptation of the word. For a full dis-
cussion of cardiac physics, however, I have the advantage of referring
the reader to the chapter on this subject from the hand of Professor
Sherrington (p. 464).
MECHANICAL STRAIN OF THE HEART 843
Cardiomotive force is equal to the output of the heart plus the resist-
ance to the travel of , the blood in the vascular system ; a resistance chiefly
due to friction, or, in other words, to the viscosity of the blood and the
diameter of the channels through which it runs. The elasticity of the
arteries adds nothing to the cardiomotive force ; by it some considerable
part of this energy is stored up in a potential form during certain
moments of the revolution, to be given out at other moments. The
elasticity of the arterial tree diminishes from youth to age, and as it
is lost the work of the heart is increased ; the work of the heart is thus
increased at a time when the powers of the body are on the wane : but
it is so difficult in later life to distinguish between lesions due to
variations of stress and those due to intrinsic degeneration in the texture
of the viscus, that when we speak clinically of strain of the heart, —
that is, of a permanent " after-strain " or " set " towards other than the
normal lines of its action, or of a permanent loss of capacity within these
lines, — we are understood to contemplate young or comparatively young
subjects, to contemplate premature tensile or shearing strains in the
causation of which degeneration has had but a small initial share or
none.
In what way or ways may stress in the heart produce strain ? What
are the conditions of abnormal pressure within or about the organ ^
How does it adapt itself to unusual stress ? In case of failure where do
the eifects make themselves felt ?
In the first place, we must realise that while, on the one hand, the
arterial blood-pressure is incessantly oscillating, yet ordinary changes of
stress do not raise blood-pressure permanently. If I lift a weight, say
of ten kilos, my blood-pressure will rise promptly, even by some 20 per
cent. After a few seconds or minutes, however (the interval depending
on incidental circumstances), the blood-pressure will have returned to
the initial level. Again, I may constrict a large artery, even the aorta,
or by injection I may increase the whole mass of the blood in the body
by as much as 20 per cent, yet in neither case will the blood-pressure (by
" blood-pressure " the mean arterial pressure is usually signified) present
more than a temporary rise. This is not the place to enter into the
wonderful mechanism — none the less mechanical that the nervous system
is largely concerned in the balance — ^by which these adaptations are made,
the heart and aorta saved from strain, and the various areas of the body
protected from irregular afilux of blood : suffice it to say that the re-
adjustment is largely determined by reductions of resistance. But there
is another factor, the factor of output ; if the output of the left ventricle
be increased, and this increase be not compensated, as is usual, by a fall
of peripheral resistance, the chamber will be under increased stress, and
may suffer strain.
Seeing then that, however transiently, blood-pressure is raised by
muscular effort, and that output likewise may undergo considerable and
■even extreme variations, are the compensatory mechanisms always ade-
quate to readjustments so rapid and so complete as to make the notion
844 SYSTEM OF MEDICINE
of injury to the heart under ordinary circumstances improbable ? If we
decide that the evidence points in this direction we, may infer, neverthe-
less, that an unhealthy heart, or one subject to other adversity, will suffer
under great exertion if these compensatory mechanisms fail, or are in-
sufficient.
A series of experiments upon the blood-pressure of persons engaged
in muscular work was projected for the years 1895-96 by the late Professor
Roy and myself, but my colleague's unhappy illness prevented this and
other investigations. One rather curious fact, however, seems to come
out in the course of the more or less desultory observations which I and
others have made upon athletic men in Cambridge and elsewhere, namely,
that in them, as a rule, the habitual blood-pressure ranges low. A few
observations were made with Roy's sphygmometer upon men given to
arduous muscular work. These observations, taken at times of complete
or comparative rest, seemed to indicate that in them the arterial pressure
ranged habitually under the average. In my own person Alpine climb-
ing and, in later life, cycling have always been followed by a fall of
blood-pressure. It is hard to say what happens during spurts or at the
outset of an excursion, but very soon afterwards the pulse not only
quickens but softens ; for the rest of the day and night, at any rate, the
pulse is soft and dicrotic. If on account of bad weather I cannot take
sufficient exercise, my pulse gives me the sense of higher pressure, and I
am conscious of a falling off in vigour and temper. I am well aware of
the difficulty of measuring the blood-pressure in man, and for the most
part we have as yet to be content with the impressions of experienced
clinical observers whose impressions must be taken for no more than they
are worth : still such impressions are not without value. If a number
of observers skilled in the pulse agree that the radial pressures of a set
of men seem to them to be low, this agreement is worth consideration ;
at any rate nothing better is to be had except a few records with Roy's
sphygmometer, which corroborated those of the finger. An interesting
passage in Dr. George Oliver's treatise on Pulse-Gauging came under my
notice as I was correcting these pages for the press. He says (p. 126) :
" Observations with the pulse pressure gauge have shown that, when
other indications are favourable, the lower ranges of pressure are not
only more salutary, but are very often compatible with the highest health."
Since these words were written. Dr. Tunnicliife, in conjunction with Dr.
Brunton, from Mosso's laboratory has published like conclusions ; and
so likewise have Tangl and Zuntz.
The converse of this proposition is seen in the rise in blood-pressure
in advancing years observed not by myself only (3), but by such experi-
enced physicians as Dr. George Balfour.
Habitual muscular exercise, then, tends in the main not to raise, but to
reduce mean arterial blood - pressure ; or persons with relatively low
pressure may be well adapted to such exertions and naturally take to
them. During the first stages of muscular exertion, no doubt, the range
of blood-pressure is high ; perhaps throughout severe exercise the mean
MECHANICAL STRAIN OF THE HEART 845
may be above normal. But during steady work it probably falls at least
to the normal mean, and during rest and on quiet days may range below
the average standard in sedentary men. If this be so, the hearts of
athletes and of ordinary labourers should be, not at a disadvantage, but
positively at an advantage.
How are we to reconcile these a,pparent contradictions ? In one
breath we say that excessive muscular exertion may damage the heart ;
and in the next, that on the whole the stress on the heart in muscular men
is not more but perhaps less than in men who lead more sedentary lives.
For while on the one hand I note that the blood-pressure of athletes
runs a little lower than the average, on the other I note that the blood-
pressure of men who lead sedentary lives, without denying themselves
a like abundance of food, often runs high. I venture to think, from
some little experience, that in members of a university or of the learned
professions the blood - pressure tends to rise as athletic habits are laid
aside. Perhaps by abstinence this disposition may be prevented ; but I
am always assured by brain-workers, and I share the prejudice, that for
them also a somewhat liberal diet is required. For my own part I have
found that I crave for food more when using my brains from day to day
in my study than when taking vigorous exercise in the open air.
We have arrived, then, at the paradoxical result that muscular exer-
tion tends on the whole to lower blood-pressure, and a sedentary life to
raise it ; yet that certain diseases of the heart are to be attributed to the
mechanical effects of muscular labour. To reconcile these opposite posi-
tions we may make a twofold reply : although the mean result of muscular
exertion may be to reduce arterial pressure, yet the initial effect of such
exertions is to raise it, often enormously. If we may make the assumption
of a man steadily working with his muscles at a uniform rate without rest
the pressure in his arteries would probably be slightly under the mean of
ordinary citizens ; and although the rate of the heart would be increased,
the total daily output might not be increased : if, on the other hand, we
assume that the same man carries eight bushels of wheat up a flight of
steps every ten minutes, although the mean of his blood-pressures for
twenty-four hours may not be very excessive, the maximum pressures,
that is, the initial rise at the outset of each effort, may be very high.
Again, let us suppose that this man does not carry sacks hour by hour
and day by day, but that he is engaged as a checkweighman and
takes a sack up occasionally ; it is likely in this case that his maximal
arterial pressure, as he shoulders the sack, will be higher than under the
same stress more regularly undertaken by a porter whose respiration, blood
volume, and vascular distributions are better adapted to the recurrent
stresses. Yet the weighman may be more or less accustomed to labour,
and, if not used to such efforts as the porters are, he is nevertheless in
something like training ; if, however, a clerk from the office were fired, by
emulation of the porters, to carry sacks, the absence of habitual adapta-
tion to such exercises might cause so sudden and relatively so great an
increase of arterial pressure as to rupture a limb of the aortic valve.
846 SYSTEM OF MEDICINE
In what, then, does such adaptation consist ? Partly in the behaviour
of the skeletal muscles ; partly in the function of the respiration. To
take the muscular system first : we readily and rightly understand that
the first effect of a general contraction of the muscular system must be
to compress the vessels embedded therein, and thus at first to raise the
blood-pressure to a degree answering to a partial closure of this vast
area of the circulation. Marey demonstrated with the sphygmograph
that even to throw the muscles of the legs into spasm (while breathing
freely) raised the arterial pressure considerably. But in the next place,
such is the exquisite provision of nature, the blood-vessels, under the
reflex influence of the afferent nerves of the muscles, or, it may be, under
the influence of an increasing acidity of their lymph when in action,
dilate, and, reopening the vascular area which was momentarily con-
stricted, they flood the muscles anew with arterial blood ; thus at once
the muscles are fed for the work and the peripheral resistance is lowered.
This afflux is independent of the general arterial blood -pressure. Even
under passive exercise also (massage), as Mitchell, Brunton, Tunnicliffe,
and others have shown (vol. i. p. 378), the flow of blood through voluntary
muscles becomes more abundant; and thus blood -pressure is reduced,
if the kneading be unattended with irritation of the skin, which
raises blood-pressure. To this compensatory mechanism we must add, in
most cases, an increased circulation in the cutaneous area and sweating,
as we see in the major epilepsy. If the blood-vessels, by the deterioration
of advancing years, or of poisons such as lead, alcohol or syphilis, be less
lively ; if the blood be more viscous, or deficient in oxygen ; or if after
some disease the nervous machinery be less sensitive, less effective, or
suffer any other disadvantageous change, the muscular reservoirs may open
more slowly or less completely, and the arterial pressure will not fall so
readily to the normal mean ; the heart may not get the relief which is
its due, and this organ and the larger arteries may suffer strain : or,
again, the output of the left ventricle, increased probably in any case as
the first acceleration of the rate subsides, may continue in a greater ratio
than the fall of peripheral resistance, and the mean blood-pressure may be
continuously higher than during rest. Dr. Weber, during an ascent at
the beginning of his holiday, stated the initial rise of his pulse-rate to
be from 74 to 122 ; but after a week's active walking the rise was from
74 to 105. He also noted that at first the systolic sound was shortened
and less distinct (the systoles probably being " fractional," and the residual
blood on each contraction large) ; but, as training advanced, the sys-
tole betrayed less interference, or even improved upon the quality of its.
tone before training began. Some cardiographic tracings taken on a
man in severe exercise indicate at first great rise of blood-pressure ; the
upstroke is much higher, and systole encroaches more on diastole. As-
the impulse quickens, although the percussion is still powerful, the
summit of the curve becomes sharper, the ascent more upright, and the
duration of systole less extended.
Once more ; an abundant supply of blood to the muscles, whatever
MECHANICAL STRAIN OF THE HEART 847
tte remittent checks of the actual muscular contractions, brings about,
after the initial moment, a large increase in the mean volume of the flow.
What becomes of this abundance ? Will it not try the heart at first in
another way by flooding the right side of it, and thus throwing stress
upon another part of the organ. This danger is, I think, as great as
the rise of pressure on the arterial side ; when the functions are duly
adjusted it is counteracted by the capacity of the muscular and pul-
monary systems, which may not only hold nearly all the blood of the
body, but are less liable to be embarrassed by incidental adversity :
moreover. Dr. Oliver has shown that as muscular exertion goes
forward a considerable transference of juices from the blood-vessels
takes place into the lymphatic areas. Nevertheless, engorgement of
the right side of the heart is an evil to be counted with, and one
which happens under exertion more often than we are disposed to
think; and thus, unless the output be enlarged, the residual blood
is excessive in one or both ventricles. As arterial blood - pressure
falls venous pressure may rise, and the pulmonary artery and right heart
may be fatally distended. In elderly people, whose lungs may be
emphysematous, grave heart disorder may come about in this way ;
but in the young and vigorous the heart, though, as I have said, it
often dilates until it beats in the epigastrium, soon recovers itself as
the lungs expand and the blood is redistributed. But if the exertion
be both hard and long continued, harm may be done even in the young,
especially in boys ; the more so as fatigue products are passed into
the blood. Hence it is that prolonged efforts, such as paper chases and
the like, are bad for boys, and murderous to the middle-aged. Such a
case I have seen recorded in a man who, at the age of 46, took to a
tricycle, and after a brief apprenticeship rode from Brighton to London
(53 miles). The physician who was hurriedly summoned on his arrival
in town, found him faint, with a pulse of 141, and cyanosed; the cardiac
dulness was extended a quarter of an inch to the right of the sternum,
the apex beat being in the 6th interspace in the mammary line.
That the respiration is an important factor in the blood-pressure, and
in the run of the circulation, is apparent to every one who has watched
the traces of the kymograph. Dr. Waller, Professor Tigerstedt, and others
have carefully discussed the effects of the respiration on the functions of
the heart ; and Dr. Morison has recently drawn the attention of physicians
to them again in the pages of a medical journal (58, p. 966).
That the respiration is quickened in exercise is a matter of constant
experience. Stimulation of the peripheral end of a muscle-nerve pro-
duces considerable increase of respiratory movement, even when the
muscles affected have been removed from the sensorium by cutting
the sensory paths. The muscles may manufacture something which,
reaching by way of the circulation some nervous element in the respiratory
mechanism, stimulates it; the respiratory centre in the bulb may be
thus stimulated. Professor Sherrington tells me that Zuntz and Goppert
have proved that this something is not CO2 ; nor again a deficiency of 0.
84S SYSTEM OF MEDICINE
Thus some waste product of the muscles seems to excite the respiration
to greater activity, while at the same time larger quantities of blood are
being injected into the venee cavse ; how large this quantity is we
may guess when we remember that on the contraction of a muscle its
blood-vessels open out so widely that it can contain at least one-third
7nore blood than when at rest ; even when at rest, the skeletal
muscles hold something like a quarter of the blood in the body. To this
forcing of successive charges of blood by the muscles beyond the valves
of the veins we have to add the suction of the respiratory movements.
The most important condition in the filling of the heart during
diastole is of course its own previous contraction ; but how far the heart
itself exercises suction upon the blood as it enters is a problem which, as
yet, is far from being solved. In the well-known experiments of Goltz
and Gaule, negative pressures in both right and left ventricles were
recorded in dogs, ranging from 100 mm. of water in the left, and from
10 mm. in the right, to numbers between 300 and 400 mm. It is not yet
known, however, what the negative pressures in a strongly acting human
heart may be. Prof. Tigerstedt, in his new work on physiology, says that
the conditions of an effective suction are so many and complicated that at
present no accurate opinion can be given on the matter.
As regards respiratory pressures, it is obvious that the pressure of
the atmosphere on the extra-thoracic veins must be greater than that
which, through the lungs, can be exercised on the veins within the chest ;
thus these veins and the heart must be distended in proportion to
the difference. In inspiration this difference must be increased : the
negative pressure within the chest must be increased, and in some pro-
portion to the depth of the inspiration. Hence the aid of orthopnoea in
venous retardation. The intra-thoracic veins, the auricles, and the pul-
monary artery must be distended, and the circulation would cease if a
sufficiently deep inspiration were held on. In expiration, on the other
hand, the negative pressure in the chest falls, and the access of the blood
to the thoracic veins is slackened. Even the systole of the heart itself, by
which movement much of the blood is driven out of the chest, must exercise
some influence in the direction of suction towards itself, or, more accurately,
towards the great venous reservoirs. Now, whatever values we put on these
several factors, we perceive that violent exertion must be attended by a
considerable oscillation of pressures in the thoracic veins and right heart,
oscillations due in part to the temporary rise in arterial pressure on the
initial compression of the intra-muscular vessels, in part to the subsequent
afflux of blood from the expanding muscular areas, and in part to the vary-
ing negative pressures of the respiration. The thick-walled ventricles and
the aorta in which blood-pressure is high " will be least influenced, and
the right auricle and the vena cava, which are thin-walled and almost at
zero pressure, will be sensibly affected, the amount of blood-flow to the
right side of the heart will be practically determined by it, and the left
side will rapidly be affected in its turn. The left side will then drive a
large quantity of blood forward soon after inspiration has begun, a smaller
MECHANICAL STRAIN OF THE HEART 849
quantity soon after expiration has begun. A violent and prolonged
expiratory effort with closed mouth and nose may even cause a temporary
arrest of the circulation, the intra-thoracic vessels being distended and
the auricles unable to contract. Conversely, an expiratory effort made
in the same way may arrest the circulation, as the venous blood cannot
enter the compressed right auricle " (Waller). Now we know that on
sudden and violent effort the chest is often fixed and the glottis
closed. Again, in prolonged exertion, such as hard and long running,
the advent of products of waste into the blood — sarcolactic acid, it may
be, and others-^must not be forgotten ; for if they do not tend directly to
increase the stress on the heart, they may do so secondarily and relatively
in so far as they weaken the muscle of the organ. The r6le of each of
these factors in the play of muscular exercise upon the heart cannot as
yet be distinguished, still less calculated.
The clinical features of heart- strain, broadly speaking, are not so
obscure as their causation. In my first paper on heart strain (1), I
stated my opinion that dilatation of the right side of the heart is an early
effect of prolonged exertion. The effect of sudden stress tells rather
on the aortic area ; that of more prolonged exertion, such as running,
hill-climbing, or steady rowing, rather on the right heart. Time has
strengthened me in this opinion ; and Eoy and Adami, Oertel, Dr.
James Barr, and other authors have given their support to it. Not only
are we strengthened in the opinion that dilatation of the right side of the
heart is an occasional consequence of these prolonged exertions, but I now
believe that dilatation of the right chambers is a frequent, I had almost
said a normal incident of such exertion. I shall not be surprised to learn,
from Rontgen rays or otherwise, that dilatation of the right heart and
pulmonary artery is a common and transient feature in the adaptation
of the heart to the variations of its work, especially in youths. The
development of the muscles of respiration and of the lungs to capacities far
beyond those of ordinary life, is a condition of training far too little
understood or sought after, and takes a considerable place in the amend-
ment of those selected cases which benefit under the Stokes, Oertel,
or Nauheim methods. The safety-valve action of the tricuspid valve
(Wilkinson King), and the apparent provision against this distension
in ungulates by the moderator band, demonstrated by the late
Professor Eolleston, are not to be forgotten in this connection. How-
ever this may be,' that dilatation of these chambers and secondarily
of the left side also is a common result of prolonged exertion, and
that it is often aggravated by the disabling effects of the circulation of
waste products of a " curarising " kind, or by the nervous exhaustion of
great fatigue, is tolerably well ascertained in a broad if not very accurate
sense. The dilatation is, I think, concerned in "second wind"; the
healthy heart increases its output, the lungs expand, resistance falls, the
^ The dUatation of the left ventricle, although it certainly occurs, cannot, I think, be satis-
factorily explained with our present knowledge. Prohably it is due to loss of tone and lar^e
residual Wood, or may be due in part to some nervous sympathy. °
VOL. V 3 I
8so SYSTEM OF MEDICINE
rigtit ventricle pulls itself together, and second wind is established. This
process, trying enough to an unsound or defective heart, to young boys,
and to elderly men, is to the healthy heart of comparatively young
adults perhaps never injurious ; I have many times seen undergraduates
and others look ghastly at the end of a long spurt of hard exercise, but
I never saw a sound young man the worse for a temporary stress of this
kind : if, as in a few cases which I have seen again and again in growing
youths, dilatation of the right heart occurs, leading to cyanosis, panting,
and confusion or vertigo, this oppression is generally sufficient of itself to
stop the exercise in time. Even in children, whose frames are immature,
and who are apt to be overdone by prolonged stress, how rarely is the brief
strife of hooping-cough attended with any, ill consequences to the heart.
In a few cases, however, — in untrained men hard driven by haste or
peril, — prolonged effort, exhaustion, heart stress, and fatigue products
come in to complicate the reckoning, and persistent harm may be done. I
have already published one carefully observed instance of cardiac dilatation
in my own person (1), 1 will now describe another. Some fifteen years
ago I was called in the middle of the night, when no doubt more or less
fatigued already, to take a mail train at a station about four and a half
miles distant ; when I had hastily dressed, I discovered that the foolish
cabman who had brought the message had driven back to town. In forty
minutes I had to catch that train ; and, running all the way on a
hilly road, I did catch it. Profusely perspiring, I stripped the instant I
sprang into the carriage, and found the transverse dull area of the heart
considerably extended, as it was on the Dom in 1869. The radial pulse
was rapid, of small volume and low pressure ; I felt a little sick, and my
face was cold. After a good rub down and an hour's rest in the train I
was quite restored, the borders of the cardiac area had receded, and
I felt no more of the stress. But it might well have been otherwise ; it
would have been otherwise if at that time I had been in bad condition.
It is thus in persons at and after middle life that the physician has to
patch up the heart thus strained ; some of these patients recover after
months of disability, others never recover, though life may continue for
some years. An old friend of mine, when about fifty years of age, thus
strained his heart by hard walking in hot weather on the Italian side of
the Alps. He broke down and came home, when we found the dulness of
the heart much extended transversely, and other signs of dilatation.
The pulse was extremely irregular and intermittent, and these characters
it never lost, though some fifteen years of a valetudinarian life remained to
him before oedema and albuminuria ushered in the closing scenes of
his life. I have notes of many such cases of strained heart, especially
in men who by years or by frailty were passing or past their prime.
Pain and constriction are felt in the acuter cases, but rarely (or never)
shooting into the arms ; though it is sometimes felt as far as the second left
intercostal space. There may be a panting dyspnoea, a cold dew on the fore-
head, yawning, and exhaustion. The pulse is proportionately irregular in
force and rate, and intermittent (vagus protection). A man of letters,
MECHANICAL STRAIN OF THE HEART 851
whose constitution had been shaken by profuse hsemorrhages in early life,
took to the bicycle in middle age, and often rode hard and far. He com-
plained to me that at times he felt some discomfort from it. On careful
examination I found no sign of disorder ; but I begged him to end his
next hard ride at my house. I then found his heart irregular and inter-
mittent, the arterial pressure low, and the right ventricle dilated.
Fortunately on his next visit he was well again, but repentant. In the
worst cases oedema of the bases of the lungs is found on the following day.
Such attacks pass off hardly and slowly ; the pulse long remains irregular
and feeble, and the breathing embarrassed by the least effort. There is
probably a large quantity of residual blood in both ventricles for a longer
or shorter time, the signs of dilatation appear on the left side also, arterial
pressure falls, and the mitral orifice may yield. Such a patient may,
indeed, fulfil the duties of a tranquil existence for some years ; but he may
remain languid and pallid, unfit for much physical exercise, and in all the
work of life soon wearied into fretfulness and depression of spirits. In
the next stage of the disease albumin appears in the urine, and oedema
about the legs and feet ; yet even then the end may not be imminent.
But on this part of the subject the reader is referred to the section on
diseases of the myocardium (p. 885).
Soldier's heart. — I venture to give this name to a disease well
known to physicians in the army, not by any means with the intention
of confining the class of cases now to be considered to the soldier, but to
indicate a state of heart which is peculiarly apt to occur in him, as its
causes are of kinds to which soldiers are more exposed than civilians.
Nevertheless if civilians, or men in other services, are exposed to like
influences, they also will be liable to "soldier's heart." Our attention
was first drawn to this condition by Brg.-Sur. Lieut.-Col. Myers more
than thirty years ago ; and his most recent views on the subject will be
found in Quain's Dictionary under the head "Exercise." In the United
States the subject was first studied by Dr. Da Costa. Many cases of the
kind, occurring in civil life, come under the notice of the general
physician, so that the condition is now well known. The degrees of the
malady range between the transient disorder of the heart seen in any
youth who in a somewhat too reckless pursuit of exercise may be dis-
turbed with some palpitation and dyspnoea for a few days or weeks only,
and a persistent disease of an incurable severity. The former transient
cases fall under the head of "Irritable Heart," in the chapter on "Functional
Disorders of the Heart " (p. 807) ; the latter fall into the present section
on " Stram of the Heart." The diff'erences are indeed no more than of
degree ; but in comparing the extremer cases we find a difference of degree
amounting to a difference in kind.
In Quain's Dictionary Myers says: "The young soldier of light
frame, with irritable, palpitating heart, who has broken down in his pre-
hmmary training, is a marked and good example of the early injurious
effect of overstrain of the heart, under the impediments, caused by tight
8s2 SYSTEM OF MEDICINE
clothing and accoutrements, to the free expansion of the chest. When at
rest he feels perfectly well, and has little or no throbbing in the chest.
So soon, however, as he puts on his tunic and accoutrements, and begins
his drill, throbbing occurs with more or less violence, accompanied with
a feeling of oppression and with difficulty of breathing, and this being
followed by a sensation of faintness, sickness, or dizziness, he has to fall
out of the ranks. At first the condition is one purely of functional dis-
turbance which, though rendering him unfit for the duties of a soldier,
does not interfere with his gaining his livelihood as a civilian." In dis-
cussing the late Dr. Morgan's evidence of the safety of athletic pursuits
afforded by the experience of University oars during the years 1820-1869,
Myers properly warns us that these were men picked for their large frames,
full chests, and exceptional strength. On the other hand, from a large
experience of University men, I must say that considering their " violent
and unguided efforts to achieve success " and their " ill-regulated emula-
tion," the ill effects are surprisingly small. Many are the "irritable
hearts" (p. 821), but permanently or gravely injured hearts are few
or none. On the other hand, I agree with Myers in his admonition
to " men who have settled down into the real business of life who, during
their nominal periods of rest from their daily labours, undertake violent
exercises without any preliminary training, and thus throw such an
unexpected strain on the heart and blood-vessels that instead of mere
functional disturbance, as in early life, they sow the seeds of organic
disease." Although I am tempted to minimise the allegations of serious
harm to the emulous young men (for among them there is now a sort of
natural selection, the weaklier taking to girls' games, such as lawn tennis,
hockey, cycling, and the like), yet I cannot enforce too strongly his
warning to older men who are not in the casual training in which all
healthy youths are constantly, if more or less unsystematically, engaged.
Bear-fighting among themselves, running and shouting with the games of
others when not themselves at work, bounding up and down long flights
of stairs, scampering, always a minute too late, to lecture or chapel, they
are always more or less in training, and, being well and plainly fed and
devoid of care, they bear what the elder brother cannot bear, who goes
to his work in a stuffy office by underground rail, loafs to his club in a
hansom, dawdles at dinner-parties and At Homes, takes his- exercise
vicariously by watching the games of others, and spends the lave of his
time with his feet on the chimney-piece with the eternal cigarette in his
mouth. This overfed and self-indulgent person, who is plucky enough
when needs must, is surprised that he goes to pieces when, on his month's
holiday, he competes with mountaineers or sportsmen who are in fit con-
dition, and who live sparingly. If this be true of the eldest son, what of
the father, who will not be forgotten but, with his nervous system corroded
by drudgery and care, is determined to scorch on his bicycle, or to climb
the Alps with any of them. These forcing kinds of effort it is which tell
for evil far more than ordinary sports by field and stream, which never
lead to strain of the heart.
MECHANICAL STRAIN OF THE HEART 853
One of our younger graduates, Dr. M'Carthy, has recently taken up
this matter of soldier's heart in an exercise for his degree. He obtained
his materials at Netley. After stating that the modern valise equipment
is less injurious to the young soldier than the old knapsack, which by its
cross belts constricted the chest, he adds that the malady is still common
enough nevertheless. He was able in a short time to collect twenty
cases, and also to examine the first batch of twenty soldiers invalided
from the campaign on the Indian frontier, and of these again five were
found to be patients of this class, though not included in his series.
In dealing with his twenty eases, M'Carthy took out in each the age,
total service, the trade of the recruit before enlistment, the habits as
to tobacco and alcohol, the climates of foreign service, and the infectious
and other diseases which he might have undergone. Fourteen of the
men were in infantry regiments, three in the Eoyal Artillery, two in the
cavalry, one in the Royal Engineers. At the date of examination two
were under the age of twenty-one ; fourteen were between twenty-one
and twenty-five ; four were of twenty-five years and over. " Taking the
statements of the men as true," the average amount of beer consumed
daily was from three to four pints. Other alcoholic drinks were taken
but occasionally. The average amount of tobacco was three to four
ounces a week, the tobacco being generally twist or plug. Twelve had
suffered from syphilis ; fifteen from malarial and other tropical fevers ;
two only from rheumatism of any kind. Some of the men figured, of
course, in more than one of these categories.
"The patients state that while not exerting themselves they feel
quite well and free from any shortness of breath ; but as soon as they
begin to march they are troubled at once with a throbbing sensation in
the chest ; and with this there is difficulty of breathing, followed in some
cases by faintness or giddiness. Rest may relieve for a time, but in most
cases all the trouble returns shortly after returning to duty."
On the other hand, many men (not in the above list) have the disease,
yet state that it has never been of any inconvenience to them whatever.
" In fact, many cases of disordered heart have been detected quite by
accident while going through the usual routine examination, when soldiers
come into hospital for other complaints, especially malarial fevers."
To take the symptoms in detail : — Cardiac pain was present in seventeen
cases, dyspnoea in seventeen, giddiness in six, sleeplessness in five,
nervousness in seven cases. Three cases were noted in which the men
were unaware that there was anything wrong with the heart.
Physical signs. — In fourteen cases the pulse was regular while the
patient was at rest, but in some of these it became irregular after slight
exertion ; in the remaining six it was irregular even when the men were
confined to their beds. In twelve cases the pulse during rest was below
100 ; in six it was between 100 and 115 ; in two between 115 and 120.
The pulse rarely exceeded 120 when the man was at rest, but would always
rise very rapidly to 140 or so on his swinging the arms three times round
the head. In nearly all the cases the pulse was of abnormally low pressure.
854 SYSTEM OF MEDICINE
The area of cardiac dulness was increased in fourteen cases ; but in
some of them the increase was so slight that it was recorded with hesita-
tion. In all the cases the impulse was diflFused, and in many the apex
was displaced — in two cases between 1 and \\ inches outside the nipple
line. Abnormalities of the cardiac sounds were uncommon. In two
cases the second sound was reduplicated at the base ; in five the pul-
monary second sound was accentuated ; in six the first sound was sharp ;
in three, prolonged and booming ; in four cases there was a systolic
murmur at the apex.
Dr. M'Carthy lays stress on the history of malarial fevers in many of
these men ; he reminds us of the evil effect of fevers on the cardiac
muscle, and urges that soldiers recovering from these fevers should be
exempted from drills and other manual work for several weeks after
discharge from hospital.
Alcohol is the next cause on which he lays stress ; and, as to tobacco,
he says that men smoke more in the tropics where they loaf more ; and
that the tobacco is bad and strong. On campaign the rations also are
often necessarily short, while the labours are excessive. Finally, the
author urges that tropical heat reduces the value of haemoglobin in the
corpuscles of the blood, and leads to ansemia. If in this condition the
soldier is called upon to do hard muscular work, is badly fed, and mayhap
attacked by some fever, the softened and flabby heart muscle yields,
dilatation occurs, and the man is invalided.
The prognosis is not good ; in the majority of cases the patients return
to hospital till they are invalided out of the service. The author found
the difficulty which might be expected in tracing the men thus invalided.
However, he obtained records of thirty cases of men discharged from the
Netley Hospital, and his impression from these returns is that in many
cases the soldier's heart ends in valvular disease. It is said in Cambridge
that influenza is very mischievous in lodging-house keepers, who cannot
keep their beds and are frequently running upstairs.
As in various parts of this article I have more or less incidentally
referred to cases of this kind as they occur in civil life, I have nothing to
add to this careful inquiry of Dr. M'Carthy. I have already said that
the obstinacy of these cases is remarkable. Those which pass the line
between " irritable heart " and " soldier's heart " rarely end in recovery,
but in permanent dilatation often resulting, sooner or later, in mitral
insufficiency. I have only to add that these cases are not only unrelieved
by cardiac gymnastics (Nauheim methods and the like), but are aggravated
by such means. Although muscular exertion is the determining, and
perhaps an indispensable, cause of "soldier's heart," yet it manifestly
depends also upon many contingent conditions.
I cannot conclude this section without a formal opinion, founded
on thirty years of close observation of heart stress, that the importance of
muscular effort as a factor in cardiac disease has been much exaggerated.
I have shown that in the sound adult organism the efiects of physical
INJURIES BY ELECTRIC CURRENTS OF HIGH PRESSURE 855
stress upon the heart are promptly counteracted by equilibrating
machinery, and especially by large expansion of muscular and pulmonary
areas. Such a statement as that made three years ago by the editor
of a leading medical journal, namely, "that the violent strams of hard
exercise bode in the end the certainty of premature decrepitude, and
that "the heart can only perform a certain total measure of work,' so
that "whether this be done by a rapid or a slow process determines the
length of days in which it is done," seems to me, both on clinical and
physiological evidence, to be unjustifiable.
The clinical story of strain in the aortic area of the heart will find its
place in a later section.
T. Cliffokd Allbutt.
N.B. — For references the reader is referred to the list on page 966.
INJURIES BY ELECTEIC CUEEENTS OF HIGH PEESSUEE
Since electricity has come to be so widely employed, and is being
increasingly used as an illuminating agent and for motive power,
accidents of varying severity have been frequent. It is desirable,
therefore, that we should be cognisant of the effects of high electrical
currents upon the human body. We know that there is considerable
danger attendant upon the generation of electricity, and we look to the
expert electrician to adopt measures to prevent accidents. During the
four years ending 1896 twelve deaths occurred in this country from
electric shock ; and when we add to these the many lesser accidents that
frequently occur, we recognise the need for careful precaution wherever
electricity is being generated and distributed. Many of the accidents
have been due to inadvertent contact with exposed parts of highly
charged metal not properly insulated. The consequences of the current
thus passed through the body vary with the amount of current entering,
the insulated position of the individual at the time, and the kind of
contact. Such conditions, for example, as standing on wet earth, the
wearing of damp boots, and a moist skin tend to increase the efi'ects of
an electrical current. The danger, therefore, is not one simply of high
potentiality of current, but of current plus the conditions under which
it has been received. The word voltage used in this article is synony-
mous with "pressure" as used by the Board of Trade, and with the
" electromotive force " of the text-books.
It is diflBcult to say what voltage is fatal to man. Speaking in terms
of voltage Dr. W. S. Hedley says that 1000 to 2000 volts will kiU. In
America, where electricity was adopted as the official means of destroying
criminals, a current of 1500 volts has been regarded as capable of
8s6 SYSTEM OF MEDICINE
causing deatt ; but there are many cases on record of persons having
been exposed to higher voltages without fatal consequences, and, on the
Ooher hand, contact with lower pressures has caused death. Of the two
kinds of electric current — the "continuous" and "alternating" — it is
impossible to say which is the more dangerous to the human body.
There is an opinion that the alternating is the more fatal ; but a larger
experience and further experimental data are wanted before any definite
conclusion on this point can be arrived at. Under either the difference
may be less (Tatum). On the relative danger to life of the continuous
and alternating currents, the Eeport of the Board of Trade states that
alternating currents are twice as dangerous as the continuous, but I
know of no evidence upon which this statement is based. As electricity
is too difficult a subject for a non-expert to handle, only those points
are here discussed which bear upon the medical aspect of the subject,
points with which medical practitioners should be familiar, as at any
time they may be called to persons injured by high electric currents.
A person, for example, may be seriously injured either by. direct
personal contact with a highly charged piece of metal, through the
medium of damp clothes or through an iron tool in his hand by which
accidental contact is made with the live metal. As an illustration I may
mention the fatal accident to a youth at St. Peter's, Newcastle-on-Tyne,
in January 1897. Carrying an iron ladder through the factory he
accidentally brought the top of the ladder into contact with the terminals
of an arc lamp. He was killed instantaneously. In regard to arc
lighting, it may be mentioned that while each arc light requires an
electrical pressure of only from 40 to 50 volts, the lamps are usually
arranged in a series and are supplied by the same current. A workman
who is himself insulated may touch the terminals of an arc light without
receiving any injury ; but should his insulation be defective, if he stand
on moist earth for example, he may receive, as did the youth at St.
Peter's, a fatal shock, since the electrical pressure between the ends
of the cable is the sum of the pressure of all the lamps in series in
the circuit (2).
"We have no positive proof that one individual is more susceptible to
electric shock than another. It is, as already stated, rather a question
of the amount of current and whether it wholly enters the body.
Where contact with currents of high potentiality has not been followed
by disastrous results, it is more than probable that at the time of contact
the skin was dry, in which state it is a bad conductor, and offers con-
siderable resistance to the penetration of the current. As might be
expected, the electrical current produces very varying effects upon the
human body. Where the voltage is low and the contact fairly good the
muscles are thrown into a state of tetanic rigidity which makes it im-
possible for the individual to relax his grasp of any charged metal he
may have seized, nor can he be released until the circuit is broken.
The effects of electric currents are experienced when they enter and
when they leave the body. It is sufficient for us to remember that
INJURIES BY ELECTRIC CURRENTS OF HIGH PRESSURE 857
effects are producpd at the moment of the entrance into and exit of
currents from the body, and that these, therefore, are periods of danger.
Hedley, in supporting the opinion that the quantity of electricity passed
determines the amount of electrolytic action and physiological eflfect,
considers that more pain is felt the higher the electromotive force, even
when the current is the same. One element entering into the causation
of pain is the local action of the accumulated products at the point of
contact consequent upon electrolytic decompositions, and the relative
resistances between the electrodes and the different layers of the skin.
The individual through whose body there is passing an electric current
of not too high potentiality generally experiences pain, but some of this
must be due to the extreme contraction of his muscles quite apart from
the influence of any products of electrolysis. If there be no immediate
loss of consciousness, terror may cause him to faint. The memory of
this plays no small part in the subsequent development of nervous
symptoms. Once liberated, the patient, as a rule, is soon well again,
but there are instances on record where for many months after exposure
to the current there was complaint of ill-defined pains and headache
which recurred with electrically disturbed conditions of the atmosphere,
and of a form of persistent nervousness which was rather the result of
the mental than of physical shock.
Another consequence of the exposure to high electric currents is
burning. That portion of the surface of the body which has accidentally
been brought into contact with the charged metal may become black
and charred, the peculiarity of such a wound being that it is sometimes
deep and apt to slough, and that while the burned part is insensitive to
pain the surrounding tissues are extremely sensitive. If the skin at the
time of contact was moist so much more severe is the burning. If a
current sufficient to produce this severe local burning pass through the
body, fatal results are the more probable ; but if the current merely
pass locally, as from the hand to the wrist, for instance, the damage
will probably be local only.
When, therefore, the pressure has been high, the contact good, and
conditions of resistance slight, the patient may at once be rendered
unconscious, or be suddenly killed. Thus stricken by a powerful current
a man suddenly falls, or he is thrown a distance of several feet before
falling. A peculiar cry is involuntarily uttered, especially when the
contact is broken, which, in electrical generating stations, for example,
at once attracts workmen to the spot where their comrade is lying,
pale, or slightly cyanosed and pulseless, apparently dead, and with
mucus escaping from his mouth and nose ; now and then a feeble and
gasping respiration is observed, but he lies helpless, his pupils keep
dilating, and unless artificial respiration is at once resorted to, and some-
times even then, death is inevitable. There is something appalling in the
extreme suddenness and severity of the shock in these cases, towards
which the unexpectedness of the accident possibly contributes largely.
Cause of death. — In conjunction with Dr. E. A. Bolam 1 undertook
858 SYSTEM OF MEDICINE
a series of experiments in the Physiological Laboratory of .the Newcastle
College of Medicine upon anaesthetised dogs, with the view of ascertaining
the cause of death by electric shock, and of testing the means of resuscita-
tion (7). Two opinions are held by the profession : (i.) that death under
such circumstances is due to respiratory arrest ; (ii.) that it is consequent
upon sudden cessation of thfe heart's beat. By placing dogs under the
influence of ether we were able to take a tracing of the arterial pressure
and respiratory movements, and thereby to record the effects of high
electric currents passed into the body. Immediately on making contact
the animal is thrown into an attitude of opisthotonos, its muscles become
extremely rigid, and as a consequence the lever recording respiratory
movement is suddenly and violently thrown up, whilst the other, which
traces the arterial pressure and heart-beats, suddenly rises owing to
general arterial constriction, and falling shortly afterwards oscillates rapidly,
but within a narrower range. On breaking the current the respiration
becomes deeper and quicker than before the shock, and in the course of
a few seconds the breathing and the beat of the heart return to the
normal. When the current proved fatal there were the same initial
respiratory and general muscular spasm, and a sudden rise of arterial
pressure followed by an immediate fall ; one or two quivering oscillations
of the lever mark the arterial tracing, and then all at once a further and
complete fall of the lever follows, indicating that the heart has ceased
to beat. Respiration deep and spontaneous may continue for several
seconds, or even for a few minutes after the heart has ceased to beat.
The experiments invariably showed that in electric shock the death
was cardiac and not respiratory. Other steps were taken to coniirm this
opinion, notably by listening to the heart of the animal with the stetho-
scope as the current entered. If the current were insufficient to kill the
dog the heart's beat was momentarily delayed and then quickened, the
cardiac sounds being well maintained ; but when, on the other hand, a
current of higher potentiality was employed, the sounds of the heart would
cease, immediately or very shortly after contact. Respiration deep and
rhythmic might continue, but if no treatment were adopted the cardiac
sounds would not return ; increasing pallor would gradually steal over
the whole surface of the body, the pupils meanwhile dilating, and mucus
being forcibly driven from mouth and nares. By exposing the heart of
other anaesthetised dogs, and inserting a canula into the trachea so as to
carry on artificial respiration, Bolam and myself had ocular demonstration
that it was the heart which was primarily arrested in death from electric
shock, and not the breathing. Dr. A. M. Bleile (3), Professor of Physio-
logy, Ohio State University, in a paper read before the American Institute
of Electrical Engineers, Niagara Falls, N.Y., June 27th, 1895, states that
" death in electric shock is really due to the fact that the current pro-
duces a contraction of the arteries through an influence on the nervous
system, and that this constriction of the arteries throws in such a
mechanical impediment to the flow of the blood as the heart is unable to
overcome, and that where drugs are given to counteract this effect, much
INJURIES BY ELECTRIC CURRENTS OF HIGH PRESSURE 859
larger doses of electricity can be borne." As to the constricted state of
the arteries, we ourselves found, with Bleile, that if nitrite of amyl were
inhaled by an animal before the electrical experiment much stronger
currents could be borne. My results, then, and those of Dr. Lewis Jones
likewise, are opposed to those of D'Arsonval, who attributes death to
asphyxia.
Morbid anatomy. — There is usually well-marked rigidity of muscles.
The skin may or may not show any signs of burning or of eschars ; it
may be pale or livid. The abdominal viscera and large veins are usually
deeply congested. The heart is usually flaccid : sometimes the right side
is flaccid while the left is hard and tense. The right auricle and ventricle
are considerably distended and are filled with dark fluid blood ; the left
auricle is generally in moderate distension and contains fluid blood,
whilst the left ventricle is firm and almost empty. The lungs present
nothing abnormal; they may be slightly congested or at places show
ecchymoses, particularly if artificial respiration has been attempted.
The brain and spinal cord are congested, but are otherwise normal. I
have seen it stated at a coroner's inquest, a diagnosis was based upon the
assertion, and the corresponding verdict of the jury returned, that in death
from electricity the blood is fluid and not coagulated after death. This
is too sweeping a statement, and not quite correct. In most cases, it is
true, the blood is found fluid after death, but in some of our experiments
we found coagula in the right side of the heart, and occasionally some of
the large veins were blocked by dense dark clot-^particularly when the
autopsy was made twenty-four to thirty hours after death. It is main-
tained that on spectroscopic examination the oxy haemoglobin of the blood
is reduced. If a strong solution of blood is examined, only one broad band
may be observed in the spectrum, and it appears at first sight as if this
were due to reduced haemoglobin ; but where the spectrum is very care-
fully scrutinised, and particularly, too, when the solution of blood is
further weakened by the addition of water, two distinct bands of
oxyhsemoglobin can be clearly discerned. It would appear, therefore,
that the blood contains both oxyhsemoglobin and reduced haemoglobin.
The blood on microscopical examination shows very marked crenation of
its coloured corpuscles. The pupils were invariably found widely dilated
immediately after death.
Treatment. — Persons who have received only a slight shock and who
have not been rendered unconscious require no special treatment. The
effects almost immediately pass away, and should any nervous symptoms
remain they must be treated on general principles. For any burns or
wounds ordinary surgical remedies will avail. It is to the treatment of
persons who have been exposed to high electrical currents, and who are
apparently dead, that the following remarks apply. D'Arsonval ( 1 ), believ-
ing the mode of death to be akin to asphyxia, recommended artificial
respiration, and of all modes of treatment, quite irrespective of whether
the death has proceeded from failure of the respiratory centre or of the
heart, I know of no treatment more likely to be beneficial than artificial
86o 5 YSTEM OF MEDICINE
respiration, systematically carried out by SylvBster's method, and con-
tinued for half an hour or longer. Bolam and myself have twice
succeeded in resuscitating a dog whose heart had ceased beating, once for
thirteen minutes, and on the second occaaion for eight. The heart, which
was exposed to view, had become rapidly distended so as to bulge out the
pericardium, and had become perfectly motionless after having passed
through a stage of fibrillary tremor ; but by persisting in artificial
respiration, aided by the occasional spontaneous inspirations which from
time to time occurred, and the rhythmic traction of the tongue, the
contents of the right side of the heart were gradually aspirated into and
through the lungs, auricular beats were re-established, at first irregularly
and feebly ; gradually, however, they became stronger and passed over
into the ventricle, so that after thirteen minutes, during which the heart
was apparently irresponsive, we had the satisfaction of seeing the normal
beat of the organ restored, the pulmonary and systemic circulation re-
established, and life return. Too often, however, the sufferer is killed
outright. Rescuers on approaching the injured must beware lest the
current be not broken.
Thomas Oliver.
REFERENCES
1. D'Aesonval. GoTnipUreridu deVmrniimAedes sciences, \?i&'l-V&^i. — 2. Dangerous
Trades Committee of the Home Office, Itid Intcri/im, Report, 1897. — 3. Electrical Beview,
Aug. 9, 1895 ; other papers in same journal, Deo. 1894, Jan. 1895. — 4. Hedlby, W. S.
Current from the Main; also Lancet, Dee. 1891 and April 1892. — 5. Jones, H. L.
" Lethal effects of Electric Currents," Brit. Med. Jomr. Mar. 2, 1895. — 6. Ministfere
des Travaux publics, Oi/rculaire du 19 ao^t 1895, Paris. — 7. Monmekque. Contr&le des
installations Uectriques. Paris, 1896. — 8. Oliver and Bolam. "Death by Electric
Shook," Brit. Med. Jour. Jan. 15, 1898.— 9. Meport of Board of Trade, 1889.— 10.
Ibid. British Medical Journal, 1885, etc., and Oct. 1896. — Tatum, Dr. Electrical
World, May 10, 1890.
T. 0.
ENDOCARDITIS
I. Acute Endocarditis
Deflnition and Classification. — By endocarditis we mean inflammation
of the endocardium or lining membrane of the heart. The inflam-
mation affects principally and often exclusively the valve segments of
the endocardium (valvular endocarditis), but other parts of the endo-
cardium may be affected also (mural endocarditis). Both clinically and
pathologically we distinguish between acute and chronic endocarditis.
The acute form is again divided into benign or simple and malignant or
infective endocarditis. Of the chronic form, likewise, we distinguish two
kinds, — one which is the result of acute endocarditis, and the other the
retractile, fibroid, or sclerotic form, which results from arterio-sclerosis or
atheroma.
In this article we shall consider acute endocarditis ; chronic endo-
SIMPLE ENDOCARDIIIS 86i
carditis, giving rise to the majority of so-called valvular affections of the
heart, will be dealt with hereafter.
Aeute endocapditis. — In the article on Infective Endocarditis I have
already considered the difficulty of separating simple from infective
endocarditis. In both forms micro-organisms have been found . in the
affected valves, though only in the infective form ■ do they play an
essential part, so far as symptoms are concerned. While the two kinds
have many features in common, in others they differ ; and as the
difference is often essential we follow the custom and consider the two
kinds separately.
Acute simple endocaeditis. — (Syn. : Benign, Papillary, Verriieose,
RhevMiatic Endoca/i-ditis.)
Causation, ^ — By far the largest number of cases occur with (a) acute
rheumatic arthritis, hence by some authors the name acute rheumatic
endocarditis is given to the disease. Its frequency in acute rheumatism
is differently estimated by different authors ; and this is readily to be
understood, for in many cases the symptoms of endocarditis may be so
slight as to escape detection ; or again persons recovering from acute
rheumatic arthritis may show signs which simulate those of endocarditis,
and yet are due only to some functional derangement of the heart. The
most trustworthy observations on this subject are those in which a large
number of cases of rheumatic arthritis have been kept under observation,
and their after-history watched for some time. Sibson analysed 32.5
cases of acute articular rheumatism which he observed during fifteen years
at St. Mary's Hospital, and found that in 79 there was no endocarditis;
in 63 endocarditis was threatened; in 13 endocarditis was probable; in
107 endocarditis was present without pericarditis; in 54 there was endo-
pericarditis ; in 6 there was pericarditis without endocarditis ; in 3 there
was pericarditis with doubtful endocarditis.
The proportion given by other observers is somewhat less : the mean
of the numbers given by older and more recent writers amounts to 20-23
per cent.
Of other noteworthy facts which have been made out regarding the
relation of rheumatism and endocarditis we may note : —
(i.) That, in connection with rheumatism, endocarditis occurs more
frequently in children than in adults. Dr. C. West estimated its incidence
at 61-3 per cent; Fuller about 66 per cent; and some authors, such as
Cadef; and Gassicourt, give as high a percentage as 80 per cent.
(ii.) The first attack of acute rheumatism is more often followed by
endocarditis than the subsequent attacks.
(iii.) Endocarditis may accompany mild as well as severe attacks of
acute rheumatism. Sibson (he. cit. p. 199) states the more severe the
rheumatic attack the greater the tendency to endocardial inflammation ;
but this is not the opinion of other observers, and in children especially
we see mild attacks of rheumatism followed by endocarditis. [Vide art.
"Acute Eheumatism in Childhood," vol. iii. p. 42.1
862 SYSTEM OF MEDICINE
(iv.) The physical signs of endocarditis usually appear early in the
attack of rheumatism. Sibson in about one-fourth of his cases noticed
the presence of a systolic bruit, which he looked upon as characteristic of
endocarditis, at the end of the first week of the rheumatic fever, and in
two-thirds at the end of the second week. Sometimes, however, the
signs of endocarditis appear much later, though probably in many of these
cases the endocardial affection had existed some time before it gave rise
to physical signs. The endocardial affection may precede the rheumatic
attack by several days.
(v.) Rheumatic fever, or acute polyarthritis, is the disease above all
others accompanied by endocarditis ; but occasionally endocarditis may
follow monarticular rheumatism and chronic rheumatism. Gonorrhoeal
rheumatism stands in close relation to infective endocarditis, though the
benign form may follow definite attacks of gonorrheal rheumatism.
(vi.) The endocarditis dependent on rheumatism most frequently affects
the mitral valve ; the aortic valve less frequently, and the right side of
the heart in very exceptional cases only.
(vii.) The pathogenesis of what we may call the meta-arthritic endo-
carditis cannot be determined as long as our views on rheumatism are as
indefinite as they are at present. The endocarditis cannot be looked upon
either as a mere complication or as a sequel of rheumatism ; it is an
integral part of the disease. As most pathologists look upon rheumatic
arthritis as an infective and most likely a microbic disease, the poison of
which chiefly attacks fibrous structures, the endocarditis may be regarded
as a localisation of the rheumatic poison in the fibrous tissue of the valves
of the heart. In some few cases the same micro-organisms have been
found both in the effusion of the inflamed joint and in the inflammatory
deposit of the cardiac valves. As in other microbic affections, so probably
here, the lesions are due to some toxic product of the microbe circulating
in the blood, as is the case in other infectious diseases ; to wit, diphtheria,
cholera, and epidemic influenza ; and if so, the absence of micro-
organisms from the deposits is quite intelligible. As the opportunity of
examining the valve often does not arrive until the endocarditis has
become chronic, the absence of all micro-organisms, even if the disease be
microbic, is not astonishing ; for this negative condition occurs in certain
other diseases which are undoubtedly microbic.
(6) Chorea. — Endocarditis is frequently met with in persons who
have had chorea ; and in fatal cases of chorea inflammatory deposits on
the valves are almost invariably found. Thus Sturges (24) collected
statistics of 80 fatal cases, and in only 5 of these were the heart valves
normal. Eeymond's figures bear out the same rule. As regards the
frequency of endocarditis in chorea authors differ considerably ; and, as
the endocarditis may not reveal itself till years after, the exact pro-
portion is not easily made out. In many cases of chorea a murmur may
be due to functional disturbance and not to endocarditis ; or, on the
other hand, as seen in some fatal cases, endocarditis may be present and
give rise to no physical signs. Osier states that of 554 cases of
SIMPLE ENDOCARDITIS 863
chorea, at the Infinnary for Diseases of the Nervous System, 170
presented heart murmurs; of these, in 149 the murmur was Etpical,
in 21 basic. Of 449 cases reported to the Committee on Collective
Investigation of the British Medical Association, 113 had heart murmurs ;
how many of these were functional and how many organic it is impossible
to estimate : a basic murmur is heard much oftener in purely functional
cases, yet an apex bruit may be present from various causes without
the existence of endocarditis. More trustworthy results are obtained
if the subsequent history of persons having had chorea is taken, an
estimate which has been made by several observers. Dr. Stephen
Mackenzie examined 33 patients at periods varying from one to five
years after the attack of chorea, and noted signs of undoubted heart
disease in 60'6 per cent ; Donkin in 40 per cent : Osier out of 140 cases
found the heart normal in 51 ; in 17 there was disturbance which might
reasonably be looked upon as functional, and in 72 cases (5 If per cent)
there were signs of organic heart lesion : it may be noted that only in 25
of these 72 cases was there a liistory of acute arthritis.
Nothing more definite can be made out concerning the relation of
chorea to endocarditis. So many cases of chorea show signs of acute
rheumatism during the course of the attack, or are followed by an arthritic
affection having all the characters of acute rheumatism, that the endo-
carditis has been regarded as a manifestation of the rheumatism only ; yet,
as will be seen from the figures given above, in many cases where heart
murmurs were noted there was no history of acute arthritis ; and this is
also noticed in fatal cases of chorea, in which endocarditis is almost
invariably found. The report of the Collective Investigation Committee of
the British Medical Association gives of a total of 439 cases of chorea 97
with a rheumatic history (about 22 per cent). Statistics on this subject,
however, are not of great use, as the joint pains occurring in chorea are
not always due to rheumatism ; and, especially in the severe cases, are
probably due to a septic condition. We must note, however, that in
children the joint affections in rheumatism may be very slight. I cannot
therefore agree with Eoger that chorea, rheumatism, and endocarditis
are three terms of one and the same pathological series; tliough un-
doubtedly in a good many cases endocarditis and rheumatic arthritis,
with other signs of a rheumatic diathesis (tonsillitis, subcutaneous
nodules, erythema, profuse acid perspiration, etc.), complicate chorea.
As yet there is no proof or evidence that chorea is due to minute cerebral
embolisms of microbic nature ; moreover, the form of endocarditis
we notice in chorea is— in by far the largest number of cases— of the
benign or verrucose and not of the malignant nature, in which latter the
microbe plays the important part. We can but surmise that chorea,
by weakening the system, and exercising some deleterious effect on the
heart valve, acts only as a predisposing agency.
(c) Acute endocarditis may be associated with the acute zymotic fevers.
Among these scarlet fever occupies the first place. Often we have
before the occurrence of the endocarditis, pains and slight swelling of
864 SYSTEM OF MEDICINE
a joint, which are apparently rheumatic in nature ; thus here again
the rjieumatic poison is the cause of the endocarditis. Some authors,
however, look upon the arthritic symptoms as an outcome of the scarlet
fever toxin, and upon the endocarditis as the result of the action of the
same toxin on the endocardium. In the other acute fevers, such as
typhoid, measles, small-pox, diphtheria or malaria, endocarditis is a very
rare complication. Pneumonia is more often associated with infective
endocarditis ; and the same is the case with erysipelas, with puerperal
and septic diseases generally, and with gonorrhoea.
(d) In cases of acute and chronic tuberculosis we meet with endocarditis
occasionally. Are we to look upon such cases as belonging to the infective
type of endocarditis, or do they belong to the benign form, the tubercle
bacillus acting as a remoter cause 1 It must be noted that in a few cases
the tubercle bacillus has been found (2) in the valve deposits ; and in some
cases of acute miliary tuberculosis vegetations on the heart valves of
recent origin have been observed. I remember in a child, who died from
general acute tuberculosis, that the pericardium was found studded all
over with miliary tubercle ; and the mitral valve showed deposits which
proved to be masses of fibrin and leucocytes, and contained tubercle
bacilli. In this, and probably in a good many other cases, the endocarditis
is of a specific nature, and therefore, as part of the general disease, belongs
to infective endocarditis ; how far, however, this applies to all cases where
valve deposits are found in persons who have died of tuberculosis can
only be settled by a microscopic examination of these masses. Even if
the old view that phthisis and heart disease are antagonistic be not
strictly true, yet it is rare to meet with either acute rheiunatic arthritis
or valvular affections of the heart in persons suffering from phthisis.
(«) Syphilis attacks the myocardium and the endocardium ; in the
former it causes endo- and periarteritis with tracts of fibrous tissue in
the midst of the myocardium, or it may lead to granular deposits. In
the latter case valvular disease may result from arterio-sclerosis, of which
syphilis is one of the remoter causes ; that acute endocarditis is ever due
to the syphilitic virus is very doubtful. Chronic endocarditis of syphilitic
nature does occur, but is a very rare occurrence (8).
(/) Of other causes of chronic endocarditis we may mention gout
and Bright's disease.
Gout. — Several cases are on record (6, 3, 9) in which endocarditic
processes showing the presence of urate of sodium crystals were found in
persons affected with gout.
In Bright's disease we often find chronic valvular heart affection from
arterio-sclerosis, yet occasionally it may be associated with acute endo-
carditis (15, 21, 7).
((/) Trawnatism. — Several cases have been recorded, amongst others
by Clifford Allbutt and Litten, where all the signs of endocarditis
followed a blow or fall on the chest. Litten tabulated the recorded
cases and added two more. The endocarditis is most likely due to a
rupture or injury to the valve ; how readily endocarditis is set up by
SIMPLE ENDOCARDITIS 865
such an injury is proved by the experiments of Rosenbach and others,
who, on injuring the valve in animals by introducing a fine wire through
the carotid, noticed distinct endocarditis to follow after a few days.
Eoy and Adami, on lightly ligaturing the aorta, and thus increas-
ing the blood - pressure, produced oedema of the valves and cell
exudation.
That infective endocarditis may be occasioned by an injury I have
already stated in my article in vol. i. p. 632. The cases cited by
Allbutt and Litten were cases of benign endocarditis, some affecting the
mitral valve and producing stenosis, and others the aortic valve ; in some
of the cases, however, the connection between the traumatism and the
endocarditis was not satisfactorily established.
(A) Endocarditis without any apparent cause, and occurring as an
idiopathic disease, has been described by some authors. Such an
occurrence is quite possible, yet it must be extremely rare; and
probably the endocarditis is in such cases the outcome of acute rheuma-
tism, for, as often happens in children, the joint affection may be quite
insignificant.
Other etiological factors relate chiefly to age. It appears that
endocarditis occurs most frequently between the ages of 15 and 40; it
is rare in old people, in whom valvular lesions are mostly due to an
atheromatous process ; it is not rare in children, as already observed by
West, who noticed it 71 times in 122 cases of heart disease (see also on
the subject Dr. Cheadle's article in vol. ii. of this Syaem, p. 42). In
very young children, however, the affection is rare ; in them pericarditis
is more often found than endocarditis.
Fmtal endocarditis is by no means a rare affection. It may occur with
or without congenital anomalies of the heart. As is well known, the
right side of the heart is generally affected in the foetus ; but according
to the observations 'of Rauchfuss stenosis of the aorta occurs as frequently
as stenosis of the pulmonary artery ; and he comes to the conclusion that
when there is no congenital malformation of the heart, the left side is as
frequently affected as the right. Apart, then, from the anomalies which
predispose to right-sided endocarditis, other factors are in play which
determine the frequency of right-sided endocarditis, as compared with
Its rarity in extra-uterine life. Such factors are the thickness of the
right ventricle, the increased pressure to which it is exposed, and the
absence of pulmonary respiration, which causes such a difference
between the blood of the right and left sides of the heart after birth •
especially as regards the amount of oxygen. Klebs, who was one of the
first to attribute all forms of endocarditis. to micro-organisms, gives
another explanation ; namely, the direct infection of the right side of the
heart through the blood coming from the placenta. Recent observations
have shown that micro-organisms do not readily pass through the
placenta ; but if the micro-organisms do not pass, the toxic substances
produced by them may do so, and thus give rise to inflammatory deposits
Foetal endocarditis cannot well be recognised before birth, and mav be
VOL.V 3j^ y
866 SYSTEM OF MEDICINE
undetected for years after birth. The foetal right-sided endocarditis affects
principally the pulmonary valves — often when there is already obstruction
or stricture ; occasionally the tricuspid valve only : similarly, left-sided
foetal endocarditis more frequently affects the aortic valve with or without
contraction of the lumen of the aorta, and the mitral valve only occasionally.
Finally, endocarditis may be secondary, being an extension of an
affection either of the myocardium or of the aorta.
Pathological anatomy. — ^Endocarditis affects principally the valves
of the heart, hence the name valvulitis ; and, except in the intra-uterine
form, it is almost always confined to the valves of the left side : here
again it affects the mitral more frequently than the aortic valve (the tri-
cuspid valve, however, is occasionally also affected in combination with
stenosis of the mitral valve). Of the mitral valve it affects the auricular
surface, and here again principally the portions of the valve which are
in close apposition when the valve closes ; when it affects the aortic valve it
is found on the ventricular surface round the corpora Arantii. That the
left side is much more often affected than the right side is due to several
causes, but principally to the higher blood-pressure and the difference in
the oxygenation of the blood : the first factor leads more easily to
abrasion of the endocardium, and other changes favouring the deposits of
inflammatory material or thrombi, and by the latter the action of the micro-
organisms is greatly favoured. That the mitral valve is more frequently
affected than the aortic may be due, as Sibson (foe. dt. p. 458) pointed
out, to the fact that the mitral flaps press against each other when
the valve is shut with much greater tension and force than the
cusps of the aortic valve. To the combined agency of a finer margin of
contact, greater pressure of blood, and the muscular force and tendinous
traction proper to the valve, another fact may be added, namely, the
absence of vessels in the aortic and pulmonary valves (Langer, Coen),
a condition which protects them, at any rate, against the invasion of
microbes by embolism. The endocarditis is localised chiefly at the part
of the valves indicated, because at these spots we have the greatest
pressure and stress.
It must be noted, however, that other parts of the endocardium,
especially the chordse tendinese, are implicated in the process. An
endocarditis affecting chiefly other portions of the endocardium, to the
exclusion of the valve, has been described by Neuwerek ; it is more or
less chronic, and leads not only to superficial cicatrices, but also to sub-
endocardial and myocardial inflammation (Rosenbach).
Appearance of the affected valves. — ^In the early stage, which we have
but rarely the opportunity -of seeing except perhaps in some ease of fatal
chorea, the endocardium at the affected parts is slightly swollen, and of
the rosy tint of increased vascularity. At a more advanced stage we
notice little pedunculated vegetations, forming a string or garland of
small beads, on the auricular surface of the mitral and ventricular
surfaces of the aortic valves ; not on the free edges of the valves, but at
some slight distance from the border, corresponding to the lines of the
SIMPLE ENDOCARDITIS 867
maximum contact of the valve segments when the valve is closed. When
the chordse tendineae are involved, the endocardium covering appears
opaque, and slightly raised ; and in rare cases may be the seat of small
vegetations.
The further progress of these vegetations varies : in rare cases they
may be completely absorbed ; in other cases the vegetations increase in
size and in extent, forming large fungating masses which may extend to
the chordae tendinese, and cause a serious obstacle to the free circulation
of the blood. In most cases the inflammatory deposits undergo fibrous
change as in inflammations elsewhere ; and these sometimes also afiect the
chordae tendinese, and even the papUlary muscles, as seen in some of the
chronic valvular affections ; or some of the cusps may become adherent to
each other or %o the walls of the heart. The fibrous and contracted valve
segments assume an almost cartilaginous appearance, and, being deficient
in blood, may give rise to degeneration of the valves ; notably to cal-
careous degeneration and the formation of necrotic ulcers.
Histologically the affection shows changes of an inflammatory nature in
the endocardium, and deposit of fibrin in the form of thrombi, both
white and mixed, from the blood. Sections of a small vegetation in a
very early stage show proliferation of the endothelial layer, increase of the
branched cells in the subendothelial tissue and infiltration of the layers of
the endocardium with leucocytes, fibrin and serum between the trabeculae,
and a deposit of fibrin on the free surface of the endothelium ; this is
deposited from the blood, and may be granular or sometimes fibrillar.
When the process has lasted some time this embryonic tissue is changed
into fully-formed fibrous tissue ; and after a time calcareous particles may
be deposited in the newly-formed structures, and the chordae tendinese and
papillary muscles then show the changes to be described under chronic
endocarditis. In the severe cases the myocardium shows indurative
changes, which may be looked upon as due to an extension of the inflam-
matory process ; the fibrous septa and the lymphatic spaces being chiefly
involved : even the muscular fibres may show changes partly due to com-
pression, and partly to myocarditis.
An examination for micro-organisms may reveal in some of the acute
cases the presence of staphylococci, or streptococci, or diplococci (12); when
the affection has become chronic, microbes are rarely found. The
organisms are found in larger numbers in the superficial layer of the
deposits, and but sparingly in the deeper.
From acute endocarditis must be distinguished —
(a) Patches of red coloration of the valves, which are sometimes seen
in persons who have died of an acute infectious disease. These patches
are simply due to blood imbibition.
(J) Certain deposits on the auriculo-ventricular valves, which are the
remains of an embryonic condition of the valves, as pointed out by
Bernays ; and in these Luschka has demonstrated pigment particles due
to old haemorrhages (Eosenbach, he. at. p. 156).
(c) A form of endocarditis probably due to sudden disturbance of
868 SYSTEM OF MEDICINE
intrarcardiac pressure, whereby the endocardium is injured. We have
here small, close, hard vegetations, firmly fixed and without adherent
fibrin (Dickinson).
Symptoms. — Acute endocarditis is sometimes easy, at other times most
difiicult to recognise ; and at times we find after death the characteristic
lesions on the heart valves without there having been any symptoms of
endocarditis during life.
The subjective symptoms vary considerably with the age of the
patients, the primary diseases, and the presence of complications such as
pericarditis, and the effects of any previous attack of endocarditis. The
physical signs may sometimes be absent or appear only when the acute
process has passed into a chronic state ; and they are sometimes difficult
to distinguish from those of a functional disturbance of the heart. In
some cases the symptoms are absent, and it is only perhaps when the
patient is brought under our notice in an attack of hemiplegia by embolism
that endocarditis may be detected.
If we take the acute rheumatic as the most common form of endo-
carditis, we find in many cases no subjective symptoms to lead us to
suspect an endocardial affection ; the febrile symptoms, such as tempera-
ture, pulse, perspiration, do not differ from those in cases of rheumatic
fever without endocarditis ; and it is by the physical examination of the
heart only that the existence of endocarditis is detected. In a second
group of cases the patient, who has generally been affected with the
rheumatic fever for a week or more, has suddenly a rise of temperature
without any fresh pains ; or he complains of oppression, uneasiness, or
pain over the region of the heart and palpitation ; the pulse becomes
small and quick, and the heart's action tumultuous : in other cases, of
subacute course, dyspnoea on exertion is the only symptom complained of,
yet physical examination of the chest reveals the existence of an
endocardial murmur. In children, when pericarditis complicates endocar-
ditis, which it frequently does (the carditis of Sturges), the symptoms are
more pronounced and fairly characteristic ; the breathing, with alse nasi
dilated, is hurried and laboured, and there is great orthopnoea ; the child
has an anxious look and is somewhat cyanotic, sleep is very much
disturbed, and . there is generally marked delirium. The pulse in these
cases is very quick, small and compressible, and there may be persistent
vomiting. It must be noticed that in children the joint affection in
rheumatic arthritis may be so slight as to be easily overlooked [see
art. on " Acute Rheumatism in Children," vol. iv. p. 40]. It may happen,
as in a case I saw recently, that the only noteworthy feature is a rise
of temperature with profuse sweating, which may go on for some time.
The daily examination of the heart shows at first nothing abnormal,
but in a short time the physical signs of endocarditis present them-
selves. In other cases in children, as in chorea, little general disturbance
is noticed.
Physical signs. — The physical signs are sometimes very marked and
admit of no other explanation ; at other times they are indefinite.
SIMPLE ENDOCARDITIS 869
Oil inspection of the thorax nothing abnormal is noticed, unless there
be pericardial effusion ; nor do we get any evidence of valvular disease on
palpation unless the affection has already existed for some time.
On percussion it is only in exceptional cases that we notice the
increase of the area of cardiac dulness due to dilatation of the left
ventricle, the right, or of both. An increase in the area of dulness, how-
ever, more especially in the transverse diameter, is often noticed in
children, and may be due to pericardial effusion ; if so, the pulse is feeble,
the apex beat is not so well felt as usual, and the area of dulness has the
characteristic outline of pericardial effusion.
The most trustworthy and important physical signs of valvular
endocarditis are noticed on auscultation. As the mitral valve is most
frequently affected, and as the fibrinous deposit is apt to prevent the
complete closure of the valve, we get the signs of mitral regurgitation ;
that is, a systolic murmur heard best at the apex, and conveyed
towards the axilla and also towards the sternum. In a good many
cases of acute rheumatic endocarditis, under my own observation, which
afterwards lapsed into chronic valvular disease, a systolic murmur,
soft and blowing in character, was noticed at the apex ; but as a rule
better heard over the lowest portion of the sternum close to its junction
with the left costal cartilages. The appearance of a systolic miu-mur is
preceded for days by an impurity and prolongation of the first heart
sound which is in itself suggestive of endocarditis. Prolongation of the
first sound is the first whisper of an " approaching murmur " (Sibson, lot.
cit. p. 493). This is probably due to the soft gelatinous deposit, which
alters the first sound while the valves are still smooth and elastic.
According to Sibson, we may notice occasionally, besides the mitral bruit,
a tricuspid systolic njurmur also ; but this is not heard at the very
beginning of the endocarditis (Sibson, loc. cit. p. 242). As regards acute
endocarditis in children, Sturges (25) gives as the earliest physical indica-
tion : " Tumultuous, quickened, and uneven heart's action and sounds,
that are changeful from day to day, especially the first ; sounds redupli-
cated, at and above the apex (not at the base) ; a temporary tricuspid
murmur ; marked accent commencing the first sound, whether mitral or
tricuspid." Occasionally, however, even in children, a loud systolic
murmur may rapidly appear ; this is sometimes only heard when the
child lies down ; in the erect position it becomes fainter and may even
disappear.
In acute febrile affections, such as the acute zymotic diseases, and in
rheumatic arthritis, a systolic murmur may be heard under conditions
other than that of endocarditis ; therefore, when we hear such murmur
we must not conclude at once that there is endocarditis. The murmur
may be due to relaxation or other changes in the heart muscle, or to a
change in the blood (hsemic bruit).
Although it is not always easy or even possible to distinguish these
conditions, certain signs will help us. The pulse in myocardial affections
is often quick, small, and irregular ; and there is marked dyspnoea and
870 SYSTEM OF MEDICINE
vertigo. The hsemic murmur is noticed when there is ■well-marked
anaemia ; it is heard not only over the mitral, but often also over the
pulmonary and aortic areas, and is accompanied by venous murmur in
the neck, while the pulse may be dicrotic. (According to Sansom, marked
dicrotism occurs only in the severe cases of endocarditis.) Besides the
mitral murmur, especially if the heart's muscle is weak and early dilatation
of the right ventricle comes on, we may note reduplication of the second
sound, accentuation of the second puLmonary sound, and sometimes also
a systolic bruit over the tricuspid valve.
If the endocarditis affects the aortic valves we may find no special
physical signs if the vegetations are very small ; at other times we
get evidence of aortic regurgitation, a diastolic bruit heard best at mid-
sternum ; and, if there be much regurgitation, we get other indications
of aortic incompetence.
The physical signs denoting stenosis of either mitral or aortic valve
are very rarely to be noticed ; as the narrowing results from a contraction
of the valves which generally takes place as the endocarditis becomes
chronic. Dr. Sansom states that in some cases he has observed re-
duplication of one or other of the heart sounds as an early sign of endo-
carditis ; and in these cases the endocarditis was followed by stenosis
rather than by regurgitation (22).
In the rare cases of right-sided endocarditis we have the signs of
tricuspid or pulmonary regurgitation.
Complications. — ^Leaving out of consideration the rare cases — which,
however, mostly belong to infective endocarditis — where there is rupture
of the inflamed valve or rupture of chord® tendineae, the most frequent
complications of endocarditis are pericarditis and myocarditis. Sibson in
161 cases of acute endocarditis noticed that pericarditis was present in
34 cases, and in children the proportion is even larger. Changes in the
myocardium varying very much in degree have, according to recent
observations, been found so often that they too must be looked upon as com-
mon ; though they do not often give rise to symptoms which lead to their
recognition. Yet we may suspect their occurrence if the heart's action
becomes weaker, or if there are physical signs of an acute dilatation of the
heart ; the pulse becomes quicker, weaker, and often irregular, the apex
beat weaker, and the murmur less distinct ; there is also marked dyspnoea,
and the patient complains of tightness and oppression, and occasionally
of pain and palpitation : these signs are often followed by vertigo, delirium,
and cold, clammy perspiration. Cheyne-Stokes breathing has sometimes
been noticed towards the end, and death takes place either from syncope
or pulmonary congestion and oedema.
Pleurisy and pnevmonia are occasional complications. The relation
of pneumonia to infective endocarditis has already been noticed (vol. i.
p. 633). Rheumatic endocarditis may, however, be associated with
croupous pneumonia, or it may give rise to embolic pneumonia.
Emholic infarcts occur more frequently in infective endocarditis, and
in chronic valvular diseases, than in the acute rheumatic endocarditis.
SIMPLE ENDOCARDITIS 871
In some rare cases (11) the endocarditis propagated to the aorta
may produce acute aortitis, a complication which is difficult to diagnose ;
it is said to produce severe paroxysmal pains behind the sternum with
radiation towards the shoulder, dyspnoea, and perhaps diastolic aortic
mui-mur.
Course and termination are most variable; in some cases the
symptoms may disappear, and the patient completely recover ; in others
the patient apparently recovers, but for some time looks very ansemic,
and the physical signs never disappear. Or the patient may enjoy
excellent health and be not aware that he has any valvular lesion till
many years afterwards, when the first symptoms of want of compensation
of the heart-defect make themselves felt ; the length of time before these
symptoms come on depends on many factors, such as the extent of the
lesion, the condition of the heart muscle, the occupation of the patient,
intercurrent diseases, and so on. In other but fortunately very rare
cases, where the valvular lesion is very severe, or the myocardium very
much enfeebled, the S3rmptoms denoting failure of compensation (dyspnoea,
quick, weak, or irregular pulse, oedema and dropsical effusion) may come
on early after the onset of the disease. When pericarditis complicates
the endocarditis the patient may pass years without any serious troubles,
till the compensation, whether of the valvular defect or of an adherent
pericardium, begins to fail.
Death may take place during the acute stage from the presence
of complications such as pericardial effusion, myocarditis, pneumonia,
embolism, or in some rare cases from hyperpyrexia; or some infective
agent may convert the rheumatic into infective endocarditis.
In children, in whom the physical signs are usually well pronounced,
and pericarditis often present, all the signs may completely subside,
and a restoration to complete health take place; in most cases, how-
ever, the child apparently recovers and may enjoy good health for
many years in spite of the presence of signs of valvular disease; yet
eventually, either without apparent cause or on the appearance of some in-
cidental disease, he manifests the subjective and objective signs of valvular
disease. In some few cases belonging to the group called active carditis
by Sturges {loc. cit. p. 506), death takes place from the associated peri-
carditis or from pulmonary oedema, embolic pneumonia, or cerebral
embolism. The cause of death in some cases of chorea with endo-
carditis is often very obscure, and not due directly to the endocarditis.
Diagnosis. — ^From what has been said of the symptoms of acute
rheumatic endocarditis, it will be clear that the diagnosis, though easy in
some cases, is occasionally impossible ; in many cases, indeed, the endo-
carditis can only be suspected. When no murmur is heard over the
precordial region we can only suspect endocarditis when, say in a case of
acute rheumatism, the heart sounds become veiled and impure (such
changes are best noticed when the heart has been daily examined), and the
patient complains of palpitation or oppression, as pointed out above. When
a murmur is heard over the region of the heart we have to distinguish
872 SYSTEM OF MEDICINE
between an exocardial and endocardial murmur, and if endocardial whether
it is due to endocarditis.
The exocardial murmur, which is occasionally difficult to discriminate,
especially in children, is a pericardial friction sound ; but the character,
the rhythm, the situation, the variability of the murmur, the direction
in which it is propagated, and some other points will help us to distinguish
pericarditis from endocarditis. Thus in pericarditis a double murmur is
heard which does not replace the heart sounds, but only obscures them ;
nor is the double murmur synchronous with them : the murmur may have
the character of a hard or soft friction sound ; it is heard usually over
the right ventricle, though it may be audible with less intensity near the
apex ; it appears to be superficial, is localised over a small area, is not
propagated either to the axilla or along the sternum, and it is variable
within short periods of time. Occasionally the rub may be felt when the
hand is placed over the precordial region. If there be much effusion the
precordial region may bulge ; the area of cardiac dulness increases, and
has a peculiar pear-shaped outline ; the apex beat is raised, displaced
towards the left and indistinctly felt ; and, on auscultation, tubular
breathing may be audible over a small area of the back. In pericarditis
pain and oppression are often noticed.
An exocardial murmur may be due to pleurisy. As a rule there is
no difficulty in distinguishing the pleuritic rub from pericardial friction
and from an endocardial murmur, since when the patient is asked to
hold his breath it disappears ; but occasionally the pleuritic rubs, though
lessened, persist and are rhythmical with the heart's contraction': as a
rule, however, the rub extends towards the left beyond the limits of the
heart, and there is often pleuritic pain.
Another exocardial murmur may sometimes be heard above the apex
beat towards the left ; it is rough, varies in intensity, begins after the
systole, and disappears when the patient sits up and bends forward.
According to Potain, this murmur is due to the intrusion of a thin
layer of the lung, close to the heart, into the space before occupied
by the base of the heart, as with each ventricular contraction the apex
is projected forwards and the base retreats slightly from the chest
wall.
Having eliminated the exocardial murmurs, we have yet to determine
whether the murmur be due to endocarditis (so-called organic murmur) or
functional ; and, if due to endocarditis, whether recent or old, benign, or
infective. The chief points of distinction between the hsemic murmur and
the murmur produced by the dilatation of the heart, and by endocarditis,
have been given above. As a ride there is no difficulty in distinguishing
recent from old endocarditis ; we have to take into account the history
of the case — whether there have been previous attacks of rheumatism or
chorea, or of some of the other diseases followed sometimes by endo-
carditis ; or whether the patient has suffered from dyspnoea on exertion
or oedema of the feet. The presence of secondary changes in the heart
due to chronic valvular disease, such as hypertrophy of the left ventricle
SIMPLE ENDOCARDITIS 873
or dilatation of the right ventricle, indicated by accentuation of the second
pulmonary sound with signs of venous stagnation (oedema, enlarged
liver, albuminuria), are of great help ; but we have to bear in mind that
dilatation of the right heart may come on occasionally in acute endo-
carditis, and that a previous attack of rheumatic endocarditis favours the
recurrence of such attacks, should the patient suffer again from acute
rheumatism ; thus we may have an acute endocarditis implanted on an
old one.
The discrimination of rheumatic or benign from malignant endo-
carditis will be considered when treating of the latter disease.
Prognosis in acute endocarditis is sufficiently evident from what has
been stated concerning the course and termination of the disease. Death
during the acute stage is generally due either to the severity of the
primary disease — be this rheumatism, chorea, or an infective fever
— or to some complication, such as .myocarditis, pericarditis, or pneu-
monia ; in some rare cases symptoms of dilatation of the right side, with
venous stasis, shown by dyspnoea, dropsy, irregularity of the heart's action,
may come on and lead to death. A very large majority of patients recover
from the acute attack, remain well for years, but become the subjects of
chronic valvular disease ; and this may occur in cases in which the murmur
had disappeared for a time ; lastly, in some few instances complete and
permanent recovery takes place. When an acute endocarditis occurs in
persons already affected with valvular disease the prognosis is still more
serious ; for often the fresh endocarditis is of the infective or malignant
kind ; or, even without this, the fresh deposit may lead to embolism or,
by increasing the weakness of the heart, hasten the downward course of
disease.
Treatment. — Prophylactic treatment. — As acute endocarditis is asso-
ciated most frequently with acute rheumatism, our attention must be
directed to prevent the occurrence of this malady in persons with a
family or personal proclivity to the disease ; such persons should wear
flannel next to the skin, avoid living in damp houses and in districts
where clay forms the subsoil and rheumatism abounds, and avoid as much
as possible those sudden changes of temperature which are so apt to
produce chills.
If a person is taken with acute rheumatism, can we by speedy and
proper treatment prevent the occurrence of endocarditis ? This question
has been the subject of many discussions, especially since the introduction
of the salicylates, which have such a decidedly beneficial effect in acute
rheumatism, often causing a speedy disappearance of the symptoms, and
cutting short the duration of the disease. There is, however, now abundant
evidence that the cardiac affections are not warded off by this treat-
ment [see discussion in the Medical Society of London, 1881]; on
the other hand, we cannot say that their frequency has been increased
by this now universal treatment of rheumatism. Some maintain that
the treatment of acute rheumatism with large doses of alkali, combined
with absolute rest in bed, has a more protective effect against the cardiac
874 SYSTEM OF MEDICINE
complications than the salicylates or salicin; and many now use this
combined treatment. So far the prophylactic treatment has had but
little success ; yet it is most important that every case of acute rheumatism
in adults, and still more the various modified and less pronounced forms
in children [see Dr. Cheadle's article on " Acute Rheumatism in Children,"
vol. iii. p. 52], should be treated at once by rest in bed, with complete
repose and appropriate medicine (alkalies and salicylates).
Local treatment. — Venesection, recommended by Bouillaud and his
school, and extensively practised for years, need only be mentioned as of
historical interest. The application of a few leeches to the precordial
region, especially in young and plethoric subjects with a quick and
full pulse, and when there is precordial pain and oppression,
indicative of early pericarditis, may be safely recommended for the
relief of these symptoms. The local application of ice, long since recom-
mended by Friedreich, and extensively practised on the Continent, has
been warmly advocated by Dr. D. B. Lees, especially when pericarditis
complicates endocarditis ; it may be tried also in simple endocarditis : it
reduces the fever, diminishes the frequency of the pulse, calms the action
of the heart, and relieves such subjective symptoms as pain and oppres-
sion. It is well to apply flannel next to the skin and the ice-bladder
over the flannel ; for dry cold is much better borne than wet cold. As
a rule it is quite tolerable, and indeed comforts the patient. It is contra-
indicated when there is marked cardiac dilatation with a small and
intermittent pulse ; but even when these conditions obtain, it may be
cautiously tried for a short time.
Other local remedies used are blisters, sinapisms, and tincture of
iodine. Large blisters have often been recommended as derivatives, and
recently Dr. Caton has spoken favourably of repeated small blisters. I
have often applied bHsters both in endocarditis and in endo-pericarditis,
and with relief of some of the subjective symptoms ; but I cannot say
that they have influenced the disease very much. Painting the pre-
oordium with tincture of iodine, repeating this from time to time, and
persisting with this for weeks or months, is asserted by some observers
to be attended with good results.
General treatment. — With the appearance of the flrst symptoms of
endocarditis some physicians recommend the administration of larger
doses of alkalies and suspension of the salicylates, which have a
depressing effect on the heart ; others see no objection to a continuance
of the salicylates, unless signs of failure of the heart or of myocarditis
appear ; others again prefer to give salicin, which has a much less de-
pressing effect. As, however, with this treatment the endocarditis, when
once it has shown itself, is rarely completely cured, I have tried from time
to time both local and general means to check, if possible, the inflamma-
tion of the endocardium and to minimise the damage done by it.
Tartar emetic, as recommended by Jaccoud, is scarcely ever employed
by English physicians ; nor do many of us give mercurial preparations
which were once so highly spoken of both by Graves and by Stokes,
SIMPLE EiTDOCARDITIS 87S
except in obedience to special indications. Iodide of potassium has
been given at a later stage of endocarditis to hasten the absorption of
the deposits.
As essential as the medicinal treatment is the general management
and diet of the patient. The patient must be confined to bed for weeks,
kept quiet, and all excitement avoided ; the diet should be light, but
nutritious, and, unless the heart show signs of failure, stimulants had
better be avoided altogether.
Other drugs than those given above may be indicated by certain
symptoms and under certain conditions. If there be much pain and
restlessness small doses of morphine may safely be given. Antipyretics
are only indicated when the temperature is high and the pulse very quick.
Quinine in fairly large doses (15-20 grains), or phenacetin (gr. 5 to gr. 10),
are preferable to antipyrin or sodium salicylate. Digitalis is not re-
quired unless the pulse becomes quick and small, or irregular ; the
tincture of digitalis or digitaUn may be given when signs of cardiac failure
appear. Besides this drug we may give strychnine, ammonia, brandy,
and ether under the above conditions. When there is much dyspncea and
cyanosis inhalations of oxygen will be found useful, especially in children.
In cases in which the pulse is quick but full, and in which the heart's
action is good, digitalis had better be avoided, as an increase in the force of
the heart might lead to a detachment of clots or parts of the vegetations,
and thus to embolism.
For the anaemia, which often persists for weeks and months after the
acute symptoms have passed off, preparations of iron are given with
quinine and arsenic ; the latter drug appears, indeed, to have a better effect
than the iron preparations. Convalescents from acute endocarditis should
be sent for some weeks into the country or to the seaside ; a dry, bracing
climate being preferred. If there be much subsequent dilatation the
Nauheim treatment may be tried, and the other measures recommended
for chronic valvular disease [see later articles].
Those cases of rheumatic endocarditis which assume a malignant type,
which run a long and protracted course, and in which fever persists, rigors
and haemorrhages appear, and further complications (septic pneumonia,
embolic abscesses) arise, require the same treatment as cases of infective
endocarditis, to which class indeed they belong.
REFEREKCES
1. Caton. Lrnicet, 17th Aug. 1895.— 2. Coenil. Les SaOeries, 1885.— 3. Cotrp-
LAND. Trans. Path. Soc. Land. 1873, vol. xxv. p. 69. — 4. Dickinson, W. H. "On
the Pathology of Chorea," Med.-Chir. Trans. 1876, p. 4.-5. Donkin. Diseases of
Ohildren, Lend. 1893, p. 302.— 6. Edwards. Lancet, 1850, vol. i. p. 673.-7. Hanoi.
Bull, de la soc. anai. 1874. — 8. Israel. Dmtsch. med. Wochensch. 1896. — 9. Lance-
KEAUX. Gaz. mM. de Paris, 1868. — 10. Lees, D. B. Laneet, 22nd July 1893. 11.
Leger. These de Paris, 1877. — 12. Lbtden. Veutsch. med. Wochenschr. 1895. 13.'
LiTTEN. Z.-CentraZU. fur klin. Med. 1897.— 14. Mackenzie. S. Tram. Internat.
Med. Congress. Lond. 1881.-15. Okmerod. Diseases of the Heart, 1862.— le!
876 SYSTEM OF MEDICINE
OsLBR. Chorea, p. 48. — 17. Potain. "Endocarditis," Dictionnaire eruyelop. des
sciences midicales, p. 501. — 18. Retmond. Dictionnaire encyclopddique des sciences
wMicales. — 19. Roger. Arch. gin. de midecine, Deo. 1866 and Jan. 1867. — 20. Rosen-
bach. Die KranJcheiten des Herzens, 1893, p. 160.— 21. Rosenstein. Path, und
Therapie der Herzkrankheiten, 1S93, p. 69. — 22. Sansom. Lettsomian Lecture, p. 18. —
23. SiBsoN. Reynolds' System of Medicine, vol. iv. p. 461.-24. Stueges, 0. Chorea.
Lond. 1881.-25. Idem. Brit. Med. Jawm. 1894, i. p. 565.-26. West, C. Dis. of
Infancy and Childhood, 7tli ed. 1884.
II. Infective Endocarditis
Syn. — Malignant Ulcerative Endocarditis
I have already (vol. i. p. 626) considered the causation and patho-
geny of this form of endocarditis ; it remains now to discuss the patho-
logical anatomy, symptoms, prognosis, and treatment.
Pathologieal anatomy. — Lesions are found in the heart and in
various other organs of the body. Some are primary, and represent the
seat of inoculation ; others are secondary, but the most important of
these are produced by the micro-organisms circulating in the blood. The
changes found in the heart vary considerably according to the microbes
which produce the disease, the extent of it, its duration, and especially
whether the infective endocarditis aflFect a healthy heart, or one already
the seat of old endocarditis or sclerosis of the valves. We may have simple
vegetations, or — and this is the most frequent occurrence — we find a more
or less extensive ulceration of necrotic character ; or, occasionally again,
the formation of one or more abscesses. Malignant endocarditis, like
simple or rheumatic endocarditis, principally affects the valves ; and much
more frequently the valves of the left side than those of the right,
though the latter are more liable to be affected than in rheumatic endo-
carditis : thence it may extend to other portions of the endocardium, and
to the aorta or pulmonary artery. Mural infective endocarditis, in which
the valves remain free, is extremely rare.
When there are only vegetations these are generally small, and
grayish or yellowish in colour ; they affect the base as well as the margins
of the valve. Such a condition we sometimes see in cases which
run a very rapid course ; histological examination of the valve reveals
numerous microbes, embryonic cells, and leucocytes ; besides the layers of
fibrin. In most cases, however, the vegetations are larger, occasionally
pedunculated, and more or less extensively ulcerated; these may be
superficial, not extending deeply into the tissues ; they are grayish,
and often partly covered with fine blood coagula ; if the valve yield to
the blood-pressure, depressions (aneurysms) may result. Sometimes the
ulceration may penetrate deeply into the valve, and perforate it ; often
the inflammation spreads to the chordae tendinese, and is followed by
further ulceration, so as to cause a detachment of the valve segment;
the valve is thus rendered incompetent, and with every cardiac contrae-
INFECTIVE ENDOCARDITIS ^fJI
tion the loose segment, flapping against a part of the auricle, sets up
fresh inflammation there, and gives rise to the formation of warty growths
on its walls. The loss of substance caused by ulceration extending to
parts of the endocardium (chordae tendinese, septum) may lead to an
aneurysmal bulging of the wall,' or even to rupture of the septum or of
the heart.
If pyogenetic organisms be the immediate cause of the ulcerative
endocarditis small abscesses may form in the tissues of the valves ;
occasionally one or more larger abscesses are found in other parts of
the heart, extending deep into the myocardium; and these again may
lead to an aneurysm of the heart, or to rupture into the pericardium.
In rare cases the pus may be reabsorbed, and leave scars or calcareous
residues (1).
In the more chronic, but sometimes also in the acute cases, we may
find deposits of lime salts on the vegetations ; but, as a rule, we find
these calcareous incrustations in cases in which ulcerative endocarditis
has attacked a person already suffering from valvular disease. It is
not always easy to distinguish these ulcerations from the atheromatous
ulcers due to simple necrosis in a valve with calcareous deposits, the
result of either chronic endocarditis or atheroma ; in most cases a
bacteriological examination will help us to distinguish the two, but not
always.
The frequency with which the various valves are affected is shown by
the following analysis from the post-mortem records of the Manchester
Eoyal Infirmary (2) for 1891-1895; 20 cases are noted: 7 men and
13 women; average age, 34| ; youngest 15, oldest 57. In 15 cases
out of 20 previous cardiac disease was noticed : the right side was
involved in 1 case only ; herein there were vegetations on the tricuspid
as well as on the mitral valve : in 7 the mitral alone was affected :
in 8 the aortic valve alone. The spleen was found enlarged in 17
cases.
From 1895 to 1897 25 cases were noted: 14 men, 7 women, 3
boys, and one girl; average age, 32; oldest 72, youngest 9. In 20 out
of the 25 previous cardiac disease was noticed: in one the right side
(pulmonary artery) was affected alone ; in 3 both right and left sides ;
in 6 the mitral valves only; in 3 the aortic only; in 6 both mitral
and aortic valves were involved. Splenic enlargement was found in 19
cases (3).
Kanthack and Tickell analysed 84 cases occurring between 1890 and
1897; of these, 51 were males, 33 females; and in all but 16 cases old
cardiac lesions were found.
The changes noted in other organs vary considerably, and may be
grouped as follows : —
(i.) Primary; such as croupous pneumonia, pleurisy, empyema, menin-
gitis, primary septic foci in the uterus or its adnexa, gonorrhoea, a primary
abscess in pyaemia, osteomyelitis, disease of the middle ear, tonsillitis,
gastric ulcer, appendicitis, gallstone, etc. (see vol. i. of this work, p. 631)!
878 SYSTEM OF MEDICINE
It must be noted, however, that septic pneumonia may be secondary to
infective endocarditis.
(ii.) Lesions due to embolism. These vary as the embolus acts
simply mechanically or has infective properties : in the first case we
meet with infarcts chiefly in the spleen and the kidney, and in the
brain ; in the brain the area of the blocked artery softens, in peri-
pheral arteries the embolus may lead to gangrene. In the second
case we meet with metastatic abscesses, which may occur either in small
or in very large numbers ; and are found in the liver, the spleen, the
kidney, the lungs (especially if there be right-sided endocarditis). In the
intestines, or even in the stomach, hsemorrhagic infarcts are found, some-
times of a septic nature infested with numerous micro-organisms, and occa-
sionally ulcerations of the mucous surface ; at other times corresponding
to simple infarcts, the intestines present intense congestion, haemorrhage,
and even gangrene.
Small capillary emboli are no doubt the cause of the haemorrhages
noted in the skin and subcutaneous tissue, the serous surfaces, the retina,
and other parts.
3. Lesions which are common to most infectious fevers, and which
may be due to micro-organisms, their toxins, or to the accompanying
pyrexia. Enlargement of the spleen, so-called " cloudy degeneration " of
the liver and kidney, and nephritis (in which the kidney is large, pale,
and shows small haemorrhages), are included in this group.
Symptoms. — The symptoms of infective endocarditis vary consider-
ably in individual cases : the heart symptoms may be quite insigni-
ficant or even absent ; as, for example, when acute infective endocarditis
complicates a septic disease, as pneumonia, empyema, or meningitis, in
which often only the autopsy reveals the endocardial lesions. In other
cases the heart symptoms are more pronounced : this is more particularly
the case in the subacute or even chronic form which complicates rheumatic
endocarditis.
Owing to the great diversity of the symptoms certain types of infec-
tive endocarditis have been formulated. We may distinguish in the first
place between an acute form and a subacute or chronic form.
The acute form includes the septic type, the typhoid type, and the
cerebral type ; the chronic form is noticed in old valvular affections of
the heart ; by some it is called the cardiac type, or, owing to the peculiar
fever curve which is noticed, it has been name(J the intermittent febrile or
malarial type. We will briefly consider the principal features of these
various types, and then note the symptoms in detail.
(a) The se'ptic, or pycemk type, which is noticed in puerperal cases and
in other forms of septicaemia and pyaemia, includes all the symptoms of
a severe septic infection. The onset is acute ; with or without preced-
ing general malaise the disease is ushered in by more or less severe
rigors, followed by heat and sweating, which may be repeated after a
shorter or longer interval ; between the rigors the temperature generally
remains high, it may, however, be remittent ; the skin may show patches
INFECTIVE ENDOCARDITIS 879
of erythema, hsemorrhage, or superficial collections of pus ; the pulse is
quick and feeble ; the respiration is hurried and superficial ; nervous symp-
toms, such as headache, delirium, somnolence, are usually present; at
times symptoms of cerebral embolism may appear ; the tongue is usually
furred, and may become dry and brown ; there may be great thirst,
anorexia,. and vomiting; there is often a good deal of tympanites and
diarrhoea. Metastatic abscesses may form in various organs and tissues,
but often do not give rise to definite symptoms, as, for example, in the
lungs.
The examination of the heart may reveal either no abnormal signs,
or audible murmurs ; from their presence alone we may not conclude
that we have to do with infective endocarditis, for such murmurs are
not uncommon in simple cases of pysemia and septicaemia, without any
ulceration of the valves of the heart. Of other symptoms common in
ordinary pyaemia I may mention albuminuria, jaundice, and pain and
swelling of the joints with suppuration. Death generally takes place
within one or two weeks.
(6) In the typhoid type infective endocarditis resembles enteric fever
as regards the general aspect of the patient, the condition of the tongue,
which is brown, dry, and furred, the presence of diarrhoea and cerebral
symptoms; but we not infrequently see rigors, petechias, and optic
neuritis — symptoms which are very rare in enteric fever: the heart
symptoms in this form again may be absent, or indefinite. The temperature
is generally very irregular; rigors may occur throughout the whole
duration of the disease, followed by profuse sweating; and attacks of
embolism in the brain, kidney, and spleen are not uncommon. The
duration of the disease, when assuming this form, varies from two to three
weeks ; sometimes it lasts longer.
(c) Cerebral type.—T}iis type is chiefly abstracted from cases of
malignant endocarditis complicated with meningitis, either cerebral or
cerebro-spinal. The afi'ection begins in these cases with cerebral symp-
toms— headache, somnolence going on to unconsciousness and coma, or
delirium and convulsions. The heart symptoms are less pronounced and
often absent. Rigors are not often present, but attacks of embolism may
occur and direct attention to the heart.
{d) Cardiac or Malarial type.—T\as represents by far the largest number
of cases ; it occurs in persons in whom the heart has ah-eady been damaged
by previous disease. It runs, as a rule, a subacute and chronic course,
and may last six months, or even more than a year. Though recovery
is extremely rare, this variety is not always fatal.
The onset of the disease is generally insidious ; the patient complains
of general malaise, and has an anaemic appearance. Sometimes an in-
crease of hody temperature, with but few other symptoms, may be the first
sign of It, as in a case under the care of my colleague Dr. Steell ■ a youne
man suflfenng from an old valvular affection of the heart, whilst in the
hospital suddenly showed a rise in temperature, and after a few days
manifested characteristic signs (rigors and so forth) of infective endo-
88o SYSTEM OF MEDICINE
carditis. At other times the affection resembles rheumatic arthritis,
pains in the joints and slight pyrexia being prominent features. After
these symptoms have lasted a few days, rigors appear, followed by heat
and sweating. During rigor the temperature may reach 104° F. or
more, and a few hours later the temperature may come down to
normal. The rigors occur at irregular intervals : two or three may
occur in one day ; at other times several days or weeks may elapse before
a second rigor is observed. In a good many cases the rigor is replaced
by a mere sense of chilliness followed by sweatings ; in others, again, a
remittent or intermittent pyrexia, going on for weeks or months
without any rigors, is a prominent feature. Thus, in one case, which I
saw with Dr. Renaud — a girl, aged 20, who at the age of 16 had had an
attack of rheumatic fever from which she recovered, but which left her
affected with mitral disease — the only noticeable feature was an intermittent
pyrexia — the morning temperature being 98°, the evening temperature
99° to 100° ; beyond this no other symptom was noticed, and the
patient felt no further inconvenience. This state persisted for over six
months, when she had an attack of cerebral embolism. From this she
had partially recovered when a second and fatal attack of embolism
supervened. At the necropsy new deposits were found upon an old affec-
tion of the mitral valve, and the vegetations showed the presence of
numerous streptococci.
A remarkable feature in the cardiac type of infective endocarditis is
the occurrence of embolism. This occasionally affects peripheral arteries
(posterior tibial, brachial, popliteal, and even abdominal-aorta), but more
often the left middle cerebral artery, or one of its branches, especially the
Sylvian artery. The blocking of the cerebral vessels may only produce
temporary paralysis or aphasia ; but often these attacks are followed
by others which leave a permanent lesion, and most frequently lead to
complete hemiplegia.
Some of the viscera also may be the seat of emboli ; thus splenic
infarcts are not uncommon, which may give rise to no symptoms : but
occasionally certain symptoms enable us to diagnose the infarction ;
namely, sudden pain in the region of the spleen, with enlargement of the
organ, and occasionally a friction sound over the spleen. It must not
be forgotten, however, that, without the presence of an infarct, the spleen
is often considerably enlarged in infective endocarditis.
Quite as common are renal infarcts, which only give rise to symptoms
when the infarct is large ; in such a case sudden pain is felt in the region
of the kidney, and hsematuria and remittent pyrexia appear.
Infarcts of the lungs can be inferred if the patient have a sudden pain
in the chest, with dyspncea, followed by the expectoration of sanguino-
len sputum. On physical examination, if the infarct be large, we
notice over a small area dulness on percussion, increased vocal fremitus,
bronchial or tubular breathing, and fine crepitations ; the temperature also
rises and assumes a remittent character. Pulmonary infarcts frequently
lead to embolic pneumonia, and often also set up localised pleurisy. If the
INFECTIVE ENDOCARDITIS 88i
endocarditis be situated on the right side of the heart we occasionally
meet with multiple metastatic abscesses in the lungs, which give rise to no
definite symptoms.
Embolism of the, mesenteric artery — a rare occurrence — ^may give rise
to severe abdominal pain, with haemorrhage from the bowels and grave
general disturbance leading to collapse.
Other symptoms often noticed are pronounced anaemia, which may be
present from the beginning : examination of blood shows the red blood
corpuscles to" be diminished ; the leucocytes are often increased, and
a few eosinophile cells may be detected. Bacteriological examination
of the blood reveals the presence of micro-organisms, notably strepto-
cocci.
PetechicB and hcemorrhage from the mucous membranes are occasionally
noted, the latter more particularly when the aortic valves are affected.
Pains in the joints are often complained of ; in many cases the joint
is neither swollen nor reddened, and the affection is probably of a toxic
nature ; at other times we meet with a definite arthritis, or again, with
suppuration of the joint.
Hcemorrhages in the retina and optic neuritis, according to some observers,
are of common occurrence. I have seen haemorrhage more frequently
than optic neuritis.
Enlargement of the spleen is very often noticed, and may reach a con-
siderable degree, so that the spleen can readily be felt ; it is not a
constant symptom, however, and in some cases the spleen, as shown by the
necropsy, is even smaller than in the normal state.
The liver is sometimes found enlarged, and jaundice may be present.
In rare cases the liver appears diminished, and the case may simulate
acute yellow atrophy. The occurrence of infective endocarditis in persons
suffering from gall-stones has already been alluded to when speaking of
the pathology of the disease (vol. i. p. 631); this may occur in persons
who have not had. rheumatic endocarditis.
The urine often shows traces of albumin and blood, and the presence
of casts, both epithelial and granular.
The bowels are often constipated ; occasionally we meet with profuse
diarrhoea, and sometimes (see above) with haemorrhage from the bowel.
The ordinary complications are pneumonia, pleurisy, pericarditis,
aneurysm, cerebral haemorrhage ; this last was noticed in two cases which
occurred in the Manchester Infirmary ; an embolus was carefully searched
for, but with negative results.
The symptoms wh^ch relate to the heart are well pronounced in the
cardiac form, and we meet with the signs of mitral or aortic disease, or of
both ; in rare cases we have evidence of an affection of the valves of the
right side of the heart. There is nothing in the character of the bruits or
in the size of the heart to enable us to diagnose infective rather than benign
endocarditis ; during the course of the disease the murmur may undergo
some change, but this may also occur in rheumatic endocarditis. The
presence of right-sided valvulitis is of greater diagnostic value, as it is of
VOL. V 3 L
882 SYSTEM OF MEDICINE
very rare occurrence in the rheumatic or benign endocarditis. Some
authors lay stress on the loudness of the murmurs, on their peculiar
(metallic) character, and on the propagation of the mitral murmur to the
axilla and angle of scapula ; but these signs are also noticed in the benign
form of endocarditis. Subjective symptoms, such as palpitation, pain
over the region of the heart, excessive dyspnoea, have no diagnostic
value.
As already stated, the cardiac form of infective endocarditis almost
always runs a chronic course ; occasionally it may occur in an acute
form. When treating of the pathology, I mentioned one instance in
which, previous to the occurrence of infective endocarditis, there probably
had been a ruptured aortic valve. Eecently I saw, with Mr. Coutts
of Blackley, a case of infective endocarditis in a compositor, aged 50,
who had always enjoyed good health, and who had never been troubled
with rheumatism ; he was suddenly seized with a rigor while at his
work; he was brought home, and his wife, who had been a nurse,
took his temperature and found it 103 '5° ; in the course of a few hours
the temperature was again normal, and the patient felt quite well. The
morning after, he had another rigor and rise of temperature ; and
in the evening he had still another rigor. When I examined the patient
soon after, I found the temperature normal, and the patient complaining
only of some oppression ; the heart's action was somewhat tumultuous,
and the arteries beating rather forcibly ; over the aorta a faint systolic
bruit was audible. The spleen was enlarged. The patient had been
taking quinine, and now some arsenic was added to this ; the rigors,
however, continued for two days, when the patient suddenly died. I
looked upon this case as one of idiopathic acute infective endocarditis.
The above types by no means represent all the clinical forms of
infective endocarditis. Thus it is found in association with pneumonia,
in which case there is very often no special symptom to lead one to
suspect its presence. It may occur with gonorrhoea, in which cases the
heart symptoms are often pronounced, whilst septic symptoms are less
obvious ; and, lastly, we meet with cases in which the distinction between
rheumatic and infective endocarditis is impossible.
Diagnosis. — In spite of our improved clinical methods, and the appli-
cation of bacteriology to clinical medicine, the diagnosis of infective en-
docarditis is still often a matter of difficulty.
Enteric fever may be distinguished from infective endocarditis by
the mode lof onset, the temperature curve, the roseolar spots, tympanites,
and so forth. [See " Enteric Fever," vol. i. p. 836.] Repeated rigors are
rare in enteric fever, and cardiac murmurs seldom appear at the begin-
ning of it. In doubtful cases Widal's serum test may be a useful help ;
if, after the sixth day of illness, this test give negative results, enteric
fever may with great probability be excluded ; on the other hand, re-
peated rigors, and especially the occurrence of attacks of embolism, speak
most strongly for infective endocarditis.
From septic and pysemic infection, unless heart symptoms are pro-
INFECTIVE ENDOCARDITIS 883
nounced and signs of embolism are present, the disease is not easily-
distinguished. This will be easily understood, for infective endocarditis
is indeed nothing more or less than a septic disease with the special
localisation of the micro-organism in the heart valves. Bacteriological
examination of the blood (see below) commonly shows us the presence of
septic micro-organisms ; and the same observation applies to the meningeal
or cerebral form. It is only in cases of tuberculous cerebro-spinal
meningitis that the withdrawal of fluid by means of puncture of the
spinal membrane in the lumbar region — which would show the presence
of tubercle bacilli — can be of any diagnostic value; as the same
organism that is found in non-tuberculous meningitis, be it suppurative
or cerebro-spinal, has been found in infective endocarditis.
In the cardiac form, when the heart symptoms are well pronounced,
several signs help us to distinguish between the rheumatic (or benign) and
the malignant endocarditis. These are : —
(i.) The presence of pyrexia. — This is often one of the first symptoms,
and may show the remittent or intermittent type ; should the pyrexia
be accompanied by rigors occurring at irregular intervals and not affected
by either quinine or arsenic, the diagnosis may be looked upon as almost
certain.
(ii.) The anaemic appearance of the patient. — Anaemia often follows
the first attack of rheumatic endocarditis ; but the persistence of anaemia
for a long time, or the occurrence of anaemia long after the attack, should
certainly make us suspect malignant endocarditis.
(iii.) Enlargement of the spleen has already been discussed on p. 881.
(iv.) Changes in the retina, whether in the form of optic neuritis or of
small haemorrhages, when occurring in persons suffering from endocarditis,
are indicative of the infective form ; and it is well to examine the eye
in all cases of endocarditis.
(v.) Haemorrhages in the skin and from the mucous membranes. —
Epistaxis is a common symptom in rheumatic endocarditis when the aortic
valves are affected ; and haemoptysis is frequently noticed early in mitral
disease, and at a later stage in other heart affections. Haemorrhages
into the skin and subcutaneous tissue, on the other hand, due probably to
numerous small capillary emboli, are indicative of infective endocarditis.
• Of haematuria from renal infarcts and of melaena from infarcts of the
mesenteric arteries I have already spoken ; but in themselves, and with-
out other signs of infective endocarditis, these haemorrhages are of no
diagnostic value, as they may be the result of the chronic venous conges-
tion secondary to chronic endocarditis.
(vi.) Bacteriological examination of the blood. — Many are the observa-
tions on this subject, and various the methods which have been devised
to obtain sufficient blood for the culture of micro-organisms. Petruschky
uses the blood obtained by cupping. Lithmann withdraws about 5 c.c.
of blood directly from a vein of the arm by means of a sterilised
syringe. A portion of this is mixed with agar-agar which has been
previously liquefied in a water-bath at a temperature of 40° C., and
SYSTEM OF MEDICINE
the mixture is poured out into Petri's capsules to secure cultivations of
the micro-organisms present. In the acute septic cases numerous cultures
of streptococci and other cocci are found ; in the chronic cases, though the
case may be one of infective endocarditis, this method does not always
show the presence of micro-organisms. Of three chronic cases of infective
endocarditis H. Cohn found a few colonies of staphylococci in one only.
In several cases of chronic infective endocarditis under my own care, in
which the diagnosis was verified by the autopsy, some venous blood was
aspirated after the method of Lithmann, and examined bacteriologically
by my colleague Dr. Deldpine, but with negative results.
Ppognosis. — The prognosis of this disease is in all cases very grave.
The acute form, be it of the pysemic, typhoid, or meningeal type, is almost
invariably fatal, death taking place sometimes within a few days. Eberth
gives the case of a man who began with typhoid symptoms, soon followed
by coma and hyperpyrexia ; the case ended fatally the next day. The
aortic valves showed ulcerations, and a metastatic abscess was found in
the brain. In other cases the symptoms may go on for several weeks.
The chronic or cardiac form may last for months and occasionally over a
year ; yet a fatal termination either by exhaustion, embolism, or complica^
tions is the rule : several recoveries of undoubted cases have, however, been
recorded. When speaking of the pathogeny (vol. i. p. 632), I mentioned
a case in which malignant endocarditis occurred after an injury, and in
which the patient recovered with a damaged aortic valve, and is at the
present time in a satisfactory state of health. Another patient, whom I
saw with Dr. Hassall of North wich, with all the signs of infective endo-
carditis implanted on a diseased aortic valve, recovered.
Treatment. — Many are the drugs that have been recommended in
infective endocarditis. Apart from the general treatment with tonics,
stimulants, and rest, the same drugs as are given in rheumatic endo-
carditis— such as the alkalies and salicylates, antipyrin, phenacetin, and
so forth— have been recommended, but the results have not been en-
couraging. Large doses of quinine appear more useful, though the
quinine does not prevent the occurrence of the rigors, even in large
doses. Fraentzel recommends large doses of quinine with arsenic, and
I have for some years given this combination ; yet, except in the two
cases quoted above, and in a third case in which the symptoms of '
endocarditis occurred after an attack of gonorrhoea, and in which
there was also a peri-urethral abscess, the fatal termination was not
averted.
Benzoate of sodium, recommended by Kleber and others, has not
given any good results in my hands.
Sulpho-carbolate of soda (half-drachm doses) is recommended by Dr.
Sansom, who records one case in which, when death took place at a
later period, distinct cicatricial tissue was found at the site of the old
ulcerations.
The subcutaneous administration of antistreptococcus serum has been
recently recommended ; judging from the successful cases published by
DISEASES OF THE MYOCARDIUM 885
Sairisbury and by Pearse, this treatment deserves a trial. Sir Douglas
Powell has tried in five cases subcutaneous injection of yeast, but without
any marked result ; and in one case nuclein was used, which caused a
temporary fall of the temperature.
J. Dreschfeld.
REFERENCES
1. ZiBGLEK. Special Path. Anat. Trans, by MacAlister, 1896, p. 53. — 2. Keltnaok.
Med. Chronicle, 1895 and 1897. — 3. Kanthaok and TiOKELL. Edm. Med. Jour. July
1897, pp. 13-36. — 4. Petrtischkt. Zeitschrift fwr Hygiene "vrnd^ InfecHonskramlc, vol.
xvii. — 5. LiTHMANN. Deutsch. Archiv f. klin. Med. vol. liii. — 6. CoHN, H. Deutsch.
iiicd. Wochen. 1897, p. 136. — 7. Ebekth. Virch. Arch. vol. Ivii. — 8. Fraentzel.
Hem-Kraiikheiten, vol. i. — 9. Sansom. Practitioner, 1891. — 10. Sainseuey. Lancet,
1896. — 11. Pbakse. Lancet, 1897, vol. li. p. 92. — 12. Powell, Sir Douolas. Brit.
Med. Journ. 1898, vol. i. p. 936.
For further references the reader is referred to the article on this disease in vol. i.
J. D.
DISEASES OF THE MYOCAEDIUM
As with other muscular organs, the heart is liable to fatigue, to overstrain,
to disturbed innervation, to impaired nutrition ; either, in the first place,
from defect in the nutritive qualities of the blood with which it is
supplied, or, in the second place, from temporary or permanent restriction
in that supply through temporary or permanent alteration of the vessels.
Fui'ther, the heart muscle may undergo degenerative changes, or may
atrophy and be replaced by fibrous tissue; and this degeneration or
atrophy and fibrous replacement may be general or localised. Yet, again,
the heart muscle may undergo physiological hypertrophy in obedience to
the demands of excessive labour, and this condition, although not one of
disease, has to be reckoned vnth, since it leads to textural changes;
finally, the heart may be invaded or occupied by growths, parasitic or
other, of various kinds. With the various diseases of the endocardium,
pericardium, and valves of the heart I have here no immediate concern'
although I shall have to refer to them incidentally in an endeavour to
give a clear account of myocardial lesions.
The several lesions of the myocardium above mentioned will be found
to group themselves naturally under the pathological headings of —
I. .Impairment secondary to general blood eonditions.— (A) Ansemia •
(B) Toxic changes. • '
II. Impairment secondary to altered blood-supply. (A) From
paroxysmal affections of coronary arteries ; (B) from permanent changes
in coronary arteries ; (i.) Atheroma ; (a) fatty degeneration ; (J) fatty
mfiltration; (c) fibroid infiltration; {d) aneurysm of the heart- (ii )
Thrombosis or embolism ; (iii.) Aneurysm. '
S86 SYSTEM OF MEDICINE
III. Impairment due to senile changes. — (a) Pigmentary degenera-
tion ; (6) atrophy.
IV. Impairment arising from functional strain. — (a) Hypertropliy ;
(6) acute dilatation ; (c) textural damage.
V. Impairment of inflammatory origin — Myocarditis. — (a) Inter-
stitial ; (i) parenchymatous ; (c) purulent ; (d) syphilitic.
VI. Growths. — (a) Sarcoma ; (6) myxoma ; (c) fibroma ; {d) gumma ;
(e) carcinoma ; (/) lipoma ; (§') cyst ; (A) myoma ; (i) tubercle.
VII. Parasites. — (a) Hydatid; (J) cysticercus cellulosae; (c) actino-
mycosis ; id) trichina spiralis.
I. Impairment secondary to general blood conditions. — A.
Ansemia. — Pathology. — In cases of marked anaemia, as in chlorosis, the
nutrition of the heart muscle suffers ; the organ is paler than natural,
somewhat glistening and wet-looMng on section, and gives less than the
normal resistance to the pressure of the finger. On microscopic
examination in persons who have died from some intercurrent malady
no change may be noticed ; but most commonly the fibres have under-
gone a certain degree of fatty change, and present a few refracting
granules. In some cases of extreme ansemia, however, a very notable
degree of fatty change may be found in the muscular fibres ; the internal
surface of the organ, especially over the left ventricle and papillary
muscles, presents a streaked or flecked appearance, due to groups of small
opacities seen through the transparent intima, the degeneration affecting
the muscular fibres having a patchy distribution.
Although the fatty heart is always somewhat increased in size, it may
not be increased in weight ; the specific gravity of muscles being reduced
by fatty change. The pericardium and endocardium usually escape
change, but the cavities of the heart are enlarged, especially the left
ventricle ; and slight incompetence of the mitral valve is often revealed
when the valve is properly tested by a fluid pressure equal to that of the
blood. I have often seen a heart inadequately tested in this respect. A
degree of regurgitation, clinically observable, may be overlooked if the
ventricle and valve are not subjected to sufficient fluid pressure.
On microscopic examination, groups of fibres are found in which the
fibrillse are more or less replaced by rows of refracting fatty granules, the
change appearing first in the neighbourhood of the nuclei of the fibres.
Besides the groups of more intensely fattily changed fibres, the other
fibres are more or less dotted with fatty granules.
Clinically, in all cases of extreme simple aneemia of any considerable
duration, one may observe a certain degree of enlargement of the heart ;
the apex beat is a little to the left of the normal, and the area of percussion
dulness extends slightly upwards ; frequently a soft murmur is to be
heard over the apex beat, which is not merely conducted from the
pulmonary area, but has the characteristics of mitral regurgitation, and is
no doubt due to a dilatation of the left ventricle, so that the base of
attachment of the papillary muscles becomes displared, and the mitral
DISEASES OF THE MYOCARDIUM 887
valve slightly incompetent at the moment of greatest intra-ventricular
pressure. The heart's action is quickened, and is peculiarly irritable to
the calls of slight effort or to reflex or emotional stimuli. These symptoms,
which constitute the cardiac features of anaemia, are of course only in
part directly due to the state of the heart muscle, they depend rather
upon the condition of the blood and the debilitated state of the nervous
system ; and to both these latter causes, as well as to the cardiac enfeeble-
ment, is also attributable that degree of oedema of the extremities which
is so common in marked ansemia.
B. Toxsemia. — Hyaline degeneration. — A peculiar hyaline swelling of the
muscle fibres of the heart in diphtheria has been described by Bouchut,
Labadie, Lagrave, and Eosenbach. The last-named author looks upon it
as an inflammation. Similar changes are met with in the voluntary
muscles in typhoid fever. Boyce speaks of it as a hyaline degeneration
of connective tissue, consisting of hyaline material similar to amyloid, but
without the chemical reaction of the latter. Hyaline degeneration
identical with that in the myocardium is more commonly observed around
the arteries, sometimes permeating, and causing extensive atrophy of the
muscle fibres of their middle coat.
Clcmdy swelling is' a condition in which the fibres of the heart lose
their striation and become finely granular ; it is met with especially in
diphtheria, typhoid and typhus, and is indeed common to all febrile states
of suflScient duration.
Fatty degeneration. — In certain poisoned conditions of blood, as from
lead, arsenic, and, in a most notable degree, from phosphorus, fatty
degeneration of the muscular fibres of the heart may be very extensive ;
and, in cases of phosphorus poisoning in which the patient has survived
the more immediate gastro-intestinal symptoms, it is the principal source
of danger. The mildest form of blood contamination — although very
important from its being so common — is the absorption of ptomaines from
the colon in neglected torpidity of the bowels, a source no doubt operative
in the production of the fatty heart of anaemia. The most intense of the
poisons of organic origin affecting the heart is that modification of the
toxine of diphtheria which is formed in the later stages of this disease,
and which appears to be responsible for that profound fatty degeneration
of the heart (in common with other organs) which is only equalled in
cases produced by phosphorus.
Repair in fatty degeneration. — Clinical observations would lead us to
suppose that repair of fattily degenerated hearts is possible, and even of
frequent occurrence; Dr. Coats is of opinion that it takes place by
absorption of the fat and an actual new formation of muscular tissue.
That such new formation is abundantly possible is evident from the
readiness with which healthy hypertrophy is established to compensate
valvular defects, or in response to other unusual calls upon the muscular
activity of the heart.
Under the heading of changes of the myocardium of toxic origin we
should certainly include those consequent upon chronic gouty conditions
888 SYSTEM OF MEDICINE
and chronic uraemic poisoning ; although, as in the less defined changes
induced by alcoholism, nicotinism, and the like, the lesions have features in
common with those induced by other causes, and will be described later.
There can be little doubt that the high-pressure pulse and consequent
increased call upon the heart which are associated with chronic affections
of the kidney are combined effects of central nervous induction, having
for their purpose such an increase of blood-pressure as shall promote
compensatory kidney function. In chronic gouty conditions the cardio-
vascular function is similarly modified; and in other cases of habitual
high arterial blood-pressure from mental strain or other causes the same
effects, although less in degree, are observed in the myocardium. These
effects are, first, hypertrophy ; and, secondly, fibro-fatty degeneration.
II. Impairment of the myocardium secondary to altered
BLOOD - SUPPLY. — A. Paroxysmal conditions of coronary arteries. —
Many authors have pointed out the occasional occurrence of angina pectoris
in young people attributable to excess in tobacco-smoking; and have
observed the anginal paroxysm of like causation in older persons.
Besides its other effects tending to disturbance of the cardiac innervation,
Dr. Huchard holds the view that nicotine has a more direct action, by
causing spasmodic contraction of the smaller vessels, and, in these cases,
especially of the coronary vessels. It is difiicult to bring evidence
sufficiently demonstrative to prove this opinion or to refute it. Dr.
Huchard relies chiefly upon the spasm of voluntary muscles and
upon the pallor and arterial contraction observed in nicotine intoxica-
tion, upon the high arterial tension often to be observed in smokers,
and upon the experiments of Claude Bernard in 1857, and by him-
self and others since, showing the local effect of nicotine in causing
contraction of the vessels in the frog's foot. There is every reason to
believe that the coronary arteries, like other vessels of equal size and
equally richly endowed with muscular tissue, are liable to spasmodic
contraction ; and it is quite possible, as maintained by Huchard, that in
some cases the abuse of nicotine may directly cause such constriction and
produce temporary anaemia and disturbed function of the heart muscle.
It has not been shown, however, that any textural damage to the heart's
substance has been caused by the vaso-motor effects of nicotine upon its
circulation. Of course, the remoter effects of nicotine in causing arterial
and muscular degeneration, if such there be, are not included in the
present subject.
B. Permanent changes in the coronary arteries. — (i.) Atheroma of
the eoronaries. — This may arise : (a) From the natural effects of age
leading to degeneration of the intima, with secondary thickening -and
softening, or calcareous deposition.
(b) These senile changes may be anticipated by constitutional con-
ditions, especially syphilis, alcoholism, and gout ; the sequence of events
being much the same, namely, degenerative impairment of elasticity,
patchy thickening, fatty change, or calcareous deposition.
DISEASES OF THE MYOCARDIUM
(c) Hereditary disposition plays an important part in determining
premature decay of the arterial system.
The above conditions are general to the whole arterial system, but
are most manifest at those portions of it at which the stress of
normal arterial pressure is most heavy. The origin and arch of the
aorta and the coronary arteries are the portions thus affected which
concern us at the present moment; and it may be noted that athero-
matous narrowing of the coronaries is generally most marked' at their
aortic origins, and is often limited to these parts.
(d) The chronic arterial strain of laborious occupations has a very
important influence in producing chronic patchy endarteritis of the aorta
and the coronary arteries ; and it operates very commonly in conjunction
with the causes of arterial degeneration spoken of under headings b and c.
There can be little doubt that the peculiar patchy distribution of
endarteritic thickening is due to small rifts at points of least resistance
of an intima rendered more brittle by degenerative changes, and to the
secondary nuclear overgrowth and subsequent degenerative changes
ensiung thereupon.
(e) Apart from the general effect of syphilis in disposing to arterial
atheroma, syphilitic granulomata may form in and about the arteries,
especially thickening their inner coats, and thus often leading to narrow-
ing or obliteration. [Fide art. "Disease of Arteries," vol. vi.]
(/) Vessels of small calibre, such as the coronary arteries when
narrowed, and with their intima changed by atheromatous or specific
arteritis, are very apt to become abruptly and completely closed by
thrombosis.
(g) The coronary arteries, like other vessels, are liable to embolic
closure, although they are much less prone to this obstruction than are
other vessels more directly in the current of the circulation. Such
embolisms when they arise may be simple or septic.
Having now enumerated the possible causes of narrowing or oblitera-
tion of the coronary arteries, let us look to the consequences of such
narrowing, which we shall find to embrace the most important lesions of
the cardiac muscle.
(a) Fatty degeneration of the heart. — A gradually increasing impairment
in the blood -supply of the heart, and a correspondingly diminished
thoroughness of the irrigation of its tissues with blood, are the most
frequent causes of fatty degeneration of the muscular fibres. I have
already spoken of fatty degeneration of the heart as a consequence of
general anaemia, and in certain states of toxaemia; the degeneration
arising from local anaemia, due to constriction of the supplying vessels, is
of the same kind, but is much less acute, and is more patchy in its
distribution. In hearts in which the coronary narrowing affects both
vessels at their origins, the distribution of fatty change would be more
uniform ; but these cases are rare. Often only one coronary vessel is
thus affected, and sometimes only certain branches within the substance
of the heart are much contracted by atheroma. Thus the change, at least
890 SYSTEM OF MEDICINE
in any serious degree, may be limited to one side of the heart, or to one
or more portions of one or both ventricles or auricles.
The change, for reasons to be mentioned immediately, besides being
much more insidious and slow in its progress, is mingled with other
changes and, in particular, with false or fibroid hypertrophy of the organ.
In very old people, 'in whom the whole process is one of senile decay,
the fatty degeneration may be simple and unattended with fibroid
changes.
The process of fatty degeneration of the cardiac muscle consists, as
already stated, in the gradual replacement of the sarcous elements by
fatty granules, the deposition of granules beginning about the nuclei and
extending linearly towards the fibre-ends. The affected tissue is thus
rendered more opaque in streaks of a tawny yellow colour, is softer and
more friable under the finger, and in well-marked patches gives a greasy
section. In some cases, in which the degeneration is extreme over a
restricted area corresponding with an occluded vessel, the fatty softening
may be so great as to resemble abscess. It is said (11a) that in many
cases the fatty change proper is preceded by a " cloudy swelling," in which
the fibres become finely granular from the deposition in them of fine
protein granules, which are to be distinguished from fatty granules not
only by their more dim and cloudy outline, but also by their reaction to
strong acetic acid or caustic soda or potash, either of which obliterates
them, whilst the same reagents bring out the granules of true fatty
degeneration in stronger relief. Both the protein and fat granules
are derived from the sarcous elements of the muscle which they replace.
As the disease advances the striation of the fibres becomes gradually lost ;
at first at the extremities of the fibres, finally towards their nuclear
centres.
In combination with the fatty degeneration there is more or less
atrophy of the muscular fibres, and in substitution for them an over-
growth of connective tissue elements resulting in the formation of fibroid
tissue (fibroid or false hypertrophy). In this respect fatty degeneration
of the heart, induced by restricted blood-supply from narrowed vessels,
difiers from the same degeneration due to general anaemia or toxic causes.
I have already indicated an exception in the case of old people, in whom
the degenerative changes are a part of general senile decay.
Although the internal surface of the ventricles may be specked and
streaked with opacities — ^much more irregularly disposed, however, than
in the case with degenerations of general blood origin — the endocardium
itself is rarely affected. The size and weight of the heart, and the thick-
ness or thinness of its walls, depend chiefly upon the amount of fibroid
substitution which is associated with the fatty change. The pericardium
is not necessarily involved, although it may be more opaque and thicker
than normal.
It was found, in speaking of the more acute fatty degeneration
of the heart due to general blood conditions, that partial or complete
repair was possible by a renewal of the muscular fibres in the same way
DISEASES OF THE MYOCARDIUM
as an extra growth of such fibres can take place in healthy hypertrophy,
whilst at the same time the fattily degenerated fibres became absorbed.
In degeneration due to permanently narrowed blood-supply, however, no
such repair can take place to any appreciable extent ; for the anastomosis
of the two coronary arteries, supposing only one to be afi'ected, is not
free enough to provide a sufiicient circulation for the purpose. Neverthe-
less, we may see in the overgrowth of fibrous tissue, of a somewhat
depraved sort it is true, an attempt to maintain the due resistance of
the heart walls to blood-pressure, without however any corresponding
preservation of contractile power.
Symptoms and signs. — The fatty heart is a weak heart, weak in its
muscular power, and weak in its resistance to blood-pressure. It is either
more or less arrhythmic in action, or readily becomes so under any extra
demand upon it from excitement or eifort. It is also (except in cases in
which the degeneration of the heart goes hand in hand with general
atrophy of blood and tissues in old age) an enlarged heart, increased in
size by the dilatation of the ventricles, and especially of the left ventricle,
under the normal blood-pressure ; and often increased in size also by false
(fibroid) hypertrophy. Hence, in a person usually beyond middle life,
with a feeble circulation and a tendency to blueness of the extremities, if
we find the superficial dimensions of the heart increased, the apex more
to the left than natural, the dulness extending an interspace higher, and
perhaps a iinger's-breadth more to the right than is proper, and if on
auscultation we find a marked indistinctness of the first sound and an
irregularity of beat both as regards time and force, we may be sure of
degeneration of the heart, and that the degeneration is more or less fatty.
A very common symptom is the occasional occurrence of attacks of
syncopal or anginal failure [see "Angina Pectoris," vol. vi.], but as these
attacks are often simulated by those of a much less serious nature, they
are always to be taken into account in conjunction with the signs of a
cardiac enlargement. In cases of anginal attack attendant upon organic
change in the cardiac muscle, and especially when such change is asso-
ciated with coronary stenosis, the immediate cause of the earlier attacks
is generally some increased call upon the heart from excessive exertion,
such as walking quickly or uphill ; and the result is to bring the patient
to a stop at once. Later attacks may occur when the patient is at rest
or asleep. In anginal seizures, when the heart is sound, the patient often
tends to move about, and if the attack be not very severe it may not
prevent the continuance of walking or other exercise.
In advanced cases of fatty heart, cases in which more distinct anginal
symptoms may not have occurred, an altered respiratory rhythm is not
infrequently to be observed, which is especially apt to occur during sleep ;
namely, an increasing shallowness of breathing down to absolute cessa-
tion for 20, 30, 40 seconds, then several profound and heaving respira-
tions take place which again gradually subside to complete pause
(Cheyne-Stokes breathing). During the pause the patient generally
wakes up with a start, and his sleep is thus much interfered with and
892 SYSTEM OF MEDICINE
becomes reduced to a succession of short dozes. The peculiar breathing
is to be observed during the waking hours also. The pulse continues
with its usually irregular action practically unaltered during the
arrhythmic breathing and pause ; it is to be noted, however, that in such
cases during ordinary or deep breathing the pulse is distinctly weaker
during the inspiratory wave. It must, lastly, be confessed that rare cases
are met with in which, even with a marked degree of fatty heart, no signs
are discovered up to the moment of fatal syncope or angina. I must state
my belief, however, that if the opportunity presents itself for a careful
examination of such cases, and the possible presence of emphysema be
taken into account as masking an increase of the cardiac area, the clinical
evidence of fatty degeneration is rarely to be missed.
The disease is most common at or beyond 50 years of age. Men more
frequently suffer than women in the proportion of nearly two to one (Quain).
All the functions of a person with fatty heart are performed in a languid
manner. He is the subject of atonic dyspepsia, with a great tendency to
flatulent distension of the stomach ; his bowel and liver functions are
torpid ; the urinary secretion, very sensitive to external surface tempera- .
ture, is of low range of specific gravity, and often contains a trace of
albumin. The brain is easily fatigued, the temper irritable. Only
gentle level exercise can be taken with comfort.
Treatment.— The treatment of fatty degeneration of the heart due to
altered blood-supply is a matter of great importance, hence the necessity
of recognising the lesions at the earliest possible stage.
In the earlier stages regular exercise short of fatigue, and adapted to
a person in whom a weakness of the central organ of the circulation is
recognised, is of importance ; quiet walking on the level, riding (not
hunting), cycling (avoiding hills), driving, sailing, quiet rowing, may all
be allowed ; and gentle incline walking, adapted to the case, may be
taken as prescribed exercise. Covert shooting may be followed, but not
rough walking or hill shooting. Golf and croquet are games well adapted
to such people. For these early cases, a course of Nauheim baths and
exercises may be taken with advantage from time to time, the exercises
being especially valuable in aiding by tonic muscular contractions the return
of blood to the heart, disgorging the venous circulation, and thus aiding
the forward movement. Cold bathing should be forbidden, and a warning
given against walking against cold winds.
A nutritious diet, rather nitrogenous than fatty or starchy, may be
allowed, distributed in three regular meals daily, eaten slowly, and adapted
in quantity to the lessened requirements of a less active life. A moderate
amount of wine is usually required.
Arsenic, iron, and strychnia are the tonics especially valuable ; but
they should not be given in more than two, or at most three doses daily
for short courses — the most careful regard being given to avoid digestive
disturbances. In all cases of lowered blood-pressure there is a tendency
to passive congestion of the organs and especially of the liver, so that
a mild dinner pill and an occasional mercurial alterative are desirable.
DISEASES OF THE MYOCARDIUM 893
In advanced cases of fatty degeneration the same general plan must
be followed still more carefully, and with narrower restrictions as regards
exercise, which should only be allowed on smooth level ground, all stair-
climbing being strictly forbidden. The diet must be closely watched,
especial care being taken to avoid overloading of stomach and acute
dyspepsia, as many fatal seizures are attributable to gastro-intestinal dis-
turbance. Persons with fatty heart are extremely sensitive to external
cold, and should be clothed very warmly. A thorough rest, lying down,
once or twice a day should be enjoined ; the best times to select are
before meals ; a short rest being taken before luncheon, and a more pro-
longed rest, of one and a half to two hours, before the late dinner. Such
patients should only use warm water for bathing, and for them the
Nauheim baths and exercises are not to be recommended.
To a strychnia and arsenic or iron tonic some digitalis, strophanthus,
or convallaria may be added ; and an aromatic stimulant and carminative
draught should always be at hand in case of syncopal attacks, and may
often usefully contain a little nitro-glycerine.
Finally, in cases of fatty heart which have advanced to the produc-
tion of any decided symptoms, the employment of oxygen inhalations
twice or three times a day is valuable as a cardiac restorative ; it operates
principally, no doubt, in stimulating cardiac nutrition and in facilitating
the removal of waste tissues from the organ by flushing it with more
highly oxygenated blood. For the Cheyne-Stokes respiration, in advanced
stages, there is no more powerful means of affording relief than oxygen
inhalations in combination with strychnia. In such cases, however, it
should not be employed with the naso-oral inhaler, but a current of oxygen
should simply be played over the mouth and nostrils of the patient for five
or ten minutes without any extra respiratory effort on his part.
(y8) Fatty infiltration of the heart. — Fatty infiltration of the heart is a
condition in which, owing to the deposition of fat in the interstices of
the muscular fibres, these fibres themselves are compressed, impeded in
action, and become atrophied.
A certain amount of adipose tissue is naturally present on the heart,
especially along the superficial course of the coronary vessels and in the
sulci at the base ; under certain conditions this tissue develops in
inordinate quantity and spreads over the cardiac surface, penetrating,
chiefly with the arterial branches, into its muscular substance. This
increase and extension of the adipose tissue is most marked over the
right ventricle, and may constitute a layer of considerable thickness
which by its encroachment upon and between the muscular fasciculi may
cause their atrophy and replacement, and thus considerably weaken and
embarrass the heart. The extension is always from the subpericardial
surface and chiefly along the arterial lines. The atrophy of the muscular
tissue which attends upon fatty infiltration is for the most part consequent
and secondary ; but it is probable that in some cases a primary atrophy
of the muscle leads to the secondary development of fat in the connective
tissue — which is everywhere present and potentially fat-bearing.
S94 SYSTEM OF MEDICINE
Thus, clinically, we have two forms of fatty infiltration of the heart :
the one in which the fat is rapidly stored and extends into and encroaches
upon a higher tissue, the function of which it embarrasses, and the nutri-
tion of which it mechanically interferes with ; the other in which the
fatty tissue merely, as it were, fills up the interstices left by an atrophy-
ing muscular tissue.
Of these varieties the first is by far the more common and important.
It is met with in persons of inactive and often indolent and self-indulgent
lives, in men at middle age, in women towards the climacteric period, or
soon after it. It is the people who have good appetites and good
primary digestion with faulty assimilation and inadequate eliminative
power that are especially liable to this disease. Indulgence in alcohol,
and especially in malt liquors and the sweeter wines, certainly favours its
occurrence ; and there are certain maladies upon which it is peculiarly
liable to ensue, especially those affections which involve a deprivation of
respiratory surface, such as chronic emphysema, or fibroid disease of the
lung in old-standing quiescent phthisis, or secondary to pleuritic efiusion
or unresolved pneumonia, etc. Defective elimination by the bowels and
kidneys is similarly efficacious. It must be carefully remembered, how-
ever, that no organic disease of any kind is necessary as the forerunner
of this affection, which may arise solely from an excess of alimentary
supply over demand, however this may be brought about.
Symptoms and signs. — Persons thus affected are stout, increasing in
weight, with a thickening layer of adipose tissue, full abdomens, and
often tender livers. Their circulation is feeble and usually slightly
quicker than was normal in them. There is some excess of venosity in
their colouring, they are short-breathed on exertion, and sweat easily.
Later they manifest functional disturbances of the heart's action, rapidly
induced on exertion or coming on without it. The cardiac dulness is
increased by an interspace upwards, but the apex beat is diflBieult to feel,
and the cardiac impulse tends to be more felt towards the epigastrium
than beyond the normal position to the left. The sounds are less clear
than natural, otherwise unchanged. There is no change to be felt in the
arteries ; the pulse is usually soft, of low pressure, and, if full, is com-
pressible. Of course this condition of pulse may be varied by other
intervening states, such as gout, to which, however, these people are not
peculiarly liable. The urine varies, but is habitually pale and copious,
and of rather low than high range of specific gravity.
Whilst in a far less dangerous condition than that attendant upon a
truly fattily degenerated heart, these patients are nevertheless very liable
to succumb to acute disease of any kind, and particularly to bronchitis,
pneumonia, enteric fever, or surgical injury.
The treatment is simple, rational, and, if loyally followed, very successful.
The dietary must be mainly nitrogenous, all superfluous starches, sugars,
and fats being discarded. Only claret, moselle, or equivalent quantities of
spirit well diluted must be allowed, and in sparing quantity. The meals
rliould be at regular times, slowly eaten and strictly moderate in quantity.
DISEASES OF THE MYOCARDIUM 895
But little fluid should be taken with the meal, but tissue change duly-
ensured and thirst satisfied by a moderate quantity of hot or cold fluid
slowly sipped about a quarter to half an hour after the meals, or, some-
times better still, half-way between the meals. A tumbler of hot water
with a little fresh lemon juice may be taken at bedtime or in the early
morning. Eaw fruits, root vegetables, and bread must be avoided, or
only very sparingly taken. Daily walking, riding, or cycling exercise
must be imperatively enjoined ; for the advantage of regulated exercise
is not merely to quicken muscular nutritive changes, and so to convert
the food taken into proper force-yielding material, but to deepen respira-
tion and to promote the respiratory and other eliminative functions.
Hence dumb-bell, fencing, or other home exercises carried on indoors,
although they may be useful supplementary aids, are not adequate to
replace open-air exercise. Medicinal treatment is of quite minor import-
ance, and may be' limited to promoting due elimination, and giving a
heart tonic if needed. Turkish baths, or a course at Homburg, Carls-
bad, Marienbad, Harrogate, or Nauheim, may be suggested in appropriate
cases.
The other form of fatty infiltration attendant upon atrophy of the
heart is met with in an altogether different type of individual, one who
commonly is already the subject of some grave organic disease, such as
tuberculosis or cancer ; and its importance and treatment are both merged
in the graver malady.
(y) Fibroid infiltration of the heart (Fibrous transformation, Coats ;
Fibroid degeneration of the myocardium, Orth. ; Myocarditis productiva
or interstitial myocarditis). — This condition essentially consists in the
separation and replacement of the muscular fibres of the heart by an
imperfect fibrous tissue generated by overgrowth of the connective tissue
of the organ. It is very closely analogous to fatty infiltration, and it
cannot rightly be described as a degeneration of the myocardium. It
would seem, therefore, that the term " fibroid infiltration " most fitly
describes the morbid state present ; interstitial myocarditis is also a
fairly accurate term, although it conveys a false impression of the disease
being an inflammatory one, which it rarely, if ever, is.
Fibroid infiltration of the heart may be described as general and
local, although even in general infiltration the disease is not uniformly
distributed.
Causes. — Besides the coronary obstruction general fibroid infiltration
has another principal cause ; namely, chronic congestion of the heart from
mechanical impediment to the return of blood from the cardiac veins.
This cause is chiefly met with in cases of old-standing emphysema, and in
cases in which the whole or a large portion of one lung is the seat of
cirrhotic change from old pleurisy, unresolved pneumonia, or fibroid
phthisis. Extensive narrowing and destruction of pulmonary vessels and
impairment of that inspiratory aid to the cardiac circulation which obtains
in healthy respiration, results in a difficulty in the pulmonary circulation,
at first overcome by greater diligence of the right heart, but gradually
896 SYSTEM OF MEDICINE
increasing until the venous return to the right auricle is seriously impeded.
A chronic congestion of the walls of the heart ensues, most marked on
the right side, but involving the left also ; and, as a result of this chronic
congestion, overgrowth of connective tissue and atrophy and degeneration
of the cardiac muscle proper. In the more advanced stages of mitral
stenosis and regurgitation the same conditions are to be observed, having
similarly a mechanical origin.
Nevertheless the most important cause of general fibroid infiltration
of the heart is the obstructive disease of the coronary arteries at or near
their origin from the aorta, under which head we now consider it. A
more marked degree of fatty degeneration of the muscular fibres is met
with in association with fibroid infiltration arising from this cause, for a
degree of blood irrigation which will suffice for the overgrowth of an
inferior tissue, such as connective tissue, will not sufiice for the nutritive
maintenance of a tissue of such activity, and requiring such frequent
renewal and restoration as the muscular tissue.
It is thus to be remarked that hearts which are the seat of general
fatty degeneration from coronary obstruction (except quite as a senile
change) are always large hearts, the seat of so-called false hypertrophy ;
and this it is which furnishes us with an important clue to their clinical
diagnosis. The increase in size is partly due to increased thickness of the
cardiac walls, in part to dilatation of the cavities of the heart ; for fibroid
infiltration, although it increases the toughness of the cardiac wall,
diminishes its resilience and contractile power ; hence a gradual yielding
to the blood-pressure, each stage of which is permanent.
Fibroid infiltration as a local affection of the heart arises from — 1.
Local obstruction to the circulation, due to local plaques of thickening,
and degenerative constriction of the coronary branches. The heart's
substance may be the seat of innumerable patches of grayish white
fibroid infiltration from this cause, or there may be one or two such
patches of larger dimensions corresponding with the territory of a larger
branch.
2. Corresponding with well - marked patches or " scars " in the
heart's substance there will often be found a complete occlusion of a
coronary branchlet from thrombosis or embolism, and in an earlier stage
the more distinct signs of a haemorrhagic infarct may be seen.
3. It is very possible that some of the heart scars which are found
may be due to a fibrous repair of partially ruptured fibres.
4. An extensive, although usually superficial fibrous infiltration of
the heart may ensue upon pericarditis and adherent pericardium, the
change beginning in the subpericardial tissue and extending more or less
deeply into the muscular interstices of the heart. Such changes are
started by direct inflammatory irritation, and are often accompanied with
a certain degree of fatty infiltration.
Pathology. — The minute pathology of fibroid infiltration of the heart
is the same, other things being equal, as that of the same process taking
place in any other organ ; that is, it begins with a proliferation of the
DISEASES OF THE MYOCARDIUM 897
nuclei of the connective tissue, so that in the earliest stage, rarely observed
except at the margins of extension, areas or groups of crowded nuclei
are to be seen which are gradually transformed into fibres ; these again
in their turn, losing their characters, form dense areas of wavy, glue-like,
interlacing processes, entangling a few nuclei. In the denser portions the
muscular fibres of the heart are completely replaced or destroyed, or
only appear as small islets of a few isolated fibres ; and towards the cir-
cumference of any local patch the muscular fibres are observed to present
broken or atrophied terminations, and to be more or less widely separated
by the intruding tissue. Here and there streaks of pigment granules
may mark the site of destroyed muscular tissue.
The process of fibroid infiltration must by no means be regarded as
in all cases a destructive lesion ; on the contrary, it is in most instances
the result of an efibrt at repair. This is most distinctly the case in
heart " scars," where the necrosed muscle, infiltrated with blood elements
which constitute an infarct, is gradually removed by absorption and
replaced in the only possible way by the growth of a living but inferior
tissue, which serves the purpose at least of healing the breach and giving
mechanical support to the heart wall. And, rightly regarded, the fibroid
infiltration more generally dispersed through the heart substance in cases
of retarded or restricted circulation is the means of maintaining the
resistance of the ventricle walls to the blood -pressure, a conservative
effort, although attended with but poor and temporary success.
In cases of local fibroid infiltration reparative of ■ necrosing infarcts,
the scars sometimes become infiltrated with lime salts, and grate under the
knife on section.
Symptoms and signs. — The symptoms of general or extensive fibroid
infiltration of the heart are those of chronic heart failure, and difiicult to
distinguish from those of fatty heart, with which, as already observed,
the disease is often associated. The patient, usually fifty or upwards,
and more commonly a man, has for some months been aware of scantness
of breath, and of oppressed feelings about the heart on exertion ; but he
has become accustomed to this, and the first symptoms compelling his
attention, and leading him to seek advice, generally supervene quite
suddenly. During some accustomed or slightly increased effort — the
walk home from business or an extra round at golf, or a tramp with the
gun over a turnip field or up a sharper hill than usual — he is seized
with severe breathlessness and oppression at the heart, which compel him
to stop and rest for a time and to get home very quietly for fear of a
further attack, of which he has some dread. The first attack may amount
to a distinct anginal seizure (see "Angina Pectoris," case 3). After this
experience his cardiac power is never on the same level as before, and often
deteriorates rapidly. His breathing fails him on slight exertion, he
becomes liable to dyspnoea on slight distension of the stomach, his face
becomes somewhat puffy and dusky in coloiu", he is apt to be awakened
at night with more or less urgent dyspnoea and wheezing, which he
regards as asthmatic. The ankles and legs become puffy and oedematous,
VOL. V 3 m
SYSTEM OF MEDICINE
and finally he is confined to his room and chair on account of the con-
stant and readily increased dyspncea.
On physical investigation the fibroid heart is always found to be
associated with other conditions in the same plane of degeneration, and
which therefore help to point to the diagnosis. Thus in extreme
emphysema, in the later stages of Bright's disease, as well as in the
early manifestations of cardio-vascular degenerations associated with
gout, intemperance, and syphilis, we often find fibroid infiltration of the
heart as a factor of importance in the illness of the patient ; indeed,
it is more than doubtful if there be such an independent disease as
fibroid infiltration of the heart.
. Diagnosis. — Having indicated sufficiently, therefore, the general
symptoms which may be attributed to this state of the heart, I may briefly
add the salient points of physical diagnosis. In the majority of cases
there is evidence of degenerative thickening of the vessels generally.
The systemic vessels are wanting in elasticity, and more or less
thickened ; the radial artery is more thick and palpable than natural ;
the pulse is not as a rule quick, it may be regular, but often it is irregular
in force and rhythm ; the pressure varies, but is not high unless it be
raised by some other disturbing condition. In cases in which the cardiac
state is secondary to emphysema, mitral stenosis, or adherent pericardium,
there may be no arterial thickening ; and the pulse is feeble, vacillating,
or compressible. Indeed, it will often interest the clinical observer to
note the big labouring heart, with no important valve lesion to waste its
force, and to contrast the work apparently done with the feeble result at
the wrist. The dimensions of the heart are increased in all directions,
the apex beat is extended beyond the line of the left nipple, the upper
margin of dulness is raised to the third space or cartilage, the right
margin of dulness extended to the median line or a finger's-breadth beyond
it. The size of the organ varies, however, of course, with the stage of
the disease, but it is always increased considerably by the time the patient
complains of symptoms. Again, in cases having their origin in cardiac
congestion from emphysema or mitral disease, the evidences of enlargement
of the right side of the heart are most considerable, the extended impulse
is most apparent towards the ensiform cartilage, and the dulness to the
right of the sternum. The presence of emphysema tends to mask the
percussion and palpation signs very considerably, and must therefore be
taken into careful account. The cardiac impulse, although somewhat
heaving, has notably less of the thrusting quality than would obtain over
a heart of anything approaching to similar dimensions from pure muscular
hypertrophy; it is also more generally diffused over the cardiac area.
In cases of difficulty in defining the limits of the cardiac outline by
palpation and percussion, a stethoscope with a small chest-piece may be
usefully employed. There is not necessarily any marked alteration in the
sounds of the heart, but the first sound at the apex is always longer,
duller, and less defined than normal, and it is often attended by a soft
murmur ; whilst the first sound at the base is barely audible, and the
DISEASES OF THE MYOCARDIUM 899
second sound there is dull, muffled, and prolonged. In mitral cases,
however, the second sound over the pulmonary area may be strongly
accentuated, although duller and less acute than in the earlier stages
of the valve disease.
There is frequently some albumin in the urine, especially in the later
stages ; and other evidence of visceral congestion from retarded circulation,
such as occasional congestion at the base of the lungs, fulness of the
hver, and the dyspeptic phenomena of slow digestion with flatulence and
loaded urine. With increasing failure of cardiac force the urine falls in
amount, and dropsical phenomena set in.
Treatment. — The treatment of fibroid degeneration of the heart is best
considered under the diseases — emphysema, angina pectoris, and failing
compensations in cardiac lesions, into the symptomatology of which it
enters as an important factor.
(S) Aiiewysm of the Aearf. ^Aneurysm of the heart is a rare condition,
and one still more rarely clinically recognisable. It is questionable
whether all the oases recol'ded by Heschl and Willigk are cases of true
aneurysm. The left ventricle is almost exclusively afiected and most
commonly (in 59 per cent) at the apex ; occasionally the septum between
the ventricles is the seat of aneurysmal bulging. The pouch varies in
size from that of a filbert to that of a large cocoarnut ; it is lined by
stretched endocardium, and contains laminated clot and more recent
coagulum.
Local destruction of the muscular fibre from any cause may lead to
aneurysm. Local softening, consequent on disease or occlusion of a branch
of a coronary artery, is commonly responsible for acute aneurysm. Cir-
cumscribed suppurative myocarditis is another cause of it. Chronic
fibrous myocarditis disposes to aneurysm when the heart wall is thin, not
when it thickens.
Dr. Wickham Legg attributes such aneurysms to fibrous degeneration
of the heart muscle, and points out that while there is abundant evidence
that this degeneration is commonly due to impaired coronary circulation,
there are yet many cases of aneurysm of the heart which occur in people
under forty years of age, in whom the coronary arteries show no change,
so that he doubts whether coronary obstruction is responsible for the
myocarditis in all cases. Hilton Fagge regarded fibrous myocarditis as
the cause of chronic aneurysm in almost all cases.
The tendency is for the sac to rupture into the pericardium, causing
death. In other cases death occurs from mechanical interference by the
sac with the movements of the heart. Spontaneous calcification and
partial obliteration of the sac may result.
(ii.) Thpombosis, Embolism, and (iii.) Aneurysm of the coronary
arteries require brief notice, although the symptomatology and diagnosis
of thrombosis and aneurysm are for the most part included in the pheno-
mena arising from atheroma of the vessels, whilst embolism is a very rare
affection, and difiicult, if not impossible, to recognise during life.
Embolism of the coronary arteries may occur under any of the con-
900 SYSTEM OF MEDICINE
ditions wWch occasion embolism of other systemic vessels; but tbe
situation of the vessels at the commencement of the aorta, the wide angle
at which they leave the vessel, and the bulk and impetuosity of the blood-
current at this portion, are all conditions unfavourable to the passage of
clot into these small side arteries.
The emboli may be of the ordinary fibrinous character, or, as in cases
of ulcerative endocarditis, may be septic. It is quite possible for debris
from a softening atheroma of the main coronary trunks to be conveyed
onwards to occlude some of their terminal branches.
Thrombosis of the coronary arteries is a frequent result of previous
atheromatous change and is also occasioned by specific arteritis. Any
portion of the vessel already thickened and narrowed by atheromatous
change may thus become more or less suddenly and completely occluded
by coagulation. Thrombosis may occur at any portion of the coronary
arteries, but is most frequently met with near their origins from the
aorta for the reason that these portions are the most common seats of
extensive atheroma. When it occurs deeper in the heart it is often
associated with gummatous arteritis.
It is to be borne in mind that although it has been shown by
Wickham Legg and West, contrary to the opinion previously current
amongst pathologists, that there is at least some intercommunication
between the peripheral distribution of the two coronary vessels, yet this
communication is very restricted, and the efiect of a complete closure
of one of the coronary arteries in any part of its course is to produce
anaemia of the territory beyond. Fringing the anaemic area and
encroaching upon it is a line of congestion or partial capiUary stasis ; but
there is no filling up of the area with blood so as to form the damson
cheese-hke appearance of recent infarcts in more vascular tissues. The
yellowish tinge of the area is that natural to anaemic muscle. A softening
from fatty degeneration and molecular necrosis of the area follows, and
haemorrhages may occur into the softened area. Microscopically the
muscular fibres are found broken up, their transverse striae are lost, and
the remains of the fibres have assumed a hyaline or waxy appearance
(Coats). The area of congestion surrounding the infarct becomes the seat
of more or less inflammatory reaction, attended with the usual proliferation
of connective tissue, and infiltration with leucocytes. The softened area
wastes (falling below the surface on section), and gradually undergoes
contraction by encroachment of fibroid growth extending from its
periphery, the semi-liquefied tissues becoming slowly absorbed ; the final
result being a heart scar of dimensions varying with the size of the
original infarct. In cases, however, where the softened territory is of
considerable dimensions, the branch occluded being large, the softened
area of the heart wall yields before the blood-pressure, and an acute
aneurysm of the heart is formed which may terminate in rupture.
The result of a partial occlusion of the coronary artery by thrombosis
or atheroma has already been described, namely, a fibrous trans-
formation of the corresponding territory ; and, in cases in which the
DISEASES OF THE MYOCARDIUM 9°!
complete occlusion of the vessel is slowly effected, the same effect is
produced.
Symptoms and signs. — The symptoms of sudden occlusion of a con-
siderable branch of the coronary artery generally begin with an anginal
paroxysm which may be fatal at once. In cases in which the first
seizure is survived, the subsequent phenomena are those of rapid heart
failure, dyspnoea with acute anginal paroxysms, rapid and more or less
irregular heart's action, dilatation of the organ to the right or left
according to the ventricle affected ; systemic and pulmonary oedema are also
correspondingly predominant. These acute phenomena almost invariably
supervene upon chronic heart difficulties already ascribed to degenerative
changes, and more or less quickly close the scene. Even the rare cases
of embolism of the coronaries have generally been preceded by the signs
of acute or chronic endocarditis, usually of the aortic valves.
Anewysm of the coronmry arteries is a disease the secondary effects of
which upon the cardiac muscle are of less importance ; the disease itself
will be treated of in the sixth volume of this work (art. " Aneurysm ").
III. Impairment due to senile changes : Pigmentary degenera-
tion; Atrophy. — (») Pigmentary degenepation. — This is a condition
seen in nearly all people above the middle period of life, but the change
is not met with in the voluntary muscles (Wilks and Moxon). The
heart weighs less than normal ; it is hard and tough, and the muscle
fibres are a dark chocolate colour. The pigment itself consists of hsema-
toidin granules of a reddish yellow colour collected about the nuclei
of the muscle fibres. Atrophic changes usually accompany the pigmenta-
tion, though the striation of the fibres is not much altered. Besides
senile states it is met with in any general emaciation (Wilks and Moxon) ;
it does not seem to impair the functions of the organ.
(i) Atrophy of the heart. — Atrophy of the heart may be part of
general wasting, as in old age or chronic disease. It may become reduced
in weight — from 9 oz. in woman, or 10 or 11 in man, to 6 or 5 oz.,
drier in texture from loss of fat and fluid, and darker in colour from the
accumulation of pigment granules about the nuclei of the muscular
fibres. Local or general atrophy may result from impaired circulation
in tortuous and diseased vessels ; but under these conditions, except
perhaps in old people, the muscular atrophy is attended with the over-
growth of another tissue — the connective. Fatty and fibroid infiltration
are both attended with more or less separation and atrophy of the
muscle proper.
TV. Impairment of the heart prom functional strain requires
little more than a reference here, since the forms it assumes are discussed
elsewhere.
Functional strain, resulting in hypertrophy, may be due to the pro-
longed endeavour of the heart to overcome some increased resistance to
the circulation, or to compensate some defect in its valve mechanism.
902 SYSTEM OF MEDICINE
Undue rigidity of the vessels, generally from atheromatous changes,
chronic heightening of the arterial blood-pressure, as in Bright's disease,
obstructed circulation through the lungs, aneurysm of the main vessel,
disease of the different valves of the heart, or congenital alteration of
one of the orifices, are amongst the chief causes leading to hypertrophy.
The hypertrophy thus occasioned cannot be strictly spoken of as disease
of the heart ; it is rather an attempt — ^for a time successful — to compen-
sate a pre-existing defect ; and the portion of the heart affected is
dependent upon the seat of obstruction in the circulation.
Hypertrophy of the heart, secondary to obstructed coronary circula-
tion or pericardial adhesions, is not real hypertrophy at all, but a
thickening of the organ due to changes (mostly fibroid) secondary to
chronic interstitial myocarditis.
Idiopathic or simple hypertrophy is a condition of muscular over-
development from excessive cardiac exercise. Allbutt has described
changes in the heart ensuing upon prolonged muscular exertion, such
as hill-climbing, athletic exercise, and the like. Perhaps the best-known
example of alleged simple hypertrophy was that recorded by Professor
Haughton in the case of the celebrated greyhound, " Master Magrath " ;
but veterinary surgeons are not yet agreed whether simple cardiac hyper-
trophy is found in horses and other labouring animals (vide p. 916).
Bollinger recorded forty-two cases of simple hypertrophy without
valvular disease — thirty-eight men and four women — in which the
hearts were one- third heavier than in health. The observations were
made at Munich, and Bollinger considers the great consumption of beer in
that eity as the chief cause of the hypertrophy, producing its effects
(a) through the toxic effects of the alcohol ; (&) by the quantity of liquid
taken into circulation ; (c) by increased nutrition. The view that the
heart (left ventricle) hypertrophies towards the end of pregnancy was first
put forward by French accoucheurs. German obstetricians denied this.
Macdonald upheld the view in this country, and Hamilton's observations
confirm the French view. The probable cause is the increased work the
heart has to do in driving blood through the enlarged uterus (Hamilton) ;
it has also been attributed to a toxic state of the blood.
Acute strain of the heart may mean either acute over-distension or
acute over-function.
In the first case, under sudden accession of the blood-pressure chiefly
arising during great effort, especially when associated with some obstruc-
tive valve defect, such as aortic or mitral stenosis, the portions of the
heart most concerned may become over-distended to the suppression of
their function. Sudden death may ensue from complete cessation of the
heart's action, or a grave embarrassment, threatening death, may only
be averted by a timely bleeding. Again, an obstructed function, less
in degree, may be to a certain point recovered from, but leaves the
heart temporarily or permanently strained. What precisely does this
mechanical strain of heart mean ? With what changes in the myocardium
is it associated ?
DISEASES OF THE MYOCARDIUM 903
In tte St. George's Hospital Reports, 1870, and in a previous paper
read before the British Medical Association in 1869, Professor Clifford
Allbutt describes the effects of overwork and strain on the heart and
great blood-vessels, especially to be observed amongst such hard labourers
as forgemen, colliers, wharfingers, etc. He also relates some cases
illustrative of the earlier stages in which, after excessive exercise in
mountain-climbing, hard gymnastics, and rowing respectively, signs of
dilatation from acute overstrain are followed by those of hypertrophy
of the heart. Professor Allbutt considers the sequence of events to
be as follows : — (i.) Dilatation of right heart ; (ii.) dilatation of left
heart; (iii.) hypertrophy of one or both ventricles ; (iv.) chronic inflam-
matory endarteritis of the aorta; (v.) dilatation of the aorta; (vi.) in-
competency of the aortic valves ; (vii.) further left ventricle hypertrophy
compensating aortic defect; (viii.) degenerative changes ensuing upon
hj^ertrophy. (Fide sltU "Mechanical Strain," p. 841.)
Mr. Myers in 1870, in a paper on "Diseases of the Heart among
Soldiers," drew attention to the effects of prolonged exertion in tight-
fitting uniforms, and especially whilst wearing the tight breast-strap, in
producing cardiac and aortic diseases from overstrain.
Da Costa has described a condition of " irritable heart " as of very
common occurrence in soldiers during the fatigues of a campaign, and
observed by him especially amongst the soldiers in the American Civil
War. A persistently quick action of heart, with precordial and left
shoulder pains, and bouts of severe palpitation under slight exertion, or
digestive disorder, are the principal symptoms. At first these are un-
attended with any notable physical signs, and they may subside without
such signs ; but in the cases of greater severity or longer duration there
is obvious enlargement of the heart. The pathology of these cases
would no doubt be for the most part the same as that described by
Allbutt, namely, a chronic myocarditis ensuing upon dilatation and
mingled with muscular hypertrophy; but probably there is also some
direct damage to the cardiac nerves, originating at the terminals of the
vagi and sympathetic. (Fide Soldier's Heart, p. 851.)
V. Impairment of inflammatory origin. — (a) Interstitial myo-
earditis. — Myocarditis most generally consists of an irritative overgrowth
of the interstitial connective tissues of the heart, which may extend from
a pericarditis or an endocarditis. In its first stages an increased nuclear
proliferation, permeating the muscular fibres, causes a " cloudy swelling "
of the tissue, and a certain degree of increased softness to the touch,
but the later result is more or less fibrous toughness of the part
involved.
Disturbed circulation, general or local, will occasion cardiac fibrosis •
such as chronic congestion of the cardiac veins, or restricted or obstructed
circulation through the coronary vessels. The cicatricial or tendinous
patches of the heart are produced by interstitial myocarditis. An
impairment even to destruction of the true muscular fibres of the
90+ SYSTEM OF MEDICINE
heart necessarily ensues upon local or general fibrous myocarditis.
Dr. Charlewood Turner has pointed out that interstitial myocarditis
may exist and extend apart from any affection of the pericardium or
endocardium, and that in cases of dilatation of the heart or failing
hypertrophy, from whatever cause, this morbid process is at work and
responsible for further changes; lastly. Dr. Turner points out that
the occurrence of recent exudative and older fibroid changes close
together in cases of valvular disease and secondary to Bright's disease,
indicate the one change as being the initial stage of the other.
(h) Parenchymatous myoearditis, which is met with in certain cases
of septic poisoning, such as pyaemia and diphtheria, is probably but
a very active form of the preceding process in its earliest stages.
Professor Leyden has studied this lesion most carefully, and regards
it as an acute myocarditis characterised by intermuscular nuclear
proliferation and by secondary atrophic changes towards necrosis and
deposition of pigment ; fatty degeneration of the muscular fibres accom-
panies it, possibly in consequence of the inflammatory changes. This
form of myocarditis is always secondary to infective fevers, such as
diphtheria, scarlet fever, and the like ; and has been met with in greater
or less degree in all acute febrile diseases, rheumatism, cerebro-spinal
meningitis, variola, erysipelas, malaria, septicaemia, influenza, and so
forth. In enteric fever and in gonorrhoea the respective specific bacUli
and cocci have been found in the heart.
(c) Purulent myoearditis is in most cases secondary to infective
embolism of the coronary vessels ; as in pyaemia, and ulcerative endo-
carditis. In all cases infective microbes are conveyed to the cardiac
muscle through the coronary arteries, and set up foci of virulent
myocarditis resulting in minute or larger suppurations.
{d) Syphilitic myocarditis. — Syphilitic myocarditis almost invariably
occurs either in the immediate neighbourhood of a gumma or secondary
to and in the territory commanded by a specific arteritis. Attention
was first drawn to the occurrence of syphilitic lesions of the myocardium
by Sir Samuel Wilks in 1856; and many isolated cases have been
reported since at the Pathological Society of London and in various
English and foreign medical journals. Our knowledge of the disease,
however, is mainly derived from the post-mortem observation of eases
in patients, by no means all of whom died with heart symptoms.
Syphilitic disease afifects the myocardium in one of three ways, and
either singly or combined : —
(a) There may be syphilitic arteritis and secondary or combined
chronic myocarditis.
(/8) There may be gummatous formation in the heart waU, around, and
extending from which chronic myocarditis takes place.
(y) There may be a difiused chronic myocarditis of specific nature
afiecting a considerable portion of the heart. It is doubtful, however,
whether this latter form of diffused syphilitic myocarditis does not
originate in scattered gummatous depositions.
DISEASES OF THE MYOCARDIUM 90S
Syphilitic arteritis of the coronary vessels does not differ from
similar arteritis elsewhere. The endocardium is only affected in cases
in which there is subjacent gumma of the muscle, and the pericardium
as a rule also only in connection with such gummata or gummatous
affections of the vessels. Pericardial adhesions in syphilitic subjects
are, however, not uncommon. Syphilitic disease, limited to the valves of
the heart, is almost unknown, but the aortic valves frequently partake
with the aorta in an endarteritic thickening having its origin in the
syphilitic cachexia.
With the undue rigidity, actual narrowing and occasional thrombosis,
with which coronary arterial diseases of syphilitic source are attended,
we find fibrous degeneration, dilatation, angina pectoris, and so forth, as
later consequences.
Gummatous formations may occur in any part of the heart, most
commonly in the ventricles or septum. They have the usual features
and ill-defined microscopic characters of gummata elsewhere ; they may
soften, or undergo fibroid change, and they are always surrounded by
more or less spreading fibroid condensation of the heart wall from
associated chronic myocarditis.
It cannot be said that any symptoms have yet been formulated which
in their grouping or individual significance are characteristic of syphilitic
disease ; and for the obvious reason that very different portions of the
heart may be affected in different cases, and that the upshot of the
morbid condition in each case is a spoiling of the cardiac muscle at the
part affected, and more or less interruption or spreading disturbance of
the cardiac mechanism therefromi.
Functional irregularity, anginal seizures, syncopal attacks, any of
which may prove fatal, are amongst the most common symptoms. It is
remarkable that sudden death has terminated a large proportion of the
recorded cases of gumma of the heart in most instances without any previous
recognition of the disease. The first case recorded by Sir Samuel Wilks
ended in death in this way, as did fourteen out of twenty-five cases recently
collected by Dr. S. Phillips. Enlargement of the heart, or displacement of
the apex beat to the left, or more marked evidence of enlargement to the
right, are amongst the later signs ; especially in cases of the more
diffused form of syphilitic myocarditis.
The absence from the history of the case of rheumatism, of gout, of
alcoholism, or strain ; and evidence — whether in the form of a distinct
history or of collateral lesions of a specific kind — pointing to a syphilitic
cachexia, are circumstances which, in the presence of such signs and
symptoms of cardiac disease, may lead us to suspect its syphilitic nature,
and to direct our treatment to that probability. When the signs and
reservations with regard to such heart diseases as are above spoken of
are found in men, and before middle life (nicotine poisoning being
also excluded), an additional argument in favour of syphilis will be
found. The success of antisyphilitic measures of treatment, which,
however, would be combined with cardiac tonics, strychnia, digitalis.
9o6 SYSTEM OF MEDICINE
iron, or arsenic appropriate to the case, would further help the
diagnosis.
VI. TuMOUES OF THE MYOCARDIXJM. — The heart is one of the
organs least commonly affected by new growths. Primary growths are
exceedingly rare, but sarcoma, myxoma, fibroma, carcinoma, and fatty
interstitial tumours have been met with. Tubercle, common in the
pericardium, is rare in the heart substance, and then occurs almost
exclusively as an accompaniment of general tuberculosis. Moreover, the
heart is but rarely invaded by secondary growths. Round-celled sarcoma
is occasionally to be met with, extending apron-like over the pericardium,
greatly thickening it, and embedding the great vessels, yet not invading
the heart itself. Carcinoma of the lung and mediastina frequently
invades the parietal pericardium in cauliflower-like excrescences, and
yet spares the heart. Sarcoma sometimes invades the heart from the
mediastina along the sheaths of the coronary vessels and their ramifica-
tions, penetrating into the intermuscular tissue and separating the cardiac
fibres, causing them to atrophy (Boyce). Secondary cancerous deposits,
both epithelial and medullary, have been met with in the substance of
the heart at post-mortem examinations.
VII. Parasites. — Hydatid is rarely met with in the heart of the
human subject, but it does occur, as does also cysticercus cellulosae.
The cysticercus of taenia solium is common in the heart of swine, and
that of taenia mediocanellata in cattle ; but they are rare in man.
Actinomycosis may extend to the heart from the mediastina and
lungs.
Trichina spiralis, according to Wilks and Moxon, is never found in
the heart, or extremely rarely.
E. Douglas Powell.
REFERENCES
I. Impairment secondary to general blood conditions, (a) Anaemia, {b) Toxic
changes: 1. Coats. ManvM of Pathology, 1895, p. 435. — 2. Hamilton. Text-Boole
of Pathology, 1889, pp. 581 and .588. — 3. Scheobttbr. Ziemssen's Cyclopaedia, vol. vi.
p. 246. — 4. ZiEGLER. Lehrluch des pathologischen Anatomie, Bd. ii. p. 38. — II.
Impairment secondary to altered blood-supply : 5. Coats. Manual of Pathology, 1896,
p. 427. — 6. Lbgg. Bradshaw Lecture, 1883. — 7. Steven". Lancet, 1887, p. 1153 ; and
Journal of Pathology, vol. ii. p. 190, 1894. — 8. Turner. Internal. Med. Congress,
1881. — 9. Weber, Hermann. Virchow's Archiv, xii. 1857, p. 326. — 10. Wilks and
Moxon. Pathological Anatomy, 1889, p. 127. In the paper of Wickham Legg will
be found references to complete literature up to 1883, and in those of Steven for the
ensuing ten years. III. Impairment due to senile change : 11. Balfour. The Senile
Heart. — lla. Oertel. " ]&-eislaufs-Stbrungen, " V. Ziemssen's Haiidiuch, B. iv. 1891.
— 12. QuAiN. " On Fatty Diseases of the Heart," Med. and Ohir. Soc. Trans, vol. xxxiii.
1850, and Dictionary, 1894. — 13. Wilks and Moxon. Pathological Anatomy, p. 123.
IV. Impairment arising from functional overstrain : 14. Allbutt, Clifford. St.
George's Hospital Reports, vol. v. 1870. — 15. Coats. Manual of Pathology, 1895, pp. 436
and 440. — 16. Da Costa. Amer. Journ. of Med. Science, 1871. — 17. Douglas Powell.
Brit. Med. Journ. 1894, ii. p. 1034.— 18. Hamilton. Text-Book of Pathology, 1894, vol. i.
pp. 649 and 650.— 19. Leyden. Zeitschrift f. klin. Med. 1886, Bd. xi. p. 105.-20.
Myers. Disease of the Heart among Soldiers, 1870. — 21. Peacock. Croonian
DISEASE OF THE AORTIC AREA OF THE HEART 907
Lectures, 1865.— 22. Seitz. Deutsch. Archiv f. Telin. Med. 1873, Bd. xi. p. 485 ;
1874, Bd. sii. pp. 143 and 297. V. Impairment of inflammatory origin, (a) Simple
or Secondary: 23. Coats. Manual of Pathology, 1895, p. 441.— 24. Hamilton.
Text-Book of Pathology, 1889, vol. i. p. 589.-25. Huchabd. Maladies du cosur,
p. 194.— 26. Lbydbn. Zeitschrift fii/r klin. Med. iv. 1882.-27. Rboklinghausbn
and others. Verhandlungen des X. internatiojialen Tried. Congress, Berlin, 1890, Bd.
ii. Abth. 3, p. 67. — 28. Renaut. Bulletin de Vacadimie de mid. vol. xxiii. 3 s,kv.
p. 345. (6) Syphilitic: 29. Coats. Manual of Pathology, 1895, p. 463.— 30.
Hamilton. Text-Book of Pathology, 1889, p. 592.— 31. Jacquinbt. Gaz. des h&p.
Paris, 1896, p. 917.— 32. Phillips. Lancet, 1897, i. p. 227.-33. Wilks. Path.
Sac. Trans. 1856, vol. viii. p. 24 ; Guy's Hasp. Rep. 3rd series, vol. ix. 1863. VI.
Growths and Parasites : 34. Botoe. A Text-Book of Morbid Histology, 1892, p.
215. — 35. Coats. Manual of Pathology, 1895, p. 464. — 36. Hamilton. A Text-
Book of Pathology, 1889, vol. 1. p. 593. — 37. Paolowsky. Berliner kUn. Wochenschrift,
1895, p. 393.— 38. WiLKS and MoxoN. Pathological Anatomy, -g.liZ.—ZQ. Zieglee.
Lehrbuch der patholog.- Anatom. 1895, Bd. ii. p. 46.
E. D. P.
DISEASE OF THE AOETIC AEEA OF THE HEAET
In formal presentation of this subject it is customary to divide it into
two parts — into aortic stenosis and aortic regurgitation. To carry out
this division, however, leads to some embarrassment : on the one hand,
by far the larger number of cases of aortic regurgitation are attended
with signs of interference with the issue of blood from the left ventricle ;
on the other hand, cases of stenosis of the aortic orifice may be attended
with regurgitation. Again, the causation of the two evils is similar if
not identical, and the determination of the one or the other event may
be accidental ; so that, although the clinical features of the two events,
taken singly, are very diiferent, as the two are often coincident it seems
more convenient to take them together except in those sections in which
their distinction becomes imperative.
Subject. — By aortic regurgitation we mean that in diastole some of
the blood driven into the aorta returns to the left ventricle ; when we
hear the sound characteristic of this disorder the inference that the aortic
valve is out of order is almost irresistible. A definite diastolic murmur
heard in the areas of the murmur of aortic regurgitation is perhaps the
surest diagnostic indication of its kind. Not so with aortic systolic
murmurs : of such signs these are perhaps the least definite. I need
not say that an " aortic systolic murmur " may not be significant of
organic disease at all ; or if significant of disease about this orifice the
alleged stenosis may be more apparent than real, the murmur may
signify no more than a roughness or other deformity of the part im-
plying no constriction of the orifice ; nay, it may be consistent with
dilatation of the orifice. Clinical clerks are far too ready to assume
aortic stenosis in all cases of organic disease of this orifice revealed by a
direct murmur ; aortic obstruction, though open to some objection, is a
better name.
9o8 SYSTEM OF MEDICINE
Causation. — The causes of the diseases of the aortic area of the heart
(omitting congenital malformation, which is dealt with in another article,
p. 697) are chiefly three; namely, infectious diseases, mechanical strain,
and atheroma.
Infectious diseases. — Of these, rheumatism, if of such it be, is the chief ;
syphilis perhaps comes second, for the poison of the other infections, such as
diphtheria and influenza, fall rather upon the muscular structure of the
heart than upon its valves or orifices. Syphilis will be considered presently.
Acute endocarditis has been dealt with already, and Dr. Dreschfeld
describes a case in which infective endocarditis fastened upon a ruptured
aortic valve (p. 882). In its liability to disease, and in the nature of it,
the aortic area of the heart is so bound up with the aorta itself that for the
consideration of some part of the present subject the reader is referred to
the chapters in the sixth volume on " Diseases of the Arteries " and on
" Aneurysm " respectively. This community of suffering is seen especially
in the cases of atheroma and of syphilis. Indeed, whether the aortic
orifice is ever attacked by syphilis primarily and more or less exclusively
is still a matter of some doubt. Pathological histology has not yet
enabled us by inspection to recognise the differential characters of
syphilitic disease. Gout and its associates, such as plumbism, seem to
produce lesions not distinguishable from " atheroma," under which easy
fitting name their agency may be included.
Acute rheumatism is by far the chief cause of aortic disease in persons
under middle age ; as is atheroma in those over this time of life. It
is admitted, however, that acute rheumatism falls first, and as it were by
preference, upon the mitral valve ; when the aortic valve is implicated
it usually suffers with the mitral, or after it. That acute rheumatism
should attack the aortic valve primarily and exclusively is not unknown
in our experience ; we see it occur thus even in women, but it is
unusual. With the mitral valve I need not say the reverse is
the case : it may almost be called a rule that acute rheumatism
of ordinary severity maims this part of the heart without implicat-
ing any other part ; though the proximity of the mitral valves to the
aortic, and the bond of fibroid tissue between them may gradually lead
to an extension of chronic inflammatory or sclerotic change from the
one area to the other — from the mitral to the aortic — without direct co-
operation of the specific rheumatic factor. In other cases the simultaneous
implication of both areas, or the rapid succession of inflammation in the
two, together with the severity of the heart symptoms, indicates that the
cause of the aortic inflammation is directly rheumatic. Yet even thus
the invasion of the aortic valve in women is so much rarer than in men
— that is, the coexistence of both mitral and aortic rheumatism is so much
commoner in men than in women — that we are led to infer the not in-
frequent presence of some other factor in the double valvular disease,
besides the acute rheumatism. This factor may well be mechanical
strain. Some cases indeed of coexistent mitral and aortic disease
after rheumatism we may regard as confirmatory exceptions ; such, for
DISEASE OF THE AORTIC AREA OF THE HEART 909
instance, as the concurrence of aortic disease in women engaged in labours
harder than those usual in the sex — in women who have worked in the
fields, in washerwomen, in women employed in brick-making, or on the
bank-tops of mines. Making every allowance in such cases for the
greater exposure to weather, there seems to be a greater prevalence of
aortic mischief in such women after acute rheumatism than among women
who have led lives of less muscular stress. I have not found that either
in alcohol or syphilis we have factors to invalidate these propositions ;
but to pursue them much farther would be to trench upon the subject of
endocarditis entrusted to abler hands than mine : suffice it to say that
I conceive that although in an unusually severe attack of acute rheumatism
both sets of valves may be attacked, whether .directly in each area or by
extension from the mitral to the aortic, yet in ordinary attacks, if the
aortic valve be involved as well as the mitral, it will often appear that
the patient, either in work or play, has been wont to put out considerable
muscular exertion. Disease of the aortic valve alone is a most unusual
event in the young subjects of chorea (of 250 cases Gowers found aortie
regurgitation in two, and obstruction in one), whose muscular efforts
are fitful, not exacting j indeed its association with mitral disease in this
disease is rare enough.
The predominance of rheumatic inflammation on the left side of the
heart is often explained likewise by the fact that mechanical stress falls
more hardly on these valves than on those of the right side, and so. it
may be ; yet it is not easy thus to explain this preference : are we to
assume that muscular labour in these persons had already produced some
cardiac strain, and that before the rheumatic attack these structures were
more or less impaired ? This would seem to be a grave charge against
the physical uses of the body ; a charge which on the face of it seems
unreasonable, if so be that without the rheumatism no harm would have
come of them. A remote suspicion of such a deterioration can scarcely
justify us in discouraging all exercises beyond nursery games. Short of
lesion one would anticipate that increased work would enhance nutrition,
and thus fend off rather than invite the approach of disease. Roy's
article on the elastic properties of the arterial wall may, however, be
usefully consulted on this problem.
Syphilis is probably concerned in the causation of many cases of aortic
disease, though, except when it exists in the form of a definite gumma,
we have no certain test of the syphilitic process, whether in the living or
in the dead body (p. 905). How large a factor, however, syphilis may be in
arterial disease will be shown by Dr. Mott in the article on this subject in
the next volume. Dr. Parkes "Weber (95) finds that syphilis is apt to be
the starting-point of atheroma. For many years I have been wont to infer
from the state of the radial artery the effects of syphilis on the vessels
of almost every man who had been saturated with this poison ; and such
surmises have been reinforced by the more direct observations of Dr. George
Oliver. We can scarcely suppose that a destructive agency, so active as
we know it to be in all other arterial regions, should be without effect in
gio SYSTEM OF MEDICINE
tte aortic area of the heart ; yet in deciding in a particular case that an
aortic lesion is syphilitic, we are confined to the inferences which may be
drawn from the story of the case or from associated changes elsewhere —
which indications may, indeed, bring us to a moral certainty. We know
that a comparatively young man of otherwise healthy habit does not suffer
from local disease of the aortic region of the heart unless it be in conse-
quence of extraordinary muscular stress, of rheumatism, or of syphilis ; so
that although there may be no direct means of detecting the syphilis,
yet if muscular stress and rheumatism be both denied, we fall back
upon syphilis as we do with some assurance in the case of aortic
aneurysm in such a person ; the inference, pathologically speaking,
may not be positive, but it is usually justified in practice. The following
case illustrates these remarks (w^« also art. "Tabes Dorsalis," in a
following volume) : —
Dr. Pye-Smith reported a case of a man, aged 32, who died with heart
disease, the physical signs being those of aortic obstruction and regurgitation.
Hheumatism and chorea were excluded. Atheroma was improbable owing to
the comparatively young age of the patient, who was, moreover, not subject to
laborious work. After death there were no signs of rheumatic or infective
endocarditis, but a patch of recent aortitis and deformity of the valve. The
lesion was soft, injected, with a swollen, crescentic margin suggesting the
advancing edge of a secondary syphilitic eruption of the skin ; there was no
atheroma. The only other evidence of syphilis was a fibroid condition of the
testicles, though this was not very marked. He suggested that the syphilitic
aortitis had spread to the valve and so produced the disease in question (70).
Atheroma. — A full discussion of the nature and fashion of this disease
or chapter of diseases of the arteries is deferred to the next volume.
Here we may ask whether the disease of the aortic orifice sheds any light
on the origin of this insidious and rather peculiarly human disease.
Does it appear that muscular labour plays any important part in the
origin or determination of the change ? For my own part I cannot say
that, likely as it may seem at first sight, there is much evidence in favour
of this hypothesis. It is true that this disease also is found more or
less exclusively on the left side of the heart — the side of stress ; it is
also true that atheroma may be the ultimate form of arteritis of
whatsoever origin — rheumatic, syphilitic, or mechanical — mechanical, as in
the pulmonary artery in mitral stenosis ; still we must admit that
atheroma is as likely to occur in the elderly lady who has spent her life
in trotting amiably about the parish, as in her husband who has ridden
for his falls, felled his own trees, and stumped about after his birds from
his boyhood.
Again, atheroma is by no means constant or approximately uniform
in its position : although well marked, no doubt, on the greater curvature
of the arch where tensile strain is highest, and at bifurcations and re-
flexions, yet it does not by any means confine itself to the parts which
receive the main stress of muscular exercise, or to parts where, elastic
tissues being most abundant, tone is least and tension most. On the con-
DISEASE OF THE AORTIC AREA OF THE HEART 911
trary, it is one of the surprises of practice to find it in all sorts of
odd areas ; and within such areas it is patchy. If in one necropsy the
cerebral vessels are like branched corals, in another, with atheroma
enough elsewhere, the cerebral vessels seem clean enough. In one body
atheroma is abundant about the region of the heart ; in another, the heart
and its orifices are fairly normal, but extensive patches of atheroma are
discovered in the abdominal aorta or in peripheral areas of the arterial
tree. Such contrasts are too well known to need the support of recorded
cases in this place.
Again, is it that the main cause of atheroma of the heart is mechanical
stress, yet stress due not to muscular exercise, but to that more persistent
high arterial pressure of constitutional origin which may be established as
well in the squire's wife, with her indolent habits and gouty inheritance, as
in the sportsman himself who works off his meat and drink day by day in
the fresh air ? Is the comparative freedom from atheroma enjoyed by
animals to be attributed to the fact that they do not suffer from chronic
high arterial pressure ; that they have exercise enough — muscular stress
enough, many of them — but are fed by their owners, and fed therefore
economically ? Certainly we see daily that hard exercise keeps the iU
effects of a too vigorous appetite at bay. This is clinical gossip, I fear,
rather than science ; but we cannot at present get much nearer to the facts.
Frequent high blood-pressure, then, as in excessive muscular stress, and
more persistent high pressure due to luxus-consumption relative or posi-
tive, to gout (especially in its non-articular forms, for the frank articular
form of gout leads less surely to high arterial pressure), to lead poisoning
(by way of gout), and possibly to certain products of metabolism engen-
dered in old and defective organs or tissues, may produce atheromatous
changes which often involve the aortic region of the heart, directly by
friction and local irritation as in central and distal arteries, or indirectly
by more immediate mechanical strain as in more central arteries. To quote
Dr. Balfour, " there is a consensus of opinion that the arterial system is
that upon which the finger of decay is first laid." We see daily in the
post-mortem room, yet still with some surprise, how readily the heart
even of an old man may take upon itself no puny hypertrophy; It is no
unusual thing to find a big heart, and one big with no bad stuff, in old
^sons subjected in later life to increased blood-pressure, even when the
corona,ry arteries have undergone some measure of deterioration ; in such
cases the aortic valves, even if competent, are practically always thickened.
Still, with all this, can we say that aortic regurgitation, common as the
disease is, is frequently found in the decay of elderly persons ? I think
not ;• on the other hand, it seems much less common in them than aortic
obstruction — by which I mean no more than the presence of an organic
direct murmur ; now an aortic systolic murmur may continue as long as
life holds together, and afford one of the many evidences of the long
story of cardio-arterial degeneration. This form of aortic disease is rarely
of itself the immediate or proximate cause of death ; we may call it
but an accident in the course of a general cardio-vascular involution,
912 SYSTEM OF MEDICINE
which was described almost as well by our grandfathers, before ausculta-
tion was a popular accomplishment, as by ourselves.
Muscular strain. — The effect of bodily exertion in producing disease
of the heart, which was apprehended by Morgagni, had again been
overlooked in the study of the effects of rheumatism until attention
was recalled to the subject by Peacock (64). Myers, Da Costa, Seitz,
James Barr, and others, including myself, followed in the investigation.
That muscular exertion is among the causes of aortic disease, and
especially of aortic regurgitgition, is now admitted on all hands. If, indeed,
a man under forty-five years of age presents symptoms of aortic re-
gurgitation without mitral disease, and without indication of syphilis,
we may well suspect that muscular effort in one way or other initiated
the disease. [Vide also art. " Mechanical Strain of the Heart," p. 841.]
That sudden muscular stress may damage the healthy aortic valve,
even to the point of rupturing a limb of it, is now well known ; the
accident is not uncommon, and the cases on record are so many as to
make it unnecessary to cite examples of it. Peacock in his Croonian
Lectures adduced seventeen such cases. It is more difficult to estimate
or to apprehend the part taken by muscular strain in the production of
aortic regurgitation of insidious origin. When a vigorous and fresh-
complexioned man of some thirty-five years of age, carrying a heavy
patient on a sudden emergency up a flight of stairs, feels a sense of some-
thing having given way inside his chest, and becomes suddenly breathless
and oppressed; when thereafter a murmur of aortic regurgitation is
heard, which murmur continues to the end of a life prematurely cut
short by this disease ; when, moreover, no trace of syphilis can be even
suspected by himself or his medical friends, we can scarcely err in deciding,
in accordance with many other cases of the kind, that by the sudden stress
he strained and ruptured a previously healthy valve. Again, when a young,
slightly-built housemaid of very healthy stock presents the ordinary signs
of aortic stenosis without any other lesion, and no rheumatism, chorea,
or other sign of infectious disorder is to bp heard of ; and when, again,
she tells a clear tale of a sudden sensation of pain and distress in her
chest, while she was lifting a heavy bed, from which moment she
became incapable of exertion, can we avoid the conclusion that during
this effort an acute valvulitis was set up with subsequent constriction ? ^
Peacock also stated that aortic disease is to be found in young women
servants subjected to straining efforts before they are fully grown.
Such cases scarcely admit of more than one interpretation. Inter-
pretation is less easy when, in a person the subject of aortic regur-
gitation, we learn first that there is no definite story of a sense of injury
on any one occasion ; that the oppression came on more or less insensibly ;
that the patient has been in the way of syphilis, of alcoholic excess, or
' This patient has been in Addenbrooke's Hospital twice at least, and during the
University examinations her case has been investigated by many physicians ; and the view
here given of the causation of the mischief generally accepted. The signs are those of
stenosis of the aortic orifice, and the symptoms those of increasing "stenocardia."
DISEASE OF THE AORTIC AREA OF THE HEART 913
of some other cause of arterial degeneration, while, at the same time,
he has been following a laborious employment : yet we may fairly pre-
sume, perhaps, that in many such cases muscular stress and decay
together have gradually impaired the valve to the point of insufficiency.
As I have said, senile decay alone does not usually cause aortic regurgita-
tion; more commonly it produces disease of the aorta with implica-
tion of the orifice, which is betrayed by a direct murmur. When,
therefore, we find that regurgitation occurs rather in persons under fifty
years of age, of the laborious sex, and especially in men who have been
engaged in heavy toil, we cannot escape the suspicion that muscular
stress, if not the sole or always the chief agent in these cases, is at any
rate a potent determining cause. Acquired aortic disease in children is
one of the rarest of clinical cases ; even in the acute rheumatism of
women and children we have noted that the mitral valve is affected first,
and that if the aortic be involved it is as it were by overflow (p. 908).
Once more, if not infrequently, yet almost exclusively in men, we dis-
cover that aortic insufficiency establishes itself in patients under the age
of senile degenerations, free from evidence of syphilis or other infection,
including rheumatism, and telling no story of sudden rupture, shall we
not be justified, at any rate in the large majority of instances, if we
suppose that the disease may be attributed to the accumulated effects of
muscular strains recurring at longer or shorter intervals over a number
of years ? Finally, if a man of irregular habits, and deteriorated tissues,
describes to us the symptoms of sudden rupture of the aortic valve,
we may reasonably infer that an effort, inadequate to rupture a healthy
aortic valve, had sufficed to rupture a valve already impaired.
Thus, in the causation of aortic insufficiency due to muscular strain,
we are led to recognise three classes, namely, acute rupture ; chronic
forcing of a valve previously impaired by some constitutional poison, such
as syphilis ; and chronic forcing of the valve by the importunity of re-
peated strains none of which alone was sufiicient to break down a healthy
valve, but all of which, by molecular rather than massive strain, con-
tributed gradually to increase valvulitis and to break down the resistance
of the part. The condition of the tricuspid valve in protracted cases
of mitral stenosis is an excellent example of chronic valvulitis due to
stress. As in the case of the housemaid mentioned in the last paragraph
but one, this strain of the tricuspid tends to stenosis. We may note in
passing that, in respect of prognosis, it is important to know whether and
for how long the ruptured valvular limb is supported by tissues other-
wise healthy. Although I have said (p. 910) that atheroma as a general
disease of the arterial tree is not due, in the main, to muscular stress, yet
local atheroma very often has this origin ; it is indeed the common result
of more than one kind of chronic arteritis.
It has been alleged that prolonged acceleration of the heart, as in
Graves' disease, may produce the valvulitis of strain ; but unless the sum
of work done be considerably increased, which is not usually the case,
such a result is not to be anticipated.
VOL. T 3 N
914 SYSTEM OF MEDICINE
External violence. — Finally, one or more of the aortic crescents may be
ruptured by a blow on the outside of the chest. Within my own ex-
perience blows or crushes resulting in the split of a vessel after this
manner have produced aortic aneurysm, not rupture of an aortic valve ;
still there are many cases of this kind on record. I distinctly remember,
indeed, in the Leeds Infirmary a case of mitral stenosis which, after the
closest inquiry, we confidently attributed to the Idck of a horse in the
cardiac area; the patient was a young man, and the symptoms were
long in declaring themselves ; yet the connection between antecedent
and consequence seemed inevitable (p. 864). Dr. L. Heidenhain of Greifs-
wald has studied these cases ; his conclusions are that, with or without
injury to the ribs or obvious external bruising, an external blow may (a)
rupture a valve in the heart, may (6) damage or rupture the cardiac
muscle, or rarely (c) set up a stenosis by insidious endocarditis. Sir
Samuel Wilks has recorded a case of this kind which occurred in a youth
aged nineteen : a blow on the chest ruptured the posterior cusp of the
aortic valve from its free margin to its base. A small deposit of fibrin
had begun to form on the raw edge. An analogous case, in which the
heart itself was ruptured in a lad of sixteen, by a blow on the chest which
caused no external bruise, has been reported by Dr. William Groom of
Wisbech, and the preparation is now at Cambridge. Potain argues that
if a blow, such as a jockey received who was heavily thrown so that his
chest smote the ground, rupture an aortic cusp, the heart at the moment
of the blow was in systole and the aorta distended. In cases of rupture of
the mitral valve in like manner, of which he records two, he conceives the
heart to have been in diastole when the blow fell, and the ventricle full.
Nervous shock. — In the earlier medical writers, not in the poets only, we
often meet with the assumption that intense emotion may be attended with
injury to the heart. In any careful consideration of this point we should
divide the question : we should first consider injury due to interference
with the circulation itself more or less directly ; as, for example, by such
an effort of the inspiration as to force the intra-thoracio negative pressures
to an extreme ; and, secondly, indirect interference through the nervous
system. Of the first kind of case I remember a strange example in
the West Riding Asylum at Wakefield. A woman, afilicted with
violent mania, one day in a fury held her breath preparatory to an out-
burst; she became livid, fell to the ground, and died (93, p. 146). At
the necropsy it appeared that death was due to extreme fulness and
dilatation of the right heart and vense cavse, though it is possible that it
was due to a fulminating shock, by way of the vagus nerve, arresting the
auricles. Of death through the heart, clearly dependent upon nervous
shock alone, I have no experience. All that we know, as yet, respecting
nervous influence on the mechanics of the heart, is that vagus shock by
diminishing auricular contractions lessens the output of the heart, which,
is also slowed, and its diastole enlarged. This for the heart is a con-
servative function, but it is conceivable that, even in a healthy adult, it may
be carried too far. The depressor effect, produced through dilatation
DISEASE OF THE AORTIC AREA OF THE HEART 915
of the splanchnic veins, could scarcely harm the heart. The accelerator
nerves are probably stimulated during emotion, which, as we all know,
quickens the rate of the heart ; but if, as we may presume, the out-
put is proportionally less, and the resistance less rather than more
(if the depressor be influenced also), no excessive mechanical strain
thus falls on the organ. Augmentor action is too little understood
to allow us to argue conclusively about it. Intense emotion might
be attended with a universal or very widespread constriction of the
peripheral vessels by which blood -pressure might perhaps be danger-
ously raised ; if such a constriction occurs, however, it is transient, and
relaxation of these vessels and of the sphincters seems to be the ordinary
eifect. Moreover, we see no great cardiac distress during a rigor, or
after many returns of quotidian ague. So far as experiment goes, it
would seem indeed that nervous shock tends to lower the blood-pressure.
Finally, it is a reasonable surmise that some deterioration of the nerves
or their centres, due to prolonged mental distress, might be followed by
fatty degeneration of the cardiac muscle ; such a process scarcely comes
under the head of aortic strain, and it is at least as. likely that such
impairments of its nutrition take place by way of the blood. What may
be the truth concerning these problems, however true it may be that
prolonged grief may invalidate the chambers of the heart, such evidence
as we have, physiological and clinical, seems to indicate that the aortic
machinery at any rate is subjected to no especial stress, but, perhaps,
rather the reverse.
Pathogeny and Morbid anatomy. — Whether the heart be liable to
undergo primary hypertrophy under normal or relatively normal con-
ditions is one of the most important problems which meet us at the
outset of this section. The answer to the question is not yet given ; but
the opinion that it is so liable is not without strong support (p. 903) : so
far, indeed, as my reading goes, I think that the affirmative opinion is
gaining ground. For my own part, I find that to be assured of the lesser
degrees of hypertrophy of the left ventricle is a much more difficult clinical
task than I used to suppose ; unless, of course, the hypertrophy be attended
with notable dilatation, and a clinical dilatation would surely forbid us to
describe the conditions even as quasi-normal. Unless the person under
observation be an inordinate drinker of fluids, alcoholic or other (p. 902),
there seems no reason to anticipate increase of the mean ventricular out-
put ; if, however, the sum of the conditions of resistance is higher in
amount than under ordinary circumstances, the supervention of hyper-
trophy may be explicable ; and in this case distension might no more take
place than under the fluctuations of output in persons leading a life in
which muscular stress is not an important condition. Prolonged exer-
tions in untrained men make themselves felt, as we have seen (p. 849),
by more or less uncompensated dilatation ; but perhaps in men such as
sprint runners, putters of weights, wrestlers, and the like, in whom
sudden and repeated efforts, under which initial rises of pressure are
frequent, bear a large proportion to more regular exercises, the mean blood-
9i6 SYSTEM OF MEDICINE
pressure may rise, as the maxima are high and of very frequent recurrence.
If this be so, simple hypertrophy may follow, though I find such a result
very difficult to verify. However, healthy men do not come to the doctor,
and in unhealthy men the conditions no longer apply. In slim, long-
chested youths with wide costal interspaces a thumping or uncovered
heart may well be mistaken for a hypertrophy ; and a great many young
men have rather thudding hearts. Whatever books may repeat, it is no
easy task to appreciate a moderate hypertrophy of the left ventricle, so
many are the sources of error, as for instance in the relation of lung to
the cardiac area, in chests of different build. Violence of impulse is by
no means directly related to the volume of the heart or to the blood-
pressure ; the " heave " in the impulse, a quality not insignificant when
the hypertrophy is considerable, may be hard to appreciate in the degrees
of hypertrophy we are now contemplating ; and a slight vertical displace-
ment of the apex is no less difficult to ascertain, seeing that the form of
the chest and its landmarks are far from constant. The researches of
Myers, Da Costa, Thurn, Fraentzel (29), and others, on hypertrophy of
the heart found .in men submitted to physical stress, were made chiefly
upon soldiers (mde p. 851). In these men, however, contingent conditions
have to be considered : omitting drink and syphilis, many ill-fed, un-
trained, half -developed recruits are (or then were) clad in ill-fitting
clothes, girthed with belts and breast-straps, loaded with 20 lbs. and more
of weapon and kit, and unavoidably sent on long harassing marches, for
which they are untrained. In civil life we see the muscular or nervo-
muscular evils which flow from like causes, and we see how tedious may
be the recovery from them. Now, if we turn to sailors, to whom drink
and syphilis are not unknown, but who are clad in easy dress and not
" trashed about," we hear nothing of cardiac hypertrophy.
It is said that in hard-worked animals, such as greyhounds and race-
horses, simple hypertrophy of the heart unassociated with cardio- vascular
disease is met with. I have referred this question to Professor M'Fadyean
of the Eoyal Veterinary College, who replies, " I have not formed the
opinion that an amount of muscular tissue notably above the average
is ever found in the heart of the horse or dog as the result of great
muscular stress, but that hypertrophy of the left heart is always the
result of some morbid condition of the valves or of the arteries. ... If
muscular effort were a cause of simple cardiac hypertrophy it should be
almost the rule in bus horses, and such is certainly not the ease."
Arguments from analogy must not have much weight until verified ;
and we must regard hypertrophy of a hollow viscus in a different light
from that of a solid muscle such as the biceps j moreover, we have in
the heart not only a hollow organ, but a hollow organ in incessant
activity ; finally we do not know that the heart of a sound man engaged
in active pursuits is over-worked on the whole, seeing that the machinery
for the equilibration of arterial blood-pressures is of miraculous efficiency
' ' p. 472 and p. 846).
The load factor of the heart, the ratio between its average and its
DISEASE OF THE AORTIC AREA OF THE HEART 917
maximum work, is ample ; as Cohnheim impressed upon us, the heart
has a large "reserve capacity." If, say, by partial ligation of the pul-
monary artery the resistance be increased to three or even four times the
normal mean, the arterial blood-pressure will remain constant, although
the left ventricle may be doing three or four times its ordinary work.
I must not delay any longer on matter which is dealt with in other
sections, but these inquiries are germane to my subject, as we are inquiring
first whether hypertrophy of the left ventricle is a quasi-normal conse-
quence of muscular exertion, and, if so, whether it can of itself provoke
aortic disease, in the adjoining section of the aorta or at the orifice itself.
If excessive pressure is thus induced we may see how muscular stress may
lead to aortic disease. Eoy and Adami noted (piAe vol. i. p. 123) that "when
the aorta of a dog is suddenly and greatly constricted, and consequently
the pressure in the proximal portion of the vessel greatly increased, the
plasma of the blood is forced into the cusps of the aortic valves, and vesicles
of lymph make their appearance on the under surface in that region where
fibroid thickening is most frequent in cases of chronic high arterial pres-
sure." This is probably the way in which the chronic inflammation of the
tricuspid valve is established which not infrequently ensues upon mitral
stenosis. Our study of muscular exertion, however, as we have seen, sug-
gested to us that such work does not create a state of abiding high pres-
sure, but of intermittent high pressures more or less compensated by a
mean pressure habitually rather low. ,
Are we not led, then, to suspect that muscular exertion, unless very
sudden and excessive, and attended perhaps by fixation of the chest
walls, arrest of breathing, and by some phase of differential pressures in
ventricle and aorta of which we know little— in which case we know that
a valve may be directly ruptured — needs some other factor to bring about
aortic disease ? This factor may be one of the causes of constitutional
high blood-pressure ; or, on the other hand, it may be some debilitating
cause, such as syphilis, anaemia, or " misfere," which so reduces the normal
strength of the cardio-vascular textures that ordinary blood-pressures
are high relatively to their feeble durability. A patient of mine, who
had certainly done all that he could to strain his heart, if by physical
stress it could be done, died of dilatation (" true aneurysm ") of the aorta,,
a result put down unhesitatingly by his friends to over-exertion ; yet I
knew well, what no one else knew, that there had been an old syphilitic
infection, and that not a few evidences of the infection, among which
had been symptoms of encephalic arteritis, had from time to time
betrayed its persistency. To my mind it was far from clear that muscular
stress had the first place in dilating the great vessel, although, no doubt,
the vessel once disintegrated by arteritis, muscular stress accelerated the
evil. If we are to form a definite opinion of the part played by muscular
stress in the causation of aortic disease with or without the intermedia^
tion of hypertrophy of the left ventricle, we must weigh with it in the
particular case all other factors which may have conspired to the same
end. If we except active destruction such as that of infective or severe
9i8 SYSTEM OF MEDICINE
rheumatic endocarditis, it may be true that all aortic disease is due more
or less to the eflfects of arterial blood-pressure.
Peter, Traube, and others have insisted upon a distinction between
aortic disease originating in the heart itself, such as that of rheumatic
valvulitis in young and otherwise healthy persons, — cases in which the
cardiac affection is in its initiation a local disease, — and implication of
the heart in a more general constitutional change such as syphilis or
arterio-sclerosis — wherein the heart disease is but an expression of a
general disease. These divisions have been distinguished by such
names as "cardiopathy" and " arteriopathy." The distinction is worth
making, though it has been made far too literary; in it too little
heed has been taken of the tendency of cases in practice to defy
these logical devices ; and much harm is done, especially by French
writers, in decorating the several phases of a continuous involu-
tion by imposing names which suggest differences in kind, or
at any rate in quality, which do not exist. While primary
cardiac disease tends to generalise itself, constitutional disease derives
much of its peril from the cardiac factor ; the series, starting, it is
true, from opposite points, meet and overlap ; thus, unless it
be in well-marked extremes in the interpretation of which we are
not likely to go astray, the distinction is often too artificial to be
of much service. Still, on paper at any rate, the contrast is worth
making as a study of origins, for reasons which have already appeared ;
and occasionally it may influence the prognosis and treatment of a
particular case. The observations of Eoy and Adami, already quoted,
throw some light on the process by which blood - pressures, relatively
excessive, set up that opacity and condensation of the valves which we
see well marked in the aortic valve, and clearly enough at times in other
valves also, under high blood-pressures ; as the heart suffers so may the
aorta (74), and atheroma may invade no small part of the intra-thoracic
arterial structures. Whether, then, the initial injury be such as this, or it
be a rheumatic valvulitis or a syphilitic, the valvular lesions may blend
into a common form which we conveniently call atheroma ; and, the line
between the aortic area of the heart and the aorta itself being no line at
all, we find this atheromatous change not only in the valve, but spread, and
often widely spread, in the neighbouring great vessel also : thus the aorta
dilates, its elasticity is impaired, its walls are diseased, and the heart,
caught in a vicious circle, has to meet an increased resistance. For a full
account of atheroma the reader is referred to the article on " Diseases of
the Arteries " in the next volume ; I may briefly say of the valves that the
milky opacity of the acuter stages of valvulitis is followed by an increase
of fibrous tissue, both in the fibrous ring itself, where it becomes exces-
sive, and in the valves themselves, chiefly about their points of mutual
contact and the corpora Arantii. With the deformities secondary to the
contraction of these cicatrised tissues we are but too familiar : induration
of the fibrous ring, or of the infundibulum below it, leads to stenosis ;
and of the limbs of the valve to their contraction, puckering, or cohesion.
DISEASE OF THE AORTIC AREA OF THE HEART 919
Thus the valve may become incompetent, or the orifice contracted ; or
these results may be concurrent.
The following remarkable case of sub-valvular constriction is pub-
lished by Dr. Langwill. The patient was a poorly -developed lad of
nineteen. He complained of pains in the chest on exertion, though he
worked as a foundry labourer till four weeks before admission. A strong,
systolic thrill was felt at the base, and a loud systolic murmur was
audible five inches from the chest. The chief cardiac disease found at
the necropsy was as follows :—
Pathological Report on Heart, by Dr. Shknnan, Pathologist to
Leith Hospital.
'Right auricle. — Normal ; tricuspid orifice, 1-2 in. Bight ventricle. — Nothing
particular to note. Left auricle. — Endocardium somewhat thickened. Mitral
valve. — Cusps slightly thickened, particularly inner cusp. Musculi papillares
small, and fibrous at apex where they join the chordae tendinese. Left ventricle. —
Walls hypertrophied ; cavity 3 in. long ; thickness of walls varies from 1 in. to
0-5 in. There are a few narrow fibrous bands stretching across the cavity, at
whose points of attachment to the wall there is marked thickening of the endo-
cardium from old endocarditis. On passing the finger up towards aorta, it
passes through a fibrous ring — 0'7 in. diameter — about 1 in. below the aortic
opening. This is continued on to the ventricular surface of the inner mitral
cusp. In this position, and extending upwards from the ring on to the lower
surface of the postero-external aortic cusp, is a narrow band of comparatively
recent vegetations. These cover the lower surface of all the aortic cusps, which
also show fibrous thickening and contraction — cone diameter of the opening
being 0-7 in. Above the valves the aorta dilates slightly — 1-2 in. — but in the
second half of the transverse part of the arch begins to contract, so that at the
upper part of the descending aorta the cone diameter is 0-6 in.
Thickening of a limb of the valve, says Prof. Hamilton, may lead to
the formation of a relatively large spur which, by intruding into the area
of the two other shrivelled cusps, may accidentally prevent regurgitation.
From such rough edges and points " vegetations " may sprout, and
form fringes on the free or ventricular edges of the valve, rarely on its
aortic aspect, whereby friction is increased and extended ; and chronic in-
flammatory changes operate on the endocardium, where the diseased valve
brushes it, on the valvular structures themselves, and on the corresponding
aortic surfaces. Below the valve "ripple-marked" thickening of the
endocardium, due to the strain of aortic regurgitation, has been demon-
strated by Dr. Glynn and other observers. Hamilton reminds us that,
in disease of the aortic valve, it is rather the base of it which is the seat
of the mischief, while the cusps may even be free ; in the mitral it
is the edge of the cusps and their substance which suffer first. Conversely
the valve may be very incompetent, while the orifice is as wide or wider
than its normal section.
Stenosis depends often, but not always, on contraction of the
fibrous ring : not always, for adhesion and condensation of the limbs of
920 SYSTEM OF MEDICINE
the valve may narrow the orifice, converting it into a slit or funnel,
as is so well known in the case of the mitral valve. In a case which
recently occurred in Addenbrooke's Hospital, under the care of Professor
Bradbury, the adherent margins were united along their surfaces of
apposition, and the blood seems to have been forced through a casual
chink so small as almost to evade discovery even on inspection. There
was no regurgitant murmur during life, nor was any regurgitation de-
tected by Professor Kanthack. In this case calcification was far advanced
in the ring, no doubt, as well as in the valve ; indeed, in stenosis attri-
buted to the valves the ring is usually concerned in the mischief also.
Similar cases have been published by other physicians.
I need scarcely say that the presence of "vegetations " and of other
detachable fringes on these dog-eared cusps is a matter of far more than
local importance, as by their means embolism may come about.
Ulceration of one or more of the limbs of the valve is always a peril-
ous process. When dependent upon micro-organisms, and we cannot say
how frequently they enter in, the process may be terribly destructive, as
the records of infective endocarditis give us too much reason to know ;
on the other hand, decay or perforation may be very gradual, and not
always due to infection : probably in chronically diseased valves it may
be a mere mechanical disintegration. Perforation of a segment is
said to betray itself by a piping quality of the regurgitant murmur.
Other rasping or "musical" qualities of these murmurs are attributed to
the projection of spurs or shreds of segments which, fluttering or vibrat-
ing as reeds, give peculiar qualities to the sounds. It is commonly said
that murmurs may be generated by a rough surface, as a brook murmurs
over pebbles ; this assertion must be taken with considerable reserve,
for to produce a murmur the column of the blood must be broken : this
a merely mammillated or corrugated, surface will not do unless
the eminences be such as to set up vortices around or behind them.
The common notion that murmurs may be generated in a rough aorta
without any contribution from the valves or orifice, is improbable and
not supported by experience. If, in the absence of any cause in the valvu-
lar area, such murmurs arise, which is rather doubtful, they are to be
attributed to dilatation of the aorta, wherein vortices may form between
the slower external and the swifter internal layers of the issuing blood.
However, wfe meet with cases every day of advanced disease of the aorta
in which no systolic murmur is heard. Again, that there is more than
the satisfaction of an anatomical curiosity in the endeavour to fix the in-
competence or the obstruction upon this limb of the valve or that I am
indisposed to believe ; nor can a leaf or stump of a diseased segment hamper
the access of blood to a coronary artery, unless, of course, it so adhere to
the wall of the aorta, or the mischief so extend from it, as to choke the
mouth of the vessel. That the propagation of a regurgitant miumur in
this direction or that can indicate the limb of the valve affected, or chiefly
affected, is not very probable in itself, nor is it borne out by experience,
and that the deformation of one particular limb of the valve should affect
DISEASE OF THE AORTIC AREA OF THE HEART 921
the coronary circulation more than the same incompetence in another
is impossible; there cannot be differential pressures within this area.
Congenital peculiarities of the aortic valve and coarctations of a con-
genital origin are dealt with in the article devoted to this subject
(p. 706). In simple rupture of a healthy valve one limb only is torn in the
large majority of cases ; but a few cases of the rupture of two limbs are
on record. Generally the limb is rent on the free edge, but sometimes
it is torn from its attachment to the vessel.
Whether these chronic changes in and about the aortic orifice lead
to regurgitation or to stenosis without incompetency, crucial as the
distinction is in clinical medicine, is pathologically a matter of accident ;
the result depends, that is, on contingent causes. At the same time
it is well to remind the pathologist that to test the competency of an
aortic valve by means of a column of water, a test which is more useful
in the post-mortem room than one might expect, is insufficient in a
doubtful case, unless the height of the column of water be equal to the
maximum aortic pressure — to the pressure, say, at the moment of aortic
diastole of 180 mm. Hg. Moreover, the water may even then escape from
the coronary arteries. Practically, as the water brings the valves into
apposition we have to judge of their competency by the eye.
Of "gouty valvulitis," of a primary kind, after the manner of
rheumatic valvulitis, and apart from the chronic sub-inflammatory and
degenerative changes in the aorta resulting from abnormally high arterial
pressure, I have no knowledge, either pathological or clinical.
It is very important to remember that these degenerative changes
involve the area and, sooner or later, the orifices of the coronary
arteries ; so that the heart, instead of enjoying that increase of nutrition
which its greater work demands, and which at first the hypertrophied
ventricle supplies, may receive, after the first stage of the malady, con-
siderably less than its normal nourishment.
It is commonly asserted that insufficiency of the aortic valve may
come about, not from any defect in its own structure, but from dilatation
of the aorta, whereby the sectional area of the orifice is enlarged.
Intermittent or temporary aortic regurgitant murmurs are thus ex-
plained. Bari6, a careful and experienced observer, reported thirteen
cases of aortic regurgitation from widening of the orifice without
disease of the valves ; but a persistent slapping second sound cannot be
taken as definitely indicative of a normal aortic valve. Vierordt assumes
that in weak dilated hearts dilatation of the aortic ostium may cause
" relative Klappeninsufficienz."
Cases of alleged temporary aortic regurgitant murmur are few and need
very careful interpretation. My own conviction is that if such cases be
followed up, the regurgitant murmur will be found permanently estab-
lished at no distant date ; as in Dr. Hermann Weber's very interesting
case (p. 946). That dilatation of the aortic orifice does often occur is
well known to every pathologist ; but I have never happened to meet with
such an increase in the sectional area of this orifice as to permit of
9^2 SYSTEM OF MEDICINE
regurgitation without disease of the valve ; however, a few specimens of
the kind are to be found in museums. Professor Osier (62), on Beneke's
authority, tells us that "the aortic origce, which at birth is 20 mm.,
increases gradually with the growth of the heart until at one-and-twenty
it is about 60 mm. Of this size it remains until the age of forty, beyond
which date there is a gradual increase up to the age of eighty, when it
may reach from 68 to 70 mm. Thus at the very period of life in which
sclerosis of the valve is most common, there is a physiological tendency
toward the production of a state of relative insufficiency." But when I turn
to Osier's opinion on the point before us, I find that "relative insufficiency
of the sigmoid valves, due to dilatation of the aortic ring, is a rare condition";
he adds, "Indeed I have myseK never met with a pure instance of the kind,
for in such cases I have always found the valve segments involved with the
arterial coats." I may repeat once more that aortic insufficiency is not
eminently a disease of old persons, but rather of persons about or under
middle age ; there is no difficulty, of course, in collecting cases of aortic
regurgitation due to senile arterial disease, — I have such a case under
my occasional observation at' present, — yet the prevalent effect of aortic
disease in the old is obstruction. Again, although in elderly persons,
and in younger men the subjects of syphilis, we meet with considerable
and even enormous dilatation of the aorta, yet even in these cases aortic
regurgitation does not generally appear unless there be disease of the
valve itself also, for the orifice is prone rather to stiffen than to yield.
Whether then regurgitation, permanent -or temporary, may arise directly
out of a mere dilatation of the aorta, if no longer an open question, is a
rare event ; and, as the accompanying tracing shows, the incompetence is
slight. I gather from Prof. Tigerstedt's new volume
that in his opinion the semilunar valves are efficient
under conditions of considerable relaxation, whether
of heart muscle or of the supporting structures ; and
Professor Sherrington (p. 466) states on experimental
evidence that the Hmbs of the valves may aid each
Pig. 60.— Dilatation of Other by mutual readjustments. Dr. Newton Pitt
Spetenorffoi, »: tas recently investigated this matter (67).
Urgement of orifice. Sometimes, as Corrigan showed, on examination
inatic case, Fig. 60. of the aortic valve after death from whatsoever
(Graham steeu.) disease, its segments are found atrophied; the flaps
are thin, and not infrequently " fenestrated," especially on a line parallel
to the free edge. It is alleged that those conditions are not necessarily
morbid or mischievous ; if on overlapping margins th,ey do not give
rise to regurgitation. Aneurysms of the parts about the valves need no
discussion here, as their pathology is dealt with in the article on Aneurysm.
Nor will I stay to discuss such pathological curiosities as morbid growths,
polypi, and the like.
The effect of aortic disease on the other valves and orifices has been
carefully studied by Professor Hamilton. Aortic regurgitation, as he
observes, is "anticipated in its injurious results on the other orifices
DISEASE OF THE AORTIC AREA OF THE HEART 923
by its own peculiar sources of mortality." From his measurements,
however, the following results appear ; namely, that, unless in addition
to the incompetence of the valve the aortic orifice be dilated, "the
effect upon the size of the other orifices is nil " ; if, however, the aortic
•orifice be dilated, a general distension of all the other orifices is apt
to follow. " Constriction of an incompetent orifice, then, exerts a salu-
tary effect " ; so far, that is, as stress on the other orifices of the organ
is concerned.
Simple stenosis of the aortic orifice, in the strict sense of the word,
seems to be a rare disease. I find that both Osier and Hamilton speak
of it as beyond their experience. Fagge and Pye-Smith speak of it as
"most rare"; Fraentzel as "ein seltener Herzfehler." As Frenchmen
will not put indexes to their books, I cannot say what their experience
may be. For my own part I should say with Fraentzel that the condition
is rare, but not excessively so. It has happened to me to see many cases
of mere aortic stenosis without any trace of regurgitation, and to have
Terified not a few after death, th« last case being that of Professor
Bradbury's, to which I have already referred. Aortic stenosis is a long
'disease, for life may continue iinder favourable circumstances until the
aperture is reduced to the size of a crow quill or less. The chink by
which the blood found access to the aorta in Professor Bradbury's case
was only discovered on the closest search after death. It is com^monly
said that aortic contraction in this simple form is the result of chronic
•endocarditis ; that aortic stenosis is connected with arterial disease which
spreads down from the aorta. But in St. George's Museum are a number
of cases of well-marked aortic stenosis, and in many of them the aorta
seems healthy. The stenosis seems to protect the aorta in spite of the
high velocity of the " choke bore." Most of these cases occur in persons
of fifty years of age and upwards, in whom the incident is usually due to
"atheroma." In younger or sounder persons it is often fibrotic. In
"these cases the effects of aortic disease upon the left ventricle are most
clearly seen ; it is in them that hypertrophy takes its simplest form. In
so far as the aortic orifice is narrow, the inner surface of the left ventricle
is protected from the pressure of "recoil."
In diseases of the aortic valve, as of other parts of the heart, our
■attention may be too much given to murmurs ; the working calculation
which we have to make is the effect of the lesion on the chambers, for
by their efiieiency the organ stands or falls, at any rate for a time. In
stenosis the left ventricle may approach that mythical type " concentric
hypertrophy." In regurgitation, especially if attended, as it is wont to
be, by dilatation of the aorta, the ventricle is at least as much dilated as
hypertrophied. The pathogeny of this event has been much discussed, and
the outcome of the discussion is that this dilatation is due to the recoil of
blood from the aorta upon the wall of the ventricle in diastole. Besides
this resistance head in the arteries, that large fraction of the force of the
systole which is stored up in the aorta in its diastole is expended not
■only upon the forwarding of the blood, but in large part also upon
924 SYSTEM OF MEDICINE
the inner surface of the ventricle. It is incorrect, then, to describe
this force so released as "wasted." It is often stated that the
dilatation is due to the filling of the ventricle from two sources ; but
it cannot matter whether the cavity be filled from two sources or
from twenty ; the matter is not one of the accessibility of blood, but
of the resultant intra-ventricular pressure. The aortic pressure is no
doubt BO much greater than the auricular that the latter may count
for comparatively little ; yet the resultant pressure is not the sum
of the two ; it will lie between them — the amount depending upon the
relative pressures at the respective orifices. If, for example, the pressure
of the current returning from the aorta = 100 mm. Hg., and that from
the auricle = 20 mm. Hg., the resulting pressure on each square unit
of ventricular surface will not be 120 mm., but a quantity somewhere
between the two numbers ; and the resistance of the aortic stream, being
greater than that of the auricular, will head back the latter more or less,
according to the degree of its excess. Furthermore, this heading back
will partially close the mitral valve, and fill the ventricle still more with
refluent aortic blood during its diastole : otherwise we should find the
auricle still more distended from the aortic head. From experiment upon
animals it seems that, on suddenly produced insufficiency of the aortic
valve, the aortic pressure may be so great as to cause rupture of an un-
prepared ventricle. The distress felt on rupture of the valve in a strain-
ing man is probably due to this distension of an unprepared ventricle.
Usually, however, " reserve capacity " — the factor of safety — sustains the
arterial pressure till the ventricle can grow up to the new call upon
its strength ; if it rupture it will give way at its weakest point,
but to speak of the regurgitating stream "impinging on the inner
surface of the apex of the left ventricle," and " of the repeated blows of a
jet of blood disabling the ventricle," is to regard the cavity as if it were the
pan of a water-closet. Writers on heart diseases are apt to lose the con-
ception of the heart and arteries as a plenum. If the heart be regarded as
a screw with reserve driving power at command, both dynamic and static,
why should not the work still be done ? We shall see, under the head of
symptoms, that the work is well done for an indefinite interval dicing
which the patient is usually unaware of any defect in his circulation.
The failure comes about, partly because " compensation " is never com-
plete, partly because of the excess of pressure of aortic blood over
auricular upon the inner surface of the ventricle : were the auricular
blood impelled under a pressure at least equal to that in the aorta
the valve might be dispensable. The dilatation is due to the abnormal
pressure of aortic blood, ■ — ■ abnormal, that is, in respect of the pres-
sure which the parts have ordinarily to bear. If the ventricle of a
frog beat in a tonometer under a supply of blood from a pressure bottle
at varying heights, curves may be taken to measure the volume of the
ventricle ; and as long as the pressure from the bottle remains constant
so long the line of the volume at diastole is remarkably level. Increase
the pressure slightly and the diastolic line immediately sinks, showing
DISEASE OF THE AORTIC AREA OF THE HEART 925
greater capacity, even though the height of each systole may be as
before (Gaskell). The distensile force being greater, the corresponding
increase follows a well-known physiological law. In like manner the
increase of the muscular coat of the smaller arteries described by Sir
George Johnson and Dr. Savill comes about in the course of resistance to
distensile forces ; and I may add that, as in the heart, this overgrowth is
intimately associated with degenerative implications.
DUatation gains on hypertrophy, as Starling clearly puts it, because,
although a loaded does more work than an unloaded muscle, the
amount of contraction (that is, the height of the lever) is less. The
cardiac muscle may be more tense, and the contraction therefore more
powerful, but it is not equal to the increased length of the muscular
fibres ; thus some dilatation remains, the residual blood is more, and the
output less. On the next diastole the heart is overfull, but even under
this increased stimulation only the normal inflow is sent out : arterial
pressure is thus kept up, but work is increased and hypertrophy should
follow. Not only has some of the output to be lifted again, but the back-
ward motion of the refluent blood has to be converted into a forward
motion. It is often said that the heart attains a larger bulk in aortic
regurgitation than in any other disease ; this is, generally speaking, true ;
but in chronic Bright's disease the "cor bovinum" — the "heart of a
pantophile," as Voltaire called that removed from Diderot's body — may
attain to no less a bulk ; that is, say, 2-3 cm. at greatest thickness and
1-2 cm. at apex. It is usual to speak of this enlargement as a com-
pensation of the defect it counteracts. There is no objection to this
expression if it be remembered that it is a figurative one ; all we know is
that increase of function within certain limits is followed by hypertrophy ;
it is not in physiology only that function creates structure : yet if in
respect of one factor the difficulty is postponed, the readjustment, as we
shall see, brings other evils in its train. We do better, then, to get rid of
these teleological connotations, and to regard the hypertrophy of the ven-
tricle simply as the result of increased function, whatever the consequences.
How does this alleged compensation break down ? The late Mr. George
Busk once reminded me that all muscular overgrowth may be transitory,
owing perhaps to the transitoriness of all conditions less stable than the
normal ; he then adduced for the first time the example of the hyper-
trophied biceps of the file-cutter, which is said to fail after a certain
number of years. But perhaps the failure is a particular instance of the
general truth that a disproportionate increase of one part of a system
disturbs the relations of all associated parts, and it begins to rock :
hypertrophied engines in swift passenger ships mean a shorter life for
the ships. Not to look beyond the immediate neighbourhood of
the heart, the aorta is strained under the immoderate stress; it dilates ;
atheroma, the effect of strain, being usually found just above the
valve, implicates in time the mouths of the coronary arteries ; from the
first these arteries, like the rest, are injured by the excessive percus-
sion, and perhaps from the first the sudden and early fall of pressure
926 SYSTEM OF MEDICINE
in the aorta may be greater than the higher pressure with which they
are filled on systole. Thus areas of the cardiac muscle come short of
blood ; fatigue is cumulative, and fibroid tissue, which is more economical
to feed, supplants the active muscular fibres. If the aorta be unhealthy
to begin with, this disintegration takes place so much the sooner. [See
also the postscript to this article.]
The only other point to which I must refer in this place is the effect
of a persistently large residuum of blood in the left ventricle on each con-
traction. The most recent observations seem to indicate that the healthy
ventricles never quite empty themselves — that there is always some residual
blood, some difference between contraction volume and output ; if this
be so, how much more must this be the case ' as the work of the
ventricle, distended under higher pressure, increases as the cube of the
radius of curvature. This consideration alone, when we recollect the
cumulative effects of fatigue and the many incidental causes of atony of
the heart, may go far to account for the wane of compensation. On.
the other hand, in aortic insufficiency the ventricle contracts against low
resistance, in stenosis against high resistance, so that the output must be
far more in the former, as indeed the upstroke of the sphygmograph shows
us that it is. In the normal state the blood-pressure falls suddenly in the
ventricle, gradually in the aorta : in regurgitation it falls suddenly in the
aorta also ; moreover, in insufficiency the pulse-rate is usually more rapid.
That dilatation is nevertheless the feature of insufficiency rather than of
stenosis would indicate that mere residual blood is not the predominant
factor in dilatation which is usually supposed : excessive contraction
volume is probably far before it in this effect. It is as cardiomotive
energy begins to fail that residual blood becomes so grave a condition in
dilatation. Finally, in regurgitation dilating stresses tell on the ventricle
when this muscle is relaxing, in stenosis when it is contracting. When
regurgitation and stenosis occur together the results will be compounded
of the characters indicated for each alone, stenosis probably having some
protective effect.
The consequences of aortic disease are so often confined to its own
sphere that disease of this part has a character of its own ; the consecutive
pathological changes which, if the patient survive, make themselves felt
sooner or later in other parts of the heart, need not detain us. It is far
from uncommon in aortic regurgitation, after long persistence even of its
extremer symptoms, not to detect any implication of other parts beyond
thickening of the mitral cusps under the effects of the hypertrophy of
the left ventricle : under increasing dilatation, however, the mitral
valve may give way, and the patient may die of mitral rather than of
aortic disease, although death with dropsy may occur without any audible
mitral regurgitation. It has been said that forcing of the mitral orifice
with moderate regurgitation gives relief to the overstrained arterial circula-
tion ; such a temporary effect it may have for a while, but it is the open-
ing of one more of the gates of death.
The pathological changes in the arteries, due to their high tension
DISEASE OF THE AORTIC AREA OF THE HEART 927
under the heavy beating of the heart, do not differ in kind from those
to be described in the chapter on "Diseases of the Arteries."
In senile aortic disease, emphysema and other evidences of decay too
frequently increase the burden of the patient's latter days. The patho-
logy of these associated degenerations is described elsewhere.
Stenosis. — Symptoms and signs. — The invasion of stenosis, as of
regurgitation, is often long latent. While speaking of the causation of
aortic stenosis I said that this disease, standing alone, is a rare one ;
aortic systolic murmurs are, indeed, among the most frequent of clinical
signs, but in many cases, even if organic, they signify no more than
a deformation of the orifice, whether sectional area be diminished or
not ; again, in many cases in which this area is diminished the valve
is also incompetent, and the case is no longer a simple one. To
understand stenosis we must study it in its unmixed form. It has
been my fortune to see not a few of these cases, and I cannot begin
better than by a brief record of one of them. Mr. X., a patient of
Mr. William Hall of Leeds, became aware of an increasing oppression in
the chest. Mr. Hall found a direct aortic murmur and hypertrophy of
the left ventricle, and was good enough to ask me to see the case. Mr.
X. was a man of about fifty years of age ; he had never suffered from
rheumatism, his life had been anything but laborious ; there was
no history of syphilis nor any evidence of this infection. He had
always been a man of correct and domestic habits. Nor was there
any sign of kidney disease or of general arterial disease ; his arterial
system, apart from the aortic valve, seemed to be no older than his
years. As no great improvement came about, nor was likely to come
about. Sir William Gull came down to meet us, the case being even for
him a rare one, and he took the greatest interest in it ; so interested
was he that he took occasion to call on me on a later day to talk
over the symptoms again and to impress the facts on his memory.
Often I recall him as he sat in my room describing with his hand
an imaginary cardiographic curve in the air — the portentously long
upstroke, percussion it could not be called, while the heart was heaving
under the hand as the back of some imprisoned monster ; the curt diastole
with faint second sound ; the irregularly protracted pause as if the heart
were slowly gathering itself together for another effort ; the deliberate
rhythm, some forty in the minute, in which each reluctant beat, stout as
it was, seemed as if it might be the last effort ; the small hard pulse ; the
substernal oppression, all these features combined to make a striking
clinical picture. The slowness of rate necessary to compass as much
output as possible was well illustrated in a case of this kind reported by
Dr. S. West, in which the pulse was 30, and in another by Dr. Parkes
Weber (96) in which the heart's beats became so slow as to give rise to
syncopic attacks.
For the most part aortic stenosis appears in persons beyond middle
life in whom this deformity is but part of a general decay : in such
928 SYSTEM OF MEDICINE
persons the compensatory reactions may be less obvious ; for, to take one
point alone, the mass of the blood to be lifted — the cardiac output — is
less in old persons than in such a subject as Mr. X.: nevertheless, as
we have seen, even the hearts of old people can attain to no inconsider-
able amount of hypertrophy; the old woman referred to on page 920
had a heart of 24 ounces, and apparently of good muscle.
Although it is true that the left ventricle, spared the recoil of
regurgitation, does not dilate in stenosis as it does in insufficiency,
yet it is untrue, on the other hand, to say that it does not dilate at
all ; the residual blood on each contraction may be large, and as the
auricle gains a little in strength to meet the increased pressure in
the ventricle, the contraction volume of this chamber is excessive,
and some dilatation is inevitable. The enlargement, however, is
more in the downward and outer than in the transverse direction; the
dulness does not cross the sternum, or at any rate not until the later
phases of the disease. Gradual and restricted as the output may be, the
mean arterial pressure is fairly high — the heart being usually slow, the
systole is not only strong but absolutely, though not relatively, pro-
tracted, as shown in the curve here reproduced ; the pulse is thus
"sustained." It may be that the arteries contra,ct upon their smaller
content. The aorta, on the other hand, is not dilated, at any rate not as
a direct consequence of the stenosis ; if there be no arterial disease to
weaken it, the vessel being less distended is, theoretically at any rate, not
increased in diameter, and may be diminished. The second sound will
vary with the state of the valvular segments ; if these be hardened the
sound may have the " parchment " character ; but it will always be short
as the blood-pressure above them, even if of normal mean owing to the
length of systole, has not a high maximum ; and unless the vessel be
drawn nearer the sternum it will not be loud because the sectional
area of the aorta at its orifice is diminished. It may indeed be quite
inaudible as in J. D. (Fig. 51). The contrast between the big heart-
beat and the small pulse may be startling, in which respects stenosis
PiQ. 51.--James D., fft. 46, acute rh. Bet. V. Loud syst. m. in aortic area; no diastolic m., no
second sound. P.M. No incompetence. (Graliam Steell.)
differs from regurgitation, wherein the pulse, although of brief
duration — "collapsing," has a very high maximum. In regurgita-
tion the " arterial tension " is enormous, as we see by the damage done
to the structures. In stenosis, then, the protraction of the phases of
the cardiac revolution makes up for the smaller delivery of blood into
the aorta per unit of time. In Dr. West's case, as I have said, the pulse-
DISEASE OF THE AORTIC AREA OF THE HEART 929
rate was only 30. Sir S. Wilks again describes the pulse in stenosis as
" small and slow." Yet many cases of positive stenosis with a quicker
pulse are recorded, wherein the rate may be due to cardiac failure or to a
call from the tissues for more blood, a call transmitted through the
accelerators. In strict stenosis, then, we ordinarily have a long slow pulse
with a low maximum, unaffected by raising the arm ; in regurgitation, on
the contrary, a short pulse not slowed, of extreme maximum pressure,
aud far more injurious to the arterial tree.
The murmur of stenosis may be heard widely over more than the
cardiac area; it is often heard at the apex and over the aorta in the
interscapular region. The character of the murmur varies to some
extent both in quality and in order. Sometimes its sound vibrations are
attended with others less numerous, not rapid enough to cause a
sound but perceptible to touch as a thrill. I need scarcely say that
these coarse vibrations need not indicate extreme stenosis. A thrill
is often to be felt in stenosis of the mitral valve, but its position is then
at or about the apex, whereas in aortic stenosis it is chiefly about the
base. A thrill perceptible over a large part of the cardiac area but rather
more towards the apex, is occasionally present in other labouring hearts
— especially when, as in the arterio-sclerosis of old folk, the vessels become
rigid while the heart itself remains vigorous and the blood -pressure
high ; but a thrill at the base is almost pathognomonic of aortic stenosis,
whether in combination with other mischief or not. Hence we expect that
the murmur also will, in part at least, be compounded of slow sound vibra-
tions, and, whether " musical " also or not, will be noisy ; we call such
murmurs sawing, rough, or harsh. As the ventricle begins to give way
under its toil the murmur will grow softer, possibly even to extinction ;
under digitalis also it may alter in quality, and the pulse may quicken
in rate ; then again the harshness of the murmur may return as the
pulse slows down. The thrill likewise depends on the vigour of the
heart; when strong, it may be felt in the vessels of the neck. As
regards the order of the murmur, I have heard it sometimes in a post-
systolic rhythm occupying the shorter pause ; I have noted two very
definite cases of this kind in private patients within the last few weeks ;
the first moment of systole was free from murmur, then followed a very
brief murmur, and instantly thereafter a clear second sound — clear of
murmur, that is, though in such cases rarely normal in tone. This is
no " pulmonary " murmur.
I am interested to find that Vulpian also reports such a murmur so
A woman, jet. 40, suffered severely from acute rheumatism ; two years later
she presented herself with mitral regurgitation revealed by the ordinary signs.
At the base a roughish bruit was also heard ; this basic bruit was placed between
the two normal sounds (" entre les deux bruits normaux "). The murmur was
heard also at the mid-precordial region, and upon the localisation of a rough
short systolic murmur. The pulse was regular, small (rate not given) " et un
peu concentre." The ascending sphygmographic line was ill-marked (trfes peu
VOL. V 3 0
930 SYSTEM OF MEDICINE
aocus^e;. Vulpian was bold enough to diagnose a contraction " sonsaortique "
" une l&ion de canalisation . . . ^ une certaine distance audessoua des valvules
aortiques."
Vulpian does not give his reason, it may lie in the increase of velocity
as the ventricle contracts. Constriction in this place might be revealed
hy a " presystolic " murmi* as recorded by Lemoine (quoted by Sansom);
that is, by a murmur coincident with the earliest ventricular effort : such
is Dr. Sansom's supposition.
In most cases, when the murmur of aortic stenosis is said to be
in part "presystolic," this apparent origin of the murmur is suggested by
the great protraction of the " prosphygmic interval." This interval may
indeed become perceptible to the finger. Ordinarily the murmur is a
long one occupying the whole of the first phase up to diastole.
The propagation of the murmur from the second right costal cartilage
depends much on the stage of the disease. If the murmur be loud — it
is often loud enough to be heard at a distance from the chest — its area of
diffusion will be considerable, both about the basic region and towards,
the periphery in the arteries. Thus it tends to gain an ascendency over
other murmurs, and quite possibly by interference vibrations to alter or
resolve them. When stenosis is extreme, however, it is said that the
murmur may fail to reach the carotids.
The anacrotic and the hisferiens pulse. — It has often been said that
the anacrotic pulse (Tracings Nos. 52, 53) is so marked a peculiarity
of aortic stenosis as to be pathognomonic of this condition. This is
certainly not the case ; for my own
part, I have found the pulse ana-
crotic in so many different cases of
cardio- arterial disease that I would
not go farther than to say that
it suggests disease of the aorta
Fig. 52. -Anacrotic pulse, sloping npstroke; o^ aortic stenosis j moreover, it is
apex of curre formed by tidal wave; ill- doublv inconstant, it is not persistent
marked dicrotic wave. Man, »t. 29, with "^ i • i
rheumatic history, loud syst. m. and thrill from day to day in the same case.
to aortic area. (Gmham steeii.) q^^ attention has been drawn more
particularly to this matter of late by Dr. Graham Steell, who is good
enough to allow me to reproduce some tracings of the anacrotic and of
the bisferiens pulse respectively. Dr. Steell reported the behaviour of
the pulse in four cases in which the observations on this formation
were interpreted by autopsy. The author concludes as follows ; " Three
of the four cases bore out the belief that the anacrotic pulse is a
valuable sign of aortic stenosis, provided the physical signs correspond.
The fourth case taught, however, that pathognomonic value must not be
attributed to this pulse, inasmuch as other conditions besides aortic
stenosis may produce it (Fig. 54). Moreover, in cases i. and iv. the pulse
was not constant in this character; in case iii., however, unalterable-
ness of the pulse was a striking feature of the most definite case of all.
DISEASE OF THE AORTIC AREA OF THE HEART
931
inasmuch as it was the least complicated. Such unalterableness of the
anacrotic pulse is probably of great diagnostic value, although it may be
rare."
Of the pulsus bisferiens (Fig. 55) Dr. Steell says that although cases of
stenosis are so often associated with regurgitation it is not easy to find
material on which to make conclusions regarding pure stenosis, yet we may
Pig. 53. — Florence ■ , set. 28, rheum. Loud syst. and diastolic m. in aortic area. Death from cerebral
embolism. Anacrotic pulse with bigeminal or alternating rhythm, possibly due to digitalis,
although none taken for two days. P.M. (Graham Stee]!.)
FtCL 54. — ^illMcnotic pul&e.traclng &om case of mitral stenosis without aortic stenosis. P.M.
(Graham SteeU.)
Fia. 65.— Margaret G., at. 25 ; rh. ait. 14. Exemplary P. bisferiens. R. radial, double beat plainly felt ■
L. radial, ordinary tracmg of aortic incompetence. Loud syst. m. and thrill in aortic area ; diastolic
m. P.M. Stenosi^of aortic orifice with incompetence of valves ; no explanation of difference
between radial pulses. (Graham Steell.)
I^G. 56.— Aortic incompetence without stenosis.
Man, ffit. 29, with history of rh. at set. 20. P.
bisferiens. P.M. (Graham Steell.)
Fig. 57. — Bisferiens pulse in case of
aortic incompetence without stenosis.
P.M. (Graham Steell.)
assert, on Mahomed's authority, that the pulsus bisferiens is consistent with
pure stenosis. In his own two cases of pulsus bisferiens there was some
regurgitation also. On the other hand, in some cases of regurgitation associ-
ated with the bisferiens pulse stenosis was scarcely present, if at all (Figs.
56, 57); and again, for our yet greater uncertainty, we read that in Steell's
cases the phenomenon was unequal on the two sides, and in one of them
chiefly unilateral, the other radial assuming the character very occasionally
932
SYSTEM OF MEDICINE
and imperfectly ; a careful examination of the arteries concerned afforded no
explanation of this peculiarity (Figs. 58, 59). In two cases, moreover, the
phenomenon was manifested in the one on the right side, in the other on
the left. Dr. Steell concludes thus : — " We are unable to explain the mode
of production of these pulses ; and I do not think we are warranted in
aflSrming either that the anacrotic or the bisferiens pulse is the direct result
of aortic stenosis ; both pulses are found, however, so often in association
with aortic stenosis that we cannot deny them diagnostic value ; of the
two the anacrotic pulse probably possesses the greater diagnostic
value."
As regards the anacrotic pulse Dr. Sansom virtually comes to the same
conclusion i he emphasises the deduction that a persistently anacrotic pulse
means organic disease, whether aortic or chronic renal ; and that in case
PiQ, 158. Left radial. C. E. W. set. 18. Loud syst. m. with thrill in aortic area ; aortic diastolic m.;
'fingers clubbed ; patient stunted in growth ; no rh. ; no chorea ; probably congenital lesion with
supervening septic endocarditis. (Graham Steell.)
FiQ. 59.— C. E. W.
Right radial, showing the limitation of bislerieus pulse%o one radial (left).
(Graham SteeU.)
of doubt an anacrotic pulse might signify that a systolic murmur at the
base of the heart is not ansemic. In aortic stenosis, as it seems to me,
anacrotism is easy to explain : the pressure in the aorta is lower than
normal, that within the ventricle is much higher ; at the first moment,
then, of the opening of the valve the blood issues readily, but as the
stenosis throttles the wave the increased velocity of the blood is counter-
acted by the rising pressure in the aorta, and the farther delivery becomes
slower and more laborious ; though so long as the heart is strong the
pulse is regular. Perhaps the most general expression under which we can
bring the anacrotic pulse is that during systole the flow from the aorta to
the periphery is at a slower rate than that from the ventricle to the
aorta : in aortic stenosis the current issuing from the choke bore is of a
high velocity ; that from the aorta to the periphery, however, is slackened
as the blood occupies 'a relatively large channel, an adverse condition
which may be exaggerated by increased peripheral resistance ; though on
the other hand it is diminished by arterial rigidity, in which case, although
the wave is accelerated, the blood-current is not.
DISEASE OF THE AORTIC AREA OF THE HEART 933
Pain is not a constant feature of aortic stenosis ; as in regurgitation
it probably depends on aortitis, and is much aggravated by cardiac stress.
In my experience neither anginal pain nor the sense of substernal oppres-
sion are so great, if as frequent, as in regurgitation. Still it is often
pain, either acute or oppressive, which sends the patient at first to the
physician. It is rarely severe, but may run down the left arm and
serve as a warning to the patient when he transgresses the limits within
which he must conduct his life. In some cases, however, the angina,
whether in obstruction or regurgitation, may harass the patient even
when at rest in bed (Douglas Powell, vol. vi.). Here I may digress so far
as to state my opinion that the seat of the distress in angina pectoris is
in the aorta, and not in the heart.
Dyspnoea. — In aortic disease dyspnoea is not so frequent nor so prominent
a feature as in mitral disease ; and this for obvious reasons. The sub-
sternal oppression of stenosis and of regurgitation is often falsely called
dyspnoea ; it is rather the complaint of the aorta and of an overworked
left ventricle in distress.
There is not the same eccentricity of symptoms in stenosis that there
is in regurgitation ; there is less tendency to gastric perturbations, to
headaches, to pangs having the degrees of angina, to cough (cough de-
pends rather on a dilated aorta), or to faltering of the mind and memory.
Diagnosis. — Latent as stenosis of the aortic orifice in its early phases
may be, on the other hand I need not repeat that to infer this deformity
in every case of basic systolic murmur would lead us into error. Not
even in persons of advanced years, in whom in all probability such a mur-
mur does indeed signify disease of this area, is it to be assumed, as too
often it is, that the aortic orifice is positively contracted. We have
already seen that aortic contraction without regurgitation is a rare condi-
tion ; yet systolic murmurs in the aortic area are of the commonest of
clinical events : in young persons they are usually due to perversions of the
blood, in the elderly to atheromatous disease. We have then in the first
place to decide whether in a given case an " aortic systolic murmur " is of
the kind known as haemic, or due to atheroma or other chronic arterial
disease, such as the syphilitic. Of murinurs due to the acuter degrees of
endocarditis I do not speak ; they are discussed in the chapter on " Acute
Endocarditis" (p. 869).
In the first place, then, is a given aortic systolic murmur, hsemic
or organic, dynamical or statical 1 Neither age nor sex is conclusive :
a young woman may suffer from aortic stenosis of a fixed organic kind,
without regurgitation, and without any history of rheumatism, chorea, or
other constitutional disease ; how are we to decide that in her the murmur
is one of stenosis of the aortic orifice ? Well, in the first place, there may
be no definite signs of ansemia, no venous hums, no characteristic blood
changes, no change of intensity on varying her position ; the first cardiac
sound is inaudible. In ansemia a murmur may be loud, occasionally
even harsh, and in stenosis the murmur may be soft ; but a sawing sound,
especially if associated with a thrill, would strongly suggest organic disease.
934 SYSTEM OF MEDICINE
In stenosis the apex of the heart is perhaps a little displaced in the
vertical direction, and the cardiac impulse not merely forcible, not merely
violent, but steady, long, and heaving. The over -action of the left
ventricle may be manifest, yet the cardiac dulness scarcely increased trans-
versely. A substernal oppression may make itself felt on exertion, or
even during rest, which diifers altogether from the painless and more
panting dyspnoea of anaemia. This oppression often amounts to pain,
and may then run into their left arm. For a broader discussion of this
part of the diagnosis the reader is referred to the article on " Chlorosis," p.
503. Again, although Bright's disease be not present, nor general arterial
disease, the pulse may be anacrotic; this feature of the pulse and its
long plateau would set aside that extremely rare affection pulmonary
stenosis. Again we shall endeavour to ascertain from the history of
the case whether the disease is congenital. Can such- a murmur be one
of mitral regurgitation, or even of mitral contraction ? As regards the
latter, the propagation into the carotids, perhaps down the aorta behind,
and the position and time of a thrill, are important distinctions, even
if we suppose a mitral disease insufficient to cause symptoms of venous
retardation ; the murmur, again, may be comparatively feeble in the
axillary line, and is usually so at the apex. But why stenosis ! May it
not be that a spur of a diseased valve in the blood-current is the cause
of a murmur within an orifice of at least normal dimensions ? May not
the cardiac hypertrophy be accounted for by arterial resistance, whether
in the aorta or elsewhere ; or again may there not be an aneurysm of one
of the sinuses of Valsalva ? This last chance cannot be eliminated ; but
against it is the hypertrophy of the left ventricle, which is not a feature
of these aneurysms; and (hereafter under regurgitation) I shall have to say
something about retardation of the radial pulse in aneurysms which may
iave some importance in this respect. Moreover, a harsh murmur is not,
in our general experience of aneurysms, characteristic of them. If, how-
ever, the systolic miu'mur be less harsh, this point loses its force, and
exclusion of aneurysm rests only on the rather uncertain basis of a
moderate ventricular hypertrophy, the absence of retardation and the
small volume of the radial pulse. Again, may the murmur be generated
in the aorta without stenosis ? I have watched so many cases of large
aortic dilatation to their close in death in which neither a systolic murmur
nor any other murmur ever appeared, that I hesitate to say that mur-
murs arise in the absence of implication of the orifice. That vortices
should form as the blood spreads into the larger channel seems likely,
and that they should thus set up murmurs seems also likely ; yet in all
cases in which I have followed organic systolic aortic murmurs to the post-
mortem table the orifice has presented disease amply sufficient to have
caused the murmur. Aortic systolic murmur with valve and orifice
virtually normal is outside my experience ; dilated aorta, even in extreme
degrees, without murmur is abundant within it. Finally, is the orifice
actually constricted, oris it merely deformed without constriction? In
stenosis I think that there are three tests of the condition : the degree
DISEASE OF THE AORTIC AREA OF THE HEART 935
of hypertrophy of the ventricle, the volume of the radial pulse, and the
diameter of the aorta.
Eosenstein, following no less an authority than that of Traube, asserts
that in aortic stenosis the ventricular impulse is weak or even imper-
ceptible ; on the whole this opinion is contrary not only to my own experi-
ence, but to that of others ; moreover, we must admit that it may not be
possible always to distinguish between cases in which a murmur is gener-
ated at the orifice without constriction in the positive sense and those of
stenosis proper. If there be any power of response in the heart at all
it seems inconceivable that an increase of resistance such as we con-
template should fail to produce hypertrophy, and that it does so is a
matter of certain observation ; moreover, in the cases in which signs of
hypertrophy are absent the pulse is of normal or excessive rapidity.
If an organic systolic murmur be heard at the aortic orifice, if the pulse is
70 or over, and there is no hypertrophy of the left ventricle, I should
say that the disease of or about the orifice has not the effect of stenosis,
or, if it has, that the nutrition of the heart is failing.
Ppognosis.- — It is said that the forecast of aortic stenosis is of all
heart diseases the least unfavourable. No doubt this is true if we
bulk together all organic mturmurs heard, at the aortic orifice ; but this
is a pell-mell classification. We see, it is true, well-to-do old ladies
leading tranquil lives up to fourscore years or more with systolic aortic
murmurs of a quarter of a century's standing ; as we see such persons
with arteries reduced to trees of coral, yet living the length of the
human span. I suppose that such survivors persist in virtue of fair
cardiac hypertrophy, and of the absence of aneurysms on their cerebral
arteries. In my eye as I write is an old lady whose carotids were
jumping to the eye, and whose radials were as tobacco-pipes fifteen
years ago, who still pursues the unbroken tenor of her existence with
no more to trouble her than a slight dry gangrene of the toes which left
her lame half-a-dozen years ago. In these patients, however, the de-
mands of life are of the narrowest and the lightest ; the expenditure is
almost nothing. In Professor Bradbury's case of stenosis — that in which
the issue of the blood was by an almost ' imperceptible channel — the
heart of 24 oz. was evidently able still to drive an attenuated stream
of blood through this tiny hole at a velocity, perhaps, of some four metres
per second ; so that the blood column in the aorta was sustained for a
long time at a pressure compatible with life. When we regard such
cases, and those again in which the aortic mischief sets up corrugation
rather than strict stenosis of the orifice, the prognosis seems better
than in that next best disease, mitral regurgitation. But a broad
division may be made which will show aortic stenosis in a less
iavourable light. If we take patients under fifty-five years of age
we shall find the prognosis much worse. In most of these cases the
stenosis is stenosis proper and of a kind to lead to further constriction ; it
probably consists in fibrous inflammation about the ring and the limbs of
the valve of a progressive kind. In them the prognosis would seem to be
936 SYSTEM OF MEDICINE
rather worse than better for the absence of atheroma : moreover, in the
young the system is more exacting in its demands, and the patient
is not becalmed in the senile torpor of body and mind. Much depends,
of course, on the rate of a subinflammatory process, but my impres-
sion is that a person who in young or middle life begins to suffer overtly
from the symptoms of aortic stenosis has but a few years to live. Of the
duration of its latent period it is of course hard to judge ; the mischief
may be detected by chance, but such discoveries are too irregular to
provide materials for prognosis. Old folks apart, then, my estimate of
the duration of a case of stenosis is not a sanguine one. The final
phase may be by dilatation and backward pressure ; but the usual mode
of death is exhaustion of the left ventricle and syncope, or degeneration
of it and asystole : the former being the predominant and sometimes the
only condition, as in the case of a boy (mentioned above by Sir E.
D. Powell) who succumbed and died suddenly while running. On the
necropsy extreme aortic stenosis was discovered for the first time.
The treatment of aortic stenosis is considered at the end of this
article.
Eegurgitation. — Symptoms and signs. — Like stenosis regurgitation
is often covert in its invasion ; moreover, the cases are many in which the
signs and symptoms of this disease are found without apparent cause. I
have said that aortic regurgitation is not the ordinary course of events in
elderly and atheromatous persons ; a systolic murmur in this area is the
ordinary result of atheroma. Eegurgitation is practically always accom-
panied by a systolic murmur, but I repeat that such systolic murmurs
do not always or even usually indicate positive stenosis; as indeed we may
readily infer from the volume of the pulse.
Whether the mischief be due to past rheumatism (acute endocarditis
is dealt with in another chapter), to strain, to syphilis, or to atheroma,
the symptoms and signs are much alike. But in the two latter cases we
expect to find, and we generally do find, by other signs and symptoms,
that the cardiac disease, pressing as it may be, is but a part of a wide-
spread arterial disease [vide "Diseases of Arteries," vol. vi.]. More-
over, in the atheromatous and syphilitic cases incidental disasters, such as
apoplexy or embolism, are more likely to befall the sufferer.
Pulse. — Aortic regurgitation is sometimes revealed, either to the
patient himself, or to an observant friend, by the characters of the
pulse, a very prominent and peculiar feature of the malady; but
it usually betrays itself in the first place by substernal oppression, a
symptom which we have already considered under stenosis.
The incomprehensible statement is commonly repeated that in aortic
regurgitation the arterial tension is low, and this in face of evidences of
tensile strain witnessed in like degree in no other disease. This tensile
strain is due to the stress of the hypertrophied left ventricle upon the
arteries, a stress often not mitigated by the bar of stenosis or by the pro-
tection of tone : the arteries are large and slack. Under conditions of
DISEASE OF THE AORTIC AREA OF THE HEART 937
high pressure, as in Bright's disease, if the arterial charge vary within
narrow limits, high as the mean pressure may be, the maxima and minima
are not widely apart. Under thes.e circumstances, especially if the
muscular coat of the arteries be hypertrophied, tone secures something
like a uniform adaptation of the vessels to the blood. If tone be
deficient in an arterial system otherwise normal, we find a wide divarica-
tion of the maxima and minima ; but this is temporary and harmless.
It is otherwise when, as in aortic regurgitation, the condition is both ex-
aggerated and persistent. In this case tensile strain, acting both in the
longitudinal and transverse directions, widens and lengthens the vessels,
tends to split them across or along ; and arterial tone, weakened by
strain or anaemia, or put in abeyance by some reflex mechanism, is unable
in any conservative degree to adapt the continent to the content ; the
extremes of volume are too far asunder. The circulation changes into
the form of a series of discontinuous discharges, as if from a catapult.
The well-known tracing of the radial pulse in regurgitation shows a
high and violent percussion, usually with an inertia " crochet " at its
summit, and as sudden a descent without
plateau (Fig. 60). Now it is not necessary
to make a long series of observations to
ascertain whether in a number of cases
the mean pressure is higher under these
extremes than in an equal number of eases
of hypertrophy of the left ventricle without
regurgitation ; nature has given us the in- ^lo-eo-— Margaret b., at. as ; rh. at.
r ,■ . , - °, . , !'• Typical pulse of aortic incom-
lormation m the state of the arterial tree, petence, showing exaggerated per-
^„ 4.1, „ 1 —L-L J J T1 J. 1 1 cussion wave, deficient dicroticwave,
m tne lengtnened and dilated vessels; and nnsustained tidal wave. (Graham
strains which eventuate in general arterial steeu.)
disease, especially in the parts most exposed to the intermittent pulses
of the blood. These results justify us in supposing that in aortic
regurgitation the mean arterial tension is higher than in any other
disease ; though as, for some obscure reason, it seems to be less modified
by tone, a deduction may have to be made in this respect. The efi'ect
of elongation of the arteries is to throw them into curves; and as
these are straightened at each diastole, the vessel is then thrown out
of its bed with a visible and palpable jerk. The wife of such a patient
told Sir Thomas Watson that for some time, on taking her husband's arm,
she had felt this uncomfortable jarring.
Whether in a normal peripheral artery, such as the radial, the pulse
should be visible is a matter of doubt. In some thin people, in whom a
fine skin allows the radial artery to be seen, the pulse is perceptible
to the eye, especially if its tone be slack. It is alleged that this beat is
made visible by the tension of the skin over the vessel, and that were
such a vessel without dimple or dint the pulse would not be visible. In
arteries such as the temporal, which are without much cushion, elonga-
tion takes place more readily ; and in men still yoimg the temporal is
often thus throwu into curves which reveal the pulses clearly enough,
938 SYSTEM OF MEDICINE
though in all other respects the vascular system may be free from any
hint of disease. After the tension of aortic regurgitation has been con-
tinued for a longer or shorter time, all the arteries exhibit the jarring im-
pulse of which I have already spoken — " danse des arteres," as the French
call it ; they start out of their beds -with each pulsation. " Sometimes the
whole of the patient's body," says Watson, " nay, his very bed, is shaken
by the strong shock of the heart during its systole." In many cases this
jerking is well seen in the tonsils. On raising a limb — the arm, for instance
— to a vertical position, the refluent character of the pulse becomes stUl
more apparent, for obvious reasons ; and if in any case of the kind the mis-
chief or the incidents of it be not such as to produce this character in the
horizontal Hmb it will surely appear in the Umb when raised. On raising a
limb the pressure in the peripheral vessels may fall to such an extent that
the pulse may actually disappear ; though entire disappearance is perhaps
always due to some constriction of the vessel at a higher point, as at
the flexure of a joint or by the fold of a garment : raise the arm of the
patient while he has an overcoat on and the radial pulse may vanish ;
remove the dress and the pulse may persist. Dicrotism does not dis-
appear so regularly as one might expect ; in the tracing, if not to the
finger, it is often perceptible. "We might have expected that with the
loss of the support of the aortic valve this recoil would wane or dis-
appear; accordingly in the degree of its persistence a prognostic test
has often been sought, but sought in vain : . we find a dicrotic pulse
sometimes in the least promising cases ; the subject needs further investi-
gation. [For other sphygmographic tracings the reader is referred to the
paragraphs on the bisferiens pulse, etc., pp. 930-932.]
It is the function of a healthy heart and healthy vessels to promote
at each beat the maximum of blood displacement with the minimum
alteration of pressures. At each beat the heart leaves a portion of its
energy in the arterial tree which, given out again between the pulsations,
converts or tends to convert the intermittent pulses into a continuous
flow : it is plain that in aortic regurgitation we have the very converse
— ^the maximum of pressure disturbance with the minimum of blood
translation. Thus, in a well-marked case, in no part of the arterial tree
is the flow made continuous, not even in the capillaries ; and Quincke's
"capillary pulse,'' although not peculiar to aortic regurgitation, is very
characteristic of it. If in any malady, even in health, the arterial
tone be so low that storage of cardiomotive force in the elastic coats
is defective, the capillary pulse may be seen. One of my pupils
once demonstrated to me the capillary pulse in his own person while
in health ; he told me that it was habitual in hita. Dr. Waller says it
may be detected in many normal persons, but that in its extremer degrees
it is characteristic of aortic regurgitation. On the other hand, in many
cases of this disease the capillary pulse is not to be seen. That its
presence or absence is of prognostic value is not yet known ; we have
not hitherto connected its phases with the course of the mischief, nor
do we clearly know why tone in this disease is so low. The readiest way
DISEASE OF THE AORTIC AREA OF THE HEART 939
of obtaining the reaction at the bedside is to press highly upon one of
the patient's finger -nails with the point of a pencil, or to depress
its edge with one's own nail ; with a little management the pulsation
becomes visible. It may be visible also in the vessels of the retina, or
in the areola about such an eruption as urticaria. The same evidence
may be obtained again by pressing a glass slide upon the mucous lining
of the everted lower lip ; or the skin on the forehead, or elsewhere, may
be rubbed until the cutaneous vessels dilate, when their visible pulsing
will prove how great is the factor of vascular tone in integrating the
circulation. In aortic regurgitation tone yields to tension, or in the peri-
pheral vessels atony may be due to lack of due nutrition.
Eetardation of the pulse. — It has been currently reported that in
aortic regurgitation the arterial pulse is retarded. Fagge held this opinion
and many other physicians likewise, among whom is an observer so dis-
tinguished as Sir WiUiam Broadbent.. As this proposition has always
seemed to me to be contrary to observation, both physiological and
pathological, it must receive some closer attention.
In the normal heart there is an interval of about O'l of a second be-
tween the beginning of the ventricular contraction and the carotid diastole.
This interval (the Anspannungszeit or prosphygmic interval) has been care-
fully studied by Chauveau and Marey, Hiirthle, von Frey, Key t, Tigerstedt,
Chapman, and others ; and its interpretation is that in this interval the
intra-ventricular pressure is rising to that in the aorta ; that not until the
contraction pressure of the left ventricle equals the resistance of the column
of blood in the aorta does the aortic valve open and the aortic diastole
occur. Generally speaking, in the normal course of ventricular systole
the relative pressures in ventricle and aorta preserve the same proportions,
and the prosphygmic interval is invariable ; but in aortic regurgitation,
the support of the valve being removed, the pressure within the aorta is
not sustained, and the relation of the pressures is altered : virtually the
aorta and the left ventricle become one chamber. Where there are no
differential pressures there can be no differential times, and the diastole
of the aorta must be coincident with the first contractile efibrt of the
cardiac muscle. On the other hand, the moment the heart relaxes the
pressure in the aorta falls to that in the ventricle. How then can there
be retardation of the radial pulse % How can the radial pulse be delayed
beyond the time of the velocity of the blood-wave ? Lest I should be
wrong somewhere in these suppositions, I have referred the matter to Dr.
Chapman of Hereford. Dr. Chapman, in supporting the arguments
used above, points out that Keyt independently foresaw and demon-
strated this order of the phenomena in 1879. In 1887 he repeated the
same conclusion, that " immediately upon the contraction of the ventricle
the blood-pressure in the aorta begins to rise." Dr. Chapman renders me
the service of tracing the history of the alleged retardation in aortic
insufficiency. Dr. Henderson, he says, first started the notion in 1832.
He was followed by authors of no less ascendency than Flint and
"Walshe. Keyt explains the discordance in this way : — " The enlarged
940 SYSTEM OF MEDICINE
ventricle suddenly filling from both the aorta by reverse and the auricle
by direct flow, communicates a shock so marked as to be mistaken
for systole. This impulse occurring in the first part of diastole, and
preceding the arterial pulse at such a distance, gives the impression
of enormous delay of the pulse." In his Goulstonian Lectures I
find that Dr. Chapman dealt with the whole question, and gave, more-
over, in one such case, the actual measurements, when the interval
between the systole and the radial pulse was 0"039" to O'OSl", instead
of the normal of O'OSO". Now if I am asked why I trespass so
long upon the reader's time and attention with details so minute
as these, I reply that in nature there is no large and small ; and that
for some few years I have anticipated that by such measurements as
these a diagnosis might possibly be made between simple aortic regurgita-
tion and aneurysm of a sinus of Valsalva : unfortunately no test case
has yet come under my notice. Perhaps ere long some skilled observer,
entering into this controversy, may light on a case of aortic regurgita-
tion in which the radial pulse is considerably retarded ; and following
it up to the post-mortem table, may decide the presence or absence of sinus
aneurysm therewith. Again, in double aortic murmur, in murmurs direct
and regurgitant, can we tell by these means whether the direct murmur be
due to stenosis proper or merely to a broken blood-stream large or small ?
Without returning to what I have said under the head of stenosis, I will
guess that, whereas in stenosis proper without regurgitation the summit
of the radial wave is retarded by conditions the opposite of those in
regurgitation, a persistence of the normal interval between cardiac systole
and full radial diastole may indicate a combination of stenosis and
insufiiciency, the pressure in the aorta which the valve is no longer able
to sustain being kept up more or less by stenosis of the orifice. [The
reader is here referred to the postscript.]
The characters of the pulse are well known ; the gifted physician to
whom we owe most of our knowledge of this subject has given a memorable
description of them. Corrigan compared the pulse of aortic regurgitation
to the " water hammer," a toy in which water, imprisoned in an exhausted
tube, falls from end to end, on every turn of the tube, with a thud.
With some such thud the charge of blood is shot along the arteries.
How this effect is intensified by raising the limb, and the effect it has on
the vessels themselves, we have seen already ; I have still to describe
some other characters which are not without interest.
In cases of extensive arterial sclerosis, or at any rate of sclerosis of
the radial and brachial arteries, the stiff walls of the vessel do not collapse
with the sudden ebb of the pulse wave as a comparatively normal artery
does. Nor, indeed, can the arterial diastole be so well marked. Yet,
unless stenosis be present, the stiffened arteries will vibrate or jar, and
the jarring in the carotids and contorted brachials will be plain enough.
The pulse during the more stable phases of aortic insufficiency
is regular. This is the rule, and a very important rule it is.
Trivial as an intermittence of the pulse may be in a healthy
DISEASE OF THE AORTIC AREA OF THE HEART 941-
heart, in . the disease before us it is of grave significance ; as grave
as it is in pneumonia or in enterica. An occasional intermittence
may be of no ill omen; but recurrent slips unmistakably indicate
dilapidation of the heart. An irresolute or dropped beat is a far
mote serious event in aortic regurgitation than in stenosis, or in mitral
disease : in the first case, as in " fatty heart," it is more likely to indicate
a failing than a merely faltering heart, or a passing inequality in blood
delivery. As in other disorders, the heart may fully intermit or con-
tract so feebly that the pulse either fails to reach the wrist, or is but a
flicker there. Irregularity of the pulse is a warning of like omen. In
the aortic insufficiency of cardio-arterial disease, intermittence occurs
earlier than in that of disease more strictly cardiac, at least such is my
experience.
The sudden distension of the collapsed and inanimate arteries gives
rise to signs which are perhaps something more than curiosities ; the
chief of these is the sign of Duroziez. We remember that for the most
part murmurs are produced in the arterial system by the passage of the
blood into a wider channel, when fluid veins are generated. If then
pressure be made on an artery in health, say with an edge of the
stethoscope, these conditions are fulfilled and a murmur is set up. This
phenomenon is intensified in aortic regurgitation, because in this state
the walls of the arteries being slack vibrate more readily, as may be
conveniently observed on the femoral artery. But in aortic insufiiciency,
as Duroziez pointed out, there is something more than this i the artery
gives out not only this single murmur, a murmur of its diastole, but a
murmur on its systole also ; there is a double murmur, and this double
murmur cannot be obtained in the normal state. As French writers
have a confusing habit of taking the word " bruit " to mean either tone
or murmur, it is well to say that a tone is produced by the diastole of
a normal artery near the heart, such as the carotid — a tone to be heard
on light pressure of the stethoscope ; but here we are discussing not the
tone, but a murmur artificially produced by stronger pressure ; and in
aortic regurgitation this murmur is followed by a second murmur generated
on the arterial systole or collapse. The causes of this latter murmur are
unknown ; it is easy to show that it is not dicrotic, but whether it be a
" recoil " murmur as surmised by Fran9ois Franok, we cannot decide. To
get it clearly, Potain directs us to press on the artery with that edge of
the stethoscope which is farthest from the heart, so that the whole wave,
if it be a recoil, passes luider the base of the instrument. He adds that
for its production there is a "most favourable point of pressure," a
degree between too light a pressure and obliteration of the vessel, which
is, of course, to be discovered in each case at the moment of examina-
tion. Now it is said that the second murmur — Duroziez's murmur —
dies out as compensation fails ; if so, it is not a mere curiosity : in any
case attention to such incidents as these encourage that painful research
in clinics which is the only way to the increase of knowledge. Duroziez's
phenomenon is not, I think, peculiar to aortic insufficiency, though
942 SYSTEM OF MEDICINE
Vierordt says it is ; I think I have found it under other atonic conditions
■when the arteries are unduly vibratile : if so, all it tells us is that the
diastole is brusque and the systole " collapsing."
If again the stethoscope be lightly laid on an artery of the size of
the carotid, a " tone " may be heard on its diastole, and not infrequently
on its systole likewise — " the double tone " ; this, though characteristic
of aortic insufficiency, is certainly not peculiar to it. If pressure be made
a murmur occurs, as we have seen ; or if an aortic direct murmur be pre-
sent, the tone is replaced by murmur without the use of pressure. Again,
under normal conditions, on systole of the carotid the second sound of
the heart is audible; now, in aortic insufficiency, and in stenosis, this
second sound is usually lost. In the smaller arteries, under normal con-
ditions, the tone of their diastole is inaudible ; but in aortic insufficiency
an arterial diastolic tone may often be heard down to the smaller and
distant arteries — in the dorsalis pedis, for instance ; so that I have been
in the habit of guessing the amount of the regurgitation from the in-
tensity of this tone in the femoral artery. Arterio-sclerosis, however,
tends to reduce it. The same phenomenon occurs in anaemia, fevers, and
other states in which the artery is slack and the diastole sudden. The
murmur of aortic insufficiency is often heard in the carotid, but by no
means always ; the conditions of its propagation thither are of some
clinical moment, in so far as they may help in the discrimination of
aortic from other diastolic murmurs.
The, Heart. — Of the dilatation and hypertrophy and their signs so much
has been said already in this and other chapters that I will not dwell upon
the subject. I may repeat that the enlargement may be greater in aortic
insufficiency than in any other disease; and usually, at least, is unmistakable.
Perhaps its size is only rivalled in certain cases of chronic Bright's disease-
In young persons with soft ribs the cardiac area may become prominent.
In cases of doubt it is better to lay the ear direct upon the wall of
the chest, whereby the heaving impulse is more readily appreciated. It
is, I suppose, conceivable that in slight insufficiency hypertrophy may
coexist with but a nominal degree of dilatation. Dr. Sansom reminds
us that the less the element of dilatation the more " triangular "
is the apex area; the superficial area of dulness is extended down-
wards and outwards, and does not extend far in a transverse direction.
Although a dull area corresponding to dilatation of the aorta may occupy
the region of the manubrium sterni, and may transgress it to the right,
the ventricular dulness may not be enlarged to the right ;• or not at any
rate until in some grievously protracted case the chambers of the heart
are involved in a common defeat. Francois Franck points out that the-
apex itself may be " dicrotic " ; the first shock being due to the reflux,
the second to the propulsion of the blood (mde p. 940). Sir W. Broadbent
gives us the useful warning not to mistake the systolic recession of inter-
costal spaces, due to atmospheric pressure acting upon the space left-
by the diminution of volume of a large heart, for a sign of adherent peri-
cardium. In cases of arterial disease the observer will not forget that
DISEASE OF THE AORTIC AREA OF THE HEART 943
causes of hypertrophy may have been in operation for an indefinite time
before the establishment of regurgitation. In such cases the hypertrophy
cannot be taken as a direct measure of the insufficiency, which accident
may be recent and inconsiderable, the chief part of the changes being,
attributable to the common causes of both ; however, whether recent
or of long standing, cardiac enlargement, considerable as it may be, is
not so large as in young and sounder persons. It is in the aortic in-
sufficiency of the young, due almost always to rheumatism, that the huge
hearts are found which lift life along for many years.
Sounds of the heart. — In a very large proportion of cases of aortic
regurgitation the first sound is impure if not actually replaced by a
murmur; whether there be positive stenosis or not, insufficiency is
generally accompanied by such changes in the structure of the ostium
as to give rise to a direct murmur also. In arterial disease the
occurrence of a diastolic without a systolic murmur is very rare, as the
regurgitation arises incidentally in the course of the atheroma. In
strain or rheumatic injury the murmur of regurgitation may exist alone,
at any rate for a time ; yet even in these cases the first sound is seldom
pure. At the apex the first sound is usually prolonged, especially if
there be coincident stenosis ;' and it takes a more " booming " quality as
the hypertrophy increases. The direct murmur is usually but not
always carried well up into the carotids, so that the carotid diastolic tone
is replaced by a murmur, or even by a thrill ; yet sometimes neither
sound nor murmur is heard with their systole. The second sound at the
pulmonary cartilage is unchanged, unless the whole heart be thrust still
nearer to the wall of the chest, when it will seem accentuated. The second
aortic sound in aortic regurgitation has not been studied very precisely.
If it persist with a regurgitant murmur, it is said, a little too readily,
to be the sound of the pulmonary valves only. That this is not the case
seems to be proved by its frequent propagation into the carotids. Again,
it is argued that if the aortic second sound coexist with a regurgitant
■ murmur there is still a substantial area of valve closure, either by
fractional parts of the valve or by the establishment of a measure of
stenosis which in aortic insufficiency may be conservative. On the
other hand, though the disappearance of it may be of iU omen, it is
certainly incorrect to say that persistence of the second sound always
means a moderate degree of regurgitation. These are points which need
verification, but after all sounds and murmurs make but a part of
diagnosis ; in quickly beating hearts indeed such points are inappreci-
able. I am disposed to regard persistence of the second sound, in some
cases at any rate, as due to the sudden systole of a slack and vibratile
aorta, such a tone as that of the systole of the femoral in this disease.
It may be audible in cases where the valve is quite disorganised.
Murmur of regurgitation. — If, on the one hand, it be true that this
murmur is usually very definite in its characters and its meaning
inevitable, it is none the less true that, with the exception of mitral
stenosis, it is the murmur most freqixently overlooked ; and not by
944 SYSTEM OF MEDICINE
pupils only, but by experienced practitioners. Sometimes the murmur
lurks in unexpected places ; sometimes its quality is so soft and evanes-
cent that a quick ear is required for its detection, especially if a rasping
systolic murmur precede it. If it be both soft and aberrant in its
site even a skilful observer may be deceived, at any rate at first. Not
only may the murmur of regurgitation be soft and distant, and may lurk
in strange places, but it may be aberrant in time also. It may occupy
fractional parts of the diastolic period, and not always the initial part.
Like the murmur of mitral stenosis, it may be perceptible only in the middle
or final third of the long pause ; and if discovered accidentally in this
rhythm, before the advance of secondary changes, it might deceive even the
elect. One such case I remember which divided three hospital physicians
in opinion. One inferred mitral stenosis ; two held to aortic regurgita,-
tion. Whether either opinion was afterwards verified I cannot say. Dr.
Douglas Stanley described an interesting case of the kind at a branch meet-
ing of the British Medical Association. In this case a diastolic murmur arose
immediately on diastole, a murmur of aortic regurgitation well marked
at the base ; at the apex was heard a mid-diastolic murmur, rougher
than that of the base, and not heard outside the mitral area, which ceased
before the first sound. After death the aortic valve was seen to have
but two cusps, and these involved in a mass of vegetation. The mitral
valve was healthy. Both murmurs were clearly aortic.
Loudness of murmur is no indication of severity of lesion ; the
reverse is rather to be anticipated. A loud murmur generally signifies a
vigorous heart ; and a refluent stream returning at a high velocity may
set up more active veins in the ventricular content than a large return
falling back through a large opening at a low velocity. If a murmur
previously loud fall in intensity we may be apprehensive of evil.
Sudden ruptures of the valve often give rise to very loud murmurs
audible over a large area of the chest; in such cases the murmur has been
audible to bystanders, and even to the patient himself. In the presence
of stenosis a regurgitant murmur is louder, other things being equal ; as
the velocity of the refluent current is greater. In these cases a small and
fairly sustained pulse is associated with a sawing double murmur. A jet
returning through a perforation of a limb of the valve is said to be attended
with a piping or mewing sound ; or it has been compared to the chirping
of chickens. A murmur direct or regurgitant, audible without contact
with the wall of the chest, is always aortic — an inference sometimes of
diagnostic value.
Prof. Sewall of Denver has investigated the behaviour of all cardiac
murmurs under increasing pressures of the stethoscope. He says that
murmurs of aortic stenosis audible at the apex disappear under pressure
there, and are herein distinct from mitral regurgitation. Also that, great
dilatation of the aorta or aneurysm apart, the murmurs of aortic regurgi-
tation may be annulled by pressure at the base but not at the apex.
"Inorganic murmurs" at the base, he says, can aU be obliterated
by pressure; and by the same means used in the second right inter-
DISEASE OF THE AORTIC AREA OE THE HEART 94S
space close to the sternum the normal second sound can be stopped,
unless the aorta be so dilated as to be in contact with the wall of
the chest.
The student is often directed to track a murmur to its origin by
shifting his stethoscope along the surface of the chest from one area
to another, in order to note where one murmur dies and another
is born. This is a misleading device, only to be used by skilled
observers. A murmur, like a river, may run underground in part of
its course, the conditions of conduction differ from place to place,
and one and the same murmur, as the stethoscope travels, may so wax
and wane, as the structures about it vary in conductive capacity, as to
appear twofold. Many a misapprehension thus arises as the observer
slips the instrument diagonally upwards ; a murmur heard at the apex
disappears to reappear at the aortic cartilage ; and thus a murmur
generated at the aortic orifice only may be regarded as indicative of two
lesions. Another error is to assume that the murmur certainly follows the
direction of the blood-current; the blood does not run in the air as water
over gravel ; the murmur we hear is due to the vibrations of surrounding
structures — chiefly the walls of the heart — set up by the vortices within
them ; the heart is the fiddle, the blood is but the bow. We must rid
our minds of these conceptions of blood running here and there in
the chambers, as if it were from a water-cock into a pipkin, and realise
that the walls are thrown into vibration by molecular collisions ' in a
plenum.
Of aortic insufficiency with regurgitation, but without a murmur,
I know nothing; but murmurs which can be extremely soft may in
very rare instances be evanescent. Weismayer, in a paper which has been
much quoted, accepts such statements, a little uncritically I think, and
proceeds to explain them. Dr. Hermann Weber's case (vide infra) is an
example of the manner in which in incipient cases the murmur of aortic
insufficiency may cease for a time with the insufficiency which gave rise
to it ; again, like any other murmur, that of insufficiency may wane with
the heart in which it is generated ; but that with a persistent insufficiency
regurgitant murmurs come and go in a comparatively vigorous heart is
contrary to experience, or at any rate to mine. As testing exceptions I
may refer to a case reported by Dr. Saundby, and to another reported
by Dr. Musser. In Dr. Musser's curious case the corpora Arantii had
been transformed into calcareous buttons (4 mm. by 2 mm.). During
the formation of these excrescences regurgitation took place and a mur-
mur was generated; but as they wore down and the free surfaces
became faceted, after the manner of gall-stones, the incompetent valve
became again competent.
Whether regurgitation is prone to occur in dilatation of the aorta with
an unimpaired valve, and without aneurysm of a sinus, has been con-
sidered already (p. 922). Eelative insufficiency at the mitral orifice is
well understood and by no means rare ; but this is known to depend
Upon the conditions of the muscular and tendinous attachments of the
VOL. V 3 p
946 SY:STEM QF MEm.CINE
limbs of this valve, a kind of attaohuieut: whioh does not exist in the
aortic val'we.
With this problem is bound up that of " intermittent aortic regurgi-
tation" considered above ; for these cases are said to depend also on con-
ditions of the aorta rather than of the valve. I believe that in cases of
intermittent aortic regurgitation the valve is nearly always diseased ;
but that in the earlier stages, say in disease of one of its limbs, the
valve becomes able, by mutual accommodation of its parts (p. 466),
to close the orifice until the blood-pressure becomes excessive, or some
other physical change supervenes. Such a patient may indeed, be ex-
amined at a time when the valvular disease is latent, or is not revealed
by a murmur at any rate ; and in such a case a grave error of diagnosis
might be committed. The following case, resting on the authority of
Dr. Hermann Weber, is most instructive : —
A very active young man, set. 32, of weak muscular development, was
examined by Dr. Weber on arriving at a height of 8000 feet. The second
aortic sound was replaced by a musical murmur at mid-sternum and a little to
the right. The first sound was rather indistinct. The pulse was 105-112,
feeble, but not characteristic of aortic regurgitation. On the following day the
murmur had disappeared ; the heart sounds' were normal, and the pulse 88.
Two days later, at 9000 feet, the same murmur became audible ; and in like
manner disappeared on the day following. Further climbing was forbidden,
and he returned to work in good health. Seven years later the patient diei
of " Herzsohlag."
Regurgitation may occur at times of high blood - pressure — as for
instance in exertion or in senile arterial plethora, and may disappear —
the valve becoming again competent — as, under treatment or otherwise^
aiTterial pressure falls.
Murmurs occurring during diastole may be heard in pericarditis and,
aneurysm ; the former murmurs are not difficult to interpret (wciJe
p^ 953).
Dilatation of the aorta is said to be the rule in cardio-arterial de-
generation, the exception (in any considerable degree) in primary aortic
regurgitation. If so, the exceptions are many ; I recently lectured,
in Cambridge on a case of mere rheumatic aortic disease in which,
tjjere was considerable dilatation of the aorta with " fireman's helmet"
dulness.
The association of aortic disease with murmurs simulating more or less
those of mitral disease remains to be discussed. The murmurs may be
divided into two classes; those suggestive of mitral regurgitation, and thoger
suggestive of mitral stenosis. First, of aortic murmur simulating that, of
mitral regur^tation four cases were brought forward by Dr. Dickinson at
the meeting of the Koyal Medical and Chirurgical Society on the 8th
of June 1897.. In them, although after death the aortic orifice
in each was found to be advanced in stenosis, a systolic murmur was
heard at the apex, so that mitral regurgitatiom was either assumed or
DISEASE OF THE AORTIC AREA OF THE HEART 947
could not be excluded. In many such cases, either my own or
shown to me from time to time in hospital wards, I have perhaps too
promptly and confidently declared my opinion — quantum valuisset — in
favour of aortic obstruction ; I admit, however, that in some of them
mitral disease can only be excluded on the principle of " ne entia
multiplicanda." Still this principle is a sound one if we do not lean too
much upon it. In two cases in which I was led to hazard such an opinion
it was borne out by necropsy ; there was no mitral insufficiency. In one
of these examples the murmur at the apex was musical, and I guessed it
to be four to one that a distinctly musical murmur is aortic. In another
the murmur was audible an inch away from the patient's chest ; it is
twenty and more to one that a murmur so audible is aortic. In another
again a thrill was perceptible at the base. That such murmurs may be
audible in the back I admit, — aortic systolic murmurs often are ; but in
the cases I have seen such murmurs were not confined to the axillary and
infrascapular regions, but were audible anywhere — -passim, not ordinatim.
Again, in such cases — and this is true, I think, of those collected by Dr.
Dickinson— the arterial pressures were in themselves almost conclusive ;
the pulse in each was not " mitral," but " aortic," regular and of fair
mean pressure. In mitral regurgitation the arterial system is ill-filled,
while signs of a rise in venous pressure, cardiac and systemic, are soon
manifested. Dr. Norman Moore has suggested that the sphygmograph
might be useful in the diagnosis of such cases ; for once in a way it
might : an anacrotic tracing would settle the question in favour of aortic
stenosis, though it might not exclude coincident mitral incompetency
of slight degree.
Secondly, an aortic regurgitant murmur may simulate that of mitral
stenosis. The murmur of aortic insufficiency generally begins on diastole,
is then loudest, and falls as the aortic pressure falls; that of mitral
stenosis generally rises up to the systole. Aortic diastolic murmurs in
the later part of the pause are very soft, because the pressures in aorta
and ventricle are then nearing equality, or have attained it, the vibrations
persisting for a sensible moment longer in the walls of the heart. If the
murmur be heard at upper and mid sternum, if it begin with the diastole
of the heart and taper ofi" during the pause, it is an easy sign to interpret.
But if the murmur, not as a rule so harsh or vibrating as that of mitral
stenosis, be so soft that it may escape an unpractised ear ; if, instead of
tapering off from the beginning of the pause, it occupy the middle, or
even the latter part of it ; if, again, it be barely audible or inaudible at
the upper sternum, distinct at the lower sternum, and loudest about the
fourth left interspace, the student of the aortic cartilage may be misled by
whispers so stealthy and devious. He may attribute the murmur to mitral
stenosis ; or he may add the case to the list of vanishing aortic regurgi-
tant murmurs, or again he may add himself to the cloud of witnesses
to "pulmonary regurgitation." However distinct the murmur may be
in the fourth left space, it dies off rather abruptly as the apex is
approached.
948 SYSTEM OF MEDICINE
Finally, tte murmur of mitral stenosis may be simulated in aortic
regurgitation. There are many cases on record in which a " presystolic
murmur " was present without mitral stenosis ; in some of them the only
perceptible lesion was aortic. From what we have seen already (p. 944), the
student is prepared to understand that murmurs occupying the long pause,
or parts of it, not necessarily the initial part, are consistent with, and
under certain circumstances significant not of mitral but of aortic disease.
Against this source of error the observer will be on his guard. But this
explanation does not cover all the ground ; observers of the highest
authority assure us that a presystolic murmur, heard in the mitral area,
such a sound as to be characteristic of mitral stenosis, is to be heard in
cases which otherwise would be regarded, even on the post-mortem table,
as uncomplicated aortic regurgitation. To these cases the late Dr. Austin
Flint first drew attention, and his lead was followed by many other
observers whose records have been well summed up by Dr. Lees. Dr.
Sansom, who recorded cases of this kind in 1881, has carefully discussed
the difiiculty again in the new edition of his work ; to this discussion I
refer the reader for further detail, as no explanation of the phenomenon is
as yet established on anything like a certain basis. Sansom and Potain
lean to the belief that the presystolic murmur (if it be generated in the
mitral area, and not in the aortic) may be due to impingement of the
refluent aortic current on the anterior mitral curtain before it is made
taut, whereby either vibrations are set up in the valve itself or, by bulg-
ing the valve, the orifice is practically narrowed. Dr. Fisher has published
two cases of this kind (one of Dr. Hale White's), in both of which
thickened endocardium upon the ventricular septum showed the formation
of the eddy was not in the region of the mitral valve. " The presystolic
thrill and bruit were well marked and mitral stenosis was diagnosed;
but at the necropsy the mitral valve was found quite normal. The
aortic valves were healthy also it is interesting to add, and the aortic
regurgitation heard during life was due to pouching of the sinuses of
Valsalva with dilatation of the first part of the aorta." A third case, of
Dr. Goodhart's, is adduced to prove that this presystolic murmur may
be heard in disease of the aortic valve without regurgitation. Other
authors suggest that a meeting of the aortic and auricular currents may
produce a murmur; if so, surely Flint's murmur should be far more common
than it is. One case shown to me in a hospital three years ago by two
physicians as one of this kind, was in my opinion a case of broken aortic
diastolic murmur, not generated in the mitral area at all. There was
no rumble ; the murmur was audible to left of the sternum, but not
in the scapular region. Still rumbling presystolic murmurs, with thrill,
do no doubt occur in aortic disease unaccompanied by mitral disease.
All I can do then is to warn the reader of this source of error ; and
that murmurs form but a part of cardiac diagnosis. It has been good
for us that these invaluable aids to diagnosis have received even a dis-
proportionate share of attention, but it has been at some loss of perception
of other aspects of cardiac disorders, some of which are of no less value.
DISEASE OF THE AORTIC AREA OF THE HEART 949
Pain. — Distressful sensations of the nature of pain are more common
in disease of the aortic area than in other diseases of the heart. The
distress may range from a slight oppression to breast pang ; while a fair
compensation is maintained, and there is no active aortitis, no discomfort
may be felt, otherwise the distress may become agonising and almost
constant. Its form is that of angina pectoris. When the insufficiency
of the aortic valve is of acute onset, as in sudden rupture, the pain and
oppression may be very great; but unless the mischief be of extra-
ordinary severity — ^bad indeed almost beyond hope — the pain wiU pass
off as the inflammation in the area subsides, the reserve capacity of the
heart comes into play, and pressures are readjusted : thenceforth, untU
the organ begins to fail, discomfort may be absent — at any rate in patients
under middle age. If it be in elderly persons, the subjects of general
arterial disease, that angina pectoris in its major or minor forms most
frequently occurs, it is by no means confined to them.. I recently
witnessed a very distressing and persistent angina in an undergraduate,
the subject of recent rheumatic disease of the valve, and probably of
aortitis. A sense of substernal oppression is the first hint of it ; it
is felt on distension of the stomach and bowels, and on ascents,
even the gentlest. In extreme cases, or in persons of the peculiar tem-
perament which favours the phenomena of angina, assaults of this kind
may come on during complete rest, probably in obedience to unseen
tides of blood-pressure. That angina pectoris comes on during effort
only is a false aphorism based upon too smart a description of such
cases ; not infrequently it comes on even during sleep, adding a
new torment to the bitterness of death. Of muscular movements those
of the arms seem to be the most efficient in producing anginose pains ;
it has been stated that movements of the arms are the most instant in
their effects upon blood-pressure. Another surmise is that persons of a
gouty habit are peculiarly liable to anginose attacks and complications,
an opinion based upon no little clinical experience ; it is but a part of
the truth, however, as angina is even more tyrannous, if less lethal,
in persons in whom the neurotic habit is conspicuous. Such sensations
are not so common or conspicuous in aortic stenosis as in regurgitation.
As the aorta is probably the seat of them this distinction is intelligible.
Another seat of pain in aortic regurgitation, and this too rather in the later
phases of it, is gastralgia, or a suffering so described. This pain is to be
discriminated from the aches, severe' and trying as they often are, which
seem to have no deeper source than the intercostal and neighbouring
spinal nerves. With the gastralgia is often associated the persecuting
flatulence which besets all cardiac affections, even the functional. To
belch up wind is attended with relief, but it is another thing to say
that the wind is the sole cause of the distress, and it cannot ex-
plain the recurrence of the " gastralgia," which I suspect is allied to
angina.
It is alleged that there is some connection between tabes and aortic
disease. Eugeand Hiitter found aortic disease in nine cases out of 138
950 SYSTEM OF MEDICINE
of tates (6 "5 per cent). In only one of these was there no probability of
syphilis, and in five this antecedent was definitely ascertained. Articular
rheumatism counted for very little. Sir W. Gowers accepts the association
as a causal one, and G-rasset and Eauzier are of the same opinion. The
probable explanation is that both diseases belong to the syphilitic series,
and may be associated in young persons before the approach of
senile atheroma. Other authors regard the connection as one of simple
coincidence. No confident opinion can be expressed at present ; but it
may be that in many cases of aortic regurgitation the gastralgic phenomena
are directly of tabetic origin. How often do we wish our cases back
again for better investigation ! It is but the other day, after I had
completed an examination and discussion of a case of thoracic aneurysm,
that my colleague in consultation was wicked enough to tell me I had
not found out that the patient was tabetic. Though the gait was scarcely
affected, I had to admit, when told, that such was the case. Here again
syphilis was no doubt the nexus, and an insidious tabes may be the
origin of some symptoms not directly attributable to the cardio-arterial
disease.
The nervous system. — ^Besides pain, which strictly speaking should
come under this head, there are other nervous disorders which are better
marked in aortic regurgitation than in other forms of cardiac disease. In
an article on cardiac delirium, published many years ago, I said that
the sufferers from aortic disease show an occasional liability to cerebral
derangements. Even in the latent or stealthier phases of aortic in-
sufficiency we may note more especially certain mental perturbations
which are not unknown in other heart diseases. We note a restlessness,
a fretfulness, a change in temper amounting sometimes, as the mischief
advances, to violence ; in rare cases the restlessness sometimes goes so far
as to urge the patient to spring from bed, to perambulate the house, or
even to jump out of the window. We may compare the delirium of such
cases of aortic regurgitation to that of alcoholic pneumonia ; and, as in
these extreme degrees it occurs chiefly in men, it may be so troublesome
as to make a male attendant necessary. That it is not alcoholic is
proved by its outbreak or persistence in patients who are and have
been under continuous observation and restriction. Much of the rest-
lessness of the delirium is due to the fact that it is usually a delirium
of place : the patient is under the delusion that he is in a strange house,
or far away from home ; pacified for a few minutes, or for a few hours, the
delusion seizes him again and again with an agitation which is fraught
with the worst consequences to the cardiac disease. Prof. Osier (62)
makes a like observation. The association of insanity with cardiac disease
has been studied by Mickle, Ball, Fauconneau, and others. Apart from
mental disorder, headache is frequent in aortic insufficiency ; and buzzings,
dizzy sensations, momentary obscurations of consciousness, twitchings, or
even convulsions, may indicate the perturbed conditions of the cerebral
functions by way perhaps of the circulation. The vascular inconstancy
is perceptible to the patient whenever he stoops. Sleeplessness, not by
DISEASE OF THE AORTIC AREA OF THE HEART 951
any means always due to cardiac uneasiness, is often very troublesome,
and is especially noticeable in aortic insufficiency.
Nutrition. — Although the arterioles cannot be contracted, as some-
times alleged, — or we should not see the capillary pulse, — yet pallor and
some falling off in flesh mark another distinction between aortic insuffi-
ciency and mitral disease, in which the face is congested ; and emaciation,
if present, may be concealed by venous turgescence or arterial oedema.
So long as dilatation of the left ventricle is compensated by hypertrophy,
so long as the cardiomotive force keeps up, there is practically no anasarca
or ascites. Filling of the pleural cavities, swollen legs, albuminuria indi-
cate a slackening ventricle and increasing residual blood ; the heart is
entering upon that final phase of demolition which has been described
under the diseases of the myocardium, and must not detain us here.
Respiratory system. — While the mitral orifice and the myocardium are
sound the pulmonary circulation is protected. It is in the final stage of
a shattered heart that the bases of the lungs begin to fill. These changes
often appear before there is definite evidence of mitral insufficiency — at
any rate before a miu-mur is generated, and even before the extension
of dulness over the right ventricle. As the ventricle is distended the
papillary muscles may fall relatively short ; or in some other of many
ways the mitral machinery may be deranged : yet even with a competent
mitral valve, as the residual blood in the left ventricle becomes more and
more, and the regurgitations perhaps larger and larger, the arterial head
will dam back the venous. When a murmur of mitral regurgitation ap-
pears the end is not far off; and therewith the case travels out of my
sphere.
Dyspnoea is scarcely to be called a prominent symptom till this last
stage is reached. The dyspnoea of the earlier stages is rather an inex-
plicable perturbation which the patient himself can hardly describe, and
which, if an exact person, he usually declines to call shortness of breath :
he speaks of it rather as a sense of oppression which impels him to sit up ;
it partakes of the nature of angina. Nay, often, as in angina, he may
evade a strong inspiratory effort. At times, however, and in later phases
of the disease, the patient may be seized with " cardiac asthma," when the
gasping and shortness of breath are distressing. Still, this is not quite
the panting of mitral disease : the excursions of the chest are less con-
spicuous, and have more of a nervous or spasmodic character. It may
be a call of the bodily tissues upon the heart for more blood, a call not
so much for the "respiratory pump" as for more driving power ; or, again,
it may have a toxic origin. If expiration becomes audible a little distance
away, and both inspiration and expiration assume a tubular quality,
such as horsemen call " roaring " or " whistling," then, however slight this
may be, the trachea is so far constricted by a dilating aorta.
Cough is often present — ^generally indeed — and may be an intolerable
evil. This cough, when it does not spring from incidental causes, is due
to pressure of the dilated aorta, either directly upon the trachea, or
upon the laryngeal nerves. Unless there be some contingent catarrh
952 SYSTEM OF MEDICINE
there is no expectoration, or no more than is hawked up by any
cough. In cases of considerable dilatation of the aorta the cough may
be of frightful severity. One patient of mine, when he felt an attack
coming upon him, used to throw himself on his hands and knees ; or
such sufferers will anchor themselves to bed or table to mitigate the
racking of it.
SphygmograpMc signs. — The ordinary tracings which adorn our
books and essays are of little worth. The more valuable ones, such
as those of Mahomed, Galabin, Riegel, Lorain, and others, present
some points of interest. Hundreds of tracings are published which
prove no more than the inadequacy of the sphygmograph to analyse
the finer components of the aberrant pulse. It is characteristic of
the tracings in aortic insufficiency to show a hook or " crochet " at
the summit of the percussion wave which, in aortic regurgitation
with a strong ventricle and little or no aortic obstruction, is of
course very high. The sharp return of this " hook " is said to exhibit
the rapid arterial recoil ; but to my eye, like many other such notches,
it exhibits nothing more than the inertia of the lever. Notches and
waves due to this cause are too often interpreted as records of this or
that secondary vascular wave. After a sharp fall of the lever in aortic
regurgitation, or in other states in which arterial resistance is low,
a second wave of inertia may also be seen, and even a third, as in
a tracing recently published and elaborately explained. Such waves
mean nothing more than the bouncings of the long and light lever
after strong percussion. It is remarkable that the dicrotic wave often
persists (Fig. 60, p. 937). Now if the dicrotic wave be due to recoil of
the aorta, we might expect that when the bottom of this vessel is
knocked out this recoil would be prevented; but this is by^no means
always the case. Dr. Samways urges that the dicrotic wave is due to
the longitudinal recoil (shortening) of the first part of the aorta ; this
may possibly explain the persistence of the wave under the circumstances
we are considering in any case stenosis would promote it. It seems
probable that as regurgitation increases the dicrotic wave would be
obliterated ; but it does not appear that this indication has any important
prognostic value. The presence of more or less stenosis might be 'indi-
cated by an anacrotic wave in the tracing. Jt is difficult to draw any
precise conclusions from the sphygmograph as to degrees of atheroma ;
the tendency in such cases is, of course, to a broader-topped wave. The
sphygmometers of Hill and Barnard and of Dr. Geor'ge Oliver seem likely
to take a practical shape, and, if so, mechanical aids of great value will
be placed at our service. By such means many difficult problems, now
obscure, will be made clearer to us.
Diagnosis. — Much has been already said indirectly in this respect.
In cases of uncertain diastolic murmur the absence of thriU or its dis-
tribution about the base, the absence, in the earlier stages, of the short
first sound of mitral stenosis, of reduplicated sounds, of evidence of rise
of pressure in the pulmonary circulation, and constancy of murmur on
DISEASE OF THE AORTIC AREA OF THE HEART 9S3
changes of position, will indicate that if there be a murmur in the mitral
area also, it is but the flapping of the upper limb of this valve (Potain
and Sansom). I repeat that in following a murmur from apex to base,
it may not only go underground for a space, but also may emerge with
a change of quality ; and that murmurs of aortic regurgitation may be
exceedingly distant or faint, may frequent strange quarters of the cardiac
area, and may be inaudible at the aortic cartilage. In the last stage
the failing systolic sound is as short as in mitral stenosis, and the liver
enlarges and hardens. The jerking of the arteries too may then subside,
and the case becomes virtually mitral. Duroziez's sign may be useful,
but is hard to make out in an oedematous thigh.
In a patient, whom I saw but once, I had some hesitation at first in
deciding whether a chafing diastolic sound at the base were due to aortic
regurgitation or to the pericarditis of chronic renal disease. A study of
the whole case, however, left no doubt of the latter interpretation.
PFOgnosis. — The course of aortic regurgitation is towards death. As
in all heart diseases the main factors in prognosis are four : the age of
the patient, his calling and habit of body, the kind of lesion, and the degree
of lesion. An accurate knowledge of the history of the patient and of
his symptoms is very important, but it is not always to be had. I have
a difiiculty in recalKng cases of mere aortic regurgitation in children ;
such cases, if rheumatic, have no doubt a long average survival.' A
deformed valve segment must in all cases be a strained segment, and
meet for chronic infiammatory and atheromatous degenerations. A clean
rent in a healthy valve segment should be a less destructive process
than a lesion of equal degree due to atheroma ; it is said that a clean
rent in an aortic cusp has been known to heal. As age advances the
prospects of the duration of life grow less and less ; the lesions may be
worse in kind, certainly adaptation is less ready. In atheroma aortic
regurgitation signifies not only progressive disintegration, but also an
accelerating rate of it, and prognosis is graver with regurgitation than
with obstruction : aortic direct murmurs being, as I have already said, the
ordinary feature of atheroma, regurgitant murmurs the extraordinary.
Death may suddenly intervene in the period of latency, primary or
secondary, but the period is one of comparative safety ; when the attention
of the physician is drawn to the disease by complaints of retrosternal
oppression or of uneasiness on ascents, the stage of dissolution has
begun ; whether the origin of the mischief be in old or young, in strain,
rheumatism, or atheroma ; though in this last kind dissolution may be
more rapid. In strain such sensations may be felt at first before re-
adaptations of cardiomotive functions have become established ; but if the
patient's life is to be a comparatively good one they should pass off for
some years, as the reserve capacity of the heart comes into play (secondary
latency). The patient may go about his work again in ignorance of the
fatal rift ; yet, when he is brought up, sooner or later, by some uneasiness
about the heart, he does not forget to tell the physician how that on a
certain occasion of effort he felt a strange and distressing sensation in
954 SYSTEM OP MEDICINE
the heart. This event may have been five years before; but usually
it is not more than two or three, and may be much less.
The duration of the latent period — primary or secondary — depends
more on the degree of insufficiency than on the soundness of the
cardio-arterial system : for, unless it be in the case of syphilis, patients
undermined by atheroma are withdrawing on account of virtual age from
heavy work ; and if in older men the conditions of nutrition may be less
favourable, those of labour are less exacting. If, however, rupture
occur in a man whose arteries are degenerate, the latent period is very
brief. In such a case, recently under my care, the consequent symptoms
of disease never receded at all. When we turn from rupture to in-
suificiency gradually established, we find, as I have already said, that too
literary a view of the matter is taken by many writers, especially in the
division of chronic aortic disease into the cardiac and the cardio-arterial.
A long survival, is not unusual in cases of general cardio-arterial disease
in elderly persons, while on the other hand " young cases " often do
poorly, and last for a briefer span than we had anticipated. That
the duration of a heart maimed by aortic insufficiency may be at least
as short in young persons as in the old and atheromatous, will be
granted in respect of younger subjects in whom the invasion of syphilis
is unchecked; it is not usually admitted of rheumatic disease, thou^
this process consists in a proliferative fibrosis which, as opposed to mere
"replacement fibrosis," too often has ruthless cicatricial consequences.
Healthy as, apart from the local disease, the heart and arteries may
otherwise be, the progress of such cases is often inexorable. It
were paradoxical to say that the outlook may occasionally be better
in cardio-arterial atheroma, but the part may not be far from the
whole truth. I have said that the capacity in elderly persons for a
fairly sound hypertrophy of the left ventricle is usually much underrated;
even in the presence of dilatation of the aorta, and of stiff vessels, the crazy
machine with a fair muscle at its centre may last many a year,
unless one or other coronary artery be blocked ; or miliary aneurysms
form on the cerebral arteries. Let sanguine prophets say what they
may, ten years is a long time in any case of aortic insufficiency ;
and, given equal degrees of insufficiency, I would not despair of such a
respite in temperate and tranquil elders, until they " be with ease
gathered, not harshly plucked, for death mature." Every physician's
experience must remind him that to be " harshly plucked " is not the
fate of the older of these patients only ; of young men who die suddenly,
no small tale die of aortic insufficiency ; and to die of syncope with
a sound or fairly sound heart muscle happens to old as well as to
young patients. To say that the disease in the cardio-arterial cases is
" progressive," and in the rheumatic or strain cases not necessarily so, is too
academic a distinction, and untrue even as that : aortic insufficiency is
always "progressive," even if the local disease is not. If the contrary
be asserted it is because observers are in a state of reaction against
the black prognosis of all and any heart disease which prevailed among
DISEASE OF THE AORTIC AREA OF THE HEART 955
our fathers ; now we are in the opposite extreme, and are buoying
up our patients with too crude a hope. Some young patients die un-
expectedly soon, some old ones live beyond expectation. Mitral in-
sufficiency is the only heart disease which, under favourable circumstances,
can be nursed to an indefinite duration. I have now under my occasional
observation persons still leading useful and active lives who have
lived a quarter of a century and more with mitral regurgitation ; but
I cannot remember the survival of any patient with aortic regurgita-
tion for fifteen. If the patient, whether in a palace or in a workhouse,
be a man of easy circumstances and tranquil occupations, he has the
greater chance of survival. Care or worry, bustle or toil will kill him.
There are men of such a temperament that they cannot form sedate
habits : recklessly, as it seems to the doctor, they skip up stairs two at a
tiine ; they puff after trains ; they climb over five-barred gates ; they
bounce up from deep sleep to pass water, and so forth : they do not mean
to run these risks, but such is their incorrigible temperament. With such
persons discipline must be attained by spending day after day in
drill, in gaining self-control, in repressing volatility. In this precaution
there is nothing false to a man's best self ; it is the way to get the most
work out of himself before he dies. Persons in toilsome callings must
change them ; and spend the perhaps no less useful remnant of their
days in some easier duties. Due vigilance may be exercised without the
encouragement of hypochondria ; as some one well put the rule : find out
what you can do, and do it ; find out what you cannot do, and never do it.
The conditions of survival are more favourable in women than in men.
The big ventricle, efficient as it is, racks the machine from the begin-
ning ; the aorta, being of elastic tissue and not of muscle, suffers under
the thrust, and the means of the heart's nutrition, instead of increasing
as demand requires, are gradually sapped. The watchful physician may
then note that muscular effort no longer raises, but even reduces the
blood-rpressure — a bad sign indeed.
Anginose pains are always menacing in regurgitation, yet even they
may be kept at bay by the nitrites, it may be for a year or two ; but
the respite is a life of troublous days — a life of pain, of slavery to
drugs, of bitter physical and mental adversity. Anginose pains seem
to signify less imminent danger in women than in men, although in
men they are more common ; this, if true, may depend on the greater
docility of women under treatment. Sometimes angina appears only for
a time, with a push of aortitis.
In insufficiency death is not always sudden ; some patients drink
the cup to the dregs ; life is protracted from phase to phase of cardiac
disorganisation. Usually, however, the thread of life is snapped before
involution is complete, before these later stages of cardiac dilatation and
rise of venous pressure are accomplished. Such patients sometimes
die of asystole, far more frequently they die of syncope : the heart, not
yet quite played out, comes to a sudden stop, probably under some reflex
interference. Although then the signs of cardiac dilapidation will be
956 SYSTEM OF MEDICINE
noted -with apprehension, gradual dissolution is often avoided : with
seeming caprice death cuts the thread after rather too good a dinner, a
quick step into a railway carriage, or a start up from bed ; or again, the
bolt may be mercifully drawn during sleep, and the last years of such
a life may be happy even in the ending of it ; for as Bacon says : " Many
times death passeth with less pain than the torture of a limb ; for the
most vital parts are not the quickest of sense."
To enter into a discussion of combined lesions of the heart would
lead to repetition of the work of other contributors; but it is almost
needless to say that in every estimate of the duration of life in aortic
insufficiency the values of the other component parts of the heart must
be estimated : such estimates are to be found in the chapters on other
diseases of the organ. Again, it is of the first importance to decide
whether a coincident lesion elsewhere, valvular or muscular, be inde-
pendent or dependent on the aortic. It is contrary to my experience to
assert, as many have done, that coexisting mitral regurgitation is helpful
in any stage of aortic insufficiency, except as a relief to the aorta in the
case of angina ; that moderate mitral contraction may be so is conceiv-
able. In rheumatic cases, aortic disease usually means a more extensive
cardiac damage, and in this respect again the prognosis is worse in aortic
than in mitral insufficiency.
That " apex murmurs " are often mere aortic direct murmurs I have
said already. Loudness of murmur, other things being equal, speaks in
favour of sustained cardiomotive force, and, although a murmur soft to
the point of indistinctness may be consistent with slight or incipient
injury, on the other hand a murmur may wane with the heart which
generates it. A quickening pulse is of iU omen ; if not due to temporary
causes, it means a larger residuum at each contraction and ill -filled
arteries, as tested by raising the arm. We are told that a fall of the
specific gravity of the blood is likewise of ill augury. If stenosis coexist
with insufficiency the peripheral arteries will be the less in diameter;
moreover, in stenosis they contract upon their contents, in regurgitation
they are slack. Increase of the area of cardiac dulness vertically may
be a good sign ; its increase transversely is a bad one ; and, speaking
generally, changes in the chambers are of far more importance than
changes in the murmurs ; as we have seen there is an element of caprice
in murmiu-s, which may rise, fall, split, or perhaps vanish for a time,
without definite prognostic meaning.
Of intercurrent diseases the infections are the most injurious in their
effects upon the lame heart ; and of these influenza and diphtheria are
the most malignant.
If possible " functional " perturbations of a transient kind must be
distinguished from changes in the myocardium ; but to estimate the value
of the myocardium in fairly stable cases of heart disease is very difficult.
The results of treatment, especially in the use of digitalis, perhaps may
give us some hints of this kind. Arrhythmia, alteration of other sounds,
diminution of urine, the appearance of albumin or hyaline casts, failure
DISEASE OF THE AORTIC AREA OF THE HEART 957
of remedies previously effective, are of sinister meaning. Neglect of
treatment until late in the disease is against the patient's prospects ;
the command of skilled treatment and the means of carrying it out are
in his favour.
Mitral insufficiency is not infrequently cured ; aortic never. As in
Hermann Weber's case, though the murmur may cease, the mischief
stealthily advances, and may bring down the stricken man when he least
expects it.
No error is worse than false precision ; none more gratuitous than
prophecy : still in human affairs we cannot get beyond moral certainties,
and patients or their friends often demand of us a fallible prediction.
Given a moderate lesion and good conditions within and without, I should
say that in a patient under five-and-thirty years suffering from rheumatic,
syphilitic, or traumatic aortic regurgitation, the prospect of life is about
ten years ; rarely more than twelve, save in cases where the lesion is
nominal in degree. In persons over fifty, in whom the arteries are
atheromatous, and the aortic insufficiency a later stage in the work of
decay, three or four years may be expected. On the other hand, if
the aortic insufficiency be an early sign of atheroma about the base of
the aorta, and the patient in easy circumstances, death may be kept at
bay for six or eight years. The previous rate of change in the individual
is of course a most important element in our judgment in each case. In
obstruction alone the expectation is much longer. If in aortic disease,
even at this later age, the lesion be syphilitic, as in a case now under my
occasional observation, the prospects are much better ; by careful treat-
ment even ten years may be added to the sum of days.
Cases of alleged recovery from aortic regurgitation are recorded from
time to time. I have said what I think of such stories : the patient was
not watched long enough ; murmurs may be evanescent, not so the
lesions they signify. No less an authority than Leyden, however, has
recorded such a case of recovery, but after a traumatic lesion (51).
Cerebral embolism is prone to occur in aortic disease of whatever
kind ; pulmonary apoplexy occurs, but does not take the place it does in
mitral disease, for obvious reasons. For an account of these events the
reader is referred to the chapters which deal with them.
Treatment. — Give your prognosis on the best suppositions, treat
your patient on the worst. The treatment of aortic disease, and I now
imply both kinds of it, falls into the natural divisions of diet, manage-
ment, and drugs. In did we have to look to three points : to the
sympathy between the heart and the stomach, to good nutrition of the
heart, and to moderation of its work. We must avert indigestion, and
administer nutritious food without either raising the arterial resistance or
increasing the heart's output. Indistinctly we are aware that there are
diets which promote arterial resistance, and so far as our lights go we
must elude this danger. Many of the elderly sufferers from aortic disease
are gouty. In such persons we should avoid all that encourages this
habit (vol. iii. p. 187). On the other hand, to reduce the diet below the
958 SYSTEM OF MEDICINE
needs even of a person who can take little bodily exercise may carry
us into the peril of pining the diligent heart; and to exclude nitro-
genous food in order to avoid goutiness may throw the patient upon a
diet of carbohydrates, a diet both bulky and provocative of flatulence
and gastric acidity. As indeed in gout itself, a careful mixed diet will
answer best ; and on two points we must especially insist — on restric-
tion of liquids during meals, and on thorough mastication of the food,
whether it be soft or hard. In more than one case I have seen great
relief to follow fine chewing and the restriction of liquid at meals.
Even between meals it is not well to allow the patient to drink largely ;
the blood - pressure can hardly thus be raised, as Huchard asserts,
enormous quantities would be required for such a result, but the output-
of the ventricle may be increased, and therewith its work. It is scarcely
needful to insist upon the use of food which is at once easy to digest-
and worth digesting ; at the same time some foods are indirectly worth
eating if they are grateful to the eater, and thus stimulate the secretions.
Alcohol is overdone in all heart diseases. The immediate relief to the-
sufferer is often considerable, and as a cardiac stimulant in time of danger
it is indispensable. As an ordinary article of the patient's consumption
its use is not without some drawbacks; it disturbs blood-pressure, its
efifects accumulate more rapidly for harm in persons who cannot take much
exercise, and the perpetual nips, in which too often they are led to indulge^
themselves, directly induce those very conditions of venous stagnation and
degeneration of the cardiac muscle which we are on our guard to avert.
On the other hand, such patients are often cheered by a little claret-
and water, a light hock or some well-diluted spirit with meals, drams
being strictly reserved for critical occasions. If on every access of
palpitation or faintness the nurse is to run for the brandy bottle, the
patient's state will grow worse rather than better.^
In respect of management it is difficult to give general directions. In
no cases are tact and experience more valuable. The young practitioner
must remember that if, on the one hand, there be a danger of injury from
the effects of a careless life, on the other the harmful effects of " valetudin-
arianism" are no less ; and the patient in gaining his life may lose it.
We must trim our treatment according to the phases and peculiarities
of the individual. Fraentzel well says that to know that one has heart
disease may be more mischievous than the disease itself. Let your patient
understand that he has a weak heart, and that he must rigidly observe
your rules of life, but not otherwise fash himself ; and to some sensible
and trustworthy friend of his tell the whole truth and the risk of sudden
death if such there be ; that like other wise men the patient may have
his affairs in order.
In the matter of exercise often lies the decision whether the patient
be allowed to follow his calling. If the occupation be one of muscular
^ In his work on " SenUe Heart " the veteran physician Dr. Balfour gives admirable
directions for treatment of heart disease, and at greater length than it is possible for me to-
give in this place.
DISEASE OF THE AORTIC AREA OF THE HEART 959
labour the patient cannot but leave it ; a working-man must seek some
quieter means of subsistence, as a caretaker or the like. A sportsman
must contract the field of his pastimes : the salmon rod must give way to
the lighter engine of the trout-fisher ; cricket to golf : the moors must be
forsaken for the stubble and the covert, and the hunter exchanged for
the nag. Cycling is by no means an unfit recreation for the subject of
heart disease, in its earlier stages ; if so be that he is already a good
rider, and will ride circumspectly. Whatever pursuit be admitted, and
much will depend on the degree of incapacity, one caution must be
remembered on all occasions, namely, that although the sense of oppres-
sion which checks exertion can be " worked off," unless very severe, by
perseverance, it is a grievous error thus to persevere. It seems then that
the heart does not so much pull itself together, as become blunted to the
persistent strain. The cry of the burdened heart must never be dis-
regarded. And yet again while we offer this necessary caution we
shall not forget that perpetual timidity is even worse for the patient
than occasional indiscretion. So long as he lives let him live, so far
as may be, the life of a good citizen. Above all do not let him mope, or
become entirely possessed by the blind and ignoble desire of the mere
prolongation of days. We who have to minister too often to these
unprofitable uses of the world, can proudly point to men, great examples
in our own profession, who showed us how to live most nobly when
death was treading in their footsteps. The physician who inspires
moral health into his patient brings comfort also to his body.
Drugs. — During the latent period of aortic regurgitation those drugs
only will be required which are of service in common ailments ; specific
remedies are rarely necessary. . In case of acute onset, such as rupture of
an aortic cusp, the measures described already under the heads of manage-
ment and diet may be all that is required. Hearken, let us say again,
to the cry of the burdened heart ; no hypertrophy can go forward
while the organ is embarrassed. Under the unwonted stress it may be
necessary, while the heart is pulling itself together, to put the patient to
bed until the heart has begun to turn its reserve capacity into the statical
condition of hypertrophy. As this is attained the patient will return gradu-
ally to the ordinary habits of life. I have not found digitalis of great
service in this stage. On the contrary, gentle mercurials, gentle salines,
a little potassium iodide — means which reduce blood-pressure — are more
helpful. In this stage too much care cannot be given to save the work
of the heart in all directions, whether of muscular work, of the digestive
and other organic functions, of cerebral and emotional activity. When
this stage is passed, and something like compensation established, the
patient will betake himself to moderated exercise and a more bracing
moral life. If during the early period there be intercurrent times of
strain, due either to indiscretion or to some fluctuations of inner health,
intervals of more or less seclusion wiU again be enjoined, and the above
indications repeated. The best all-round medicine for heart disease in
these phases is blue piU.
96o SYSTEM OF MEDICINE
In preparing this section I saw before me the duty of reading over the
multitudinous arguments which have been written upon the use of digitalis
in aortic insufficiency, a grievous prospect : this intention I have given
up. After all that is written, the subject lies in a good deal of physio-
logical obscurity, and it is best for the present that each observer should
give the results of his own impressions as simply as possible. Against
its use in aortic insufficiency we have the eminent authority of Corrigan ;
in favour of its use that of Balfour.
Let me repeat that if the excised heart of a small animal be so attached
to a pressure bottle, that pressure can "be increased gradually, it will be
seen that with each increment of pressure the base line of the cardiographic
curve will fall ; the ventricle dilates. Why does not the ventricle in all
cases, in health or in disease, dilate to its extreme limits at once ? Because
of its " tone " ; probably also because of the well-known reaction of the
"loaded muscle." A loaded muscle, although prevented from lifting the
lever so high as before loading, contracts more strongly. For what we
know of tone, a property of the highest importance in cardiac functions,
we are largely indebted to Dr. Gaskell. My own view is that if the
property of tone be fundamentally one with that of contractility, it
has become so far differentiated from it that the two virtues may be dis-
cussed separately. Tone we may define as that property in heart, artery,
or other hollow viscus which preserves the mean diameter of the part ;
contraction, as that which enables the organ, nevertheless, to obey stimulus
and to perform particular acts. The vermicular movements of the bowel
and of ail arteriole are due to the quality of contractility ; their tone
preserves their mean diameters in spite of distension or contraction.
Were it not for tone a hollow organ, often subject to extravagant demands,
would be strained and perhaps ruptured. In the heart it is tone which
does much, if not all, to prevent loss of form under the great variations
of internal pressure.
In the year 1868, when Dr. Milner Fothergill was the resident
medical ofiicer to the Leeds Dispensary, I placed a large collection of
cases of heart strain imder his superintendence, and in order to test
our remedies for these patients, we carried out together a series of
experiments on digitalis, which Fothergill afterwards published in his
Jacksonian Essay. We demonstrated the effects of digitalis on the hearts
of frogs and small mamnmls, effects which are now too well known to
need narration here. Suffice it to say that the chief effect is an increase
of tone, which may be pushed to a degree inconsistent with normal
function. When a solution of digitalis is dropped on a frog's heart we
see an increment not of contraction but of tone. The heart goes
on contracting with a smaller and smaller volume till for lack of blood
the animal is moribund ; when other variations, such as fibrillar contrac-
tion, may supervene. In aortic insufficiency, the regurgitant stream does
not exactly "impinge upon the inner wall of the ventricle at a moment
of relaxation," for it can scarcely be said that the ventricle is " relaxed " ;
the mischief is that the pressure is abnormally increased at a moment
DISEASE OF THE AORTIC AREA OF THE HEART 961
when the muscle is at the disadvantage of greater cubic capacity, and
when the direction of motion is with the regurgitant stream. The
"loading" indeed, if not excessive, stimulates the organ to stronger
contraction (reserve capacity), and this dynamical reinforcement becomes
statical as hypertrophy. The same process being repeated again and
again, the heart attains the huge dimensions with which we are familiar ;
and in the muscle itself there may be no limit to such increase, the
limit being imposed by the scale of the associated structures. Were
tone absolute, there would be no dilatation ; hypertrophy alone would
take place, and the output would be too small ; on the other hand, if, as
in chronic strain, the tone is overborne little by little, dilatation ultimately
soon surpasses hypertrophy.
Tone, then, is the quality to be watched and supported ; and in
digitalis we have a means of intensifying tone, of moderating distensibility.
Now tone, like any other quality in excess, may be injurious, and the
output of the constringed ventricle may fall short of the demands of
the system. That the residual blood should become less and less after
each contraction, and possibly vanish, is good ; but if the shrinkage of
volume goes on farther, the output may fall farther below the needs of the
system than it did in the case of excessive residuum. On the body the
result is practically the same. Hence one chief reason why digitalis
should be used with especial precautions is lest diminished capacity come
to the same thing as asystole. Again, when the muscle falls into
degeneration digitalis seems to have other injurious actions, the nature
of which is obscure. We cannot get fatty hearts of frogs for experiment.
It would appear that digitalis acts not only on the tone of the cardio-
arterial muscular coat, but also on the vagus. In tachycardia, and other
conditions of rapid pulse, digitalis by giving tone to the arterial system
often causes diuresis without reducing pulse-rate — without, that is, being
able to get a hold on the vagus. Conversely in a degenerated heart digi-
talis often seems to stimulate vagus
action while tone is failing ; then we
get slowing, coupled beats or inter-
mittence of the heart without diuresis
(Fig. 61). Indeed the vagus inter-
ference by slackening such a heart
may conspire to its further dilata-
tion with increase of residual blood. Fiq. ei.-Aortic incompetence with bigeminal
This perilous result of digitalis is but |J^|J ^^ *° ^°*'™ °^ digitalis. (Sraham
too well known to us not only in
aortic regurgitation, but also in other kinds of failing left ventricle.
If, then, diuresis do not soon appear, the drug must be stopped and a little
alcohol substituted for it. So long as the cardiac muscle is in fair condi-
tion, the working of digitalis counteracts the distension of the left ven-
tricle and lessens the volume of residual blood, an aid too valuable to
neglect if contingent dangers, such as an undue reduction of output,
vagus meddling, or oppression of degenerate muscle, can be avoided.
VOL. V 3 Q
962 SYSTEM OF MEDICINE
If we can use the drug so far as to pull the heart together without
constricting its cavity or arousing the vagus too much, we shall gain
ground so long as the muscle is sound. Now we find, prolonged diastole
or not, that in practice digitalis, used with discretion bo as to brace
the heart and not to string it up too tight, is indeed the most valu-
able weapon in our armQia?y while the cardiac muscle is sound. The
advent of degeneration of the muscle cannot well be detected save by
administering the drug experimentally in single doses, say in one dose of
10 minims of the tincture once every second day, taking the flow of
urine as our guide. As to the " prolongation of diastole," in so far as
propulsion is better, refluence is less ; in so far as the ventricular cavity
is less, residual blood is less ; moreover, the pause is not all active dia-
stole; during it the pressures in aorta and ventricle approximate, and
during the later part of it are indifferent, or even reversed. Again,
acceleration of the blood is almost entirely an abbreviation of the dia-
stole, yet acceleration is not a help to the heart, but a sign of its undoing.
The organ is then dependent for its integrity on its tone, and if, as we
have seen, by digitalis the residual blood may be reducible by moderate
constriction of the ventricle, the abnormal pressure at the first part of
the diastole, when it is highest, tells upon the walla at a moment of less
cubic capacity, and at a moment of greater resistance. In a word, as
the ventricle dilates, the output, other things being equal, remains con-
stant, and the mass of residual blood increases ; if by digitalis tone can
be enhanced, output and contraction volume will approximate again.
What are, then, the rules for the administration of digitalis in aortic
insufficiency % No one would give digitalis when a big heart is thunder-
ing along its course and the arteries bounding under its pulses. But if
the left ventricle be relatively too capacious, and the apex beat becomes
diffused, put the patient to rest with his feet up, so as to diminish blood-
pressure ; and put him on tender meats, avoiding much carbohydrate and
much liquid. Gentle deobstruents will probably be required also. Now if
under these means the symptoms and signs of dilatation continue, ad-
minister one dose of digitalis, and if it is at least harmless, administer
another twenty-four hours later, noting the rate and rhythm of the pulse
and the volume of the urine ; thus watchfully a safe judgment may be
made as to the further use of the drug. Although a pulse over 80 may
suggest, it does not dictate the use of digitalis ; some evidence of dilatation
is required ; on the other hand, it can rarely or never be well to give
digitalis if the pulse be at or below 75, I have a prepossession against
digitalis in any case in which the heart intermits : it may be more than
justifiable to give it in cases in which the intermission is but a subordinate
element in a rhythm otherwise quick and irregular ; but if intermission be
the sole or a leading feature the drug is better avoided. If in later stages
the right side of the heart seem disturbed, digitalis can rarely be other-
wise than helpful. In such cases, indeed, we do not look too curiously
to murmurs or even to valves ; we watch the apex beat, the area of
cardiac dulness and the volume of the urine.
DISEASE OF THE AORTIC AREA OF THE HEART 963
Perhaps digitalis is least needed in aortic stenosis ; yet even in this
malady, if the stenosis be constant or increasing, and the heart yielding,
it may be necessary to introduce it occasionally, remembering, however,
that, if the obstacle in front be very great, to spur on the heart is to
ride for a fall.
The preparations of digitalis are so many, and the advantages and
the drawbacks of this and that are so many, that I must refer the reader
to works on pharmacology for full discussion of these very practical
points. In a case to which I was called in consultation three or four
years ago, Nativelle's granules were used by the medical man in charge
of the case, one of dilated heart ; these proved so helpful that I have
prescribed them occasionally since that time, and certainly can confirm
my friend's good opinion of the preparation. I see Dr. Balfour also uses
these granules, or a syrup made by Nativelle. I believe in the " cumu-
lative action " of digitalis, but have no notion in what it consists ; what-
ever preparation be used, it is well to use it intermittently. Death is so
often sudden in aortic insufficiency, that its occurrence during the use of
digitalis, or of any other means, must not be attributed too readily to
medicine. If the stomach be disordered, digitalis, if given at all, must be
given subcutaneously.
Strophanthus is sometimes of great service ; more frequently it dis-
appoints us altogether. I have little experience of it in aortic disease ;
generally speaking, I should say that it is much more useful in young
than in old people ; it is in patients under thirty years of age that I can
recall many cases of heart disease, chiefly of mitral regurgitation, in
which the drug acted with celerity and efficiency.
Arsenic and strychnine come to our assistance at times when drugs
which should be more directly potent fail or are inadmissible. If
strychnine be prescribed at a critical moment and rapid effects be
desired, doses much larger than those regularly given are required. For
an adult fifteen drops of the liquor are not too much thus to prescribe as
a single dose. If the patient complain of some slight rigidity the dose
is intermitted, and no harm comes of the reaction. Arsenic is more
adapted, of course, to chronic medication, and, whether as a nervine
or muscular tonic, is very useful. Sir William Broadbent, I see, regards
the virtue of phosphorus as even superior to that of arsenic. Caffein —
the pure caffein of Merck, not the citrate — is an old ally of mine ;
it stimulates the heart when it flags, and it promotes diuresis. It
is also useful in " cardiac asthma." From 1 to 3 grains may be
given for a dose; and in some persons it is better to push the drug
early in the day, pretermitting it of an evening lest it disturb sleep.
Caffein is useful as a cardiac stimulant in cases of slow pulse in which
digitalis is out of the question. Good and strong coffee taken black
may be substituted for the caffein if no great precision of dosage be
necessary.
The nitrites are perhaps never required until symptoms of an anginose
kind arise; then they are invaluable palliatives. The researches of
964 SYSTEM OF MEDICINE
Professor Bradbury and Dr. Marshall indicate that of these agents the
erythrol tetra-nitrate is the most useful, as its effects are easily calcu-
lated and more persistent. The amyl nitrite, being the most rapid in
action, is to be preferred at critical moments ; but its effect is fleeting.
In cases of severe angina these agents are very precious to us, probably
by relieving the stress upon the aorta wherein the pains originate ; an
end attained by slackening the heart as well as by expanding the peri-
pheral vessels. I cannot but suppose, however, that these agents have
some anodyne virtue besides the mechanical, for I have seen angina
relieved by a nitrite, while my finger was unable to detect any change
in the blood-pressure. In extreme cases of aortic disease the assaults of
angina may be so frequent that the life of incessant suffering and appre-
hension is almost more than can be borne ; in these cases the use of the
nitrite of amyl may become almost a slavery. A craving seems to spring
up which is not easy to discriminate from the sinking of the angina itself.
Bradbury and Marshall have made researches into a method of combin-
ing the use of vaso-dilators with digitalis which seems to be of con-
siderable promise (48).
I suppose that chloral is a dangerous remedy in heart diseases,
especially in degenerate heart. Sir W. Broadbent proscribes it altogether ;
Dr. Balfour, on the other hand, speaks of the drug with appreciation.
When chloral first came out, being less troubled with modern speculations
about blood-pressures than we are now, and undisturbed by Gaskell and
Shore on chloroform, I used chloral freely in the restlessness of heart
diseases, not excluding those of old people. Indeed, to many old people
with degenerate hearts I gave the drug year after year, and certainly
with the greatest comfort. The anxious, perturbed nights of these
sufferers are full of trouble and peril, and sedatives cannot be forbidden.
I now use chloralamide, which, I am told, is safer than chloral, and
certainly it acts well, though scarcely so well perhaps as the latter.
Balfour, while clinging a little to chloral, suggests the use of chloralose
or paraldehyde instead. Trional is perhaps better than sulphonal ; but
neither is so useful as the drugs just named.
It is now thirty years since, in the third volume of The, Praciiiiorwr, I
recommended the hypodermic injection of morphine in heart disease ; and
testimony of the best kind, such as that of Dr. Balfour, has supported
my advice. Dr. Leonard Hill says " morphine is one of the best vaso-
constrictors and cardiac tonics we possess," By the mouth opium
is behind other sedatives in value, its use being attended by grave
drawbacks ; but hypodermically, in doses beginning at one-tenth of
a grain and gradually ascending to a quarter of a grain if necessary,
it is a precious means of relief. The physicians who still protest against
its use are unfamiliar with the practice. There is no remedy which calls
forth so warm a tribute from the patient himself, who, after nights
of watching and agony, sleeps a peaceful and natural sleep, and awakes
almost forgetful of his plight. Of the drawbacks to the continuous
use of morphine I may refer to the article on the subject (vol. ii.
DISEASE OF THE AORTIC AREA OF THE HEART 965
p. 887). Like any other potent remedy, it must be used seasonably and
discreetly.
Ammonium bromide is sometimes of service in the minor degrees
of restlessness, but, if long continued, is apt to be depressing. All the
salts of potash are to be avoided, even the nitrate. Convallaria,
sparteine, cactus, and the like, are only known to me in the blind uses of
despair.
In this section I have spoken almost entirely of the treatment of
insufficiency ; of stenosis, I need not say more than will be gleaned
incidentally, here and under the head of Diseases of the Arteries.
Indeed, if there be no means of dealing with the local process, as by the
use of potassium iodide, the management of stenosis is an eminent
example of " expectant treatment."
P.8. — As these pages are being printed oflf, I hastily intervene to qualify or
indeed to contradict my statements in the text concerning pulse delay. It seems
probable that Sir William Broadbent and other authors are right after all in as-
serting that there may be cardio-radial delay in aortic regurgitation. The mis-
understanding is one more instance of the drawbacks of making tracings without
time lines. The error and its correction may be reconciled by the elevation of
the whole problem into a wider generalisation. Throughout this article I have
assumed that, except in advanced decay and toxic states, the systole of the heart
is relatively constant in duration ; this, on the researches of Cohnheim, Roy, and
others, has been generally accepted. But it appears that the proposition is open
to grave doubt in respect of more than one kind of heart disease. Dr. Chapman,
who is good enough to keep me informed of his researches on the physiology
of the circulation, sends me (1st April 1898) tracings taken from a case of
pure compensated aortic regurgitation, which prove that in this case, at any
rate, the systole was relatively prolonged. This observation, if well founded,
will throw a new light on the failure of compensation in aortic insufficiency ;
it means, of course, exhaustion in a proportionately shorter period of years. The
prolongation of the heart's contraction accounts for the slower transmission
of the wave. The details of Dr. Chapman's case are as follows : — The
pulse-rate in the tracings was (about) '75. Two tracings were taken (among
others). In the first the systole occupied 0'40" (the normal systole for this
pulse-rate being 0-32" to 0-33"). The diastole was 0-36" to 6-39". In the
second tracing the systole occupied 0-50" to 0-53"; the diastole 0'33". To
apply this observation, in Dr. Chapman's language, " the duration of the heart's
work (on this basis) is about fifteen hours of the twenty-four, instead of ten or
eleven hours." On the first tracing the cardio-radial delay was as great as 0'4".
The time measurements were made with a reed vibrating at 64 per second. If
I am naturally disconcerted to find, when it is too late, that much of my text
in respect of these points ought to be modified, I trust I need make no
apology for our common fallibility. It would seem, from Dr. Chapman's records,
that cases of aortic regurgitation differ widely among themselves.
T. Clifford Allbutt.
966 SYSTEM OF MEDICINE
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Feb. 26, 1897.-97. Weber, Hermann. "Hygiene of Climbing," Lancet, Oct. 28, 1893.
—98. Wbismatbr. Zeitsch. f. klin. Med. vol. xxxii. 1896. — 99. West, S. Dis-
cussion at Clinical Society, Feb. 26, 1897. — 100. Wilks, Sir S. Trans. Path. Soc. vol.
xvi. p. 77. — 101. Wilson, Surg.-Capt. " Disordered Heart in Young Soldiers," Arrmy
Med. Bep. 1896.
T. 0. A.
968 SYSTEM OF MEDICINE
DISEASES OF THE MITEAL VALVE
Mitral Insufficiency
Definition. — A diseased condition of some of the structures constituting
the mitral valve ; or a defect at the left auriculo-ventricular orifice, pre-
venting the normal closure of the orifice during the systole of the left
ventricle, and occasioning a backward flow of a portion of the output into
the left auricle.
Morbid anatomy. — (i.) In the chronic stages of rheumatic endocarditis. —
The curtains of the mitral valve are thickened and comparatively rigid ;
the neighbouring endocardium is also denser and more opaque than
the normal, especially in the portion extending from the great anterior
flap of the mitral valve to the base of the aortic semilunar valves.
Many of the chordae tendinese, together with their columnae camese,
are thickened and shortened ; there are often adhesions between the
curtains, the cords and the columns, as well as in some cases between
these and the endocardium of the wall of the ventricle. In some instances
the chordae tendinese, especially the finer cords which are inserted near
the free border of the curtain, are lengthened instead of shortened ; prob-
ably this is due to yielding under the pressure of the blood upon the
under surface of the mitral flap, so that the edge of the latter is inverted
into the auricle during the systole of the ventricle. Whether the chordae
be shortened or lengthened, the result is an imperfect apposition of the
curtains at the time of ventricular contraction. The endocardium lining
the left auricle is also thicker than normal, especially at the ring bounding
the auriculo-ventricular aperture. From this ring extends a whitish or
milky patch of the fibrously transformed endocardium into the auricle above
and the ventricle below. Such thickening may involve the structures
subjacent to the endocardium, and tend to narrow the orifice, though the
signs may be entirely those of mitral insufiiciency and not those of obstruc-
tion. Duroziez (14) says, that if the orifice be large enough to admit the
passage of the thumb the signs will be those of insufficiency, and not of
stenosis. Much, however, depends on the condition of the internal surface ;
if this be smooth, as in many cases it is, there will be signs of mitral
insufficiency only ; if rough, there will be those of stenosis in addition.
The thickening of the endocardium is due to fibrous proliferation of
the original inflammatory exudation, a process of development of con-
nective tissue extending into surrounding structures. Repeated attacks
of endocarditis affecting the already diseased tissue cause fiu-ther
thickenings and retractions; the thick fibroid material compresses the
blood-vessels, and tends to induce degeneration. Fatty degeneration
is not often observed, but calcareous change frequently, even in the
DISEASES OF THE MITRAL VALVE 969
case of young children. The calcified portion of the valve structure
may act as a mechanical irritant producing inflammatory or necrosing
changes in the tissues adjacent. A fragment of the calcareous or the
necrosed material may become detached and form an embolus. Very
rarely a change of the firm fibrous material into cartilage has been
found (72).
(ii.) In the chronie forms of ulcerative or septic endocarditis. — The valve
curtains, the cords and columns, or the endocardium of the ventricle may
show the lesions of ulcerative or septic endocarditis, the tissues in the
aifected areas being destroyed by necrosis. Usually the ulcerated surfaces
are covered with large vegetations. These changes in a large majority of the
eases of ulcerative endocarditis — about three-fourths of the total — are
found on valves previously diseased. In all such cases some of the forms
of pathogenetic micro-organisms are to be discovered. It is to be borne
in mind, therefore, that on the chronic morbid products at the mitral
orifice a destructive disease which has no relation with rheumatism may
be engrafted. In a minority of the cases the necrosing changes are slow ;
there is evidence to show that the process may be arrested in some areas,
cicatricial tissue covering the portions showing loss of substance.
(iii.) In rupture of the mitral valve.— The valve curtains, cords, or
columns may be ruptured. It is improbable that such an accident can
occur from strain where the structures had been previously healthy.
Post-mortem evidences of the rupture of a tendinous cord are not
infrequent; an occurrence which has sometimes changed fairly com-
pensated mitral inadequacy into a hopeless disablement (72). In the
majority of cases I think it probable that the rupture is due to ulcerative
changes. In some of them it seemed to have been due to the direct
irritation of a calcareous plate or firm fibrous band operating during the
movements of the ventricle ; in others ulcerative endocarditis has effected
the rupture. In the case of a curtain of the valve there may be first
aneurysmal pouching, and' secondly perforation. A vegetation on the
curtain, if it induce softening of the endocardial surface, brings about a
yielding under the blood-pressure within the ventricle, and a pouch is
formed which projects into the left auricle ; further pressure may cause
rupture (perforation), when of course the valve is no longer competent.
(iv.) In papilliform endocarditis. — A form of chronic endocarditis is
sometimes observed in which there are small, firm, warty outgrowths from
the surface ; these are fibrous proliferations of the endocardium, usually
attached by a broad base but sometimes pedunculated. They are covered
by smooth endothelium to which fibrin does not adhere ; the sclerous
changes of rheumatic endocarditis are not associated with them. They
have been most frequently observed in cases of chorea ; Lancereaux has
found them also in alcoholism and in malaria. I have seen an example
in a case of tuberculosis. Sometimes in newly -born infants small
spherical outgrowths are observed on the free border of the mitral ; they
are probably hsematomata due to rupture of blood-vessels situated under the
most superficial layer of the endocardium (36, 44) ; usually they disappear
970 SYSTEM OF MEDICINE
in the first few months of life, but in some cases they may initiate the
warty excrescences above described (Cruveilhier). I have considered it
probable that in some cases of chorea, determined by sudden fright,
similar ruptures of intra-valvular vessels with subsequent fibrous warty
transformations occur.
(v.) In dilatation of the left ventricle. — There may be considerable
dilatation of the ventricle, and yet the mitral curtains be quite competent
to close the aperture. In many cases, however, when there is no disease
of the structures constituting the valve, the cavity is so greatly dilated
that it is demonstrably impossible that the aperture between auricle and
ventricle could be adequately closed during, the ventricular systole. Amongst
the post-mortem associations of the latter condition are the following :
{a) there may be disease at the aortic orifice causing obstruction or
regurgitation or, as very frequently is the case, the combined lesion. The
ventricle has become hypertrophied and dilated on account of the
abnormal pressure to which it has been subjected, and the dilatation
continues and progresses until the mitral curtains are no longer capable
of closing the auriculo-ventricular orifice ; (J) the signs of chronic disease
of the kidneys (chronic interstitial nephritis) may be found. In some
cases there is great hypertrophy of the muscular wall of the ventricle ;
in others dilatation, even at early periods of the disease, preponderates
over hypertrophy. Microscopical investigation has shown that the
causes for the changes in the cavity and the walls of the left ventricle
are complex. The obstruction to the general arterial circulation due to
the thickening of the arterioles in various situations causes abnormal
intra-ventricular pressure during systole and thus there is a mechanical
cause of dilatation ; but the muscle of the ventricle also suffers from
the process of disease. The morbid changes in the ventricular wall
have been described as an excessive proliferation of the connective
tissue (3, 16, 29), a special quasi-inflammatory afiection of the smaller
branches of the coronary arteries — endarteritis and periarteritis (13,
26, 33, 39), or a fibrosis extending to the general connective tissue, but
starting from the arterioles and capillaries — arterio-capillary fibrosis (69).
The muscular fibres are altered, the transverse strise are obscured, some
fibres are atrophied and encroached upon by the fibroid tissue, others are
hypertrophied. Similar changes are sometimes noted in the walls of the
ventricle in persons at and after middle age, when there are no signs of
chronic Bright's disease, (c) As a sequence to inflammation of the peri-
cardium, the pericardial surfaces being found adherent. An excess of
fibroid tissue not only extends amongst the muscular bundles and fibr«s,
but also compresses the blood-vessels ; this is especially seen after
general rheumatic disease of the heart (carditis) in children; the left
ventricle may be extremely hypertrophied and dilated so that the mitral
valve is incompetent, and yet there may be no sign of endocarditis affecting
the structures of the valve. Dilatation of the left ventricle to the extent
of mitral incompetence is also observed occasionally after rheumatic fever
in childhood, with no evidence of pericarditis or endocarditis, (i) In
DISEASES OF THE MITRAL VALVE 971
syphilitic affections of the ventricle the muscular fibrillse have probably
been weakened by myocarditis. In rare cases small gummata have been
found in the wall of the ventricle; in others bands of fibroid material, prob-
ably the sequels of syphilitic endarteritis, and obliterations of the vessels,
have been seen (e) in Graves' disease, and other kinds of long-continued
morbid acceleration of the heart's contractions, such as tachycardia. In
some such cases the left ventricle has been found so hypertrophied and
dilated that the mitral curtains were incompetent ; it must be remembered,
however, that in many of the fatal cases of these diseases the ventricular
cavity had not been dilated, and the muscle of the heart was quite normal.
The dilatation of the left ventricle must be regarded only as an occasional
sequel of the disturbance of the nerve-mechanism of the heart.
(vi.) In degenerations or transformations of the structures of the left
ventricle. — In a large number of instances the various forms of degenera-
tion of the heart — fatty, fibroid, and granular — are associated with
dilatation of the left ventricle ; and the mitral regurgitation, which is a
feature of their history, is thus explained. In a minority there is no
such dilatation. In fibroid degeneration bands of firm fibrous tissue,
replacing more or less the muscular fibres, are observed, on section of
the ventricular wall, to spread out in certain tracts ; they often extend
into the musculi papillares, and some of these may be wholly transformed
into fibrous tissue. In granular degeneration, " dissociation segmenteuse "
(30), the heart-muscle is observed to be disintegrated, and to present the
appearance of an aggregation of fine particles ; the cement substance
which normally binds the fibres together being softened. This morbid
condition is to be demonstrated in the musculi papillares. In fatty
degeneration pale spots or streaks are observed on section, not only in
the wall of the ventricle but in the papillary muscles also ; then micro-
scopic examination shows the absence, in greater or less degree, of the
proper muscle elements, and the presence of minute oil globules. These
transformations or degenerations may be the consequences of obliteration
of the arterioles. In cases where there is sudden and recent infarction
of these vessels the appearances are those of the softening known as
myomalacia cordis. Where the process has been more chronic, fibrous
transformations or fatty changes are observed. In some cases the two
forms of transformation, fatty and fibrous, are seen together.
In another form of fatty degeneration of the heart>-muscle the pale
spots and the mottlings indicating the areas of metamorphosed muscular
fibres are scattered throughout the ventricular wall and the fleshy
columns, having no relation with any tract of vascular supply. These
constitute the majority of cases known as " fatty heart." In some they
are associated — especially in fat persons and drunkards — with infiltration
of fatty tissue amongst the muscular bundles. Fatty degeneration of
the muscular fibres of the heart is found also in chlorosis, ansemia, and
blood-deteriorations. In some of these cases there has been evidence
of mitral regurgitation. If there be local degeneration resulting from
the obliteration of arterioles the condition leads to a fatal issue. In
972 SYSTEM OF MEDICINE
the majority of cases of fatty degeneration in anasmia the heart
regains its structural integrity, and any consequent mitral insufficiency
disappears. When the heart thus recovers it must be inferred that
many of the diseased fibres actually disappear, the fat which is the result
of their disintegration becoming absorbed, whilst new formation of normal
muscular tissue takes place. In cases in this category, where death does
not occur from the fatal forms of ansemia, careful search should be made
for disease in other organs, and the formula, "death from fatty degeneration
of the heart," should not be delivered too hastily.
(vii.) In some cases in which there has been strong evidence of
mitral regurgitation during life the heart has been found on postmortem
examination to present perfectly normal appearances. The pathology of
such cases will be considered later.
In mitral insufficiency from all causes the left ventricle is dilated
and its muscular walls hypertrophied. The dilatation and hyper-
trophy proceed hand in hand, and both are the direct and salutary
results of the regurgitation through the mitral orifice. As the late Dr.
Herbert Davies pointed out, the process whereby, in sequence to mitral
insufficiency, the cavity of the left ventricle becomes enlarged and the
muscular tissue hypertrophied should not be considered morbid. The
enlargement may be in just such degree that the amount lost to the
aorta by the leakage into the auricle is compensated ; and the increased
driving power of the ventricle is precisely regulated to deliver the
normal supply to the great artery (12).
In mitral insufficiency the left auricle is dilated and hypertrophied,
and the endocardium lining it is thicker and more opaque than normal.
In some chronic cases the muscle of the auricle wastes, and is replaced
by fibrous tissue. The pulmonary veins also may be much dilated.
Occasionally in chronic cases globular fibrinous coagula are found adher-
ing to the lining membrane, and projecting from between the fleshy
columns and trabeculse into the cavity of the ventricle or the auricle.
These thrombi are firm and dense in their external portions, and often
soft and fluid in their interior ; cysts thus formed may rupture or become
detached, and their fragments may cause embolism of systemic arteries.
In some cases the coagula undergo fibrous and calcareous transforma-
tions.
The right auricle and ventricle in cases of mitral insufficiency are also
found dilated and hypertrophied. Hypertrophy is found to preponderate
in the earlier stages, dilatation in the later. The wall of the ventricle is
in some cases found thick and leathery, in others thin and flaccid. The
tricuspid valve may be incompetent on account of extreme dilatation of
the ventricle. The globular thrombi, described as sometimes visible in
the left cavities, are much more commonly observed in the right. The
detached coagula cause embolisms of branches of the pulmonary artery.
The dilated condition of the right chambers of the heart is obviously
associated with general venous engorgement. In the heart itself the
coronary veins are turgid and dilated.
DISEASES OF THE MITRAL VALVE 973
The pericardium may show signs of disease, recent or remote, and
there may be fluid effusion in the pericardial sac.
Morbid anatomy of other organs in mitral insuffieieney. — The
limgs in cases where there has been long-continued mitral regurgitation
are found engorged with dark blood, and their fibrous tissues abnor-
mally dense. The lung is tough; the capillaries of the alveoli have
become dilated and varicose, their walls thickened. Patches showing
the signs of broncho-pneumonia may be scattered throughout the
toughened lung. Blood escaping into the surrounding connective tissue
produces brownish pigmentation (brown induration of the lungs) ; it may
transude into the alveoli, causing the tinged, sputa and haemoptysis
observed in some cases. The lining membrane of the bronchi often
shows extreme engorgement, and blood exudes from the surface. The
blood-tinged sputa, therefore, may be derived from the lung capillaries
or from the bronchial mucous membrane. The lower lobes, or the more
dependent portions of the lung in chronic cases, become engorged, dense,
and often oedematous. In many cases there are multiple pulmonary
lesions, with evidence that these arose at different dates. Effusions into
the pleurse may have caused collapse of various portions of the lungs. The
signs may indicate that local pulmonary infarctions have occurred in
different areas at various dates. There may be the blood-clot and pro-
minence of the pleural surface indicating a recent embolism of a branch of
the pulmonary artery (pulmonary apoplexy) ; the sites of old infarctions
may be indicated by pigmented indurations of portions of the lung- tissue,
with, perhaps, some depression of the pleural surface corresponding to
the indurated portion. In cases of comparatively recent embolism the
corresponding area of the pleura may be covered with the yellowish
exudation of pleuritis. All pulmonary apoplexies, however, are not due
to infarction. The abnormal strain of the pulmonary artery may lead to
degeneration of the vessel and dispose it to rupture. Old adhesions of
the pleurse or of pleura and pericardium are often observed. In many
cases there is fluid effusion in the pleural cavities.
The stomach manifests greatly dilated veins ; its mucous surface shows
much congestion ; the venules are often varicose ; mucus, tough or
fluid, is seen in abundance. The liver is enlarged; the intra-lobular
capillaries are very greatly dilated and their walls thickened ; on section
it shows the characteristic appearances of "nutmeg liver," the dark
brownish-red stellate spots marking the centre of each lobule on the
yellowish ground formed by the bile-stained liver-cells. The bunch of
greatly dilated capillaries in the centre of the lobule encroaching upon
the hepatic cells may cause atrophy or fatty degeneration of the latter,
some brown pigment granules being seen amongst them. The most
marked signs of venous engorgement with increase of bulk of the liver
are seen in cases in which tricuspid incompetence has followed mitral
insufficiency. It is to be remembered that the size of the liver in such
cases may become greatly reduced soon after death, the organ being
partially emptied of blood by gravitation.
974 SYSTEM OF MEDICINE
The spleen in mitral regurgitation may be enlarged from passive
hypersemia, its connective tissue being mucb increased and causing it to
feel much firmer than under normal conditions. In some cases it shows
infarctions old or recent. "When recent, wedges of hard tissue with their
bases at the circumference (that is, the capsule) are felt on manipiila-
tion. Old infarctions are indicated by shallow depressions of the surface
of the viscus.
The intestines show venous engorgement. In some cases embolisms
of the small arteries supplying the intestinal wall have been found, with
consequent necrosis of the bowel. The veins of the mesentery are
engorged. The glands, within the abdomen are enlarged and con-
gested.
The Mdneys are abnormally firm from cyanotic induration ; the
pyramids are especially engorged ; blood may exude from the glomeruli
into the tubules. In some cases they show on section pale, wedge-
shaped, recent infarctions, their base towards the cortex and their apex
towards the hilum; or deep depressions of the surface, with cicatricial
tissue visible on section, may indicate the situations of old embolisms.
There may be much fibrosis in these kidneys.
The peritoneal cavity may be more or less filled with ascitic fluid.
The membranes of the brain and spinal cord may show much venous
engorgement. Signs of embolism of the cerebral arteries are found in
some cases.
The subcutaneous tissue generally, especially in the lower extremi-
ties, may be found infiltrated with dropsical fluid. In some cases patches
of the superficial layer of the epidermis are raised in large bullae. In
other chronic case's the fibrous elements of the skin are thickened —
there is a brawny oedema.
Meehanism of mitral regurgitation. — ^In normal conditions of the
structures, after the filling of the ventricular cavity from the auricle, the
muscular wall of the ventricle immediately contracts; the musculi
papillares do not begin their contraction until after an appreciable
interval, then these muscles act with sudden energy, drawing down the
mitral curtains and completely closing the auriculo-ventricular aperture,
the apposed curtains presenting a convex surface in the auricle ; the
energetic tug of the papillary muscles gradually ceases and they relax,
whilst the muscle of the ventricular wall remains contracted (54).
The contraction of the muscle of the ventricle has a direct effect upon
the auriculo-ventricular aperture. Before the beginning of the systole
of the ventricle this orifice is circular; during the period of systole
the contraction of the surrounding muscular fibres causes it to become
narrower and of oval form (35, 37). At the acme of systole the auriculo-
ventricular orifice has an area not much more than half that which it
presents in diastole (35). The shape of the papillary muscles is such
that in the complete contraction of the ventricle they are accurately
applied to each other (63).
The ventricular systole, therefore, consists in a series of co-ordinated
DISEASES OF THE MITRAL VALVE 975
rhythmic movements. There may be many causes of disturbance of the
normal association and sequence of these actions, the result of which is
insufBcient closure of the mitral orifice and reflux into the left auricle
occasioned by the ventricular systole, (a) There may be such structural
disease in the curtains, cords, and attachments of the valve that due
apposition is impossible. (J) The fibrous ring to which the flaps of the
valve are attached at their circumference may be so much thickened that
the muscles at the base of the heart are unable to compress it sufficiently
to cause accurate closure by the curtains during ventricular systole, (c)
The insuflicient narrowing of the auriculo-ventricular aperture during
systole may be due to no structural alteration of the ring, but to en-
feeblement of the muscle of the ventricle, {d) The ventricle may be so
greatly dilated, and with it the fibrous ring to which the mitral curtains
are attached, that these latter fail to meet at their borders during the
period of contraction of the ventricle, (e) The papillary muscles may be
so enfeebled by disease that they fail to perform their function of approxi-
mating the valve curtains. (/) Owing to disturbance of the nervous
mechanism the movements may not be performed in their due association
and sequence.
Consequences of mitral regurgitation. — It is probable that in cases
in which very small amounts of blood are regurgitated into the auricle
from the left ventricle the consequences are inappreciable. The mechanical
results are directly proportioned to the amount of reflux. The immediate
efiects may be regarded as simultaneous upon the left auricle and the left
ventricle. The auricle is distended in proportion to the force of the
ventricle and the amount of fluid regurgitated. The auricular wall
becomes dilated, and its muscle, subjected to abnormal stimulus, hyper-
trophied. The left ventricle, receiving during its diastolic expansion an
abnormal quantity of blood from the dilated auricle, is subjected to
unusual pressure; the muscle yields and its cavity becomes enlarged.
Such increase of capacity is a necessity if the normal supply to the aorta is
maintained. In systole it is called upon for more work, in order to deliver an
adequate amount into the aorta. Hypertrophy of its muscle ensues, and is a
favourable condition. The efiect of the regurgitant stream is manifested
upon the right chambers of the heart. The current impelled by the
right ventricle, which in normal condition should flow unimpeded through
the pulmonary vessels, is met by the reflux current from the left ventricle.
The capillaries of the lung, the branches and trunk of the pulmonary
artery, and the right ventricle itself, are thus subjected to abnormal
strain. The effects are hypertrophy of the muscle and dilatation of the
cavity of the right ventricle. Hypertrophy of the right ventricle also is
essentially favourable, for the more vigorous action antagonising the back
flow into the left auricle helps the delivery of an adequate supply to
the aorta.
Thi maintena/nee and the failwe of compensation. — If the changes in the
cavities and in the myocardium thus sketched out are nicely balanced,
a condition of restored equilibrium ensues ; thus a stationary lesion of
978 SYSTEM OF MEDICINE
compensated mitral regurgitation may persist for long periods, the subject
thereof presenting neither morbid sign nor symptom. An adverse change,
however, may be effected by many causes : the dilating strain upon the
left cavities may impair the muscular power of the left auricle and
ventricle ; renewed disease of the endocardium may increase the degree
of valvular imperfection ; intercurrent diseases may affect the structural
integrity of the cardiac muscles, vessels, or nerves ; affections of the lungs
(from extrinsic causes, or from causes, such as embolism, intrinsic to
the cardiac imperfection) may induce direct and mechanical as well as
indirect and enfeebling difficulties. The result of any of these inter-
ferences is a break of compensation — a failure of the cardiac forces of
circulation ; the supply to the aorta and thence .to the tissues becomes
inadequate, then the muscle of the left auricle and the ventricle becomes
more and more enfeebled, their constituent structures degenerate, and
their cavities contain more and more residual blood. The force of the
right ventricle now fails, and both right auricle and right ventricle
become engorged with venous blood; the systemic veins are dilated,
and the tissues suffer from venous stasis. The hepatic veins (which are
in such immediate relation with the inferior cava), being destitute of
valves, are especially congested, and their engorgement becomes mani-
fest in enlargement of the liver. As the distension of the right
ventricle continues, the right auriculo-ventricular orifice may become so
much dilated that the tricuspid valve becomes incompetent to close it ;
then the pulsatile action of the right ventricle is communicated to the
valveless hepatic vein, and thus to the liver, as well as to the veins of
the neck, if the walls of these have been sufficiently dilated to render
their valves incompetent. The interference of the general and the
lymphatic circulations at varying stages of this period of failing com-
pensation may induce dropsy.
Diagnosis. — The chief sign by which the diagnosis of the in-
sufficiency of the mitral valve is to be made is a physical sign
obtained by auscultation — a systolic murmur heard at the apex of
the heart, or having a maximum intensity in this situation. It is an
essential preliminary that the position and outline of the apex be deter-
mined by palpation and percussion. The abnormal sound, is often in
some degree musical, varying in different cases from a very low to a very
high pitch ; in some it may resemble the sound of a whispered " who," in
others a musical note of varying pitch and quality, and in no inconsider-
able number a shrill whistle. In many it has the sound as of a puff of
steam. A characteristic to be especially noted is that it fades off gradu-
ally, and does not come to a sudden, abrupt stop. The murmur begins
with the systolic contraction of the ventricles ; this may be determined,
at the time that auscultation is practised, by the observer placing his
finger over a point where the apex beat is to be felt; or, if this be impracti-
cable, over one of the carotid arteries in the neck. The bruit may be very
short, ceasing at an early portion of the systole, or may be prolonged
nearly throughout the whole of the systolic contraction, ceasing just
DISEASES OF THE MITRAL VALVE 977
before the second sound. It may wholly replace the first sound, or the
dull sound of valvular tension may be heard to precede it, virhen it " tails
off" from the first sound. The murmur may be of very slight
intensity, and may be localised at the exact apex, or it may be audible
over the whole precordia with maximum intensity at the apex. In some
cases it is audible from the apex in a line which extends into the
left axilla, and then it often has another area of audibility at the back
between the spine and the angle of the left scapula. In other cases
the conduction is to the left border of the sternum above the ensiform
cartilage, and the cartilages and the interspaces as far as the second
left costal cartilage. I have observed cases in which the explanation of
this cohduction of a systolic murmur has appeared to me to be afforded
by discovery at the necropsy that the disease was chiefly confined to
the anterior flap of the mitral valve with the attached chordae and the
papillary muscles. Firm fibroid or calcareous material conducted the
vibrations towards the septum ventriculorum, whence they were trans-
mitted to the sternum and superficial parts adjacent. It is probable that
conduction towards the axilla and the back may indicate an implication
of the posterior flap in the disease.
It has been thought by some observers (41, 1, 53) that mitral
regurgitation may be evidenced by a systolic murmur in the second
left intercostal space, not quite close to the sternum but about two centi-
metres to the left of it; the murmur being due to vibrations communicated
by the reflux current to the left auricular appendix (1). Many con-
siderations seem to me to render this view untenable. The left atpicular
appendix, as has been pointed out by Russell, Byrom Bramwell, and
others, does not approach the surface at the spot where the murmur
is audible ; in many necropsies it has not been visible on an anterior
view of the heart ; when seen it is at least an inch and a quarter to the
left of the left border of the sternum, and is for the most part on the
posterior aspect of the heart (55). It is more probable that the vibra-
tions of the reflux current, if transmitted to the auricle, would be audible
at the back. Duroziez has used this argument to explain the audibility
of the murmur of mitral regurgitation at the back : — " L'oreillette gauche
plac^e en arrifere contre la colonne vert6brale transmet en arriere le
soufile form^ a la mitrale." I consider it most probable that, when the
murmur of mitral regurgitation is audible in the second left interspace,
it is by means of vibrations communicated to the great anterior flap of
the mitral valve, or to the morbid structures in contiguity therewith.
The chief practical difiiculty in the diagnosis is that of discriminating
a murmur due to mitral insufficiency from one to be ascribed to the
influence of the movements of the heart upon the portions of lung in
front of it and around it. Cardio- pulmonary murmurs have been
described by many observers (51, 64, 28, 18, 42, 48, 40). Of these
Potain has made a careful and elaborate study.
The first sound of the heart to the right of the apex and over much
of the area occupied by the right ventricle is often observed to be rough
VOL. V 3 R
978
SYSTEM OF MEDICINE
under conditions in which cardiac disease has no part. Such rough
sounds have been referred to many causes which it seems unnecessary
to discuss. As a rule they are readily to be distinguished from murmurs
due to mitral insufficiency, because they are not heard at the exact
apex nor over the situations mentioned as those to which a mitral
regurgitant murmur is conducted.
In some cases, however, the difficulties are greater. In order to
make the distinction clear, certain steps should be methodically taken.
First, the relation of the murmw to the movements of respiration should be
observed. The cardio-pulmonary murmur is usually much influenced by
the respiratory movements ; for the most part it is intensified both during
expiration and inspiration, especially during the latter ; but it often
becomes inaudible at the end of an expiration. If, therefore, rhythmical
crescendo and diminuendo in the sound of the murmur are heard during
the respiratory acts, it is probable, though not certain, that the murmur
has its cause in the lung outside the heart.
The position of audibility of the murmv/r must be carefuUy noted.
Cardio-pulmonary murmurs are not heard at the exact apex of the left
ventricle, but over a small area at
the level of the apex to the right
and to the left. Instead of corre-
sponding exactly to the centre of
the outline of the apex of the left
ventricle, as does that of mitral
insufficieiicy from organic causes,
these murmurs have their maximum
from a quarter of an inch to an inch
and a quarter away from the point
of apex beat. Above the exact apex
there is a doubtful zone, where a
precise diagnosis cannot readily be
made ; but if a systolic murmur has
its site of maximum audibility ex-
actly over the apex, it must be
ascribed to intra-cardiac causes.
The rhythm of the murmur must
be determined. A cardio-pulmonary
murmur does not replace the first
Fig. 62.— Sites of systolic murmurs at or near the SOUnd. The Valvular flap is heard,
apex of the heart. A, Murmur nearly always J ^.i^ Tniirrrinr ia nViaei-irprl to nppnr
organic ; B, 0, murmurs always non-oiganio ^^^ ''"^ murmUT IS ODSerVCQ tO OCCUr
(cardio-pulmonary of Potain) ;i) doubtful ; subsequently, after an appreciable
murmurs usually non-organic. (Potain.) . -*■, ''^ i p ^
interval, and to cease before the
second sound ; it is manifested during a portion only of the ventricular
contraction, and is meso-systolic (Potain).
In the next place, auscultation should he practised in various positions of
the patient. A cardio-pulmonary murmur, as a general rule, is very
evident when the patient is recumbent, diminishing in intensity, and
DISEASES OF THE MITRAL VALVE
979
even disappearing when the sitting or erect position is assumed. In a
minority of cases this rule is reversed. It. has been shown by Cuffer
that though the bruits which have their causes outside the heart are in
the greatest degree modified by changes of position, yet systolic apical
murmurs, due to organic mitral disease, are sometimes similarly influenced.
Potain says that if the change from the dorsal decubitus to the sitting
Fig. 63. — A, Portion of heart and pericardium uncovered by lungs. (After Aitken.)
position causes the complete or almost complete disappearance of the
murmur, it can be confidently ascribed to extra-cardiac causes ; the same
may be said when a murmur well marked in the erect position disappears
on recumbency. On the other hand, it is not true that every murmur
which is uninfluenced by changes of position is necessarily organic.
Potain has adduced a great amount of evidence to show that the
cardio- pulmonary murmur is caused by an aspiration of some of the
alveoli of the lung produced by the cardiac movements. When the heart
98o SYSTEM OF MEDICINE
is distended in diastole certain portions of the adjoining lung are com-
pressed against the thoracic wall, and the air is squeezed out of them.
When the systolic recession ensues the comparatively airless tongue of
pulmonary tissue quickly becomes inflated, provided always the muscular
contraction is accomplished rapidly.
Estimation of the degree of mitral insufficiency. -^'Whsn. the amount of
Wood regurgitated into the left auricle at each systole is very small,
there may be no physical sign to indicate the existence of any lesion
other than the systolic murmur having the characters and areas of audi-
bility already described. In the cases where the amount is sufi&cient to
disturb the normal physical conditions vrithin the chambers of the heart,
there are signs which indicate, in greater or less degree, the amount as
well as the existence of imperfection. In the attempt to make this esti-
mation, in the first instance the second sound of the heart should be
carefully observed. If, in any case in which a murmur indicating mitral
regurgitation is manifest, the second sound, as heard in the second left
intercostal space or the second and third left intercostal spaces, is noted
to be of a sharp, loud, metallic, or tympanitic character, or by its loudness
(" accentuation ") to contrast with the second sound heard in the course of
the aorta and great vessels of the neck, as well as in the positions below the
third interspace as far as the heart's apex, it must be concluded that the
regurgitant stream, antagonised by the adequate force of contraction of
the right ventricle, causes abnormal pressure in the pulmonary artery and
the vessels of its circuit. This sign, as Skoda pointed out, indicates a
compensated mitral insufficiency ; when the right ventricle becomes
feeble or the tricuspid valve inadequate, the accentuation of the pulmonary
second sound is no longer heard. The observation of an accentuated
pulmonic second sound, with no sign of pulmonary embarrassment, no
abnormality discovered by auscultation, except the murmur of regurgita-
tion through the mitral orifice, and no physical signs of dilatation of the
muscular chambers of the heart, will indicate a moderate and not an
extreme degree of mitral insufficiency.
Any deviation of the ventricles and auricles from the normal shoiild
be noted and considered. The left ventricle should be investigated by
palpation and percussion. In cases of mitral regurgitation, the apex
may be felt to Uft the finger of the observer considerably below the
normal fifth interspace, and in a greater or less extent to the left ;
so that it may overpass the vertical mid-thoracic line, and be palpable
in the axilla. The forcible heaving or thrusting movements of the
ventricle constitute a measure of the degree of hypertrophy of the
muscle. In young subjects the ribs and cartilages corresponding to the
area occupied by the ventricles may be bulged forwards and prominent.
It is very rarely that a systolic thrill is to be felt over the apex. The
rhythm of a thrill must be carefully noted — one felt near the apex is nearly
always presystolic, and pathognomonic of mitral stenosis. Determination
of the outline of the left ventricle by percussion adds to the informa-
tion obtained, and indicates the shape and position of the apex, when
DISEASES OF THE MITRAL VALVE gSr
these are not perceptible on palpation. The line of dulness or deficient
resonance on percussion, indicating the outline of the left ventricle, may
be found to extend to the left of the mammillary or mid-thoracic line, even
as far as the axilla at the level of the seventh rib, and thence in a line
inclining upwards to the level of the second left intercostal space. The
upper limit of deficient resonance has been found above the second
rib (19).
At post-mortem examinations, even -when there is clear evidence of
much hypertrophy and dilatation of the left ventricle, the latter is
generally observed only as a mere margin to the left of the right ventricle
on an anterior view of the heart ; the left auricle is often invisible on
inspection of the front, and only discovered on so turning over the heart
that a back view is obtained. It must be remembered, however, that
the conditions during life differ from those observed after death; the
heart-muscle contracts in rigor mortis : nevertheless, it is no doubt correct
that the left auricle and left ventricle occupy but a small portion of the
left border of cardiac dulness.
In cases in which a notable accentuation of the pulmonic second sound
and the physical signs of enlargement of the left ventricle are manifested
with no evident deviation of the right chambers from the normal, it may
be inferred, that though regurgitation through the mitral orifice may be
considerable, the lesion is compensated by augmented force of the right
ventricle.
For the due estimation of the extent of the lesion the right cavities
must be carefully explored. Palpation may detect a forcible heaving of
the right ventricle to the left of the ensiform cartilage. Percussion parallel
in direction with the long axis of the sternum may indicate a line of defi-
cient resonance extending to the right of the mid-sternal line in various
degrees in different cases. The dulness . exceptionally extends to two
and a half inches from the median Hne ; it delimits the right border of
the right auricle.
In some cases I have found on plessimetric percussion that the right
border of dulness does not meet the line which indicates the upper border
of the liver at a right angle ; but, from one to two inches above the
liver, a sloping line of dulness extends from the auricular border to meet
the liver dulness an inch to an inch and a half to the right of the sternum.
There is a wedge-shaped area of deficient resonance to the right of the
vertical line which indicates the limit of the right auricle. I believe this
to be due to a distension or dilatation of the venae cavse as they open into
the auricle ; it is only observed in cases of great dilatation of the right
cavities. The upper limit of dulness may reach as high as the lower
border of the second right costal cartilage. The extent of the dulness
from right to left may be determined by percussion over the first part
of the sternum in a horizontal direction ; this line crosses the sternum to
the second interspace on the left side. Such a line of dulness over the
sternum at the level of the second rib still indicates the right auricle,
which may even encroach on the second interspace on the left side. The
982 SYSTEM OF MEDICINE
remainder of the upper limit of dulness is due to the right ventricle and
the pulmonary artery.
The evidence of the outline of the heart obtained by percussion must
not be accepted without the due estimation of causes of fallacy. Dis-
tension of the stomach with air will cause a tilting of the ventricles to a
higher plane, and a dislocation towards the right of the right chambers.
The content and consequent bulk of the right auricle and ventricle vary
with the varying turgescence of the Uver. Such distension may be pro-
tracted and due to a lasting or temporary and evanescent morbid con-
gestion ; for it is well known that the Uver presents great variations in
bulk even during brief periods of time. A dilatation of the blood-vessels
within the abdomen (that is, in the splanchnic area) also may reduce the
content and consequent bulk of the right auricle and ventricle when there
is no obvious change in the volume of the liver. Another cause for
reduction in the observed size of the right cavities is expansion of the
lungs. In such cases there are two causes of a recession of the area of
deiicient resonance indicating the bulk of the heart ; namely, the inflated
air-cells of the tongues of pulmonary tissue overlapping the heart which
give rise to a clearer note on percussion, and the augmented volume of
blood circulating in the pulmonary blood-vessels which reduces the
content of the heart chambers.
The apparent bulk of the heart, as determined by the means of
physical diagnosis, may be temporarily increased by congestion of the
vessels of the pericardium and neighbouring pleura as well as of those of
the coronary blood-supply ; and there may be fluid exudation into the
spaces of the surrounding tissues.
The testimony of many observers has shown that the bulk of the
heart may be much reduced in a brief space of time — in some cases, as
in acute rheumatic diseases, without relation to the therapeutic means
adopted ; in others in response to special methods of treatment, such as
baths and certain methods of muscular exercise.
When in a case manifesting the murmiu' of mitral regurgitation it is
found that the right chambers are persistently dilated, and especially
if physical signs of tricuspid incompetence be present, it must be inferred
that the degree of valvular imperfection is great and the muscle of the
heart gravely approaching failure.
The investigation of the bulk of the liver is also important as a
guide to the estimation of the degree of valvular imperfection in a case
manifesting the murmur of mitral insufficiency. When there are signs
of dilatation of the right chambers of the heart, and the Uver is felt as
a thickened rounded tumour below the right costal margin, it must be
inferred that the mitral valve is gravely incompetent — the imperfection
is still greater if the Uver be felt to pulsate.
Important evidence is afibrded by the observation of the characters
of the pulse. If in a case manifesting the systolic apex murmur and other
physical signs of mitral insufficiency, the hand of the observer applied to
the precordia is sensible of a forcible ventricular contraction, whilst the
DISEASES OF THE MITRAL VALVE
983
radial and other arterial pulses are found to be small and -weak, the
inference is legitimate that much of the volume of blood which should
have been delivered into the aorta is lost by regurgitation into the
auricle. The pulse of a slight mitral regurgitation differs inappreciably
from the normal : when the lesion is considerable the volume is small
and the tension low. The sphygmograph often shows dicrotism when
the evidence of impaired tension is not obvious to the finger. Not in-
frequently, even when compensation is maintained, the low-tension pulse
presents marked fluctuation of the base line which shows that the normal
correlation between circulation and respiration is disturbed.
The cardiogram in a case in which there is free mitral regurgitation
sometimes presents special features. There is a pronounced dip or notch
FiQ. 64. — Cardiogram and sphygmogram from a case of free mitral regurgitation.
Fig. 65. — Cardiograms in mitral insufficiency showing dip or notcli in the upper portion of the trace,
in the upper part of the tracing giving the summit a forked appear-
ance.
It would seem probable also that the relative durations of the systolic
and diastolic periods, as expressed in the cardiogram, are altered ; the
diastolic period being relatively shortened. In compensated mitral regur-
gitation in many cases neither cardiogram nor sphygmogram presents any
notable deviations from the normal.
Irregularity of the pulse is not, in my experience, a characteristic of
mitral insufficiency.
Clinical groups of eases of mitral insufBeieney. — Group I. Mitral
insufficiency the remit of rhevmatic endocarditis. — It will be convenient
to consider this group in two divisions : the first of children, the second of
adults. .
In children of twelve years of age and under, who have suffered either
from a well-marked attack of rheumatic fever, or from repeated attack^
984 SYSTEM OF MEDICINE
or from one attack with subsequent subacute manifestations, it is in the
highest degree probable that the signs of insufficiency of the mitral valve
will be observed. Such insufficiency is nearly always due to the sclerous
alterations at the left auriculo-ventricular orifice and to a retraction of the
valve curtains, the cords and the muscular columns which are the results
of the progressive morbid changes of rheumatic endocarditis (9). These,
however, are not the only changes in such cases. Pericarditis usually
coexists ; the layers of pericardium become united, oftentimes through-
out their whole extent, by adhesions. The muscle of the heart is in-
flamed and infiltrated, and rapidly becomes extremely hypertrophied.
The whole heart participates in the rheumatic inflammation ; there is
general carditis (Sturges), the result of which, though life may be pro-
longed for months and years, is a crippling of the heart while such life
lasts. In the course of development of this severe heart disease
subcutaneous rheumatic nodules are frequently observed (Barlow, Warner,
Cheadle). Such severe general rheumatic heart disease is rarely met
with in children under six years of age, it is most common between the
ages of six and twelve years. As a general rule, of the children admitted
into hospital for acute or subacute rheumatism 50 or 60 per cent are
discharged with valvular disease, the most frequent form of which is
mitral insufficiency. This, however, by no means represents the full
efiect of rheumatic endocarditis as a cause of the valvular imperfection,
for the cases discharged without evidence of such disease are often foimd,
after the lapse of months, or perhaps years, during which no rheumatic
phenomena have been manifested, to present undoubted evidence of
mitral regurgitation. The process of the changes in rheumatic endo-
carditis is slow and is not necessarily betrayed by symptoms.
In a considerable number of cases of mitral insufficiency in children
no evidence of rheumatism is to be obtained. For instance, in a series
of 11 8 cases of mitral regurgitation under my observation I found an
absence of any evidence of rheumatic association in 40. In 8 of these
there appeared to be a definite relation in sequence to scarlatina, in
6 to measles, and in 3 to scarlatina and measles. In 13 cases there
was no evidence of any antecedent disease to account for the valvular
imperfection. Post-mortem evidence showed that the morbid changes
in these were identical with those observed in cases known to be
rheumatic (59).
In the cases in which there is no evidence of rheumatism the child
may be brought under notice for a disorder of nutrition — especially wast-
ing and anaemia — or for a disturbance of respiration, such as cough and
dyspnoea, the results or concomitants of the heart disease ; or for an ajBfec-
tion of the nervous system, such as chorea, epilepsy, or hemiplegia. In
some of them there is cerebral embolism, the plug being derived from the
diseased endocardium. Not infrequently the valvular disease is discovered
by accident. No notable discomfort may be caused by the movements of
the child in play nor on running upstairs ; and Henoch says that in many
cases the disease is first discovered by the mother observing the violent
DISEASES OF THE MITRAL VALVE 983
motion of the heart when she strips the child to give the bath. The
evidence points to the conclusion that a form of endocarditis which has
the essential characters of the rheumatic may occur in infancy and child-
hood without any other manifestations of rheumatism (17). Endocarditis
then may occur as a solitary expression of the rheumatic disease (Archi-
bald Garrod). [Firfe art. " Acute Rheumatism of Childhood," vol. iii. p. 42.]
The symptoms observed in childhood during the progress of un-
compensated mitral inadequacy are very varied. The age of the child
has some influence in regard to these. As a general rule, the signs
in infants and very young children are chiefly those of inanition, —
emaciation, anaemia, and deformity of the thorax. There are in many
cases frequently-recurring attacks of bronchitis or broncho-pneumonia,
cough being a prominent symptom. In children after the age of four
years symptoms more directly indicating disorder of circulation become
manifest : bleeding at the nose may be cited as one of these. Difficulty
of breathing becomes apparent, and in some cases most distressing ortho-
pncea. Precordial pain and discomfort are severe symptoms in some
cases, and these may be associated with lumbar pain. Palpitation may
be a distressing symptom. Dropsy is by no means uncommon, but it
rarely follows the gradually ascending course usual in the adult ; the
oedema is either more general, or more variable in the sites of its mani-
festation. In cases with oedema or ascites albuminuria is a frequent
complication : this may be transient and due to venous congestion, but
in the majority of cases it is dependent on the coexistence of inflamma-
tion of the kidneys, and is a sign of dangerous import. In the later
stages of the disease vomiting and diarrhoea may be observed as most
serious indications ; hsematemesis occurs in some cases. A marked
anaemia, occasional vomiting, restlessness followed by apathy, and partial
unconsciousness are symptoms which in many cases . mark the weeks or
days preceding the close of life.
In the form of mitral insufficiency attended with general carditis the
prognosis is bad. The pericardial adhesions and the consequent hyper-
trophy and dilatation of the whole heart are a constant menace, and
prevent satisfactory treatment. On the other hand, an uncomplicated
mitral insufficiency in childhood often has a favourable issue \ and the
results of treatment even when the severe symptoms of threatened
failure are present are often very satisfactory. Henoch considers that
children recover from rheumatic endocarditis better than adults, and that
in them the valve is more likely to regain its structural integrity.
Cadet de Gassicourt has given his opinion that, whilst in the adult the
valvular thickening increases, and the sclerosis at the auriculo-ventricular
opening becomes more and more considerable, so that incurable disease
remains, in the child there is more probability of absorption of the
morbid products ; then, the obstacle being removed, the growth of the
cardiac muscle ceases to be exaggerated, and the heart, at one time too
large for the child, comes by degrees into due proportion with the needs
of the adult (71).
986 SYSTEM OF MEDICINE
In the treatment of mitral insufficiency in the child when compensa-
tion fails and the symptoms are those of progressive cardiac enfeeblement
-^the condition being one of chronic disease uncomplicated by acute
rheumatism — the following are the chief points to be observed : — (i.) Rest
in the recumbent position, or in the semi-recumbent with the shoulders
supported, must be maintained as much as possible, (ii.) Precordial pain
and discomfort or difficulties of respiration call for the application of
warmth to the chest by warm moist flannels, spongio-piline, or the
jacket poultice. On some occasions a digitalis poultice may with ad-
vantage be substituted for the ordinary linseed meal poultice : this
is made by boiling two ounces of digitalis leaves in a pint of water
for ten minutes, about two ounces of linseed meal being gradually added
until the proper consistence for a poultice is attained. The mass is of
course to be spread upon suitable material and applied in the usual way.
(iii.) Means for inducing good general nutrition are of the first importance.
A child with mitral incompetence is often intensely anaemic. Cod-liver
oil, by itself or in an emulsion, or in combination with some of the iron pre-
parations, is very beneficial. In some cases small doses of arsenic (Fowler's
solution), with tincture of nux vomica or liquor strychnines, succeed better
than iron. In not a few I have seen a plan of supplementary alimentation
by nutritive enemas turn the scale towards amendment. One of the best
of such enemas is made by shaking together in a bottle one egg, an ounce
of hot milk, and an ounce of cod-liver oil, and administering very slowly
through a large soft rubber male catheter, with a funnel attached and held
at a sufficiently high level, or by an india-rubber enema tube. The
administration should be twice or three times daily. (iv.) Cardiac
tonics are to be prescribed with judgment. In some cases rest, carefully
regulated diet, and the tonic methods just mentioned suffice, and all
agents which directly influence the cardiac rhythm are unnecessary or
even injurious. Of all cardiac tonics digitalis is of the greatest value ; it
is especially so when dyspnoea is a marked feature. The drug may be
given in the form of the tincture in doses of from one to five minims, or
the infusion, ten minims to one drachm, or the leaves in powder, one-
fourth of a grain to half a grain, repeated three times a day. There is
some difference of opinion whether the administration should be con-
tinuously for long periods or in larger doses with omissions for several
days. In some instances digitalis is not well borne, and in children this
intolerance is usually shown by the occurrence of vomiting : it should be
omitted whenever vomiting appears. In cases when digitalis adminis-
tered by the mouth seems to be inert, rapid improvement may follow
the hypodermic injection of digitaline y^ to -j^ of a grain for a
child of from six to twelve years of age. In any case such hypodermic
injection should not be repeated for at least forty-eight hours. As an
alternative to any preparation of digitalis caffein citrate dissolved in
water or in the ordinary saline mixture, in doses of from one to three
grains three times a day, may be given. The administration should not
be continuous, but for a period of four to six days, with similar periods
DISEASES OF THE MITRAL VALVE 9^7
of suspension ; for all cardiac tonics, thougli tending at first to increase
the excretion of urine, by their prolonged action often tend to diminish it.
In cases where as a consequence of mitral regurgitation the right cavities
of the heart are much dilated — especially when the tricuspid valve is
rendered incompetent — digitalis and other cardiac tonics may be power-
less for good. Their inefficiency is readily to be explained, for it must
be remembered that their action is on both ventricles, and that they
augment the force of the right ventricle as well as that of the left : now
increased action of the right ventricle means so much the more reflux into
the general venous system and further disasters. In many cases where
there is such distension of the right cavities (an occurrence which may
supervene as an acute phase in a case of chronic mitral insufficiency), the
relief of venous pressure by leeching is a most valuable auxiliary to
treatment. One or two leeches may be applied to the precordia, and
the leeching may be repeated on several occasions at intervals of two or
three days. Exceptionally, half-a-dozen leeches may be applied at the
first. I have often observed that digitalis, which has been powerless for
good before the application of leeches, proved of great service there-
after (58).
Dropsy, in cases of chronic mitral insufficiency in the child, may be
transient, and yield to the medicinal treatment already sketched out ; or it
may become a far more serious symptom. There may be general anasarca,
and pronounced ascites and effusion may rapidly take place within the
pleural cavities. In a considerable proportion of cases desquamative
nephritis is manifested in the course of the mitral disease. In the treat-
ment of such cases, sponging of the skin with hot water made alkaline with
sodium carbonate, the child being afterwards wrapped in a hot blanket, is
often a more practicable and efficient measure than the administration of a
hot-air bath or a vapour bath. Purgatives, as compound jalap powder, are
essential ; at first calomel may advantageously be administered therewith.
Saline diuretics are to be combined with digitalis and decoction of
broom. The removal of all traces of dropsy in the child is sometimes
rapid. In some cases medicinal means fail. As a rule, punctures of the
skin of the lower extremities and the use of Southey's tubes in the treat-
ment of dropsy in the child are not to be recommended ; there is a
danger that restless movements may cause chafing and irritation. If there
be ascites, paracentesis abdominis should be performed : sometimes rapid
convalescence follows this operation. Sedatives and medicines to procure
sleep must be used with caution, but in many cases they are indis-
pensable.
In mitral insufficiency, the result of rheumatic endocarditis in the adult, we
find associations differing from those in the cases of children. In adult
life the occurrence of general carditis and the implication of pericardium,
endocardium, and myocardium in the rheumatic disease are much less
common. In this sense the disease is less formidable than in the child.
On the other hand, repeated storms of endocarditis in the adult increase
the sclerosis at the mitral orifice and the imperfection of the curtains,
SYSTEM OF MEDICINE
cords, and columns ; the thickened fibrous structures tend also in pro-
gressive degrees to undergo degeneration and calcareous transformation.
The already diseased endocardium may be attacked by pathogenetic micro-
organisms ; the endocarditis may be septic. This is especially probable
in women after parturition, and in both sexes when there are dangers
of septicaemia ; but the disease may arise insidiously without traceable
infection. The causes of overstrain, both physical and mental, which
aifect the adult warrior in the battle of life adversely modify the con-
ditions. Emotions disturb the rhythm of the heart and tend to spoil the
compensation. Severe physical efforts may rupture curtains or cords
already diseased. Diseases of various forms may alter the nutrition of
the heart-muscle. There are probably many forms of disease affecting the
coronary arteries and their branches within the heart ; arteritis and peri-
arteritis occur in many forms of infectious disease, and notably in syphilis.
Arterio-sclerosis involves the coronary arterioles (especially in chronic
Bright's disease), and the larger branches in the later periods of adult
life become affected by atheroma. The result of all such morbid altera-
tions of the walls of the arteries is an impairment of the force of the
cardiac muscle with subsequent degenerations. Intercurrent diseases of
the lungs,, again, may rudely interrupt a compensation hitherto satisfactory.
In some cases causes of inflammatory irritations are imported from with-
out. In others infarctions or so-called pulmonary apoplexies are both
consequences and causes of cardiac failure. Any considerable interference
with the function of the lungs imposes a direct obstacle to the work of
the right ventricle. It is the energy of the right ventricle that, by im-
pelling an abnormally large volume of blood through the pulmonary
vessels, and thus antagonising in the left auricle the regurgitant stream
from the left ventricle, is the effective agency of compensation.
The symptoms in the adult of a failure of the compensatory conditions
in cases of insufficiency of the mitral valve are briefly, and in an approxi-
mative way chronologically, difficulty of breathing, especially upon effort,
but also paroxysmally ;' cough, with physical signs of oedema of the bases
of the lungs, and often of localised consolidations ; and dropsy, gradually
extending from the more dependent portions of the body. From all
such symptoms and from the epiphenomena of embolism and infarction,
pulmonary and systemic, there may be recovery. When the limits of
possible restoration of the powers of compensation are reached, the picture
is one of suffering and sadness. The recumbent position is intolerable,
the lower limbs are persistently cedematous and their integuments indur-
ated ; the countenance wears the hue of combined sallowness and
lividity, the expression is one of anxiety and of a restless craving for
sleep, alternating with a feeble, helpless wandering of mind; there is
abdominal discomfort from a large and tender liver ; the arterial pulse
becomes feebler and nearly imperceptible, and by slow degrees, with
occasional awakenings to the reality of suffering and distress, life be-
comes extinct.
In the treatment of a case of mitral insufficiency in the adult, when
DISEASES OF THE MITRAL VALVE
compensation is failing, rest is of the first importance. For a practitioner
to prescribe digitalis or other cardiac tonics in a routine fashion for
patients who manifest morbid heart symptoms is a dangerous error.
Eest, careful dieting, and judicious purgation may turn the scale towards
recovery, even when dropsy, and signs of much venous engorgement of
the viscera, have supervened (see case by Dr. Vivian Poore, 46). In a large
proportion of cases, however, the difficulties are not to be thus sunnounted,
and recourse must be had to drugs, whose influence is especially upon the
forces of circulation ; of these digitalis is the chief. Digitalis may be
administered in the form of the powdered leaves, the infusion, or the
tincture. One grain of the powdered leaves is equivalent to one-third of
an ounce of the infusion and to eight minims of the tincture. The leaves
may be administered in doses of half a grain to a grain and a half three
times a day in wafer cachet or pill, alone or combined with other agents
such as mercury, iron, or aloes, or other aperients. The infusion may be
given in doses of a quarter of an ounce to half an ounce, or the tincture
from five to thirty minims.
In many cases the daily administration of digitalis can be continued
for long periods, for a considerable number of months at any rate ; but
great care must be taken to ascertain that the patient is perfectly tolerant
of the drug, and at the outset of this treatment the effects must be
noted daily : the treatment should not be continued for more than three
or four days vrithout the control of a skilled observer. Digitalis has
a complex action. It has a tonic effect upon the pneumogastric
nerve, whereby its power of moderating and slowing the heart's move-
ments is increased ; but further, it increases the energy of the myo-
cardium by a direct effect upon the neuro-muscular mechanism of the
heart itself. It also augments the contractility of the walls of the arteries
by an influence upon the vaso-motor centres and upon the local nervous
mechanism of the muscular coat of the vessels. The good effects of
digitalis are manifested by its so lengthening the diastolic pause that the
ventricles become more completely filled, and deliver ampler blood-
waves into the general arterial system. The arteries, when moderately
contracted, do not impede the blood-flow ; in fact, a larger amount of
blood traverses the circulation in a given time. The ventricles emptying
themselves more completely, the previously dilated heart diminishes in
volume. The beneficial effect of digitalis is also shown in the production
of diuresis. Neither the heightened arterial pressure nor the augmented
urinary outflow produced by the drug is, however, by any means constant.
Variations of arterial blood-pressure under the action of digitalis have
been noted by many observers to be quite independent of the slowing
effect upon the heart; indeed the diuretic results are confined almost
entirely to those cases that manifest oedema. It seems probable that
the fluid absorbed from the lymph-spaces, drawn within the capillaries
on account of the augmented rapidity of the circulation, and carried
to the renal capillaries, so stimulates the kidneys as to provoke diuresis.
When there is no effused lymph to be absorbed, diuresis does not result ;
990 SYSTEM OF MEDICINE
in fact, the urinary outflow in some cases diminishes even to arrest,
and there may be hsematuria. Digitalis is contra-indicated when nausea,
vomiting, and diarrhoea form part of the symptoms, and when the pulsa-
tions of the heart are rendered inordinately slow. When the administra-
tion of comparatively small doses is continued too long there may be a
sort of chronic poisoning ; the signs are pallor of surface, coldness, and,
sometimes, attacks of faintness ; it would seem that cerebral ischsemia
is thus produced (Duroziez, 14). I am of opinion that the dangers of
the prolonged administration of digitalis are too often ignored. Certain
effects of digitalis may persist long after cessation of the administration.
Abnormal retardation of the heart's contractions has been noted ten days
after omission of the drug (Raven), three weeks (Potain), 28 and 29 days
(Duroziez). The practical rule should be that average doses of the pre-
parations of digitalis, repeated at intervals of four hours, should not be
continued, in the earlier stages of treatment, for more than three days ;
then the drug should be suspended for a like period. It is only when
a patient manifests a perfect tolerance that the protracted administration
should be permitted.
The employment of digitaline is preferred by many physicians, especi-
ally by the French.' It is to be remembered that the various digitalines
vary greatly in strength ; that of Nativelle has about fifteen times the
strength of the digitaline of HomoUe, weights being equal. Potain
prescribes for a case of cardiac failure with dropsy one milligramme of
Nativelle's crystallised digitaline. This may be administered in one
dose, or, if tolerance be doubtful, it may be divided into four or five
doses given in as many days. After the administration there is often
profuse diuresis. There should be no readministration for many days —
the interval may be from ten days to three weeks ; renewed acceleration
of the pulse is to be taken as an indication for repetition of the
treatment.
Digitaline may be administered hypodermically. When satisfactory
effects have not followed administration by the mouth, I have seen excel-
lent results follow the hypodermic injection of digitaline in the form of
a solution of the discs of Savory and Moore. Each disc contains -^^
of a grain. The dose should not exceed two discs {^-^ grain).
In cases in which the right chambers of the heart are much dis-
tended the abstraction of blood is indicated. A bleeding from the arm
to the extent of six or eight ounces eoincidently with the administration
of digitalis, or subsequently to it, will often turn the scale towards
recovery.
In some instances of mitral insufficiency, the consequence of rheumatic
disease, the treatment by digitalis entirely fails ; there seems to be no
good effect upon the left ventricle, the right cavities continue to dilate,
dropsy increases, and the drug in combination with ordinary diuretics
fails to increase the outflow of urine. Other cardiac tonics and various
combinations of these may then be tried.
Gaffein or its citrate may be given in doses of from three to five grains
DISEASES OF THE MITRAL VALVE 991
every four hours, but, as in the case of digitalis, it is better that it should
not be used for more than three days continuously. I prefer to administer
it in the ordinary saline mixture (solution of ammonium acetate). Its
action is in many points similar to that of digitalis, but it has a much less
effect in retarding the pulse and also in causing contraction of the arteries.
Its diuretic influence is decided, and, unlike digitalis, it stimulates the
renal epithelium to the excretion of solids. I have found the diuretic
effect to persist after the suspension of the drug. In some cases this
result is coexistent with good and rapid recovery from all distressing
symptoms ; but diuresis may occur and persist, and yet the result be
unfavourable. The drug very rarely induces insomnia ; I have more
frequently observed that by lessening the dyspnoea it has promoted sleep.
In some subjects, however, it produces agitation, headache, vomiting,
purging, and sleeplessness. The combination of digitalis and caffein may
act more favourably than either drug alone (4).
Theobromine, in the form of the sodio-salicylate (diuretin), may be
substituted for caffein. It is to be administered in doses of 15 grains six
times in the twenty-four hours. It is freely soluble in water. It has a
stronger diuretic action than caffein, and does not cause nervous agitation
and sleeplessness. The diuretic effect is manifested between the second
and sixth days of its administration.
Strophanthm may be administered in the place of digitalis, caffein, or
theobromine. It is given in the form of tincture (two to ten minims, in
chloroform water or with alcohol), or of tabellse, each of which is equiva-
lent to two minims of the tincture. The dose may be repeated every
four hours ; the same care in watching effects and suspending the
administration at intervals of a few days should be used as in the case of
digitalis. The action of strophanthus upon the heart by the way of the
vagus and through the local neuro-muscular mechanism resembles that of
digitalis (Fraser, Popper, Bucquoy) ; but, according to Roy and Adami, it
stimulates the contraction of the papillary muscles to a far greater
degree than that of the ventricular wall ; these observers have shown
that on repeating the dose so that the more pronounced toxic action of
the drug is manifested, the papillary muscles become notably weakened,
and even their power of contraction annulled. Fraser concludes that
strophanthus acts upon the heart more forcibly than digitalis, but on the
calibre of the arteries infinitely less. It has often a very favourable effect
upon the difficulties of breathing, and, used with care, is an efficient and
useful substitute for digitalis ; but it is not without its dangers. Its
protracted use may cause dyspepsia with diarrhoea and wasting (Lemoine),
and there are some probabilities that it may lead to sudden death in the
course of its administration for heart disease (Gottlieb). I cannot doubt
that the protracted injudicious administration of digitalis and strophanthus
— especially in those who absorb these drugs without skilled medical
supervision — has often been productive of dangerous and fatal results.
The other substitutes for digitalis, Adonis vernalis, Cactus grandiflorus,
etc., are not of proved importance. Sparteine has no notable advantage
992 SYSTEM OF MEDICINE
over the broom tea (decoctum scoparii) which contains it ; the latter is
useful as a diluting agent for the heart tonics already considered. Con-
vallaria majalis will be considered in reference to the therapeutics of
mitral stenosis.
Treatment of dropsy. — By the means already indicated, together with
the administration of such purgatives as produce watery evacuations —
one or two purgative doses of calomel are often of service in the early
stage of treatment — may suffice to remove all traces of dropsy and to
restore compensation. In other cases where the dropsy does not disappear
the mechanical removal of the effused fluid may be necessary. Incisions
by a lancet or punctures by a needle may be made into the skin of
the lower extremities, the limbs being wrapped in flannels or other
absorbent material to take up the fluid which, copiously drains away ; or
the fine trochars and canulas known as Southey's tubes may be used. In
either ease the skin should be previously sponged with alcohol, ether, or
an antiseptic solution. The former plan is to be preferred in the case of
a delirious or very restless patient ; the latter when the patient is tranquil
enough to allow the fluid to flow gradually through the fine flexible
tubes into the receptacle underneath the bed for many hours. The
trochar should be inserted very obliquely beneath the skin ; the opening
of the canula should be at the extremity (and not at the sides), and the
flexible exit tube in the portions nearest the inserted canula should be
fixed to the skin of the leg by strips of adhesive plaster ; it should also be
arranged so that it does not kink and obstruct the flow. It is best, when
the anasarca is considerable, that two canulas with tubes attached be
inserted into each lower extremity. When ascites exists, the fluid within
the abdomen may be drawn off by the slow process of draining through a
small canula and fine tube, or by the more rapid process of paracentesis
abdominis. I prefer the more speedy withdrawal by a comparatively
large trochar. When ascites coexists with general anasarca it may be a
a question whether draining the subcutaneous tissue or tapping the
abdominal cavity should be first performed. When the abdomen is not
much distended the former should be practised first, for after the draining
the intra-abdominal effusion may become absorbed. When the ascites
is considerable paracentesis abdominis should take the precedence.
Effusions within the pleural cavity should be withdrawn at once.
Agents for producing sleep or calming nervous agitation are of high
importance in the treatment of the failing heart of mitral insufficiency.
In some cases chloralamide has been useful, as it is always a harmless
hypnotic. It may be given in doses of from 20 to 50 grains in wafer
cachet or in weak spirituous or acidulated solutions. Each draught should
be made up separately. I prefer a combination of 20 or 30 grains of
chloralamid with 30 minims of dilute hydrobromic acid with a drachm
of syrup of orange flowers and an ounce of pure water, administered
at bedtime. Another harmless agent is urethane (ethyl carbamate), which
is freely soluble in water, the solution having a saline but by no means
unpleasant taste. In doses of 15 to 20 grains at bedtime I have found it
DISEASES OF THE MITRAL VALVE 993
induce a calm, natural sleep lasting in a case of severe cardiac failure for
more than five hours, the patient being manifestly refreshed on waking.
Paraldehyde is perhaps a little stronger as a hypnotic. It may be adminis-
tered in doses of from 30 to 90 minims in diluted syrup or in almond
mixture, or in capsules (each containing 40 minims) ; it has a powerful
and unpleasant taste.
In a considerable number of cases manifesting distressful symptoms of
dyspnoea and insomnia no agent succeeds so well as morphia. By far the
best way of administering it in cases of cardiac disease is by hypodermic
injection. The solution of the acetate or the hydrochlorate or the solution
of morphia and atropia may be used. The first dose should be small —
one-sixth or one-fourth of a grain — but this may be increased subsequently
to half a grain. Care should be taken that the administration shall not
become habitual.
In regard to diet the aliments in the condition of failing compensa-
tion in mitral insufficiency should be very simple. Milk is the best
of all foods, but in some cases is hardly tolerated. In the gastric crisis
accompanying the failing heart there is often a complete disinclination for
food. Then peptonised milk or milk gruel may be swallowed in sipping
fashion, the patient being never permitted to take a distinct meal, nor a
particle of solid food (Sir Wm. Roberts). In such cases I have seen great
benefit follow the administration of peptonised enemas or the cod-liv6r
oil milk and egg enema already mentioned in the treatment of children.
Brandy, if given at all, should be in teaspoonful doses with milk and wine
only. Sherry, marsala, or tokay may be given in jellies. At the
subsidence of the crisis, as soon as milk can be well borne, an all-milk
dietary, especially if there be dropsy, should be prescribed until con-
valescence.
The diet and hygiene during the stage of comparative convalescence
will be considered with the third group of cases.
Group II. Mitral regurgitation in chorea. — In the majority of cases
of chorea a systolic murmur, having the characters which indicate regur-
gitation through the mitral orifice, is manifested at some period of the
disease or throughout its whole course. In a large section of such cases
the signs and symptoms are such as to leave no room for doubt that the
imperfection of the valve has been caused by rheumatic endocarditis. In
many instances of chorea there has been antecedent rheumatism ; the
proportion varying, according to the beliefs of individual observers, from
8 per cent (Hughes) to 30 per cent (Pye Smith), 31 per cent (A. E.
Garrod), and 32 per cent (Sir Andrew Clark). There is a consensus of
opinion that about one-fourth of all the subjects of chorea are or have been
rheumatic. In many also of those who have personally shown no
evidence of rheumatism there has been a family tendency to the disease.
The doctrine has been formulated that chorea is in all instances a rheu-
matic afifection (Roger) ; other observers (Stephen Mackenzie, Barlow,
and Cheadle) have estimated that in from 45 to 75 per cent of the
cases there are sufficient evidences of rheumatic tendency ; it may be
vol.. V 3 S
994 SYSTEM OF MEDICINE
concluded, therefore, that in the majority of cases chorea is a phase of
rheumatism. It must be allowed that in many of the cases the diagnosis
of rheumatism (reposing as it necessarily does on the statements of
unskilled observers, with whom as a matter of common experience almost
every painful aflfection is rheumatic) can be by no means precise. If
causes of fallacy be excluded we may perhaps take it as a fair working
hypothesis that about half the total cases of chorea are rheumatic, and
that the endocardial murmurs manifested in these patients are due to
structural disease of the valves, the result of the rheumatic form of
endocarditis. In this section of the cases the mitral incompetency which
is the concomitant of the disease is to be estimated and treated — ^when
any failure of compensation renders such treatment necessary — according
to the rules already laid down. The therapeutics of chorea are discussed
elsewhere.
Nearly all observers, however, are agreed that some cases of chorea
are non-rheumatic. It is well known that a sudden shock or terror may
be the precursor of chorea : such a cause may operate in a case undoubtedly
rheumatic, but, in common with many other observers, I have seen many
cases of chorea where a sudden and violent emotion preceded the attack
in a person who showed no sign of rheumatism, nor any proclivity thereto.
Dr. Stephen Mackenzie's statistics showed rheumatism and fright to be
nearly equal, numerically, as antecedents of chorea (38). Observers are
generally agreed that emotional and mental disturbances have a large share
in the immediate causation of the disease (A. E. Garrod). " The only
immediate cause of chorea that can be traced with any frequency is emotion,
usually fright, rarely mental distress " (Gowers, 20). The heart affection,
in Dr. Stephen Mackenzie's statistics of cases of chorea, was associated with
rheumatism in 50 per cent ; whilst in 35 per cent no such association was
recorded. In non-rheumatic chorea I consider that the symptoms and
signs of mitral insufficiency differ from those in the rheumatic cases. In
some of these, careful examination for many days may detect no evidence
of valvular disease ; then a soft and slightly pronoimced systolic murmur,
localised at the position of the heart's apex, may become audible. There
is no accentuation of the pulmonic second sound ; the ventricles do not
become dilated ; yet the murmur, having its original characters, persists
for several years. At later periods it may become completely inaudible.
The late Sir Andrew Clark held that the murmurs of mitral regurgitation
so frequently observed in cases of chorea disappear, in the great majority
of cases, within eight or nine years of the attack (10). These clinical
features greatly differ from those of mitral insufficiency due to rheumatic
endocarditis. The evidence of morbid anatomy completes the distinc-
tion. In cases of fatal chorea wherein a soft, apical, systolic murmur has
been observed during life, the left auriculo- ventricular orifice on its
auricular aspect has been found studded and fringed with small, firm
outgrowths having the signs of papilliform elevations of the endocardium.
These outgrowths are firm to the touch, and are not detached by rubbing
with the finger. The endocardium is smooth over them. They do not
DISEASES OF THE MITRAL VALVE 99S
begin, as in rheumatic endocarditis, with a change in the epithelium
and an attachment to the roughened surface of fibrous caps, but they are
firm outgrowths showing fibrous hyperplasia. Their formation is not
followed by the sclerous changes, the widely-spread fibrous proliferation, the
retractions of valve curtains, cords, and columns so frequent in rheumatic
endocarditis. On the other hand, they interfere but little with the closure
of the orifice in systole, and in process of time, the endocardium remaining
quite smooth, they come to have no pathological significance whatever.
It seems to me probable that they may be the immediate results of a
sudden overstrain and rupture of the terminal arterioles distributed to the
valve structures. The immediate symptoms induced by terror or by any
sudden mental shock is a blanching of the surface of the body, a contrac-
tion of the arterioles, a stimulation or over-action of the sympathetic nerve
mechanism.^ The eifect on the heart at first would seem to be arrested
action, afterwards palpitation. In the case of the delicate arterioles of
the endocardium of the valves the result might well be ruptiures ; — minute
haemorrhages, followed by thickenings analogous to those observed after
the experimental production of overstrain in animals (Roy and Adami).
In cases of chorea in which there is no evidence of failure of com-
pensation, but only a systolic murmur at the apex to indicate some
incompleteness of the closure of the mitral orifice during the ventricular
systole, all treatment by cardiac tonics, or by means specially directed to
the valvular imperfection, is unnecessary, and probably mischievous. The
therapeutic methods adopted should be those for calming the tumult of
the nervous system and for ministering to a healthy nutrition.
Groni,]) III. Mitral insufficiency the result of dilatation of the left
ventricle. — This group must of necessity be subdivided. In some cases
the dilatation of the ventricular wall is from mechanical causes. This can
be traced in the case of disease of the aortic valves, which has caused
obstruction, regurgitation, or the combined lesions. For long periods no
murmur is heard at the apex, but later the systolic bruit of mitral regur-
gitation becomes audible, and the case, which formerly presented no such
signs, begins to manifest the venous congestion, the rising dropsy, and the
forms of dyspnoea of mitral disease. A similar sequence may be observed
ill chronic Bright's disease with arterio-sclerosis. The left ventricle may
for long periods show signs of hypertrophy ; then signs of dilatation
are manifested more or less rapidly ; later the murmur and the signs of
mitral insufiiciency are observed. The ventricle has become hypertrophied,
or dilated and hypertrophied, from the resistance in the aorta and the
^ Witness the words of the poets : —
I could a tale unfold whose lightest word
Would harrow up thy soul, freeze thy young blood,
Make thy two eyes, like stars, start from their spheres,
The knotted and combined locks to part
And each particular hair to stand an end.
Like quills upon the fretful porcupine.
Shakespeare.
Obstupui, steteruntque comae ; vox faucibus haesit.
Virgil.
996 SYSTEM OF MEDICINE
peripheral vessels on account of the thickening and contraction of the
smaller arteries. The intra- ventricular overstrain continuing and in-
creasing— because of the augmenting arteriole-obstruction — the left
ventricle yields to such an extent that the mitral curtains fail to coapt
during ventricular systole.
In another set of cases there may be none of the ordinary signs of
chronic Bright's disease, nor of thickening of the walls of the systemic
arteries ; and yet, in patients who have manifested no signs of rheumatism
nor of endocarditis, the physical signs show dilatation of the left ventricle
and finally mitral insufficiency. In some of these it is found after death
that there have been arteritis and periarteritis in the vessels of the heart
itself ; in others atheroma of the coronary artery of the left ventricle
and tracts of degeneration, molecular, fibrous or fatty, corresponding to
the area supplied by the branches of the artery. In another subsection,
these patients being usually obese and often alcoholic, there is fatty infiltra-
tion amongst the cardiac muscular fibres, and the left ventricle yields
because of the imperfection of its muscle. In yet another subsection in
this group the heart becomes dilated to the degree of incompetency
of the mitral valve from a morbid afiection of the nervous system.
Probably the nervous influences disposing to dUatation of the left
ventricle have been too much overlooked. I have traced a rapid and
extreme dilatation of the left ventricle coincidently with signs of neuritis
of the vagus. In several cases the complete signs of dilated ventricle
and mitral insufficiency have come on in the course of Graves' disease ;
these will be considered hereafter.
It is obvious from these considerations that dilatation of the left ventricle
with mitral insufficiency, apart from structural disease of the valve, may
be the result of various and complex morbid states. It must be re-
membered that these complex morbid conditions may coexist with
structural disease the result of rheumatic endocarditis, which has abeady
been discussed.
These considerations must have their due weight in questions of
treatment. In cases of arterial obstruction in the subjects of chronic
Bright's disease, and often in patients after middle life, digitalis and all
forms of cardiac tonics fail,, or even do positive harm. In such cases good
may result from the administration of arterial relaxants, and with these
digitalis may often be associated. Dr. Balfour considers that digitalis
cannot be safely given in cases of senile heart without a simultaneous
unlocking of the arterioles. The cardiac tonic, therefore, should be
combined with iodide of potassium or sodium, or with a nitrite, such as
nitrite of ethyl (nitrous ether), nitrite of sodium, or nitro-glycerine. In
cases in which there is reason to suspect thickening of the walls of the
arteries — in the general arterial system, or in the heart itself — a long
course of the iodides is to be advised. Digitalis may be also administered
for periods of two or three days at long intervals. Trinitrine should
be prescribed if any sign of intolerance of the iodides be noticed ; or if
these seem to be inefficacious, it may be administered in one-minim doses
DISEASES OF THE MITRAL VALVE 997
of the one per cent spirituous solution ; or in the form of tablets in
which x^ grain of nitro-glycerine is combined with chocolate. For
continuous administration I prefer very small doses (-ij^ grain) three
times a day. A combination with amyl nitrite is in some cases a distinct
advantage, for example, nitro-glycerine 3-^ grain, amyl nitrite \, menthol
•Jj- graih, capsicum y^ grain, with chocolate to form a tablet (Pharma-
copoeia of the Westminster Hospital).
When a case in this group shows signs of marked cardiac failure,
such as severe dyspnoea and dropsy, complete rest in bed should be
enjoined. Before the administration of any cardiac tonic it is well that
purgatives be administered. A dose of calomel, three to five grains, is a
good beginning ; or the patient, having abstained from liquids for some
hours, may take two to four drachms of sulphate of magnesia in hot
water (Matthew Hay). A considerable watery discharge may rapidly
reduce the oedema. The patient should be cautioned against getting
out of bed, or even assuming the sitting position during the relief of the
bowels, lest syncope be thus induced. The trunk should be supported
by pillows and the bed-pan used.
In cases in which dropsy is not extreme, massage may be of great
advantage. The muscles of the extremities and of the thorax should
be gently kneaded. Abdominal massage should be practised with caution ;
to dilate the vessels within the splanchnic area may induce anaemia of
the brain. Massage of the extremities aids the venous circulation,
quickens the function of the absorbents, and tends to bring about a more
deliberate and efficient ventricular systole.
In the grave conditions of failure of compensation it is best that the
diet be exclusively milk, diluted with barley-water or peptonised. Small
quantities should be swallowed at a time. Milk is a notable diuretic, and
in the dropsical stages it should form the staple diet. All strong
extracts of meat, which contain many products of retrograde meta-
morphoses, are to be forbidden ; but chicken or veal broth and jellies
may be permitted in some cases. In the stages of recovery three to six
pints of milk may be taken in the twenty-four hours.
When the patient begins to be able to take some walking exercise,
and the probability of resuming ordinary avocations comes into con-
sideration, the question of limitation of the ingestion of fluids has to
be settled. Oertel permits only 34 to 36 ounces of water, including that
contained in the solid food, per diem. The best proportions of food are
said to be about 1 ounce of fat, 3J ounces of carbohydrates, and not
less than 5 ounces of proteids. A cup of tea morning and evening,
about half a pint of claret, from %\ ounces to rather more than a pint
of water, and a little over 3 ounces of soup, should constitute, besides
that contained in the solids, all the fluid taken during each day. The
solid diet should be rich in nitrogen — for example, bread 4 to 5 ounces,
meat or fish 6 to 7 ounces, with 5 ounces of chicken or game, one or two
eggs, a little salad, cheese, etc., and 3 J to 7 ounces of fresh or cooked
fruit (43).
998 SYSTEM OF MEDICINE
As compensation is recovered, and during its maintenance, system-
atised muscular exercise is a valuable therapeutic means. Stokes, in
1854, said that " the symptoms of debility of the heart are often
removable by a regulated course of gymnastics, or by pedestrian exercise
even in mountainous countries such as Switzerland or the Highlands
of Scotland or Ireland " (66). This opinion sounded the note of reaction
against the routine practice of a long series of years of keeping a patient
who presented any sign of heart disease in the most complete muscular
repose attainable. Supposing that active disease be not going on
in the cardiac tissues, a " coddling " policy, whereby the heart muscle is
kept at a minimum exercise of function, is contrary to sound physiology
and good practice. Saeterburg of Stockholm and Zander used gymnastics
in the treatment of diseases of the heart, and described their experiences,
which appeared to be very favourable in the period between 1862 and
1872. The Swedish system for the promotion of good physical develop-
ment— the chief exponent of which was Professor Ling — rbecame an
important agency for preventive as well as curative treatment ; the
essentials being a forced action of the voluntary muscles for given periods.
The order proposed by Ling for these exercise movements was (i.)
respiratory, (iL) lower extremities, (iii.) upper extremities, (iv.) abdomen,
(v.) trunk, (vi.) movement of lower extremities repeated, (vii.) respira-
tory movement repeated. In the Zander system mechanical appli-
ances were used for the special exercising of certain groups of
muscles. Oertel in 1884 extended the doctrine and practice, and
advocated, in a regulated and graduated manner, the promotion of
vigorous muscular effort in mountain-climbing. The effort of ascend-
ing a hill is much more potent for good than that of walking on level
ground. There is an increased flow of venous blood to the right side
of the heart ; the lungs become more fully expanded, the channels of
the pulmonary circulation to the left auricle are more free, and the
volume of blood delivered to the arteries by the left ventricle is greater.
The perspiration causes a reduction in the volume of the fluid blood, and
a relative augmentation of the haemoglobin. The lymphatics are
stimulated to their task of absorption. Many cautions, however, are
necessary in the prosecution of this plan of treatment. If the efforts
induce unduly rapid breathing, the patient should at once come to a
rest and make deep inspirations. It seems to me that the plan is only
good when, with the increased muscular effort, there is no considerable
increase of the breathing-rate — the lungs must be adequately but not
rapidly, imperfectly, and deceptively inflated. No effort must be sudden.
It is the sudden overstrain, such as occurs in running to a railway
station, that kills. Again, great caution must be exercised in sending
cardiac patients to considerable altitudes. Dangerous and fatal symptoms
have occurred even at moderate elevations above the sea-level.
The climbing of hills is not to every patient a possible method of
treatment. Systematised gymnastic exercises exclude the necessity of
hill -climbing. The exercises recommended by Dr. Schott of Nauheim
DISEASES OF THE MITRAL VALVE 999
are known as resistance gjrmnastics (Widerstandsgymnastik). The
patient, loosely and lightly clothed, is instructed to breathe quietly, and
to make certain movements which are gently resisted by a skilled attend-
ant, who uses for this purpose the palms of the hands, without grasping
or constricting the limbs. The movements made are (a) various flexions
and extensions of the forearm and upper arm ; (6) movements of the lower
extremities, the patient maintaining his position by resting his hand upon
a chair ; (c) flexions, extensions, and rotations of the trunk upon the hips.
A short interval is enjoined after each movement, during which the
patient sits down ; the exertion should be only moderate in degree, and
should cause no flushing nor pallor, nor quickened breathing.
It is not possible in aU cases for a patient to have the assistance of
a skilled attendant, yet much good often results from a course of
systematic movements executed without such aid. These should be (a)
exercises of the arms and coinoidently of the upper thorax muscles, (6)
of the legs both in walking and with the body at rest, (c) flexions and
extensions of the trunk ; thus movements are communicated to the
abdominal viscera. No heavy weights, such as clubs or dumb-bells, should
be used, and the muscles of one side of the body should not be exercised
disproportionately to those of the other. So far as the movements of the
upper extremities are concerned, these may be accomplished by the patient,
standing erect or in the sitting position with spine straightened, hold-
ing lightly in the hands a rod or cane, and lifting this by deliberately
calculated actions to the fullest extent above the head the rod is then
brought down behind the shoulders, the chest being thus thrown forwards.
The position of the rod is to be always maintained at right angles to the
spinal column ; the movements are to be repeated slowly and deliberately
until there is a slight sense of fatigue.
The eflect of exercise of the voluntary muscles is an accumulation Qf
blood in their vessels of supply, and a corresponding derivation from
congested areas — for example, from the right chambers of the heart and
engorged veins (34). "The vessels which supply the muscles of the
body are capable of such extension that when fuUy dilated they will
allow the arterial blood to pour through them alone nearly as quickly as
it usually does through the vessels of the skin, intestines, and muscles
together" (Lauder Brunton, 7). The conditions, however, induced by
muscular exertion are very complex. There are alternate contractions
and relaxations, the former compressing the blood-vessels, the latter
freeing these channels ; concurrently there are increased activities of the
absorbents and reflex nerve-stimulations. In the movements of the
trunk upon the lower extremities another set of factors comes into play.
The alternate compressions and relaxations of the abdomen aff'ect the
blood-supply to the abdominal viscera. The tendency must be in the
main to cause the vessels in the splanchnic area to dilate and so to
co-operate with those of the muscles in relieving any turgescence of the
right cavities of the heart.
The MS« of haths and bathing in the treatment of ill-compensated mitral
SYSTEM OF MEDICINE
insuflSciency can be very useful. In years past there has been no
doubt too great fear lest a patient presenting the signs of mitral re-
gurgitation should catch cold ; thus the ablutions have often been
insufficient or injudicious. The use of cool or cold water has been
proscribed, and possibly hot baths have been too freely indulged in. The
effect of a hot bath is evident to ordinary experience — causing dilatation
of the vessels of the skin it may induce cerebral anaemia with symptoms
of faintness. The debilitating eflFect of repeated hot baths is well known.
On the other hand, the invigorating effect of cold tub in those who can
bear the shock, and of cool sponging in those who are more susceptible,
are matters of common experience. For a long period the sending
patients to any health resort for a course of treatment formed no part of
the therapeutics of heart disease. Beneke in 1859 and 1861, and Groedel
in 1878, adduced evidence to show that the baths of Nauheim, near
Frankfort, in Germany, were beneficial in increasing the force of the
heart and in restoring compensation in cases of valvular disease. Dr. L.
Blanc in 1886 recommended the course of treatment at Aix-les-Bains by
douches (temperature about 90° F.), together with skilled massage ; and
he cited 52 cases of mitral regurgitation in which this plan was pursued : in
15 of these all signs of disease disappeared, in 21 there was improvement,
and in 16 the signs remained stationary (5). The chemical constitution
of the water of Aix-les-Bains has probably but little to do with its thera-
peutic effect as used externally in these cases. Its chief value lies in
its soft, unctuous quality, due mostly to the presence of organic matter
(bar^gine), which, when at the agreeably warm temperature at which it
is used, adapts it admirably for the douche-massage. The therapeutic
conditions of the employment of the Nauheim waters are more complex.
These come from hot springs (temperature 83° to 100° F.), and are
charged with saline matters, chiefly chlorides of sodium and calcium, and
free carbonic acid gas. In marked feebleness of heart, and generally in
the earliest stages of treatment, the patient takes a saline bath from which
the carbonic acid has been allowed to escape ; the duration of the bath is
six to eight minutes, the temperature of the water being 95°. A rest of an
hour is enjoined after each bath. The periods of immersion are increased
during the course of treatment to twenty or thirty minutes, and the tem-
perature is lowered by degrees to 85 "5° F. The water used is allowed to
retain its carbonic acid in less or greater proportion, as it is exposed for
longer or shorter periods to the air, or used as the Strombad foaming with
its full content of the gas. The effects of the various agencies thus put in
force have been studied experimentally by Dr. R. F. C. Leith and others
(31). In regard to temperature, simple thermal baths at 90° F. or
under commonly tend to reduce the pulse-rate by five or seven beats a
minute. The effect of the addition of sodium chloride to the bath is
generally to emphasise the change in the pulse, and to make the bath
more agreeable to the patient ; when the bath is charged with carbonic
acid gas (Sandow's effervescing tablets being used) the pulse-rate is
further reduced, whilst the force of the heart's action is increased ; the
DISEASES OF THE MITRAL VALVE
pleasantness and buoyancy of the bath are also enhanced, and the patient
experiences an agreeable sensation of warmth. The result of a bath at a
temperature below body-heat is contraction of the cutaneous vessels
of the area immersed, higher temperatures cause their relaxation ; the
lymph-circulation is necessarily modified, the internal vascular conditions
are changed, dilatations of the vessels occur in various regions — ^notably
in the vascular districts of the brain, and probably there are some
rhythmic alteration of dilatations and contraction. Furthermore, there
are reflex efi'ects upon the vaso-motor and cardio-inhibitory centres.
When the bath contains free carbonic acid gas the fine bubbles adhering
to the skin protect the body from the colder surrounding water, and
constantly impinging upon the surface stimulate the cutaneous nerve-
endings. Probably also some of the gas permeates the skin ; carbonic acid
has been shown to be a notable and valuable local anaesthetic (Ozanam).
The effects of the combined treatment by baths and muscular exer-
cises as carried out at Nauheim are said to be increased strength of the
pulse with diminution of its abnormal frequency, decreased rate of
respiration, together with fuller inspirations and greater ease and comfort
in breathing, and diminution in the size of the dilated heart. There is
sufficient testimony to show that in a large number of cases there has been
a great improvement in the subjective conditions. The evidence is less
generally conclusive as to the reduction in size of the heart. From
examination of a considerable number of outlines purporting to be those
of the heart before and after the Nauheim treatment, I am of like
opinion with Dr. G. V. Poore, Sir William Broadbent, Dr. Leith, and Dr.
Herschell, that many are the results of a fallacious plan of physical
examination, and cannot be held to represent with any degree of accuracy
the size and position of the heart (24, 31, 45). On the other hand, there
is a very high probability that in some cases the situation and shape of
the heart have become changed, and the right chambers reduced in
volume. Careful observations have shown that the bulk of the heart
may greatly change under varying conditions within very short periods
of time. In the case of mitral disease, whilst the patient has been at
rest, and when no special therapeutic means could be invoked as causes, I
have observed signs of very considerable variations in the bulk of the
heart in less than twenty-four hours (61). Sir W. Broadbent says : "That
a diminution in the volume of the heart may take place under the
influence of saline baths and certain movements there can be no doubt,
but such diminution is an occurrence which is perfectly familiar to all
who are in the habit of noting the changes in the size of the heart
under other methods of treatment or from various causes. In a heart
dilated from over-exertion, for example, the apex beat may often be felt
to come in for half an inch towards the normal situation, when the
patient is simply made to walk two or three times across a room " (6).
Not only the positions of the apex (Leith), but also the outlines of
precordial dulness, have been found to vary at intervals during the day.
Heitler considers from his observations that there are rhythmic changes
SYSTEM OF MEDICINE
in the volume of the heart, the pulse remaining unaffected by these (22).
All these considerations must have their due weight, and too much
reliance must not be placed on the evidence derived from the ordinary
means of physical examination as to the space occupied by the heart at a
given time. The concurrence of signs, — the evidence of rational as well
as of physical diagnosis, — however, shows that a combination of judicious
bath treatment and physical exercises may be a valuable agency for good
in cases of mitral insufficiency with failure of compensation.
One factor in the therapeutics of a health resort must not be over-
looked. The change in surroundings must produce an effect upon the
higher attributes of the nervous system — the will, the emotions, and the
intellect. It is no slight advantage for a patient to be taken away from the
little worries of home to a place where, with clear sky and pure air, there
are facilities for systematic self-management, a prescribed and regulated
dietary, and the associated hope and faith inspired by the favourable
experiences of others. Mental and emotional impressions can strongly
influence the trophic nervous mechanism of the heart. It is true that
there is a reverse to this picture. Patients are sometimes deceived by
false hopes and fallacious arguments ; persons, for example, the subjects of
mitral insufficiency, well compensated and causing no adverse symptoms,
have been persuaded by so-called friends that calcareous incrustations and
fibrous thickenings about their heart-valves would by the operation of a
certain " cure " disappear as crystals dissolve in water. Long and arduous
journeys have been undertaken by those who were totally unfit to leave
the comforts of their home, and there has followed a sad awakening
from the delusive dream. These agencies are potent for good or for
evil, and every case in which the use of them is contemplated, must be
careful considered.
Group IV. Mitral insufficiency from ancemia. — A systolic murmur
over the apex of the heart is heard not infrequently in the subjects of
the various forms of anaemia ; in some cases it is also audible at the back
internally to the angle of the left scapula. Dr. A. G. Barrs found an
apex systolic murmur alone in 13 out of 115 cases of anaemia. In 60
examples of chlorosis Potain observed a murmur, which he considered
to be cardio-pulmonary, in nine cases above the apex, and in one case near
the apex. Byrom Bramwell and Stephen Mackenzie have recorded cases
of apex-systolic murmurs in cases of pernicious anaemia. I have myself
found an apex systolic murmur in 7 per cent, and coexisting
murmurs at the apex and over the site of the pulmonary artery in 9
per cent of cases of anaemia. The first question to determine is whether
a bruit having such characters be due to causes operating externally
to the heart itself. Potain describes all the murmurs heard in the
neighbour-hood of the heart which are causally related with anaemia and
chlorosis as cardio-pulmonary ; he finds that they do not begin with
the systolic contraction of the ventricle as organic murmurs do, but are
meso-systolic (occupying a portion only of the systole), that they are
soft and superficial, greatly modified by the act of respiration, that they
DISEASES OF THE MITRAL VAL VE 1003
are influenced by the attitude of the patient, so that they sometimes dis-
appear when the recumbent is changed for the erect position, and that they
vary from day to day. He considers that chlorosis tends to the pro-
duction of cardio-pulmonary murmurs by influencing the nervous system,
and so enhancing the cardiac excitability. When in a case of anaemia a
systolic murmur is heard at or near the situation of the apex, it is of
importance (a) to determine by palpation and percussion the position of
the apex beat of the outline of the left ventricle, and the relation of the
observed murmur to the area thus determined; (J) to consider the
various signs already noted which diflerentiate the cardio-pulmonary from
the organic mitral murmur. A certain proportion may be found to
answer to Potain's criteria of non-organic murmurs. I can have no
doubt, however, that in some cases the apical murmur is due to veritable
mitral regurgitation ; first, because it has the site and characters iden-
tical with those due to organic causes, and, secondly, because it may be
followed by all the symptoms of failure of compensation in mitral in-
sufiiciency. I have observed an apical systolic murmur to arise in a
healthy woman after profuse uterine haemorrhage (from fibroids), severe
dyspnoea with abundant dropsy to follow, and ultimately complete
recovery to take place, "with the disappearance of all the physical signs
of disease (56).
From the well-known association of fatty degeneration of the muscular
fibrillse of the heart with anaemia, it must be inferred that the mitral
insufficiency is caused, the valvular apparatus being normal, by the
resulting enfeeblement of the myocardium. The incompetence may be
from impairment of the muscle of the ventricular wall or of the musculi
papillares, or of both. Positive dilatation of the left ventricle has been
described by some observers (Goodhart, Stephen Mackenzie, Niemeyer).
In these cases the incompetency of the valve is readily explained by the
passive dilatation of the auriculo-ventricular orifice ; on the other hand,
the ventricle, and the heart generally, have been found by other observers
to be abnormally small (Duroziez, Potain). I have observed cases in which
there have been the physical signs of mitral regurgitation in anaemia
when the outline of the heart has been markedly smaller than the
normal. The regurgitation in such cases may be explained by enfeeble-
ment of the papillary muscles. In fatal cases of anaemia these muscles
have been observed to be profoundly affected by fatty degeneration.
The treatment of cases of mitral insufficiency, the result of anaemia, is
practically the treatment of the form of anaemia which is the proximate
cause. Though there may be very extensive fatty degeneration of the
myocardium, there is good evidence that there frequently occurs a
"restitutio ad integrum"; new and healthy muscular fibrillae being
developed. The good effects of tepid and cool baths in such cases may
be briefly mentioned ; the use of baths, spongings, and spinal affusions
of cool or even cold water has been a routine practice with many
physicians, myself included, in cases of anemia. The occurrence of a
systolic murmiu: at the apex is no contra-indication to this mode of
I004 SYSTEM OF MEDICINE
treatment. The carbonic acid and saline baths, such as those of
Nauheim, so much extolled of late, have been used very successfully for
many years at Schwalbach, in co-operation with the internal administra-
tion of ferruginous water, in the treatment of ansemia. The modes in
which such baths influence the heart and blood-vessels have been already
discussed.
Qrowp V. Mitral insufficiency in Graved disease and allied affections.
— Murmurs in the precordial area are heard in a large number of
cases of exophthalmic goitre. In the majority of these the maxima of
the murmurs are over the base of the heart, and especially over the
pulmonary artery. In a minority the systolic bruit is heard over the
situation of the apex. I found an apex-systolic murmur in six out of a
series of twenty-nine cases of Graves' disease. In some of these the
bruit varied much and the diagnosis of mitral insufficiency was doubtful.
In one case, however, that of a lady who had previously shown no sign of
rheumatic change in the valve, the onset and course of the disease were
carefully watched, and there could be no doubt of the establishment of
mitral insufficiency. The disease was initiated by a sudden fright : after
violent palpitation the pulse-rate rose to 160 per minute, a systolic
murmur became evident over the apex, and general dropsy supervened with
the usual signs of failure of compensation in mitral regurgitation. Com-
plete recovery, however, succeeded, and the murmur disappeared, health
being maintained for at least thirteen years after the acute manifestations
(60). It is probable that in such a case the insufficiency of the valve was
due not to endocarditis but to a disturbance of the nerve-mechanism of
the heart. In some cases of Graves' disease dilatation of the left ventricle
has been indicated during life and proved at the autopsy. In others the
heart has been found to be quite normal. In one case of Graves' disease
in a man, observed by myself, the dilatation was shown chiefly in the
right chambers ; the signs of tricuspid regurgitation were manifested in
well-marked systolic venous pulsation in the neck. The evidence pointed
strongly to the conclusion that the morbid conditions of the heart
advanced step by step with the exophthalmic goitre, and that there was
no pre-existing disease of the heart. I have found that dilatation of the
heart has been by no means commensurate with the rapidity of its action.
In cases of extreme tachycardia the outline of the heart has remained
normal, whilst in the case of Graves' disease in the man, where the
rapidity of the heart's action was far less, there- occurred distinctly pro-
gressive hypertrophy and dilatation of the left ventricle. I consider it
probable that the insufficiency of the mitral valve, which occurs in a
minority of cases of exophthalmic goitre^structural valvular disease being
excluded — has a like pathogeny with that which obtains in ansemia. The
valve curtains fail to. coapt in some cases on account of dilatation of the
ventricle ; in others because of enfeeblement of the papillary muscles, or
faulty correlation between these muscles and those of the ventricular
wall. In the treatment of these cases, supposing that there are signs of
failure of compensation, the rules already laid down may be followed ;
DISEASES OF THE MITRAL VAL VE 1005
but another therapeutic agency demands consideration — the employment
of electricity.
The treatment of the cardiac symptoms occurring in the course of
exophthalmic goitre is notoriously unsatisfactory. The rapidity and
irregularity of the heart's contractions in the majority, and the dilatation
of the cavities in the exceptional cases, are not favourably influenced by
digitalis or any form of cardiac tonic. Only those agencies which tend to
calm the nervous perturbations can be relied upon. Yet I think that
there is good evidence that patient and systematic electrisation, carried
out in such a manner that the pneumogastric nerve and the surrounding
nervous elements can be directly influenced, is of therapeutic value. The
inten'upted current (faradisation) as well as the continuous galvanic
cmTent were employed by the late Professor Charcot and by Vigouroux. I
have not found benefit from the treatment by the interrupted current,
the immediate effects of which have indeed been objected to by many
nervous patients ; but I consider that in the employment of the con-
tinuous current the results have been good (8). The current should be
weak — two to four milliampferes as given from three to eight Leclanch^
bichromate or chloride of silver cells : the anode should be placed at the
nape of the neck, just above the vertebra prominens, and the cathode
on the groove external to the larynx and trachea. The current should
be allowed to pass for from six to ten minutes three times a day, the
cathode, which may be moved over the skin, without lifting and re-
applying, towards the clavicle, being adapted to each side of the neck
alternately. This treatment in cases of Graves' disease manifesting severe
and distressing cardiac symptoms has seemed to me more efficacious than
any other, and a considerable number of patients have completely re-
covered. Although in many cases the heart-rate is often reduced after
each application it is long before continuous improvement is obtained. I
have seldom seen much amendment under six months of treatment.
The continuous galvanic current may also be of value as an aid to
treatment in cases of failure of compensation in mitral insufficiency other
than that which is manifested occasionally in Graves' disease. I have
employed it in cases of chronic endocarditis undoubtedly of the rheumatic
form, and it has seemed to turn the scale towards recovery. I have
recorded the case of a young man who suffered from rheumatic endocar-
ditis involving the mitral and aortic valves, and in whom extremely
severe symptoms occurred during seven months. At a time when the signs
were very grave the constant galvanic current from eight Leclanch^ cells
was employed in the manner already described. Improvement soon ensued,
the abnormal rapidity of the pulse was subdued, strength returned, and
but for the warning note of a murmur indicating aortic regurgitation, the
patient became a strong, well-nourished man (62). Potain writes concern-
ing electrisation of the vagus : " Its efficacy is not limited to the tachy-
cardia which accompanies exophthalmic goitre. We have been able to
apply it advantageously in cases of cardio-arterial disease accompanied by
marked excitability of the heart where heart remedies had absolutely
ioo6 SYSTEM OF MEDICINE
failed. It was always applied in the form of tte constant current
(descending), the positive pole being applied over the sides of the neck,
and the negative on the anterior surface of the chest with an intensity
varying between 10 and 15 milliamperes " (47) It is probable that in the
constant galvanic current we have a valuable therapeutic means for the
treatment of some cases of mitral insufficiency.
A. Ernest Sansom.
EEFEKENCES
1. Balfour, G. W. yAc^em'feJeari, London, 1894, p. 56. — 2. Baelow. "Rheu-
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and Philippe. Remw de wM. 1891. — 4. Baer, James. "Cardiac Tonics," iiwrpoo?
Medico-Chirurgical Jowrnal, July 1886, p. 307. — 5. Blano, L. Des affections cardiaques
d' origine rheumatismale traities aux eaiix d' Aix-les-£ains, Savoie, 1886. — 6. Broadbbn'J',
Sir William H. ' ' Note on Auscultatory Percussion and the Schott Treatment of Heart
Disease," British Medical Journal, 28th March 1896, p. 769. — 7. Beunton, Lauder.
"Harveian Oration," Lancet, 20th Oct. 1894, p. 895.-8. Cardew, H. "W. D. "The
Practical Electro-Therapeutics of Graves' Disease," Lancet, 4th and llth July 1891. — 9.
Chbadle, "W. B. The various Manifestations of the Mheumatic State as exemplified in
Ohildliood and Early Life. London, 1889. — 10. Clark, Sir Andrew. "Substance of
some Remarks concerning cases of Valvular Disease of the Heart known to have existed
for oyer five years without causing Serious Symptoms," British Medical Journal, 19th
Feb. 1887, p. 379. — 11. Cuffer. Bes causes qui peuvent modifer les bruits de souffie
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Templer Davies. The Mechanism of the Circulation of the Blood through Orgcmically
Diseased Hearts. London, 1889. — 13. Debove and Letulle. " Recherches anatomiques
et cliniques sur I'hypertrophie cardiaque de la nephrite interstitielle," Arch, de mid.
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On Rheumatism and JiJieumatoid Arthritis, London, 1890, p. 123. — 18. Geehahdt.
Lehrb. der Auscult. und Percuss. Tubingen, 1884. — 19. Goodhart. "Anaemia as
a Cause of Heart Disease," Lancet, 1880. — 20. Gowers, Sir W. R. A Manual
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Thomas. "Some Clinical and Post-Mortem Observations on the Cardiac Dulness in
cases of Mitral Disease and Cardiac Dilatation, and on the relative Size and Position
of the Cavities of the Heart," Medical Chronicle, February 1893. — 22. Heitler. Die
Percussionsverhaltnisse am normalen Herzen. Wien, 1891. — 23. Henoch. Lectures
on Children's Diseases, translated by John Thompson, M.B., F.E.C.P. Edin. vol. i. p.
475. New Sydenh I m Society, 1889. — 24. Heeschell, Geo. " Critical Remarks upon
the Nauheim Treatment of Heart Disease," The Lancet, 15th Feb. 1896, p. 413. — ■25.
HuoHAiiD, Henri. Traiti clinique des maladies du cmur, etc., p. 170. Paris, 1893.
— --6. Huchard and Weber. Huchard, Maladies du cceur, p. 167. — 27. Hug.
" Maladies du coeur et nevroses," Thise de Paris, 1891. — 28. Kreisner. Cf Potain,
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Batlis anil Resistance Exercises in the Ti'catment of Chronic Heart Disease ; the
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do'phia, 1888. — 34. LuDWio and Hafiz. Henle and Pfeiffer's Zeitschrift, 1863. — 35.
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DISEASES OF THE MITRAL. VALVE 1007
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Science, 1st June 1886. — 43. Oertel. " Handbuoli der allgeineinen Therapie derKreis-
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Rheumatic Carditis of Childhood," Ibid. 27th August 1892, p. 469. — 68. Idevi.
Lumleian Lectures on Heart Inflammation in Children, Ibid. lOth March 1894, p. 683 ;
17th March 1894, p. 653 ; 24th March 1894, p. 723.-69. Sutton, H. 6. Lectures on
Pathology, p. 372. London, 1891. — 70. West, Charles. Lectures on the Diseases of
Infancy and Childhood, 7th edit. London, 1884, p. 566.^71. WiLKS arid MoxoN.
Pathological Anatomy, 1875.
A. E. S.
Mitral Stenosis
ileflnition. — A morbid condition of the structures at the left auriculo-
ventricular apertiu-e, causing a constriction of the latter and an obstruc-
tion to the normal flow of the blood from the left auricle to the left
ventricle.
Morbid anatomy. — The appearances of the mitral valve and the
structures adjacent to the orifice in mitral stenosis may conveniently be
considered as they are manifested («) in infancy and childhood, (b) in
maturity and advanced life.
(a) In wifanty and childhood the comparatively slight degrees of
obstruction at the mitral orifice are marked by a ring of vegetations — in
some cases friable and easily detached, in others sclerous and firmly fixed
— situated around the orifice on its auricular aspect. The fibrous
structures subjacent to the vegetations are firmer than the normal, the
thickening frequently involving the mitral curtains, the chordae tendineae,
and the musculi papillares. In a more advanced stage the marginal
portions of the curtains are joined by fibrous adhesions. At a still later
stage the two curtains are so completely fused together that the valve
presents the form of a hollow cone or membranous funnel, the wider
portion of which is at the auriculo-ventricular orifice, and the narrower
ioo8 SYSTEM OF MEDICINE
points downwards within the ventricle near the apex of the heart. The
funnel form of mitral stenosis, and the smooth polished membrane, regular
in its conformation as a hollow cone, have suggested that the malforma-
tion of the valve is a congenital anomaly. It is undoubtedly true that in
rare cases such an obstruction of the mitral orifice has been found in associa-
tion with congenital malformation. In a case of this kind recorded by
Parrot, the aorta and pulmonary artery were united in a single trunk.
In one of my own cases the aorta arose from the right ventricle, and there
was a communication between the ventricles. In these, and in all cases
the records of which I have examined where the mitral orifice was found
on post-mortem examination to be obstructed in infants who died shortly
after their birth, the vegetations of endocarditis were found. In one of
my cases, a b.ibe of two months, a ring of granulations was found
encircling the mitral orifice, and the valve was thickened. I consider that
mitral stenosis, as observed in these cases, is not a congenital malformation,
but the result of intra-uterine endocarditis — the smooth and regular
conformation of the funnel constituted by the cohering curtains of the
valve being due to the even pressure of the fluid blood both on the
auricular and ventricular surfaces during the rhythmic movements of the
heart. The terminal aperture of the funnel, by which the blood issued
into the ventricle, may be extremely small, allowing the passage of
nothing thicker than a goose-quill.
The fibrous thickening of the valve, of the chordse tendinese — which
may be much shortened as well as thickened — and of the muscuH
papillares is in some instances very dense ; in one patient, a girl aged
eleven, these structures presented the characters of cartilage. Though the
" funnel " form of transformation of the valve is by far the more
common in childhood, the " button-hole " form is sometimes observed ; it
has been noted in the case of a boy aged seven (Hayden). The auriculo-
ventricular orifice as seen from the auricular side then presents the
form of a slit or chink, or a crescentic opening in the firm, thick, fibrous
septum of the welded valve-structures. The division of cases of mitral
stenosis into the " funnel " and " button-hole " forms, first made by Sir E.
Douglas Powell, is a very practical one from the point of view of morbid
anatomy. In some cases, however, the auriculo-ventricular aperture on
its auricular aspect presents a very irregular form. It may be surrounded
by thickenings and nodosities, and the opening may have a puckered
appearance resembling, as a French observer has aptly said, the normal
anus.
(6) In adults and in persons of advanced years the "button-hole" form of
mitral stenosis is observed with much greater frequency. In childhood
the proportion is about one " button-hole " to eight " funnels "; in adult
age and later life twenty-five "button-holes" to one "funnel." The
associations with the rheumatic form of endocarditis are abundantly mani-
fested in the necropsies of cases showing constriction of the mitral orifice in
adults. I have seldom, I think I may say never, observed cases of chronic
endocarditis or repeated endocarditis affecting the mitral valve — ^whether
DrSEASES OF THE MITRAL VALVE 1009
the signs during life have indicated combined stenosis and regurgitation,
or regurgitation only — ^without the necropsy demonstrating that the left
auriculo-ventricular orifice was more or less constricted, and the surround-
ing fibrous ring firmer than the normal.
In many instances in adult age and later life the fibrous material is
infiltrated with calcareous salts, the resulting plates having the hardness
and general characters of bone. In rare cases the curtains of the valve
have been found normal, whilst calcareous plates have been observed in the
adjoining muscular wall of the ventricle. These may be associated with
atheromatous changes, or may represent syphilitic gummata which have
become calcified. In a case of chronic interstitial nephritis the vegeta-
tions surrounding a stenosed mitral orifice have been found to contain
urates (Lancereaux). Dr. Goodhart, on an analysis of the post-mortem
records of 192 cases, showing the changes of chronic interstitial
nephritis, found that about one-fourth of the whole number presented
either thickening or contraction of the mitral valve. Dr. Newton Pitt
observed, on examination of the records of the post-mortem department
of Guy's Hospital, that the cases of mitral stenosis in the subjects of
granular kidney were to those not manifesting renal lesions in the pro-
portion of three to one. In many cases in this category atheroma of the
aorta was also found, more rarely atheroma obstructing the coronary
arteries. Huchard has designated the cases as " r6tr6cissement mitral
art6rio-scldreux." In some instances, as in a case of my own, chronic
fibrotic changes have been found in various situations — in the pleurse, the
lungs, the capsules of the kidneys, the liver, the spleen, and the intra-
cranial membranes. In this last, which was that of a woman aged 52, the
mitral valve presented the funnel form of stenosis. This form is excep-
tional in the subjects of chronic renal disease, but other such instances
have been recorded. It is obvious that the funnel form of transformation
of the mitral valve, the so-called " pure mitral stenosis " of Duroziez and
other French observers, is found not only in childhood (when it simulates
a congenital malformation), but also in advanced life. In some cases it
is certainly associated with rheumatism ; in others such association is
not proved ; but it may be found in the subjects of chronic renal disease
and of arterio-sclerosis.
The left auricle in cases of this affection is frequently hypertrophied and
dilated. In some cases the cavity is greatly enlarged, but the walls are
thin. In a child of nine years old I have found hypertrophy so far
advanced that the muscle was a quarter of an inch thick (the normal
being about -^^ of an inch) ; in another case, that of an aged woman, it
was as thin as an ordinary visiting-card, almost destitute of muscle, and
lined with laminated coagula. The appendix of the auricle is usually the
portion which manifests hypertrophy in the greatest degree. When on
opening the pericardium the heart is viewed in position, the hypertrophy
of the auricle is in some cases very striking : instead of being flaccid it
stands out firm and muscular. On section it does not collapse, and
pronounced reticulations mark its internal surface. In other cases, when
VOL. V 3 T
SYSTEM OF MEDICINE
dilatation preponderates, the capacity of the aiuricle is increased, in some
cases enormously. The pulmonary veins are also greatly dilated. In
my own records of 40 cases of mitral stenosis at all ages observed after
death, the left auricle was found dilated in 18, dilated and hypertrophied
in 10, and hypertrophied without notable dilatation in 3. Dr. D. W.
Samways (21), who examined the register of necropsies at Guy's Hospital
for four years, found that in 70 cases of mitral stenosis the left auricle
was hypertrophied in 36. In 36 cases of well-marked stenosis — the
mitral orifice admitting only one finger or the extremity of a finger — the
left article was hypertrophied in 26, dilatation coexisting in 14. In 3
cases only was there dilatation without hypertrophy. In the cases of less
pronounced stenosis the state of the auricle was precisely noted in 1 1 only,
and of these 5 showed dilatation without hypertrophy. The conclusion
is probably correct that hypertrophy is the rule ; with the hypertrophy
some dilatation nearly always coexisting. When compensation fails,
the muscle becomes enfeebled, and dilatation progressively increases.
The endocardium lining the auricle is usually thickened ; in some
cases all over — the probable cause then being the excess of blood-pressure
to which it is subjected, and in many cas.es in patches by chronic endo-
carditis or atheromatous change. The posterior wall of the auricle is
most frequently thus affected. On the internal surface of this part of the
axu-icle coagula are frequently observed. These are sometimes stratified
and composed of alternating layers of coloured and colourless fibrin closely
adherent to the endocardial surface. In some cases the whole auricle,
thus distended with layer upon layer of coagula, resembles an aneurysm
(Potain and Rendu).
The vegetations observed on the lining membrane of the auricle may
be sessile or pediculated — warty, globular, or polypoid (Coats). The
warty vegetations are simply coagula of fibrin on the diseased surfaces of
the endocardium. Globular thrombi are found especially in the auricular
appendage, and between the muscular bundles ; in rare cases they almost
fill the auricle. Their external portion is smooth and tough ; on section
they are found to contain a creamy fluid. Polypoid thrombi are more
rare ; they are attached by a pedicle to the wall of the auricle or to the
auriculo-ventricular ring. Some, like the globular thrombi, are masses
of firm fibrin \ others are hard and calcified. Thrombi at the left
auriculo-ventricular aperture are found with greater frequency in mitral
stenosis than in mitral regurgitation. They may be detached and become
emboli, which are arrested at some point in the arterial channels ; or one
or more may persistently block the aperture ; or, again, one may obstruct
the orifice, in the manner of a ball-valve, during certain periods of the
cardiac cycle.
The pulmonary veins are in some cases much dilated ; their coats may be
thickened and atheromatous. Dr. James Barr of Liverpool has described
well-marked atheroma of the pulmonary veins in cases of mitral stenosis.
The left ventricle in the majority of cases presents characters which do
not obviously diifer from the normal ; its cavity is not enlarged ; in some
DISEASES OF THE MITRAL VALVE
instances its capacity is less than the normal. In the cases of young
children the smallness of the left ventricle is striking ; in some of these
patients the whole heart is correspondingly diminished in size, the lungs
are small, and the thoracic capacity reduced. On account of the imperfect
blood-supply to the ventricle the whole organism has been impoverished
(Wilks), and the entire economy has suffered from arterial starvation. In
other cases the contrast with the large and muscular left auricle is very
obvious. In about three-fourths of those which I observed after death the
wall of the left ventricle was not hypertrophied. When hypertrophy
is manifest, as in the remaining fourth of the cases, there is usually an
obvious concurring cause — in the young pericardial adhesions, in the old
chronic renal disease or arterio-sclerosis. Globular thrombi are sometimes
found in the interstices between the musculi papillares of the left
ventricle remote from the valve.
With the exception above noted, when death has occurred in the
period of childhood, the right cavities are dilated in marked degree, and
the walls of the right ventricle and right auricle are hypertrophied. The
hypertrophy is often evidenced by the massive muscular columns in the
ventricle and the thick interlaced muscular bands in the auricle. The
orifice guarded by the tricuspid valve is usually abnormally wide ; the
valve in some cases is competent to close this orifice, in others its incom-
petence is obvious ; indeed, cases have been recorded of such dilatation
that auricle and ventricle appeared to form one enormous cavity.
Thrombi are observed in the right auricle and right ventricle in many
cases ; the surfaces of endocardium, on which they are formed, are not
necessarily diseased. Such thrombi, when they become detached, plug
the larger or smaller branches of the pulmonary artery. Their inception is
no doubt due to the retardation of the blood-flow. The chain of conse-
quences is as follows : — Obstruction at mitral orifice, abnormal tension of
the walls of the left auricle, auricular hypertrophy and dilatation, obstruc-
tion to blood-flow from pulmonary artery to pulmonary veins, increased
labour of right ventricle, tension of its walls, hypertrophy and dilatation
of right cavities.
In some cases of mitral stenosis vegetations are observed on the
tricuspid valve, and these are evidently the results of endocarditis. An
induration of the structures at the right auriculo- ventricular aperture
may take place, and lead to a series of morbid changes producing a
stenosis of the tricuspid aperture closely resembling that of the mitral.
Tricuspid stenosis is nearly invariably associated with mitral stenosis, and
the morbid changes producing it are more recent in the right heart than
in the left. When mitral and tricuspid stenoses coexist, the tendency to
the formation of thrombi and emboli in the right cavities is more pro-
nounced than when mitral stenosis exists alone.
In some cases the venoe cavce have been found greatly dilated ; the
inferior in greater degree than the superior vense cavse.
The lungs generally present the appearances — congestions, consolida-
tions, brown and pigmentary degenerations and scleroses — already de-
SYSTEM Of MEDICINE
scribed in mitral insufficiency. In cases of stenosis, however, tsemorrhagic
extravasations in the lungs, and infarctions of the pulmonary artery, are
observed to a greater extent and with greater frequency. Not seldom
there are signs of pulmonary infarction, old and recent. From an analysis
of the post-mortem appearances in 36 cases of mitral stenosis, I find that
infarctions of branches of the pulmonary artery, or so-called pulmonary
apoplexies, were observed in 22 instances. In rare cases a coagulum,
evidently detached from the auricle, has plugged the pulmonary artery
itself. Cases of mitral stenosis have been recorded in which an extremely
dilated left auricle has compressed the left bronchus to such extent as to
reduce its calibre to a mere chink (Friedreich). In no inconsiderable
number of cases of mitral stenosis the lesions of tuberculosis have been
found in the lungs. In the case of a woman aged 29, observed by myself,
the necropsy showed a very narrow mitral aperture, with much thickening
of the adjacent structures ; both lungs were studded with tubercles,
some miliary and others yellow and softening. I observed a well-marked
case also under the care of my late colleague Dr. Sutton. These are the
only cases of tuberculosis in association with mitral stenosis which have
come under my own eye, but according to Potain the coexistence is
frequent. In 35 autopsies, in which mitral stenosis was demonstrated,
tuberculous changes were found in 12 instances. Taking the cases
recorded by Teissier, Kidd, and other observers, I find a total of
31 in which the association of mitral stenosis with tubercle was proved
after death : of these cases 1 1 presented also the signs of tricuspid
stenosis or of endocarditis affecting the tricuspid valve, and 5 others
manifested disease of the aortic valves. Uncomplicated mitral stenosis,
therefore, was present in 1 6 cases only. Potain has stated his opinion
that the occurrence of mitral stenosis in the course of pulmonary tuber-
culosis is so frequent that there seems to be a causal relationship between
the two diseases. Teissier has gone much farther than this ; he
considers that some form of tuberculosis is the cause, direct or hereditary,
of the " pure " form of mitral stenosis. Nevertheless, his own observa-
tions agree with those of LetuUe, that the search for bacilli and for any
lesion demonstrably tuberculous in the diseased structures surrounding
the mitral orifice has always been fruitless. To ascribe the origin of the
fibrous thickening to an attenuated tuberculosis seems to me an extra-
ordinary example of special pleading. A more tenable hypothesis, in my
opinion, is that in some cases the anaemia resulting from the delivery of
an insufficient volume of blood from the imperfectly supplied ventricle,
especially in the case of coexisting aortic disease, disposes to the tuber-
culous invasion ; and in others the failure of the right ventricle, or the
obstruction to the supply to the pulmonary artery in the cases of con-
currence of tricuspid stenosis, disposes to tuberculosis of the lungs;
for it is to be remembered that in stenosis of the pulmonary artery,
where there is a like physical impediment to the blood -current to the
lungs, pulmonary tuberculosis is almost invariably the mode of death.
The stomach, liver, spleen, and other abdominal viscera in mitral
DISEASES OF THE MITRAL VALVE 1013
stenosis show, for the most part, the appearances already described in
mitral insufficiency. Embolisms and their consequences are much more
frequent in mitral stenosis. Taking post-mortem evidence alone, I find
that embolism is most frequently observed in the arteries of the brain
and the kidneys, and these in equal proportions. Next in order of
frequency are pluggings of the splenic arteries. In a small minority of
cases the arteries of the pancreas, stomach, and intestines have been
blocked by emboli.
In the cases in which emboli have obstructed the intra-cranial arteries
the infarctions have been found almost invariably in the vessels of the left
hemisphere. In seven. out of eight cases the left middle cerebral artery
was the vessel occluded ; in two cases the anterior cerebral artery
also was plugged. The resulting softening was found chiefly in the
frontal and parietal convolutions and in the corpus striatum. In a case
recorded by Hallopeau, in which the left vertebral artery was blocked by
an embolus, softening of the left eminentia teres was observed. According
to the evidence which I have obtained, fatal cerebral embolisms, which are
the result of the chronic conditions of mitral stenosis, are invariably left-
sided. In cases in which acute endocarditis, especially infective endo-
carditis, has supervened, the limitation to the arteries of the left
hemisphere is not so decided. When there is necrosis of the tissues
adjacent to the valve there are often multiple emboli. The clinical
evidence in cases of mitral stenosis sometimes indicates a lesion of the
right hemisphere, but the emboli which are fatal — probably slowly formed
and comparatively large — are those which plug the arteries of the left
hemisphere. There can be no doubt that the well-known physical
explanation of their occurrence in the arteries of the left hemisphere is
correct. The left carotid has its axial current in the same direction as
' that from the ascending aorta ; the stream, therefore, carries the dislodged
coagula most readily through the aorta into the left common carotid, the
internal carotid and the middle cerebral, the current continuing in these
vessels without deviation. If the embolism be large, it is sufficient to
block not only the trunk of the middle cerebral artery, but also that of
the anterior cerebral at its bifurcation with the former. If small, the
embolism may be only in one of the branches of the middle cerebral.
The right hemisphere is practically immune, because the right carotid,
arising from the innominate, is placed at such an angle with the aorta as
to lie off the axial current.
The working of the heart in mitral stenosis. — In the slighter forms
of obstruction the mechanism is precisely that obtaining in the sclerous form
of mitral insufficiency. The orifice may be so narrowed as to admit only
two fingers or even- the thumb only ; but the thickened curtains of the
valve are retracted, and the physical signs, symptoms, and consequences
are those of mitral regurgitation.
The conditions are characteristically different when the mitral orifice
is so narrowed or obstructed that the outflow from auricle to ventricle is
seriously impeded ; and when, as may be inferred with great probability.
I0I4
SYSTEM OF MEDICINE
there is no regurgitation at the time of the systole of the left ventricle.
The most pronounced eifect in such case is upon the left auricle. The
muscular wall may he greatly hypertrophied, while the diameter of the
chamber remains not notably greater than the normal. Or, again, the
auricle may be greatly enlarged, so that in some cases its capacity is more
than double the normal ; its muscle in some cases is hypertrophied,
in others atrophied, even so far as to be represented only by a few
muscular fibrillse scattered through a shell of fibrous tissue. Observers
have differed as to the relative preponderance of hypertrophy and
dilatation in the auricle. Potain and Rendu consider that, suffering as it
immediately does a " contrecoup " on account of the obstructive lesion,
the left auricle dilates and liypertrophies simultaneously, and these
15 10
Repletion Distension
0/ Ventricle ^
25
25 25
Repose Auricular Systole Ventricular Systole
Fig. 66. — Schema of a cardiac revolution. (After Potain.)
changes are never wanting in mitral stenosis. It is obvious that the
muscular auricle is strong enough to inject its blood-content forcibly into
the ventricle even though the mitral orifice be considerably stenosed.
I have myself found, in the case of a child, the muscular wall of the
auricle as thick as that of the right ventricle. Cases have been recorded
in which the left auricle has maintained life for a long time when the left
ventricle, converted into a completely calcified chamber, had been
incapable of any active contraction (Burns, G-6rard).
It has been generally considered that the auricle ceases its active con-
traction before the systole of the ventricle begins. This was the doctrine
deduced from the graphic records obtained by the experimental methods
of Chauveau and Marey in the horse. Subsequent investigation, how-
ever, has demonstrated that the auricular systole may continue after the
commencement of the contraction of the ventricular muscle, both auricle
DISEASES OF THE MITRAL VALVE 1015
and ventricle continuing to contract simultaneously until the moment
when the sigmoid valves are opened and blood begins to be expelled from
the ventricle into the aorta. Potain considers that the auricle is in
action from the beginning of its systole until the precise moment of closure
of the auriculo-ventricular valves — that it is this muscular contraction of the
auricle which ordinarily causes the propulsion of the heart's apex against
the wall of the chest, and that thus it plays a notable part in the produc-
tion of the impulse which is felt by the hand applied over the situation of
the apex beat (Fig. 66). In stenosis of the mitral aperture this lifting of the
apex by the force of the contracting auricle may be greatly exaggerated.
In investigating cases of mitral stenosis by the cardiograph, I have
repeatedly observed that in some the eminence which alone can be
ascribed to the auricular systole has contributed to the general elevation
due to the systole of the ventricle ; one of the most remarkable is here
figured (Fig. 67). , It is to be remembered that the pen of the cardiograph
is guided by the apex of the left ventricle ; the record of the auricular
systole is written by an impulse communicated from the auricle to the
ventricle. It is obvious not only that the auricle contracts in a manner
PiQ. 67. — Cardiogram in a case of mitral stenosis. Auricular systole (a) greatly exaggerated and
contributing powerfully to the elevation completed by the systole of tlie ventricle.
much more powerful and much more prolonged than under normal con-
ditions, but also that it contributes in very marked degree to the general
elevation which is completed by the systole of the ventricle. Professor
Potain has entirely corroborated my observations and conclusions. Dr.
D. W. Samways (19) has advanced the ingenious hypothesis that the
abnormally powerful contraction of the left auricle prevents regurgita-
tion in compensated mitral stenosis. He shows from mechanical and
experimental data that the force of the auricle, seeing that its active con-
traction is continued until the aortic valves are opened and a free outflow
is permitted into the aorta, is adequate to prevent any reflux during the
ventricular systole. It seems to me very probable that this view is
correct. It affords a good explanation of the post-mortem appearances
when a contracted mitral orifice, evidently of slow pathogenesis, is
accompanied by a very small left ventricle. If mitral regurgitation had
occurred in such a case the ventricular cavity would in all probability
have become dilated. Yet in the early stages of the transformation of
the mitral orifice it would seem that such regurgitation would have been
inevitable unless prevented by some cause apart from the sclerosis of the
structures at the periphery of the valve. A compensatory hypertrophy
of the muscular wall of the auricle — ^whence an abnormally prolonged
ioi6 SYSTEM OF MEDICINE
and powerful auricular systole — occurring early in the morbid process
would explain not only the absence of the characteristic signs of mitral
inadequacy during life, but the absence of hypertrophy and dilatation of
the left ventricle observed after death.
It is obvious that the enhanced force of the auricle, evidenced by the
muscular h3rpertrophy, is an important, if not the chief factor in main-
taining compensation during the survival — many months or many years
it may be — of the subjects of mitral obstruction. It is equally certain
that it is not the only factor, for hypertrophy of the right ventricle may.
be looked upon as a constant sequel of mitral obstruction. Dilatation in
most cases accompanies the hypertrophy, but for long periods the tricuspid
valve is competent to close the right auriculo- ventricular orifice.
Abnormal pressure is thus maintained in the pulmonary blood-circuit.
The hypertrophied right ventricle co-operates with the hypertrophied
left auricle in augmenting the force by which the blood is urged through
the narrowed mitral orifice. In the later stages of the affection, however,
the right ventricle may become dilated on account of the exaggerated
blood-pressure to such degree that the tricuspid is no longer competent,
and there is reflux into the great veins. Compensation is then no longer
maintained. The failure of compensation, however, in a given case may
be not by failure of the right ventricle, but on account of enfeeblement
of the left auricle. We have seen that the auricular cavity may be
enormous, but with practically no effective muscle in the wall. The
evidence, especially the deposition of layer upon layer of fibrin, shows
that failure has been slow and life has been prolonged without any active
participation of the auricle in the work of the circulation. The kinetic
energy of the right ventricle must have operated with the elastic recoil
of the distended auricle after its injection by the right ventricle, and the
suction power of the left ventricle during diastole.
In a case of compensated mitral stenosis we may thus summarise the
work of the heart — Systole of the ventricles. Left unimpeded, quantity
delivered minus or else sufficient for the needs of the organism. Eight
abnormally forcible, thus distending the pulmonary veins and the left auricle.
Left auricle over-distended after right ventricular systole ; this distension
in greater or less degree relieved immediately on diastolic relaxation and
suction action of ventricle ; its own elastic recoil probably aiding the
inflow into the ventricle in the earliest stages of diastole. Probably
muscular contraction of the pulmonary veins a concurring cause ; pos-
sibly such contraction in the manner of a sphincter preventing reflux
from the auricle into the pulmonary veins ; the proper auricular systole
following and, being abnormally forcible and protracted, contributing to
produce the apex impulse.
Diagnosis. — The diagnosis is in many cases easy, in some attended
with considerable difficulty ; at any ra-te all the ordinary means of physical
investigation should be put in force.
Inspection may reveal no signs. The apex beat may be invisible or
observed in the normal situation — if displaced to the left, causes external
DISEASES OF THE MITRAL VALVE 1017
to the heart being excluded, the explanation may be enlargement of the
right cavities or a general increase of bulk of the heart due, in the early
periods of life, chiefly to adherent pericardium ; in the later periods to
the hypertrophy and dilatation of the left ventricle accompanpng arterio-
sclerosis. In some cases the precordial region over the right ventricle is
rendered prominent and visible; pulsation is seen below the ensiform
cartilage. In any case where there is this prominence over the right
ventricle, whilst the left ventricle is not observed to pulsate to the left of
the normal position, mitral stenosis is pima facie more probable than
mitral insufficiency. Inspection of the veins of the neck may show a
pulsation in the venous sinus just above the right clavicle coincident with
the systole of the right auricle ; or, when the tricuspid is incompetent, a
definite pulsation of the jugular veins coexistent with ventricular systole.
Pulsation may be observed in the second interspace, or second and
third left intercostal spaces near the sternum, and if a vibrating flag or
lever be affixed over the spot of pulsation and another over the visible
apex beat of the heart, it may be seen that the movement of the former
(auricular) is distinctly in advance of that of the latter (ventricular),
i'hus there may be evidence of abnormal force of the left auricle. It
must be remembered that this is capable of demonstration only in rare
cases ; it has not been observed in adults but in children only.
Palpation may reveal some very important evidence or may be negative.
In a case of marked mitral stenosis of long standing a heaving impulse
may be found over the position of the right ventricle, under the false
ribs to the left of the ensiform cartilage, whilst there may be no palpa-
tion-signs of a forcible ventricular systole abnormally to the left. Palpa-
tion may thus confirm inspection in indicating that the right side of the
heart is enlarged and the right ventricle hypertrophied, whilst the left
ventricle does not show these abnormalities. Any such deduction, how-
ever, must be made cautiously, for the left heart may be more enlarged
than the signs indicate, as it may be covered by inflated lung -tissue.
There is one sign obtained by palpation to be observed in a considerable
number of cases of mitral stenosis which, provided it has certain essential
characters, may be regarded as almost a crucial sign of the afiection.
This is thrill — " fr^missement cataire." The feeling of vibration communi-
cated to the finger lightly laid in the intercostal space close to the point
of the apex beat or slightly to the right thereof may be fine or coarse, pro-
tracted throughout the whole diastole and ceasing (usually) at the instant
of the shock of the apex beat, but sometimes very shortly after the com-
mencement of this event, or occupying a very brief period just before the
systole of the ventricle. It can best be timed by the finger of the
observer's free hand placed over the carotid artery, when the thrill is
found to cease at the moment of the carotid pulse. If in the case investi-
gated there be well-marked signs of incompetency of the aortic valves, it
is to be borne in mind that the diastolic-presystolic thrill may be present
without mitral stenosis. Such cases are, however, rare ; in a larger
number mitral stenosis coexists with the disease of the aortic valves.
ioi8 SYSTEM OF MEDICINE
In the absence of signs of aortic-valve disease a well-marked diastolic-
presystolic or presystolic thrill when observed in the apex region is nearly
always indicative of mitral stenosis. It is important that thrill be investi-
gated in varying positions of the patient. Vibrations which are scarcely
felt when the patient is in the recumbent position may become much
more marked in the sitting posture with the body bent forwards. The
observation, however, does not excuse the omission of all other ordinary
means of investigation. It is to be remembered that thrill may be absent
at some periods and present at others during the observation of a case.
Sometimes it is absent when the patient is at rest, and developed after
exertion or when the arms are elevated. Percussion is chiefly of import-
ance to determine the outline of the heart : it gives more precision to
the evidence obtained by inspection and palpation, and when dispropor-
tionate enlargement of the right chambers of the heart is thus indicated,
this method of investigation is valuable for diagnosis not only of the
nature of the affection, but of its extent and significance. The signs
obtained by auscultation are of chief importance in the diagnosis of
mitral stenosis — they are murmurs, double shock-sound during the period
of ventricular diastole (reduplication of the second sound), accentuation
of the pulmonic second sound, loud and sudden snap at the acme of ven-
tricular systole, and inaudibility of the second sound at the heart's apex.
The murmur characteristic of mitral stenosis is that known as the pre-
systolic murmur. It is generally of rough quality, vibratory or bubbling.
Potain states that it rarely has the characters of a blowing sound (souffle) ;
most frequently it is snoring or rolling. It may begin almost immediately
after the second sound of the heart, be prolonged through the whole
period of ventricular diastole, become reinforced towards the end of this
period in a "crescendo" manner, and end with a sudden tap or snap.
This terminal tension sound is in some cases coincident with the impulse
of the apex as felt by the finger ; in others it is noted to occur very
shortly after the first shock of the impulse ; but it is always synchronous
with the pulse felt in the carotid artery. The sound of the murmur
may begin long before the proper systole of the auricles (see Fig. 69)
— ^it may therefore be correctly designated diastolic -presystolic. The
evidence leaves no room for doubt that the reinforcement towards the
close is coincident with and due to the muscular contraction of the auricle.
Sir Wm. Gairdner uses the term " auricular systolic " (A. S. murmur) to
denote the bruit. Whether the term " presystolic " or " auriculo-systolic "
be used, it must be remembered that the active muscular contraction 'of
the auricle is not the only force on which the murmur depends. In some
cases the bruit is not prolonged throughout the periods of diastole and
presystole (the entire diastolic murmur of Bristowe), but is audible as a
short murmur closely following the second sound (early diastolic murmur),
or isolated with a pause before or after (mid-diastolic or meso-diastolic
murmur). Usually these disjointed murmurs are found in a case which at
some periods of observation manifests the more typical presystolic murmur.
The sudden snap which generally terminates the murmiu: is peculiar
DISEASES OF THE MITRAL VALVE 1019
and characteristic. In some cases it is observed without any bruit leading
up to it. It is evidently an unusually short and sudden first sound of the
heart ; if in any case it be observed in the near neighbourhood of the
apex — in some cases I have noted it at the back under the angle of the
left scapula — mitral stenosis should be suspected and the concurrent signs
searched for. The cause of this phenomenon is not definitely settled.
It closely resembles the sound of sudden tension which may be imitated
by abruptly stretching a piece of moist membrane. In the left ventricle
of some hearts with stenosed mitral aperture observed after death, in
which the phenomenon had been manifested during life, it would seem
that there are no structures likely to give rise to this sudden sound of
tension at the moment of contraction of the ventricle — the mitral curtains .
being thick and leathery, the chordae shortened, and, with the papillary
muscles, forming thick fibroid bands ; the muscle of the ventricle not
obviously differing from the normal, and the ventricular cavity small
rather than large. On the other hand, the tricuspid valve is seen to be
thin and membranous, and it seems probable that to its sudden tension
by a forcible right ventricle the loud snap may be ascribed.
Another very important auscultatory sign for diagnosis is the double
sound heard during the period of the diastole of the ventricles. This
phenomenon, which vividly recalls the " postman's knock," has been
generally named the reduflicated second sownd. To avoid speculation as to
its mode of production we may be permitted to call it a double-shock
sound in diastole. It may be manifested in the neighbourhood of the
apex or at the base of the heart. When audible in the neighbourhood
®f the apex of the heart and not over the base the double-shock sound
iadicates an early stage of mitral stenosis. This view which I enunciated
in 1880 was confirmed by Cheadle. As a sigQ of mitral stenosis in later
as well as earlier stages, it has been noted by many observers (Potain,
Eouchfesj Gerard, Phear, Boyd). The explanation of the mechanism of this
sound first recorded by myself has been for the most part accepted. It is
not a true doubling of the second sound, and cannot be ascribed to the
asynchronous closure of the semilunar valves of the aorta and the pul-
monary artery, but is of mitral origin. It is a sound of tension due to
the first inrush of blood into the ventricle, such inrush being more sudden
and forcible than under normal conditions from the increased blood-
pressure in the left auricle due to the constriction of the mitral orifice.
Potain, Rouchfes, and other French observers have described this sound
as the "claquement d'ouverture de la mitrale." Potain thus explains
the mechanism of the sound. The opening of the mitral valve is norm-
ally noiseless ; but in the subject of mitral stenosis the valve curtains at
the moment when they separate, moved by the blood- wave that enters
the ventricle, are abruptly cheeked by the adhesions of their free borders ;
the sudden tension which results produces the sound, which is the more
dull as the normally thin curtains have become more dense and have lost
their elasticity.
"When the double-shock sound is audible over the base of the heart
SYSTEM OF MEDICINE
and not in the close neighbourhood of the apex the problem of its cause
by no means admits of a ready answer. It is undoubtedly over the base
of the heart that the double sound, when manifested in mitral stenosis,
is heard in the majority of cases. The diagnostic value of the sound is
very great ; the double sound either at base or apex is found in more
than one-third of all cases of mitral stenosis. The generally accepted
view of its mode of production is that the semilunar valves of the aorta
and the pulmonary artery respectively do not close in normal synchronism,
but those of one vessel coapt in advance of those in the other according
to the relative degrees of blood-pressure. The objection to this hjrpothesis
I take to be that it involves an admission of an asynchronous action of
the two ventricles which physiologists are not able to accept. The sound
of tension of the aortic valves cannot be produced until the left ventricle
begins its. diastolic expansion; if this sound be followed by that of the
tension of the sigmoid valves of the pulmonary artery, it follows that the
diastolic expansion of the right ventricle is not synchronous with that of
the left, but is in all cardiac revolutions delayed. Potain has, however,
more recently minimised or overcome this difficulty by advancing the
following hypothesis : Premising that the precession of the two sounds of
tension is aortic in the earlier, and pulmonic in the later phases of the
disease, he considers it probable that when the obstruction at the mitral
orifice is slight, but yet sufficient to bring about some difficulty in the
entry of blood into the left ventricle, the aspirating power of the latter in
diastole is augmented (" elle est moins ais6ment satisfaite "), and the semi-
lunar valves, drawn upon with more force than ordinarily, close more
rapidly. Later, when the obstacle at the left auriculo-ventricular orifice
has notably impeded the circulation in the lung, and the right ventricle
has become hypertrophied, the over- pressure in the pulmonary artery
compels the semilunar valves of this vessel to close more forcibly and
more rapidly at the beginiung of ventricular diastole. For my own part,
though there is room for much difference of opinion, I think it more
probable that the phenomenon has a similar cause at base and apex of
the heart. The first element of the double shock-sound is the normal
second sound often accentuated as to its pulmonary artery component ;
the second element is a sound of tension produced by the forcible entry
of blood into the ventricle, the shock being communicated either to the
wall of the ventricle or to the anterior curtain of the mitral valve close
to the aortic cusps, and thence to the sternum and especially its left
border.
Accentuation of the pulmonic second sound is a sign to be noted in mitral
stenosis as in mitral regurgitation. The cause — over-pressure in the
pulmonary artery — occurs in both morbid states, though from differing
causes. In mitral stenosis, however, the irregular rhythm of the heart
in many of the cases prevents a due appreciation of this accentuation ; the
sound then is very loud in some cardiac cycles, in others feeble or almost
inaudible.
Another auscultatory sign to be noted in a section of the cases is
DISEASES OF THE MITRAL VALVE
inaiidibiUty of the second sound of the heart at the apex. This extinction of
the second sound at the apex is usually manifested in the later stages of
mitral stenosis (Broadbent, Acland) ; its causes are — (a) a diminution
of blood-supply to the aorta, and consequent feeble recoil against closed
aortic valves (it is the aortic element of the second sound that is audible
over the heart's apex) ; (b) the enlargement of the right auricle and ventricle
which, coming more and more to the front, displace the left ventricle, the
chief conductor of the sound.
In the latest stage of mitral stenosis the presystolic murmur may
be inaudible, the second sound absent, and the short and sudden first
sound, to which attention has been already called, the only notable
auscultatory sign. More frequently, however, in later as well as
in earlier stages, a systolic murmur is to be heard in the neighboxir-
hood of the apex. This murmur may have the ordinary characters
of that of mitral insufficiency, audible over the apex and at the back
under the angle of the left scapula, or may be a short systolic "pufF"
having a very limited area of audibility, but over the site of the apex. It
may coexist with the presystolic murmur, which in such case is usually
heard for the most part slightly to the right of it ; or it may be heard
when no presystolic or diastolic-presystolic bruit is audible. Nearly
always in these cases the sudden tap indicating the first sound is heard
over some part of the apex region. In another section of the cases the
systolic murmur has an area of audibility to the right of the apex,
encroaching more and more on the tricuspid region, and in some instances
localised at the base of the ensiform cartilage, that is, the area of a tricuspid
regurgitant murmur. It has been considered (and the contention has a
great show of validity) that in some of the cases in which a systolic
murmur has been ascribed to regurgitation through the mitral orifice
the real cause of the phenomena has been tricuspid reflux (Samways,
loc. cit. pp. 64 et seq.). In some instances, however, there are
two areas of audibility of the systolic murmurs, when it is most
probable that there is regurgitation through both mitral and tricuspid
orifices. If the hypothesis be correct, that the abnormally powerful
muscular contraction of the left auricle prevents regurgitation in the
compensated stages of mitral stenosis, it is probable that some such
regurgitation is inevitable when compensation fails and the auricular
muscle has become feeble.
It is to be noted that a very marked irregularity of the heart's rhythm
is by no means infrequent in mitral stenosis, and that this irregularity
may modify all the physical signs already described. The murmurs, the
so-called reduplications of normal sounds, the snap sound, and the thrill
may be observed in some cardiac cycles, and may be absent in others.
The irregularity of rhythm is evident to the auscultator. Such irregu-
larity may be entirely due to disturbances of the nervous mechanism,
and may be quite independent of structural changes in the heart ; but
when signs of organic valve disease coexist with it, mitral stenosis is the
lesion in the great majority of cases.
SYSTEM OF MEDICINE
Cardiographie evidence. — The use of the cardiograph has in many-
instances afforded valuable evidence not only for the diagnosis of
the condition of mitral stenosis, but for the elucidation of some of the
difficult problems connected therewith. The chief signs recorded by
the cardiograph have been — (a) An abnormal magnitude of the eleva-
tion denoting the auricular systole. It has been shown in some cases
that the power of the auricle is sufficient to lift the ventricle in a pro-
FiG. 68. — Cardiogram in a case of hypertropliy of the left ventricle. Anricular systole (a)
contributing very slightly to the elevation completed by the ventricular systole.
~J ^ -^ ^ -wJ -^ ^
Fig. 69. — Cardiogram in a case of mitral stenosis with presystolic murmur and thrill. The cardiogram
shows the auricular systole in the normal position. The lower line indicates the position in the
cardiac cycle of the vibratory murmur and presystolic reinforcement. * First sound.
HEART
RADIAL ARTERY
Fig. to. — Trace in mitral stenosis, a. Second sound ; S, diastolic roll ; c, presystolic reinforcement ;
d, first sound. (Potain.)
nounced manner (Fig. 66). This can only occur when the narrowing
of the mitral orifice is not considerable, the auricle being hypertrophied.
(J) An increase in breadth of the auricular eminence, the summit of which
is seen to be broken by undulations, a condition felt by the finger as
thrill, (c) Repeated elevations denoting rise and fall of pressure during
ventricular diastole, not necessarily indicating any muscular contractions
of the auricle, but probably expressing graphically the interruptions of
the flow of blood through the diseased valve-structures which are audible
as a rolling or bubbling murmur, ii) Fine serrations in the diastolic and
DISEASES OF THE MITRAL VALVE
1023
,presystolic periods audible as harsh murmur, and due to the causes already
considered. This iorm of cardiogiam denotes a considerable degree of
stenosis contrasting with (a), in which the orifice is only moderately
constricted. It has already been noted that in some cases (e) the cardio-
gram in mitral stenosis differs in no appreciable way from the normal.
It would be legitimate in such case to infer that the stenosis is slight
in degree.
Sphygmographie evidence. — In a large number of cases of mitral
stenosis the sphygmograph indicates a very notable irregularity ; this
irregularity may be observed when the lesion is compensated and the
patient appears to be in perfect health. In some instances in which the
-^v\A^-^^/^-vVVv-v\y\A/WVvAvAAj\
Fig. 71. — Sphygmograms in mitral stenosis. A, In stage of compensation ; man aged 44, observed during
five years. B, Case manifesting typical presystolic murmur ; no signs of failing compensation ;
patient in good health. 0, Mitral stenosis with failure of compensation (tricuspid regurgitation,
pulsating liver). D, Late stage of extreme mitral stenosis (female aged 17). E, Regular anacrotic
pulse ; mitral stenosis in a female aged 41, with rheumatic antecedents.
rhythm of the heart is apparently regular, a slight exertion serves to provoke
the irregularity. The administration of digitalis may produce or increase
it ; but it is often found in cases in which the drug has not been
administered. The most frequently observed form of irregularity is that
evidenced in the sphygmogram by a repeated elevation in the down-
stroke. There may be two or three of such elevations before the base-
line is reached. It is evident that these excursions from the down-stroke
contain all the elements of a complete pulsation effected by the ventricle.
They show that after a comparatively effective emptying of the ventricle
there may be repeated systoles following at very brief intervals. In late
I024 SYSTEM OF MEDICINE
stages of the disease the irregularity may be extreme. The irregular
pulse of mitral stenosis has been noted by many observers (Balfour (2),
Mahomed, Foster, and others). I consider that the sphygmographic
indication of irregularity in a case in which compensation appears to be
perfect may aid in the differentiation between mitral stenosis and mitral
insufficiency, for the latter lesion during the stages of compensation is
not attended by irregularity of the pulse unless there be some coexisting
neurosis.
In another large series of cases the sphygmograms show a perfect
regularity in the heart's rhythm. Many observers have considered such
regularity to be the rule in mitral stenosis (Hayden, Fagge, Broadbent).
The up-stroke of the tracing indicating the volume of the artery is
inconsiderable, and the indications are that the vessel is full between the
beats. Sir W. Broadbent (5) considers that this modified high tension-
pulse is almost constant in mitral stenosis, and indicates resistance in the
capillaries. Such resistance may be due to contraction of the arterioles
consequent upon the overloading of the blood with impurities arising
from defective elimination or, possibly, from the backward pressure in the
veins effected through the capillary network, or from the contraction of
the entire arterial system upon a diminished supply of blood from the
imperfectly filled left ventricle.
Practically the observation of a heaving impulse of the right ventricle
without signs of dilated left ventricle, together with the evidence of a
pulse having the characters above stated, may have a valuable bearing in
the diagnosis of mitral stenosis. That the arteriole resistance is in some
cases increased is proved by the anacrotic form of pulse which is some-
times observed (see Fig. 71, E). The association with arterio-sclerosis,
well proved in a section of the cases, is in these a sufficient explanation.
Some, difficulties in the diagnosis. — Although th§ presystolic murmur
and the thrill observed in the positions mentioned close to the heart's
apex are indications of mitral stenosis, in the great majority of cases they
are not absolutely pathognomonic.
Austin Flint was the first observer to show that a murmur having the
characters of that of mitral obstruction could be produced in cases of
insufficiency of the aortic valves in the absence of mitral stenosis. These
observations were confirmed by many observers. I have shown that the
presystolic thrill of mitral stenosis also can be exactly simulated under
conditions of aortic regurgitation. Dr. Phear (15) has carefully analysed
the records of forty-six cases in which there was presystolic apex murmur
without mitral stenosis ; in twelve of these, thrill, presystolic or diastolic,
was present. In seventeen of the cases the aortic valves were incompetent;
in twenty the pericardium was adherent ; in the remainder there was no
valve-lesion, but in some of these there was dilatation of the left ventricle.
The hypotheses which have been adduced to explain these phenomena are
the following : (i.) That in the cases of aortic regurgitation the regurgitant
stream tends to lift the great anterior mitral curtain, and so to obstruct
the mitral orifice at the end of diastole as to impede the current from the
DISEASES OF THE MITRAL VALVE 1025
auricle ; (ii.) That the mitral valve is thrown into vibration by the two
currents, the regurgitant from the aorta and the direct from the auricle,
such vibrations lasting until the commencement of ventricular systole ;
(iii.) That in the absence of aortic valve disease, but in the presence of
adherent pericardium, vibrations may be set up by the current propelled
from a dilated and hypertrophied auricle into a ventricle whose muscular
walls are deficient in their normal nerve-tone ; (iv.) That shortening
of the chordae tendineae, or dilatation of the left ventricle, may bring about
a virtual narrowing of the aperture through which the blood passes from
auricle to ventricle, the auricular muscle continuing to be sufficiently
powerful to generate a fluid vein. It must be admitted that these
opinions are for the most part conjectural, but the fact remains that in
some cases the physical signs have led most competent and careful
observers to an erroneous diagnosis of mitral stenosis. The practical
lessons I take to be the following : — In cases where the concurrent signs
indicate dilatation of the left ventricle, and where the previous history
tells of au antecedent pericarditis, we must be cautious in interpreting a
presystolic murmiu- as pathognomonic of a stenosed mitral orifice. In all
cases careful investigation must be made into concurring signs of incom-
petency of the aortic valves. If the murmur of aortic regurgitation be
absent from the base of the heart and the line of the sternum, it may yet
be found alone at the apex, and may then closely simulate the murmur of
mitral stenosis. In such case, however, according to my experience, the
terminal tension sound, the tap or snap, is not marked — the sound is dull.
All available means, including the use of the cardiograph and sphygmo-
graph, should be used to effect the differentiation.
It must be remembered that aortic insufficiency and mitral stenosis
may coexist, and the diagnosis of the combined lesion may present great
difliculty. Dr. F. J. Smith found on examination of the post-mortem
records of the London' Hospital evidence of the combined lesions in thirty-
nine instances. Uncomplicated, aortic insufficiency was to aortic in-
sufficiency plus stenosis as 88 to 39. The association of the two valvular
affections therefore is not very rare, and the diagnosis of such association
can only be made with an approach to certainty when there are decided
physical indications of each separate morbid condition.
Clinical groups of cases of mitral stenosis, their symptoms
AND TREATMENT. — Group I. Cases associated with rheumatism. — The
intimate relation between mitral stenosis and rheumatism is shown by
a large series of cases. In some of these the rise and progress of the
endocarditis, the cause of the obstructive lesion, can be traced by clinical
observation. The patient may show all the signs of acute rheumatism, an
occurrence comparatively rare in children, the acute symptoms being often
very slightly pronounced, though in some instances they are fully mani-
fested, and then usually the first sign of implication of the valves is the
systolic murmur of mitral regurgitation. The child in the course of months
or years may suffer from repeated attacks of acute rheumatism, and after
VOL. V 3 U
1026 SYSTEM OF MEDICINE
a longer or shorter interval the systolic murmur is preceded by a
presystolic murmur, the other signs of mitral stenosis concurring. In
some such cases, and in course of time, the murmur of mitral re-
gurgitation becomes replaced by that of mitral stenosis. Many such
instances have come under my observation (27). In other cases the
presystolic murmur of mitral stenosis after repeated attacks of rheumatism
has been very decidedly modified — ^it has been followed by a systolic
murmur. The significance of such a change it may be difficult in
some cases to estimate. The murmur may be very loud, and heard in
the left axilla and at the back : if so, there can be no doubt that it is due
to regurgitation from organic disease. Or it may be heard over a
very restricted area, not conducted to the axilla, but just over the
apex itself. In such case the auriculo-ventricular orifice may not be
widened by any retraction of curtains or columns, but the anatomical
lesion may be stenosis nevertheless, and the auricular muscle have be-
come weak ; therefore regurgitation, which previously had been prevented,
is now permitted. Or the murmur may be observed to the right of the
position of the apex close to the tricuspid area ; in such ease the
probability of tricuspid regurgitation must be borne in mind.
In some cases rheumatic phenomena are declared, not in the early
stages of the affection, but subsequently, during the observation of the
case. For instance, a girl of fourteen, without any rheumatic antecedent
— though there was hereditary tendency thereto on the mother's side —
manifested a prolonged systolic and a short presystolic mitral murmur.
There were no rheumatic phenomena for thirteen months when poly-
articular rheumatism appeared. At that time a marked thrill was felt at
the apex ; a grating presystolic and a prolonged blowing systolic murmur
were heard, and the heart was enlarged, especially as regards the right
chambers. The autopsy showed a funnel-shaped transformation of the
mitral valve and a ring of small vegetations (recent rheumatic endo-
carditis) encircling the auriculo-ventricular orifices. This affords one
of many pieces of evidence that the rheumatism which is associated
with mitral stenosis may be attended for long periods by no obvious symp-
toms.
A sign of the advent of the structural change in the valve
inducing obstruction at the mitral orifice is a double shock sound
heard during the period of ventricular diastole, and resembling a
doubling of the second sound over the apex of the heart. I noted this
simulated doubling of the second soimd at the apex in a large number of
cases which eventually manifested all the usual signs of the lesion. Dr.
Cheadle found "33 cases with presystolic murmur, and 24 with re-
duplicated second sound at the apex, indicating commencing stenosis out
of 273 cases of organic heart disease in children" (8). He adds:
" There can be no question as to the connection of this morbid sound
with early mitral stenosis, and of its clinical significance." Potain has
confirmed these observations, ascribing it, as I do, to causes affecting the
mitral valve. The first element is the normal second sound heard at the
DISEASES OF THE MITRAL VALVE 1027
apex, the second element occurring soon after it, the "claquement de
I'ouverture de la mitrale."
In a large number of cases the clinical signs of association with
rheumatism are insignificant. The evidence of many which I have
analysed shows that in a considerable proportion the origin and progress
of the morbid changes in the valves and the adjacent structures are
insidious and gradual. The disease which initiates these is not inde-
pendent of rheumatism, but is often unaccompanied by pronounced
rheumatic phenomena. The endocarditis which results in mitral in-
sufficiency is more violent and more obviously associated with ordinary
acute rheumatism ; that which induces stenosis is more protracted and
symptomless, giving rise to a gradual welding of the curtains and a slow
formation of fibrous tissue which, under the even pressure of the blood
within the auricle and the ventricle, tends to the production of a smooth
septum. This septum becomes gradually thicker, for it has to bear the
chief strain of the auricular pressure — not the ventricle, as in the case
of mitral insufficiency.
When the acute signs of rheumatic endocarditis have passed away, or
when, in the absence of any obviously acute manifestation, the obstructive
lesion has been gradually induced, compensation enduring for protracted
periods may ensue. Such compensation is a simpler matter than in the
case of mitral insufficiency, for an increase of power in the muscle of the
right ventricle and of the left auricle only is necessary to maintain it ;
enhanced force and increased capacity of the left ventricle not being also
required as in the structural lesion inducing mitral regurgitation. The
left ventricle may deviate but little from the normal, and a strong right
ventricle, aided by a hypertrophied, or at least not enfeebled, aiuricle, wiU
urge a sufficiency of blood through the narrow orifice.
The symptoms of failure of compensation diifer in many points from
those in cases of mitral insufficiency. In the latter the signs are more
uniform — ^the dyspnoea of effiart, or the paroxysmal dyspnoea progressively
increasing in intensity, the gradual oncome of dropsy, and other signs
which have already been considered are evidenced ; in mitral stenosis,
on the other hand, the symptoms are more erratic, the accidents of the
disease predominate, and it is these rather than the gradual heart failure
that have in the greatest degree to be reckoned with.
One of the earliest symptoms to attract attention in cases of mitral
stenosis is epistaxis ; Duroziez has noted this, and I confirm his observa-
tions. Probably we are not told of this symptom in many of our cases in
hospital because it is considered trivial. In some, though in a less pro-
portion than I should have imagined, there have been complaints that
the patient is soon " out of breath." Precordial pain and distress are
noted, however, in a considerable number of patients, and in some Of
these palpitation. My notes show these symptoms in 21 out of 54
cases. Haemoptysis was recorded in nine of these cases ; it occurred
in the course of the lung affections in many more. The most fre-
quent of all the induced morbid states is that evidenced by dyspnoea,
X02S SYSTEM OF MEDICINE
cough, and other symptoms referred to the lungs. In some cases there
is a general bronchitis; but in the great majority there are signs of a
localised pneumonia, in the course of which the sputa are frequently
blood-stained. The bronchitis can be referred to the general venous
engorgement of the lungs, but the localised consolidations are proved, by
morbid anatomy as well as by clinical evidence, to be due to infarctions
of branches of the pulmonary artery. These occur with the highest
degree of frequency in mitral stenosis ; and in at least half the cases I
have observed they have been manifested at some time of the life-history.
The haemoptysis and the lung signs often suggest the probability of
pulmonary tuberculosis ; but in the vast majority of cases this is negatived.
I have mentioned, however, the fact of its occurrence in a small
minority ; so that investigation should be made for tubercle bacilli in the
sputum, and the other related signs should be duly weighed. Other
symptoms which occur in the course of mitral stenosis, increasing the
dangers of the disease and adding new difficulties to its treatment, are
those due to embolic infarctions of the systemic arteries. These will be
considered in the next group of cases. In only a few cases are they
clinically observed in the spleen, though morbid anatomy teaches that
this is a very frequent site of embolism. Probably the symptoms thus
occasioned pass in many cases unnoticed and unknown. It is otherwise
when an intra-cranial artery is thus blocked — then the danger of the
condition is proclaimed. It is to be remembered that these embolisms —
whether in the pulmonary or in the systemic circulation — very rarely
occur in mitral stenosis from detachment of the vegetations of acute
endocarditis, but most frequently from plugs passively formed within the
chambers of the heart. Frequently, therefore, they are the first
manifestations of disease, and not symptoms developed during an acute
or subacute illness. They occur both in the cases which are obviously
associated with rheumatism, and those which present no such evident
relation. Of course they tend further to disturb compensation, though in
many cases there is recovery for long periods.
G-enerally speaking, in the cases of mitral stenosis oedema is not nearly
so marked a symptom as in the cases of mitral insufficiency. A fugitive
and slight oedema occurs in many of them, but general dropsy rarely until
the final stages, when the right chambers of the heart have become dilated
and the tricuspid valve incompetent ; and many patients die before this
stage is reached. Sir W. Broadbent notes that great enlargement of the
liver with true pulsation of this organ is more frequently found as a con-
sequence of mitral stenosis than of other valvular affections ; and it is not
uncommon to find fluid in the peritoneal cavity before oedema of the feet
and legs. The oedema will disappear with rest in bed while ascites remains
for a time ; whereas cardiac dropsy in mitral and tricuspid insufficiency
begins, as a rule, in the connective tissue of the most dependent parts
(6). My own observations confirm these conclusions.
In the rheumatic group of cases the influence of sex in the disposition
to the obstructive mitral lesion is well marked and difficult to explain. Of
DISEASES OF THE MITRAL VALVE 1029
264 cases of all forms of mitral stenosis collected by Sir Dyce Duckworth,
177 were female and 86 male. In Hayden's cases the proportion of
females to males was two to one. In Broadbent's list of 53 cases examined
post-mortem, 38 were females and only 15 males. Sir Dyce Duckworth
concluded that in 70 per cent of the cases of mitral stenosis tabulated by him
there was a certain or strong presumption of rheumatic antecedents ; and
he considered this estimate of the relation to rheumatism to be rather under
than over the mark. In regard to my own cases, in 17 autopsies £ii
children manifesting mitral stenosis in conjunction with pericarditis or
endocarditis, which I judged to be of the rheumatic form, 10 were female.
Of 35 children under 12 years clinically observed, 22 were female;
of 31 adults with mitral stenosis in distinct association with rheumatism
observed by myself, 18 were female. It would appear, therefore,
that the preponderance of cases in the female sex in my own experience
is not so great as in that of other observers. It must be remembered
that I have taken those only in which I considered the rheumatic associa-
tion to be strongly accentuated : the groups of cases not decidedly
associated with rheumatism will be considered hereafter.
Prognosis. — I have found the average age at death of 61 patients
with mitral stenosis to be 32"7. The late Dr. Hayden's cases — 42 in
number — gave an average age of 37 '8. Sir W. Broadbent states that
the average age at death, deduced from 53 cases abstracted from the post-
mortem records at St. Mary's Hospital, was 33 for males and 37 and 38
for females; and he adds : " Mitral stenosis stands next to aortic regurgita-
tion among valvular affections in the order of gravity." I have records of
17 eases fatal before the age of 12 years, the average being 9| years ; 10
of these at the age of 10. The association with rheumatism is shown by
the fact that, in addition to the valve-lesion, in 14 of these either pericar-
ditis or recent endocarditis of rheumatic characters were found in necropsy.
The rheumatic associations of the majority of cases of mitral stenosis
constitute a very great, if not the chief element of danger. The other
causes of fatality will be pointed out in the consideration of the other
groups. It must be accepted as a general proposition that the subjects
of mitral stenosis (discovered at an early age) rarely survive the age of
40 ; the disease, therefore, when dating from childhood and adolescence,
and in such cases having its origin, as I believe, in a rheumatic aflFection,
is of grave significance.
Treatment. — The recognition of the rheumatic association of mitral
stenosis is of much importance in treatment. In childhood and ado-
lescence a slight febrile attack in the subject of mitral stenosis, or in one
who presents signs of the advent of the lesion, should be held as a
probable indication of a subacute rheumatism ; and treatment by com-
plete rest with the administration of salicin or the salicylates should be
enjoined. If cough and difficulties of breathing are also present, symptoms
of bronchitis or pneumonia, the systematic administration of ammonia in
addition is valuable. The frequency of infarction of branches of the
pulmonary artery in cases of mitral stenosis has already been pointed
1030 SYSTEM OF MEDICINE
out. The late Sir Benjamin Eichardson advocated the frequent adminis-
tration of liquor ammonise, well diluted, as a means not only of inducing
fluidity of the blood, but also of dissolving a coagulum already formed.
There may be diflferences of opinion whether such solution be thus
possible ; but there are many reasons in favour of the treatment. Besides
increasing the alkalinity of the blood-plasma, ammonia is a valuable
stimulant of the nervous mechanism of the heart and of the respiratory
centre ; and, by increasing the bronchial secretion and rendering it more
fluid, it acts very favourably as an expectorant. I have witnessed a
case in which death seemed impending from plugging of the pulmonary
artery when the frequent administration of ammonia seemed to be the
means of saving the patient's life ; and I have observed many cases in
which there were signs of partial embolism when recoveries were very
satisfactory. The best mode of administration in young subjects is the
liquor ammonias fortior in doses of one to five minims, with liquid
extract of liquorice well diluted with water ; the dose being repeated —
according to the urgency of the case — every half-hour, every hour, or
every two hours until signs of improvement appear. It may then be
continued every four hours for several days. Whether there be bronchitis
from venous congestion or local consolidations of the lungs from infarcts,
the ammonia treatment is valuable. It may be well to issue a caution
against the use of digitalis during any febrile manifestation in these cases.
I have found it worse than useless. The haemoptysis which may occur
should not be treated by styptics or opium. As a general rule it is
better that any haemorrhage which breaks out in the course of mitral
stenosis should not be checked by drug treatment. A like medicinal
treatment to that just mentioned may be put in force in cases in which
precordial pain or distress is manifested in the subjects of mitral
stenosis. It is to be remembered that pericarditis arises not infrequently
in this connection, when the special treatment for this disease must be
carried out. The occurrence of pericarditis or of lung complications of
any kind may rapidly break the compensation in mitral stenosis ; and
inadequacy of the right heart, with dropsy and other signs of heart
failure, may occur. In such case the treatment should be as already
described under mitral insufficiency. The symptoms, however, are
frequently recovered from, and compensation is restored.
Whilst there are any indications of acute changes — of endocarditis,
of pericarditis, of rheumatism, or of any symptoms attended by pyrexia
— perfect rest in bed should be enjoined. It is otherwise, however, in
convalescence, when it is to be presumed that sclerosing changes in the
valve structures are going on. Then systematic exercises, gradual and
tentative at first, should be recommended, for they fulfil important
indications ; they not only aid the venous circulation, but by expanding
the thorax they tend to aspirate the heart, increase the outflow from
auricle to ventricle, and perhaps prevent the imminent danger of the
progressively increasing contraction of the auriculo-ventricular aperture.
It may be urged that a danger of such exercises may be a detachment of
DISEASES OF THE MITRAL VALVE 1031
a vegetation left by the jheumatic endocarditis ; this is possible, but it is
proved that the greater danger is the passive formation of thrombi within
the heart in consequence of retarded circulation within it. The patient
should be cautioned against violent movements, but there can be no
doubt, I think, of the value of systematic exercises. These have been
considered in the treatment of mitral insufficiency. During convalescence
from any acute febrile manifestation in the subject of mitral stenosis, the
first method employed should be gentle massage and movements of the
legs, the patient being quiet in bed ; next in order the arms and thorax.
Later, expansion movements of the thorax, made by the patient himself
cautiously and deliberately, should be practised, with judicious intervals
of rest. Concurrently, or, as I prefer, just subsequently to these move-
ments, there should be spongings, first with warm and afterwards with
cool water, followed by dry towel friction. Later the systematic muscular
exercises, as prescribed by Ling and Schott, may be used. An excellent
summary of methods of muscular movement is given by Dr. Lauder
Brunton (7).
Although moderate exercise in the fresh air in the subject of fairly
compensated mitral stenosis is salutary, sudden overstrains are dangerous.
In some cases breathlessness does not come as a warning, and patients
persist in overtaxing their strength. The subject of mitral stenosis
.should be protected from chills by suitable apparel, and no clothing is
better than pure woollen. A light woollen night-dress is also to be
recommended. Heavy overcoats and sealskins, which weigh down the
shoulders and thus prevent good expansion of the thorax, are, in my
opinion, to be deprecated.
The late Sir Andrew Clark, in a clinical lecture which was published after
his death, gave some valuable hygienic rules f orapatient with mitral stenosis.
In the daily dietary fluids should be restricted, for after their absorption
they distend the vascular system, and increase the bulk without increasing
the nutritive value of the blood -within the vessels. The ingestion of much
liquid enfeebles the heart and increases the labour of the right ventricle
and left auricle in the transmission of blood through the narrowed aperture
into the left ventricle. The patient should have three good meals a day
as dry as he can make them ; over-eating and indigestible foods must be
'strictly guarded against. I consider it a good plan to advise that the
two meals of the day of which meats form a portion should be taken
without alcohol, and with a little pure water or toast water only ; and
subsequently to each of these a wineglassful of milk with two teaspoonf uls
of good old brandy or whisky may be allowed. In some patients there is
a slight appearance of jaundice, the liver is embarrassed ; there is often
constipation. There may be basic congestion of the lungs. Sir Andrew
Clark said, "To relieve the lungs give something to relieve the bowels.'
Sulphate of soda and phosphate of soda, equal parts in powder, may be
administered in doses of two or three teaspoonfuls dissolved in water in
the morning, or a teaspoonful of sulphate of magnesia may be taken
in hot water. Such aperients relieve the portal system, and so the right
I0J2 SYSUEM OF MEDICINE
side of the heart and the lungs. Mercurial purg9,tives are occasionally of
service.
The routine administration of digitalis in cases of mitral stenosis is to
be condemned. Very often it does harm. When once a patient manifesting
the physical signs of mitral stenosis has recovered from any intercurrent
disease which has disturbed the compensation, careful hygienic treatment
and the administration of ordinary tonics are all that is necessary ; all the
special heart tonics should be avoided. When, however, the right heart
begins to fail, or dropsy to appear, some special heart treatment becomes
necessary. Even then in many cases the administration of digitalis
cannot be advised with the same confidence as in cases of mitral
regurgitation. In many it causes the heart's action to become irregular,
or increases an already existing irregularity ; in some it induces nausea
and vomiting, in others precordial oppression. I have found convallaria
to act more beneficially in these cases than digitalis ; it favourably
influences the irregularity, and acts as a powerful diuretic. The extrac-
tum convallariae fluidum in doses of 5 to 10 minims, or the tinetura
convallarise in doses of 10 to 20 minims, may be administered every four
hours, or three times a day, in adults. Strophanthus is useful in some
cases, but, like digitalis, should not be continued for long periods. When
there are serious symptoms of heart failure — the radial pulse small and
irregular, whilst the right ventricle is felt to beat forcibly, and the veins
of the neck are seen to be distended, and perhaps pulsating, the patient
being pale or dusky and breathing badly — relief of the venous engorge-
ment by venesection is a valuable means of treatment. The ordinary method
of opening the vein in the arm and permitting the flow of about six
ounces of blood is the best, but this is often objected to ; if so, six or
eight leeches may be applied over the epigastrium. In children the relief
given by the abstraction of blood by two or three leeches is very well
marked. After abstraction of blood digitalis and other heart tonics often
act more favourably than they would have done before the relief of the
venous engorgement.
Group II. Cases in which the disease is first declared by symptoms
of lesion of the nervous system. — Not uncommonly a patient comes
under medical care for a lesion of the nervous system which has suddenly
shown itself and then the diagnosis of mitral obstruction is made for the
first time. If rheumatic manifestations existed at any period of the
previous history of the patient these were trivial and unnoticed. The
physical signs indicate a pure mitral stenosis; there is no evidence of mitral
regurgitation. In fatal cases, for the most part, the funnel form of
mitral constriction is found. In many there is good reason, from the
hereditary bent, or from the occurrence of some symptoms which suggest
a rheumatic proclivity, to suspect that these insidious morbid changes
had their origin in rheumatism ; but it may not be so in all cases. It is
possible that the hsematomata of the delicate mitral flaps in infancy may
be the starting-points of the fibrous proliferation ; or vascular dilatations
or hssmorrhages from the fine vessels of the growing valve may be the
DISEASES OF THE MITRAL VALVE 1033
earliest changes. At any rate the only cause concerning which we have
precise evidence is rheumatism.
The most characteristic among the severe lesions of the nervous
system is right hemiplegia. In one of my cases, a girl of 10, the first
detected sign was sudden paralysis of the right arm and leg ; the child
recovered completely from the paralysis, but died seven months afterwards
after having manifested much precordial distress. Mitral stenosis was
demonstrated at the autopsy, and there was universal adhesion of the
pericardium. In another patient, a woman aged 22, who had never
manifested any symptom of rheumatism, and who had no hereditary
tendency thereto, sudden right hemiplegia occurred with aphasia. There
were pronounced physical signs of mitral stenosis without regurgitation.
The patient made a perfect recovery from the paralysis of motion, but
complete aphasia persisted (28). In another of my cases, also a woman,
left hemiplegia occurred ; after full recovery from this lesion right hemi-
plegia came on suddenly ; from this latter attack the recovery was but
partial. In Duroziez's 43 cases of " pure " mitral stenosis in females, 1 1
manifested right hemiplegia with aphasia, and 4 hemiplegia without
aphasia ; there were no such cases in the male sex.
Another nervous disorder which may suddenly arise in subjects of
the affection is hemichorea. In 38 cases of mitral stenosis I found
4 of hemichorea. Duroziez records a case of a woman, aged 24,
with mitral stenosis declared by right hemichorea in which the con-
vulsive movements of the limbs ceased, but chorea of articulation
remained, so that the beginning only of each word was uttered.
One of my patients, a boy aged 3|, was suddenly seized with
epilepsy, the unconsciousness lasting twenty minutes. Nine months
afterwards chorea became manifested ; recovery took place, but after a
second period of nine months another attack of chorea occurred ; there
were well-marke4 physical signs of mitral stenosis. In a boy, aged 5,
who manifested presystolic murmur and thrill, a fit had occurred eighteen
months previously attended with unconsciousness so profound that the
child was thought to be dead ; nine months afterwards chorea appeared.
In another case, a girl aged 5, epilepsy occurred, and the attacks were
repeated and severe. In a lad, aged 18, in whom I had the oppor-
tunity of watching the physical signs of the gradual establishment of
mitral stenosis, from the manifestation of a soft apical systolic murmur to
that of complete and characteristic presystolic murmur, thrill, and doubled
second sound, there occurred during his exercise in the garden a sudden
unconsciousness, which was complete for a minute or two, but was not
attended by muscular spasm.
It is, I think, reasonable to conclude that these sudden perturbations
of the nervous system are caused by infarctions of branches of the intra-
cranial arteries ; in some instances this was positively proved by necropsies.
It is clear that the consequences of such embolism may in some cases
pass away completely ; in others the plugging of the vessel is followed
by necrosis of the nervous structures thus supplied.
I034 SYSTEM OF MEDICINE
In the treatment of such cases complete rest should be promptly
enjoined. There is fair evidence that the ammonia treatment, as described
in relation with embolisms of the pulmonary artery and its branches,
may fulfil a useful purpose.
Group III. Cases presenting disorders of nutrition. — Children
are not infrequently brought for treatment on account of their pro-
gressive wasting. The parents, or those who have charge of them,
think they are "in a consumption." On removal of the clothing the
emaciation is seen to be considerable ; the ribs stand out and the inter-
costal spaces are sunken, except in some cases over the situation of
the right ventricle, where there is a marked prominence ; on further
examination the physical signs of mitral stenosis are in fuU evidence. In
those who have arrived at adolescence or adult life there are other signs
of ill development. The patients are indisposed for exertion (though
they seldom complain of breathlessness) ; they are unstable and infirm of
purpose, are accounted very nervous, and in some instances are demented;
they are frequently dyspeptic. The elucidation of the condition is in
fatal cases made by the post-mortem examination ; constriction of the
mitral orifice is found, and the enlarged right chambers of the heart
contrast with a small left ventricle and small aorta. The normal arterial
blood-supply has been gradually diminished by the contraction of the
mitral orifice, and has continued to be in minus quantity during the
periods of development and growth. As Sir Samuel Wilks has pointed
out, " The lungs are small as well as the chest, and the respiratory
process is correspondingly lowered, and with this probably the whole body
is impoverished. At aU events, the organism is working with a diminished
amount of blood " (30).
In young women — and in the great majority of such cases, even in
childhood, the patients are of the female sex — ^there is frequently, though
not invariably, an association with anaemia and chlorosis. The frequency
with which a chlorotic patient has presented physical signs of mitral
stenosis has been noted by many observers. Stokes in 1854 was the
first to record this in describing the case of a young girl, aged 18,
who was anaemic and chlorotic, and showed the physical signs of organic
mitral disease, the precise form of the lesion being then undiscovered.
Death occurred after the manifestations of anasarca and congestions of
the lungs, and at the necropsy the funnel form of mitral stenosis was
found, with an auriculo- ventricular aperture that scarcely admitted a
goose-quill. This case may be regarded as an exemplary one. I have
observed many instances of very marked anaemia, some not presenting
signs of wasting, in which there has been well-marked physical evidence
of mitral stenosis without regurgitation. Duroziez, who has given the
notes of many cases, goes so far as to say that pure mitral stenosis is a
feminine and a chlorotic malady (9). Teissier points out that a similar
anaemia occurs, though more rarely, in the male subjects of mitral
stenosis.
In any of the cases in this group haemoptysis may occur, and local
DISEASES OF THE MITRAL VALVE 1035
consolidations may be found in the lungs — the group of symptoms
closely resembling those of pulmonary tuberculosis. In the great
majority the diagnosis of pulmonary consumption is not justified ; the
symptoms are the accidents of the mitral disease itself. I have given
my reasons for dissenting from the view that mitral stenosis can be
considered as standing, even remotely, in any causal relation to tuber-
culosis ; but I think it probable that the deficient arterial supply which
is a consequence of the disease disposes to the occurrences of tubercular
changes in the lungs in a small minority of cases, and the remote proba-
bility of this should be present in the mind of the observer. The
presence or absence of tubercle bacilli in the sputa will settle the question.
In the treatment of this group of cases physical training should hold
a first place. It is evidently of the highest importance that the blood-
flow from the right to the left ventricle should by judicious means be
increased. It is possible that if this be accomplished by systematic
muscular movements and careful hygiene at an early period of the mani-
festation of the morbid condition, the insidious contraction of the orifice
may be averted. The means to this end are frictions, massage, carefully
planned muscular movements, baths and bathing, the selection of suitable
climates, and the regulation of diet. Medicinally iron, arsenic, small
doses of liq. strychninse, and cod-liver oil are the chief agents to be
employed. The treatment of complications and of failure of compensation
"will be as in other groups of the disease.
Group IV. Cases associated with ehronie renal disease and
arterio-seierosis. — As I have already stated, the association between
mitral stenosis and chronic renal disease was first pointed out by
<jroodhart (11), and confirmed by Pitt in 1887. The observations
were made chiefly from the standpoint of morbid anatomy, though Pitt
contributed some clinical data. It was made clear that the cases demon-
strating the coexistence of the two morbid states are by no means
infrequent. Nevertheless G6rard and others hold that mitral stenosis,
having its origin in arterio-sclerosis, is rare. I cannot doubt that the
■explanation of this apparent conflict is to be found in the fact that the
cases demonstrating the conjunction of the diseases are most frequently
found after death ; they come under clinical observation with compara-
tive rarity. The two morbid affections progress insidiously, and either
the patient is suddenly stricken down with apoplexy, or some sudden
complication which precludes any physical examination, or, if such
examination has been possible, the physical signs were supposed to
indicate some form of disease other than mitral stenosis.
I have notes of six cases observed by myself, in which, without any
evidence of rheumatism or other predisposing malady, there have been
signs which should bring them into the group under consideration. In
three other cases aortic valvular disease was conjoined with the mitral.
Several others could be regarded as mixed cases, these having rheumatic
antecedents ; but the subsequent evolution was after the manner of
arterio-sclerosis. In my cases the most advanced age was 70, the only
1036 SYSTEM OF MEDICINE
male ; the youngest was 35. The cases recorded by Blind (four) and
Gr6rard (five) which should come into this group are nine in number, five
men and four women, the oldest patient 67, the youngest 32. In the
cases taken as examples there is no rheumatic antecedent ; but in the
majority the usual signs of chronic Bright's disease are present. The
radial and other arteries are firm and incompressible ; the usual hyper-
trophy of the left ventricle of the heart, however, is not manifested. In
some of the cases, in addition to the signs of thickened arteries, there are
obvious evidences of gout with deposits of urates in the joints and else-
where. In some there are well-marked signs of arterial atheroma. There
may be emphysema of the lungs or pulmonary fibrosis. Fibroid changes
may occur about the viscera, the perivisceritis of Huchard. The origin
of the disease is not to be traced, the progress is slow and imperceptible.
The physical signs of mitral stenosis in many of the cases do not differ
from those ordinarily observed — the presystolic murmur, the entire diastolic,
or the early or mid-diastolic murmur, the sudden, loud first sound and the
double shock sound in diastole. In some cases there is no presystolic
murmur, but a systolic. This may be heard at the apex and the back,
thus answering to the criteria of mitral regurgitation ; in such case it is
probable that the auricle has become dilated and weak. The diagnosis
of stenosis can only then be made from the evidence of a heaving and
enlarged right ventricle, contrasting with the absence of signs of enlarge-
ment .of the left ventricle, perhaps also from the absence of any second
sound at the apex (Broadbent). Exceptionally there is no loud, sharp,
short, sudden first sound, but a dull sound as in the case of a hyper-
trophied left ventricle. In the cases manifested between the ages of 30 and
40, there have been the evidences of the gradual oncome of chronic renal
disease with thickened arteries or undoubted gout with deposits of urates.
There is no evidence of any pre-existing disease of the valve due to
rheumatic or other causes ; but there must be a remaining doubt whether
any change in the valve preceded the fibrous proliferations intrinsic to the
Bright's disease. It is, I think, improbable, seeing that the great majority
of cases due to rheumatism are fatal before the age of 40, that chronic
Bright's disease is a superadded factor, for if so the scene would be more
speedily closed, and death would ensue. It is at first sight more likely
that the changes are independent of rheumatism and due to a slow form
of sclerosis.
In one case, that of a lady aged 52, I had opportunity of observing
the gradual involution of the disease as evidenced by the physical signs
and confirmed by post-mortem examination. There was at first no sign
whatever of cardiac disease, but gradually all the usual signs of mitral
stenosis were manifested. The urine showed normal characters for nearly
the whole period of observation, and the case was observed during
thirteen years. The symptoms were those of dyspepsia, with gradual
implication of the nervous system, first evidenced by an epileptic attack
and afterwards by dementia. The necropsy showed funnel transformation
of the mitral valve, with much fibrous thickening of the surrounding
DISEASES OF THE MITRAL VALVE 1037
structures. There were chronic fibroid thickenings in the pleurae, the
left lung, the spleen, the liver, the capsules of the kidneys, and the mem-
branes of the brain. The granular changes in the kidneys were but
slightly pronounced, and no doubt comparatively recent. The chief
morbid change was the widely-spread fibrosis, the progress of which had
been very gradual ; and it seemed legitimate to infer that the stenosis of
the mitral orifice and the fibrous transformation of the surrounding
structures were due to a similar morbid process. This case is no doubt
exceptional in that the fibroid changes in so many situations long pre-
ceded any signs of interstitial nephritis. In the majority of cases the
evidence of chronic renal disease is well marked when the case comes
under observation. The age 50 to 70 renders it improbable that
obstruction of the mitral orifice from any cause had preceded the gradual
evolution of the chronic renal disease with its attendant arterio-sclerosis.
In all cases the progress of the disease must have been very gradual and
insidious. In many there have been signs of cerebral disease ; indeed, it
is for symptoms indicating such disease that the cases usually come under
notice. Epileptiform seizures, apoplexy, dementia, or ursemia, are the
chief forms. In several instances the signs of albuminuria retinitis have
been recorded. That the morbid changes have been slow and gradual is
shown also by the post-mortem evidence. In the case of a woman of 65
there has been found a funnel transformation of the mitral curtains ;
just as observed in the cases in earlier life ; but in the majority the
button-hole form of mitral stenosis is manifested with great thickening
and firm fibrous transformation of the papillary muscles.
The treatment in this group of cases is subordinate to that of the
chronic renal disease and the attendant thickenings of the arteries. It is
important to realise that the prognosis is very grave. When a patient
manifesting the signs of mitral stenosis at whatsoever age presents signs of
firm and thick arteries, and the urine is found to be continually of low
specific gravity and occasionally albuminous, it is well that for a few weeks
an entire milk dietary be enjoined. It may be a little difficult to convince
a patient past middle age, whose stomach has been the receptacle of foods
of many and various kinds far more than adequate to the needs of his
organism, whose nerves of taste have been frequently and abnormally
stimulated, and whose absorption of nutritive material and excretion of
effete products have been after the manner of periodic and irregular
thunder-showers which have deluged the land and blocked the drains, that
he must return to the sweet simplicity of the earliest months of his life.
Yet it is best so. It is the absence of the irritation to the arterioles
caused 'by the complex albuminoids which turns the balance towards
amendment. It may be necessary, however, to make some concessions.
In the early morning, or on waking, the patient may take half a pint of
milk with half an ounce of rum, or of cognac and an ounce of lime water.
In some cases one to two ounces of fluid magnesia may be substituted with
advantage for the aqua calcis. Three or four hours afterwards a second
half-pint of milk may be taken flavoured with a little hot coffee ; the third
I038 SYSTEM OF MEDICINE
half-pint, after a like interval, may be taken as a blancmange made with
isinglass or gelatine. At similar intervals, during the r.emainder of the
waking hours, the changes may be rung with the various flavourings ;
but no solids should be permitted other than light biscuits.
The total amount of milk taken in the twenty-four hours should be
three to six pints. The total quantity of cognac or spirits of any kind
should be limited to two ounces. To break the monotony of the purely
milk diet, it is a good plan to allow occasionally a firm jelly fully
flavoured with madeira, rum, kirschwasser, or chartreuse. One or two
tablespoonfuls of isinglass are to be melted in very hot water, and the
mUk added thereto ; the small quantity of gelatin thus mingled with the
milk is sufiicient to prevent any firm curdling of the casein in the stomach,
the coagidum being rendered much softer and its digestion facilitated (25).
In regard to medicinal treatment, the rule of Dr. G. W. Balfour should
be followed, that no cardiac tonic should be administered without a
simultaneous unlocking of the arterioles. The therapeutic measures
should follow the lines already described in the consideration of Group
II. of cases of " Mitral Regurgitation." As Sir Wm. Broadbent has said,
" Nitro-glyeerine and other vaso-dilators may sometimes be given with
good effect for many weeks or even months in conjunction with general
tonics, such as iron, quinine and nux vomica " (5).
A. Ernest Sansom.
REFERENCES
1. AoLAND, J. D. "Mitral Stenosis, a Clinical Lecture," Lancet, 20th July and
27tli July 1889. — 2. Baifotib, G. W. Clinical Lectwres on Diseases of the Heart,
2nd edition. London, 1882. — 3. Blind, F. A. " Le r^tr^oissement mitral des
art^rio-scUreux," Thise de Paris, 1894. — 4. Boyd, Feancis D. " Apparent Reduplica-
tion of the Second Sound in Mitral Stenosis," Paper read before the Edinburgh Medico-
Chirurgical Society, Lancet, 12th December 1896, p. 1685. — 5. Broadbent, Sir Wm.,
and Broadbent, J. F. H. Heart Disease viith special, reference to Prognosis and Treat-
ment, London, 1897, pp. 192-194. — 6. Broadbent, Sir Wm. "Mitral Stenosis,"
International Journal (^Medical Sciences, January 1886. — 6a. Idem. Heart Disease,
1897, p. 197. — 7. Brunton, Lauder. Lectures on the Action of Medicinies, p.i 368.
London, 1897. — 8. Chbadle, W. B. The Various Manifestaiions of the Rhewmatic
State as exemplified in Childhood and Early Life, Harveian Lectures, p. 114.
London, 1889. — 8a. Clark, Sir Andrew. Lancet, 2nd December 1893, p. 1367.
— 9. DuROZiEZ. TraiU clinique des maZadies du ccewr, p. 259. Paris, 1891. —
10. Fisher, Theodore. "The Presystolic Apex Murmur of Aortic Regurgita-
tion," etc., Lancet, 9th March 1895, p. 609. — 11. Goodhart, J. F. "Anaemia as a
cause of Heart Disease," Lancet, vol. i. 1880, p. 479. — 12. G^irard, E. A.
" L'oreillette gauche dans le r^tr&issement miiiral," Th^e de Paris, 1894. — 13.
Lanoereaitx. Atlas d'a/natomie pathologigue ; texte, p. 214, Paris, 1871. — 14. Pheak,
Arthur G. "On the Reduplication of the Second Sound," Lancet, 9th January 1897.
— 15. Idem. "On Presystolic Apex Murmur without Mitral Stenosis," Lamcet, 21st
September 1895, p. 716.— 16. Pitt, G. N. "On the Association of Mitral Stenosis
with Gout and Granular Kidneys," British Medical Journal, 16th July 1887, p. 108. —
17. PoTAlN. Clinique medicate de la charitS, Fa.ris, lS9i, p. 5i. — 18. RoucHte. "Du
claquement d'ouTerturedelamitrale," Th^e de Paris, 18SS. — 19. S.vmwats, D. W. Le
r6le de l'oreillette gauche notamment dans le ritricissemeni mitral. Paris, 1896. — 20.
Idem. "The Influence on the Action of the Auricle of Variations in its Capacity," British
Medical Journal, 23rd January 1897, p. 199. — 21. Idem. "The Left Auricle in Mitral
Stenosis, Hypertrophy, and Dilatation," British MedicaZ Journal, 28th November 1896,
DISEASES OP THE MITRAL VALVE 1039
p. 1567.— 22. Sansom, a. E. "The Pathological Anatomy and the Mode of Develop-
ment of Mitral Stenosis in Children," Transactions of the Medical Society of London,
1890, p. 143. — 23: Idem. " On the Difficulties of Diagnosis in Cases in which Disease
of the Aortic Valves is associated with Mitral Stenosis," Liverpool Medico-Chirurgical
Journal, January 1892, p. 6. — 24. Idem. Diagnosis of Diseases of the Heart, 1892, p.
383.-25. Idem. "Diseases of the Blood-Vessels," Twentieth Cent. Syst. Med., New
York, 1895, p. 477. — 26. Idem. Lettsomian Lectures on Valmdar Diseases of the Heart,
London, 1886, p. 137. — 27. Idem. Keating' s Oyclopcedia of Diseases of Children, vol. ii.
p. 831. Philadelphia, 1889.-28. Idem. Clinical Society's Transactions, 1894, p. 268.
— 29. Teissier, Pieree. "Rapports du r^tr&issement mitral pur avec la tuberculose-
ftiologie, pathogenic, clinique," Clinique mMicale de la charity., p. 913. — 30. Wilks,
Sir S. " Consequences of Narrowing of the Mitral Valve when occurring in Chil-
dren," Lamcet, Jan. 1886, p. 7.
A. E. S.
LIST OF AUTHOEITIES
AoLAND, T. D., 1020
Adami, 465 et seq., 849, 865, 917, 991
Addison, T., 92, 150, 243, 519 et seq.
Affleck, 538
Albers, 59 (note)
Albuoasis, 648
Alison, 121
AUbutt, T. C, 294, 469, 759, 864, 902
Alsaharavius, 548
Andral, 54, 153, 222, 521
Andrew, 237
Arbuthnot, 108
Arcangeli, 490
Aretseus, 202
Arkle, C. J., 258
Arnold, 3
Ashby, 557
Ashwell, 482
Auenbrugger, 97, 150 (note)
Babes, 663
Babington, B. G., 349 (note)
Bachstron], 588
Badham, 1
Baer, von, 712
Baginsky, 663
Baillie, M., 92, 692
Balfour, G. W., 121, 506, 735 et seq., 829,
844, 911, 960, 1024
Ball, 950
Baly, 619
Balz, 24
BambergeT, H., 62
Banti, 624, 539
Bar, 563
Barclay, 521
Barie, 921
Barlow, T., 604, 633, 984. 993
Barlow, W. S. Lazarus, 671
Barnes, 587
Barr, J., 849, 912, 1010
Barrs, A. G., 1002
Barth, 30, 60
Barthez, 64
Bastian, 66
VOL. V
Baumgarten, 166, 464
Baumler, 750
Baunboltzer, 722
Bayle, 109, 150 (iiote), 222
Beau, 63
Beck, Marcus, 776
Becquerel, 597
Beevor, H., 166
Begbie, W., 728, 802
Behier, 645
BeU, 950
Bemmelen, von, 648
Beneke, 173, 707, 922, 1000
Bennett, Hughes, 121, 243, 257, 635
Berkart, 293
Bemabei, 34
Bernard, Claude, 888
Bert, Paul, 298
Besnier, 581
Biermer, A., 20 et seq., 60, 287, 298, 519 et
seq.
Bihler, 500
Billard, 562
BiUings, 112, 420
Binswanger, 830
Binz, K, 308, 489
Bizzozero, 645
Blackley, 300
Blanc, L., 1000
Blane, Gilbert, 586
Bleile, A. M., 858
Blind, 1036
Block, 458
Bockemiahl, 648
Boerbaave, 120
Bohn, 604
Bollinger, 25, 9C2
Bond, 460
Bondsynski, 659
Born, 715
Bouchut, 887
Bouillaud, 120, 756, 874
Bouveret, 827
Bowditch, 157
3x
1042
SYSTEM OF MEDICINE
Boxall, 713
Boyoe, 258, 887
Boyd, F. D., 1019
Bradbury, 963
Bradford, J. R., 237
Brakeoridge, 522
Bramwell, Byrom, 83, 522, 977
Bree, 300
Bremer, 413
Brigstooke, 550
Briquet, 34, 61
Bristowe, 106, 257, 509, 628, 713
Broadbent, J., 740, 743, 780 et seq.
Broadbent, Sir W., 805. 834, 939, 1001
Brodie, T. G., 416, 451
Broeck, 584
Brown, Graham, 461, 474
Bruce, Mitchell, 206
Brucke, 466
Bruhl, 539
Brunton, Lauder, 127, 200, 844, 999, 1031
Bryant, J. H., 130
Bryson, 587
Bucbanan, G., 157
Buchholz, 835
Buch, Schebey, 577
Buoquoy, 58^ 991
Budd, 566
Buhl, 64, 175
Bunge, 488
Burns, A., 1014
Busey, 562
Busk, G., 597, 614
Buzzard, 588
Cabot, 410
Cadet, 861
Calvert, J., 344
Campbell, CoUn, 83
Canali, 35
Canon, 457
Oantlie, J., 776
Canton, 707
Carr, W., 55
Carta, 546
Cash, 127
Caton, 874
Cayley, W., 237
Cazeaux, 30
Ceradini, 466
Chalret, 597
Chambers, 649
Champneys, 285
Channing, 521
Chantemesse, 257
Chaplin, A., 45, 73, 82, 84, 167
Chapman, P. M., 939
Charcot, 150, 1005
Chauffard, 366
Chauveau, 939, 10^4
Cheadle, 733, 984
Chevers, N., 697
Cheyne, Watson, 178, 569
Chomel, 150 {note)
Christison, K, 121, 243
Church, W. S., 740
Chvostek, 490
Clark, Andrew, 37, 153 206, 244, 300
489, 993
Clark, J., 222
Clarke, R., 27
Clement, 490
Coats, J., 251, 887, 1010
Coen, 866
Cohn, H., 71, 884
Cohuheim, 173, 474, 533, 670, 917
Combe, 521 '
Copeman, 424, 528
Coppola, 496
Cornet, 167
Cornil, 227, 638
Coirigau, D., 30, 64, 150, 243, 922
Corvisart, 150 (note), 697, 834
Councilman, 317
Conpland, S., 109 647, 702
Couty, 581
Craig, 622
Crocker, Eadoliffe, 574
Cruveilhier, 92, 150, 970
Cuffer, 979
Curnow, 602
Curschmann, 296
Da Costa, 820, 861, 903, 912
D'Arsonval, 859
Davies, H., 38, 972
Dean, H. P., 237
Debove, 232
Degler, 27
Del^pine, 321, 884
Delpech, 588
Demelin, 564
Demoor, 421
Dickinson, W. H., 605, 777, 868, 948
Dieballa, 536
Dieffenbach, 559
Diesing, 25
Die-olafoy, 257, 776
Dittrich, 35
Dixon, J., 31
Dobell, Brian, 85
Donders, 336
Donkin 863
Dorsch, 697
Downie, J. W., 83
Drouin, 448, 491
Druitt, E., 629
Drummond, D., 64
Duchek, 593
Duohenne, 549
Duckworth, Dyoe, 703, 1029
Duclaux, 181
Duncan, Johann, 482
Dungern, 563
Durham, H. B., 458
LIST OF AUTHORITIES
1043
Duroziez, 968 tt seq.
Dusser, 565
Ebkrth, 884
Ebstein, 547, 654
Ehilich, 178, 366, 412, 528, 636
Eichhorst, 522
Eichorst, 649
Eisenlohr, 524
Ely, 458
Engelmann, 169
Bppinger, 562
Eross, 562
Everard, 421
Ewart, W., 32 (note), 182, 744 et seq., 798
Faoqe, Hilton, 159, 512, 669, 899, 923,
1024
Parre. 697
Fauconnean, 950
Fenwick, Samuel, 194, 524
Ferdinand, Prince Ludwig, 366
Filehne, 35
Finny, 522
Fisher, T., 948
Fleischl, von, 430
Flexner 259
Flint, A., 205, 803, 939, 1024
Forbes, John, 121
Forster, C, 699
Fdrster, 311
Foster, W. B., 1024
Foumier, 580
Fowler, J. K., 75, 173 et seq., 712
Fox, Wilson, 20 et seq., 109, 162, 288, 569
Foxwell, 920
Fraentzel, 828, 884, 916
Franck, F., 796, 941
Franoke, 58
Frankel, 68, 95, 366
Frankenhauser, 526
Eraser, T. E., 522, 991
Frazer, 712
Frey, von, 939
Friedlander, 112
Friedreich, 791, 874, 1012
Fritzsohe, 27
Fruitnight, 605
Fuller, 267, 861
Gaibdher, W. T., 58, 218, 257, 264, 1018
Galabin, 952
Galen, 27, 202
Gamaleia, 113
Garagee, A., 35
Gardiner, 522
Garrod, A. B., 590, 614
Garrod, A. E., 714, 985, 993
Gartner, 663
Gaskell, 812, 837, 842, 925
Gassicourt, C. de, 861, 985
Gaitle, 848
Gee, 202, 549, 605, 773
Gerard, 1014
Gerhardt, 61, 205
Gerlach, 296
Gibson, G. A., 65, 522, 722
Gilbert, 60, 366, 498 {note)
Glynn, 919
Golding-Bird, C. H., 559
Goldscheider, 420
Goltz, 848
Gombault, 366
Goodhart, 605, 948, 10C3
Goppert, 847
Gottlieb, 659, 991
Gowers, W. R., 430, 509, 642, 834, 909,
950, 994
Graber, 414, 491, 600 {note)
Gram, 414
Granboom, 648
Grandidier, 553, 561
Grasset, 950
Graves, 22, 874
Grawitz, 58
Greenfield, 699
Greenhow, H., 159, 243 {note), 294
Griffith, G., 534
Griffith, W., 708
Groedel, 1000
Groom, 914
Griinbaum, 417
Gull, W., 121, 500, 624
GuUand, 415
Gunn, D., 596
Gusserow, 521
Habebshon, S. H., 220, 800, 804
Habershon, S. 0., 521
Haig, 489
Hall, Marshall, 521, 68S
Halliburton, 416
Hallopeau, 1013
Hamilton, D. J., 2 et seq., 60, 251, S02.
919
Hammerschlag, 425, 484
Hanaii, 220
Handford, H., 504
Hanot, 60, 367
Hardy, 411 et seq.
Hare, C. J., 38, 705
Harley, G., 627
Harris, T., 244
Harris, V., 351
Harvey, 842
Haspel, 598
Haughton, W. S., 902
Hay, Matthew, 997
Haycraft, 426
Hayden, 1008
Hayem, 427, 482 et seq., 522, 576, 597
Head, H., 510
Hedley, W. S., 855
1044
SYSTEM OF MEDICINE
Heidenhain, L., 914
Hememann, 491
Heitler, 1001
Heller, 58, 313
Hendsrson, 939
Hennige, 491
Henooh, 581, 721, 984
Henocque, 498 {note)
Henry, 522
Hdrard, 227, 576
Herniary, 560
Heron, 167
Herriugham, 824
Hersohell, 1001
Herxheimer, 58
Herz, 823
Hesohl, 899
Hess, 709
Hesse, 507
Heubner, 605
HUl, L., 478, 819, 964
Hilton, 676
Hindenburg, 645
Hinds, F., 258
Hippocrates, 91, 156, 350, 383
Hirsch, 156, 484, 586
Hirsohspring, 604
His, 715
Hitzig, 34
Hoohsinger, 313
Hoffa, 366
Hoffmann, F. A., 27, 71, 482, 589
Hofmeier, 625
Hofmookel, 87
Holt, 558
Hope, J., 697
Hopkins, Gowlland, 529 (note)
Hoppe-Seyler, 630
Horbaczewski, 647
Howard, R. P., 522
Hubert, W. A., 32 (morie)
Huohard, 888, 968, 1009
Huerthle, 461, 470, 939
Hughes, 993
Hugner, 268
Hunter, W. (Junior), 230, 522 d se
Hunter, W. (Senior), 719
Huss, 136 (note)
Hutchison, 449
Hiitter, 949
Huxham, 91
IMMERMANN, 491, 522, 588
Ingeler, 605
Irvine, Pearson, 326
Jacooud, 231, 874
Jackson, 267
Jacob, 420
Jaffd, 35
Jaksch, von, 460
James, 480
Jamieson, 83
Jani, 174
Jenkins, J. F., 565
Jenner, W., 121, 201, 264
Joffroy, 499
Johnson, G., 631, 672, 925
Johnson, Wyatt, 458
Jones, Lloyd, 424, 481 et seq., 723
Kannbnberq, 35
Kanthack, 411 et seq., 543, 877
Kaposi, 659
Kast, 661
Kelly, 157
Kelsch, 366
Kennedy, 158
Kessler, 68
Keyt, 939
Kidd, P., 652, 1012
King, Wilkinson, 849
Kingscote, 306
Kinnioutt, 622
Kisoh, 30
Kleber, 884
Klebs, 112, 230, 562, 865
Klein, E., 113, 562
Klemperer, F., 122
Klemperer, G., 122
Kletzinsky, 489
Kling, 560
Kobert, 489
Koch, E., 27, 113, 164
Koettnitz, 569
Kohn, 260, 468
Koplik, 367
Kossel, 647
Kotliar, 261
Kracht, 366
Kraus, 491
Krehl, 464
Krefsohy, 31
Kussmaul, 795
Laaohe, von, 522, 576
Labadie, 887
Laboulbene, 597
Laenneo, 1 et seq., 59, 92 et seq,, 180 263i
868, 383, 697, 739
Lagrave, 887
Lancereaux, 969
Landau, 662
Landois, 448
Landouzy, 160, 366
Landwehr, 648
Langer, 866
Langwill, 919
Lasser, 448
Latham, P. M., 190
Latham, P. W., 615
Lazarus, 289
Lebert, 20 et seq., 59, 166, 267, 521
Lee, B., 44
Lees, D. B., 722, 774, 874, 948
LIST OF AUTHORITIES
I04S
Leffevre, 296
Legg, Wiokham, 566, 570, 899
Leichtenstern, 484
Leith, E. F. C, 1000
LemoiDe, 930, 991
Lupine, 413, 521
Leroy, 65
LetuUe, 1012
Leveii, 698
Levy, 366
Leyden, 384, 566, 647, 904, 957
Lichtheim, 71
Liebreioh, 447, 646
Limbeck, von, 419, 649
Lind, 586
Lindes, 715
Ling, 998
Lion, 366
Lister, M., 27
Lithmann, 883
Litten, 864
Loewy, 449
Loffler, 412
Lombard, 156
Lorain, 311, 952
Louis, 63, 171
Lovibond, 431
Lower, 669
Lowit, 420
Lucas-CJhampionniJre, P., 30
Luciani, 419
Lndwig, 465, 507, 842
Lumniczer, J., 34
Lusohka, 867
Maoalister, D., 507
Macdonald, 902
Maokay, 489
Mackenzie, S., 522, 711, 863, 993 et seq.
MacMunn, 455, 629
M'Carthy, J. M'D., 852
M'Fadyean, 916
M'Munn, 532
M'Nutt, S., 558
Mader, 27
Maffucci, 174
Magnlaux, 27
Mah^, 588
Mahomed, 631, 931, 1024
Maissiat, 63
Manaon, P., 24
March, 42
Marey, 842, 939, 1014
Marfan, 34
Marie, P., 62
Markham, 121
Marshall, C. R., 963
Martin, C. F., 484
Martin, S., 175
Massart, 421
Matthes, 646
Mead, 120
Meckel, 487, 697
Meerbeck, van, 30
Meinert, 485
Mendelssohn, 63, 164, 264
Meyer, 58
Mickle, 950
Milroy, 157
Mitchell, S. Weir, 418, 570, 846
Model, 30
Moens, 469
Mohler, 604
Moore, N., 699, 947
Morehead, 600
Morgagni, 92, 346, 487, 722, 912
Morgan, 852
Morison, A., 847
Mdmer, 491
Mosler, 656
Mosso, 829
Mott, F. W., 522, 909
MouUin, C. Mansell, 801
Moxon, 153, 901
Mracek, 562
Muir, E., 533
MuUer, 297, 522, 544
Munok, 22
Murchison, 566
Murray, 675
Murrell, 38, 234
Murri, 633
Musser, 622, 534, 945
Myers, A. B. R., 821, 851, 903, 912
Naohet, 442
Netter, 347 {note)
Neumann, 522, 663, 636
Neuwerck, 866
Nielsen, 457
Niemeyer, 197, 485, 1003
Nikeforoif, 412
Nocard, 166
Noordeu, C. von, 291, 490, 815, 835
Northrup, 605
Nothnagel, 490
Obrtel, 849, 997
Ogle, C, 31, 58
Ogle, J., 838
Ogle, W., 160
Oliver, G., 430 et seq., 516, 819, 844, 909
Oppenheimer, 429
Oppolzer, 28
Ord, W. M., 460
Osier, W., 106, 158, 500, 622, 575 640,
834, 862, 922
Oui, 565
Owen, Isambard, 36
Ozanam, 1001
Page, H., 605
Paget, S., 775
Pancritius, 311
Fansini, 366
1046
SYSTEM OF MEDICINE
Panzieri, 8
Parker, 27, 704
Parkes, 615
Parrot, 1008
Pasteur, L., 174
Pavy, 627
Payne, J. F., 157
Peacock, T. B., 27, 243, 552, 697 et seq.,
729, 912
Pearce, 521
Pearse, A. C, 105 {note), 885
Peiper, 491
Pepper, W., 522, 991
Perls, 337
Peter, 200, 918
Petersen, 559
Petrescu, 127
Petruschky, 883
Phear, 1019
Phillips, S., 905
Picohini, 27
Pick, 490
Piorry, 112, 521
Pitt, Newton, 922, lOOS
Plehn, 457
Plutarch, 91
Podack, Max, 258
Politzer, 660
Pollard, B., 559
Pollock, J. E., 162, 222
Pomorski, 562
Ponfick, 632
Poore, G. V., 82, 989
Portal, 171
Porter, W. T., 465
Potain, 294, 503, 816, 872, 914, 941, 977
et seq., 1011
Powell, R. Douglas, 212, 810, 837, 933,
1008
Power, D'Aroy, 559
Preuschen, von, 562
Pringle, J. J., 574
Probsting, 829
Prout, 689
Prussak, 570, 589
Purser 522
Pye-siith, 487, 521, 910, 923, 993
QUAIN, E., 530, 892
Quekett, 521
Quincke, 428, 522
Quinquand, 576
Rainet, 264
Rake, Beavan, 532
Ralfe, 592 et seq., 614, 631
Ransome, A., 156
Ranvier, 669
Rapp, G., 60
Rauchfuss, 698 et seq., 865
Rauzier, 950
Raven, T. F., 990
Rayer, 257
Rehn, 662, 605
Reifseissen, 298
Rendu, 1010
R^non, 25, 257 et seq.
Renvers, 366
Rethers, 491
Reymond, 862
Reynaud, 65
Riberaont, 560
Richardson, B., 503, 1030
Richet, C 812
Rieder, 419
Riegel, 288, 952
Rllliet, 54
Rindfleisch, 177, 252, 269
Ringer, Sydney, 38
Roberts, F. T., 6, 237
Roberts, W.j 993
Robin, 311
Rodier, 597
Roger, 504, 566, 863, 993
Rokitansky, 63, 92, 164, 264, 487, 698 etseq.
RoUeston, G., 849
RoUeston, H. D., 42, 712, 800
Romberg, 707
Romme, 562
Rosenbach, 366, 865, 887
Rosenberg, A., 83
Rosenstein, 35, 935
Rossbaoh, 7
Rotch, 763
Rouch^s, 1019
Roux, 166
Roy, C. S., 424, 465 et seq., 835, 842, 865,
909, 991
Rubenstein, 480
Ruge, 949
Rumpf, 491
Runge, 560
Russell, A. E., 451
Russell, Risien, 522
Russell, W., 506, 522, 977
Sabatier, 718
Sacaze, 367
Sack, 568
Sa«terburg, 998
Sainsbury, 885
Salomon, 647
Salter, Hyde, 62, 287 et seq., 304
Samson, 810
Samways, D. W., 952, 1010
Sansom, 502 et seq., 762, 870, 884, 930
Sargent, 259
Sasaki, 524
Saundby, 945
Saussier, 378
Savill, 925
Sohafer, B. A., 447
Schafifer, 563
Scheimpflug, 524
Schmaltz, 427
LIST OF A UTHORITIES
1047
Sohmidt, A., 297, 516
Schonlein, 548, 577
Schott, 998
Schreiner, 647
Schrott, 490
Sohulz, 422
Sciola, 546
Sears, 777
Sfe, G., 34
Sehrwald, 83
Seitz, 205, 912
Senator, 604, 649
Sewall, 944
Sharkey, 55
Shattook, 706
Shattuck, 736
Shennan, 919
Sherrington, 409 et seq., 922
Shore, L. E., 964
Sibson, 728 a seci., 782 el seq., 861
Silbermann, 582
Simon, C. E., 483
Sisley, 321
Skoda, 121, 792, 980
Smith, F. J., 1025
Smith, S., 824
Smith, T., 605
Sorensen, 484
Souza-Leite, 62
Spaundis, 312
Spencer, H., 557
Stanley, D., 544, 944
Starling, 671, 925
Steell, Graham, 922 et seq.
Steer, L., 605
Stengel, 421
Sternberg, G., 113
Steward, F. J., 130
Stewart, T. G., 61, 776, 825
Stills, 722
Stockman, 479 et seq., 522, 648
Stoker, G., 39
Stokes, 22, 59, 111 {note), 769, 874, 998
Stolnikow, 35
Storok, 300
Strauss, 670, 575 (note)
Streng, 35
Strieker, 589
Striimpel, 546
Sturges, 0., 99, 733 et seq., 862 984
Suter, 708
Swayue, L., 294
Sydenham, 91, 499
Talamon, 113
Talma, 467
Tappeiner, 167
Taylor, P., 522, 542
Taylor, J., 522
Taylor, W. H., 591
Teissier, 1012
Thierfelder, 31
Thoma, 441
Thomas, Davies, 805
Thompson, H., 386
Thompson, R. E,, 162 ■
Thomson, J., 644
Thorowgood, 307
Thurn, 916
Tickell, H. M., 877
Tiedemann, 34
Tigerstedt, 848, 922
Toeniessen, 722
Tomaselli, 625
Tooth, H. H., 261
Townsend, 515, 561
Traube, 127, 300, 745, 841 918
Trojanowski, 62
Trousseau, 237, 382
Tunnioliffe, 844
Turner, Charlewood, 800, 904
Turner, W., 712
Tyndall, 826
Unna, 568
Vaillaed, 366
Vavandal, Jean, 479
Vay, 496
Vehsemeyer, 652
Vierordt, 414, 468, 921
Vigouroux, 1005
Villemin, 165, 264
Virohow, 9, 112, 159, 243, 257, 311, 487,
635, 707
Vulpian, 929
WAOHSMnTH, 560
Wagstaffe, 700
Waldenburg, L., 30
Waller, 810 (note), 833, 847, 938
Walshe, W. H., 13 et seq., 53 et seq., 171
316, 504, 939
Warfvinge, 489
Warner, F., 984
Washbourn, 116
Watson, T., 121, 502, 814, 937
Weber, E. H., 476
Weber, H., 311, 846, 921
Weber, Parkes, 909, 927
Weichselbaum, 113, 366
Weigert, 174, 562
Weismayer, 945
Welch, W. H., 311
Wertheim, 477
West, C, 861
West, S., 27, 212, 759, 777, 779, 900, 927
Westphal, 647
Wheaton, 258
White, Hale, 105, 522, 948
Whitelegge, 109
Widal 257 458
Wilks,' S., 318, 521, 797, 901, 914, 101'
Willan, 581
Williams, C. J. B., 63, 99, 222. 298
Williams, C. T., 167 et seq., 282, 294
I04S
SYSTEM OF MEDICINE
Williams, Roger, 163
Williams, Watson, 824
Williamson, E. T., 448 541
Willigk, 62, 899
Wilson, 698
Winckel, 626
Wintricli, 205, 298, 467
Wolfenden, 239
Wollaston, 467
Wood, H. C, 830
Woods, 522
Wright, A. E., 237, 447 et seq., 584
Wunderlich, 31
Zaleski, 496
Zander, 488, 998
Ziehl, 196
Zuckerkaiidl, 3
Zuntz, 448, 847
Zwaardemaker, 477
INDEX
Abscess in the thoracic walls, diagnosis from
pleurisy, 371
Abscess, pleural, 357
Abscess, subphrenic, diagnosis from pleurisy,
370
Achlorhydria in pernicious ansemia, 529
Actinomycosis of ba«e of the lung, diagnosis
from pleurisy, 369
Albumin in cedema fluid, 667
Albuminuria in purpura, 574
Albumose in clotting of blood, 404
Alimentary canal in leiicooythaemia, 645,
656 ; in pericardial adhesion, 788 ; in
phthisis, 214
Alkalinity of the blood, estimation of, 447 ;
method of Haycraft and Williamson, 448 ;
of Wright, 449
Altitude, influence on phthisis, 157
Amenorrhcea in chlorosis, 609 ; in pul-
monary tuberculosis, 220
Anaemia and mitral stenosis, 1034 ; as cause
of disease of the myocardium, 886 ; as
cause of dropsy, 680, 688 ; as cause of
mitral insufiicienoy, 1002 ; in purpura,
576 ; specific gravity of blood in, 429
An£emia^ encephalic, as cause of fainting,
839
Anaemia, myelogenic, 533
Anaemia, pernicious, 519 ; age in, 525 ;
bibliography, 538 ; definition, 519, 531 ;
diagnosis, 534 ; diagnosis from scurvy,
601 ; etiology, 522 ; favouring conditions,
523 ; history, 520 ; morbid anatomy, 530 ;
pathology, 631 ; prognosis, 535 ; signs,
527 ; specific gravity of blood in, 429 ;
symptoms, 625 ; treatment, 536
Anaemia, splenic, 539 ; age and sex in, 542 ;
bibliography, 548 ; case, 540 ; complica-
tions, 646 ; diagnosis, 547 ; diagnosis
from pernicious anaemia, 536 ; diagnosis
from scurvy, 601 ; duration, 547 ; morbid
anatomy, 545 ; pathogeny, 546 ; prognosis,
547 ; symptoms and signs, 539 ; treat-
ment, 548
Aneurysm, cardiac, 899
Aneurysms in phthisis, 184
Angina pectoris, 891
Anthracosis, 248
Aorta, congenital atresia or stenosis of, 706,
720 ; stenosis, 923 ; diameter o^ com-
pared with renal artery, 476 ; elasticity
of, 477 ; hypoplasia of, 707 ; transposition
or malposition, 708, 720
Aortic area of the heart, disease of, 907 ;
bibliography, 966 ; causation, 908 ; patho-
geny and morbid anatomy, 915 ; regurgi-
tation, 936 ; stenosis, 927 ; sub-valvular
constriction, 919
Aortic insnfliciency, 921, 936 ; death in,
955 ; murmur of, 943 ; diagnosis from
murmur of mitral disease, 946, 1024 ; as
cause of cardiac dropsy, 684
Aortic spindle, 707
Apex beat in pericardial adhesion, 790
Apoplexia neonatorum, 567
Appetite in chlorosis, 485, 499
Arteries in phthisis, 184
" Arteriopathy," 918
Arterio-sclerosis and mitral stenosis, 1035
Ascites, 677 ; causes of, 678
Aspergillosis, pulmonary, 257 ; bibliography,
263 ; diagnosis, 261 ; etiology, 268 ;
morbid anatomy, 260 ; primary form,
259 ; prognosis, 262 ; secondary form,
262 ; treatment, 262
Asthma, 286 ; age in, 292 ; bibliography,
310; diagnosis, 301; etiology, 292;
heredity in, 292 ; immediate causes, 293 ;
morbid anatomy, 295 ; pathogeny, 297 ;
prognosis, 309 ; results, 295 ; sex in, 292 ;
symptoms, 287 ; treatment, 302
Atheroma as cause of aortic disease, 910
Auricle, left, in mitral stenosis, 1009
Baths for bronchiectasis, 88 ; in treatment
of mitral insufiiciency, 999
Baths, compressed air, for emphysema,
282
Beriberi, diagnosis from scurvy, 600
" Bleeders," 549
Blnoil, alkalinity of, 447 ; coagulation time
of, 451 ; oxidising activity of, in chlorosis.
loso
SYSTEM OF MEDICINE
498 (note); spectroscopic examination of,
454 ; viscosity coefficient of, 475
Blood, clinical examination of, 408 ; biblio-
graphy, 462 ; blood crystals, 459 ; colour
curves (figs.), 431 ; determination of co-
agulation time, 451 ; of isotonic coefficient,
461 ; of viscosity coefficient, 461 ; enumera-
tion of corpuscles, 440, 461 ; estimation
of colouring matter, 430 ; of reaction, 447 ;
of specific gravity, 424 ; of specific gravity
in shook, 430 ; in various diseases, 429 ;
examination for parasites, 456 ; histological
examination, 410 ; of red corpuscles, 413 ;
of white corpuscles, 415 ; microscopic
techniijue, 409 ; spectroscopic examination,
454
Blood, general pathology of, 391 ; changes
effected by the tissues, 395 ; changes in
blood during circulation, 398 ; clotting,
403 ; corpuscles, red, 399 ; white, 401 ;
reaction, 393 ; specific gravity, 394 ;
volume or quantity, 393
Blood in congenital heart disease, 722 ; in
diabetes, 413 ; in infective endocarditis,
883 ; in leucooythsemia, 637, 654 ; in
paroxysmal hsemoglobinuria, 629 ; in per-
nicious ansemia, 527 ; in purpura, 570 ;
in scurvy, 597 ; in splenic anaemia,
542
Blood parasites, examination for, 456
Blood - plates, 405; in spleno - medullary
leucOcythsemia, 640
Blood, specific gravity of, 394 ; estimation of,
424 ; in chlorosis, 483 ; charts of, 493 ;
in shock, 430 ; in various diseases, 429 ;
method of Hayoraft, 426 ; of Hammer-
schlag, 425 ; of Roy, 424 ; of Schmaltz,
427
Bone^marrow in .leucocythaemia, 641, 656 ;
in pernicious ansemia, 531
Bones in infantile scurvy, 611
Bradycardia, 832
Brain, abscess of, secondary to empyema,
363
Brain in phthisis, 221
Bright's disease, acute endocarditis in, 864
Bronchi in emphysema of the lungs, 273
Bronchi, secretion in bronchiectasis, 61
Bronchial catarrh, chronic, 19 ; relation to
pleurisy, 25 ; with pleuritic adhesions, 26
Bronchial glands in syphilitic disease of the
lungs, 321
Bronchial lymphatics, 3
Bronchial mucosa in bronchiectasis, 60
Bronchial tubes, anatomy, 1 ; parasitic
affections, 24
Bronchiectasis, 53 ; age in, 79 ; biblio-
graphy, 89 ; congenital, 58 ; cystic, 61 ;
diagnosis, 76 ; general and clinical etio-
logy, 62 ; hypotheses, 65 ; in phthisis,
181 ; morbid anatomy, 58 ; physical
examination of the chest, 74 ; prognosis,
78 ; symptoms, 71 ; treatment, 79 ;
climatic, 87 ; of complications, 80 ; sur-
gical, 87
Bronchiectasis, capillary, 54 ; acute form,
55 ; chronic, 54 ; treatment, 57
Bronchiolectasis, 17, 54
Bronchitis, 1 ; acute gouty, 43 ; acute
suffocative of adults, 13 ; treatment of,
39 ; bibliography, 49 ; capillary of infancy
and old age, 16 ; treatujent of, 41 ;
chronic, 19 ; treatment of, 43 ; classifica-
tion, 4 ; dry chronic, 21 ; intercurrent, 21 ;
mechanical, 24 ; parasitic, 24 ; plastic,
27 ; treatment of, 31 ; prophylaxis, 47 ;
putrid, 33 ; relation to pleurisy, 25 ;
secondary and special varieties, 21 ; symp-
tomatic, 43 ; treatment, 36
Bronchitis, paroxysmal, of children, in
asthma, 290
Bronchitis, simple, 5 ; acute catarrhal, 8 ;
causes, immediate, 6 ; remote, 5 ; chronic,
• 9 ; etiology, 5 ; of larger tubes, 10, 37 ;
pathological anatomy, 8 ; physical signs,
9 ; treatment, 36
Broncho-pneumonia, acute, 17, 140 ; chronic,
150
Bronchorrhcea, 19 ; purulent, 20
Bruit de diable in chlorosis, 502
" Button - hole " form of mitral stenosis,
1008
Byssinosis, 248
CALcnu, "cardiac," 731 ; pulmonary, 193
Cardiac disease, specific gravity of blood in,
429
Cardiac dulness, area of, in acute peri-
carditis, 762 (figs.), 760
Cardiac physics, 464 ; bibliography, 478 ;
mass movements, 468 ; sounds, 467 ;
valves, 464
"Cardiopathy," 918
Cardio-pulmonary murmurs, 977, 1002
Carditis, 733
Caseous glands in phthisis, 218
Cat asthma, 293
Catarrh, dry, 21 ; influence on bronchiectasis,
70
Cephalhsematoma, 556
Charcot - Leyden crystals, 296 ; in blood,
460 ; in leucocythasmia, 647
Chemiotaxis, 401
Chest, change of form after empyema, 362 ;
in emphysema of the lungs, 275 ; physical
examination in bronchiectasis, 74 ; shape
and size in bronchitis, 9
Chlorate of potash as cause of hsemo-
globinuria, 625
Chlorosis, 479 ; age in, 484 ; bibliography,
517 ; Bunge's hypothesis, 488 ; causation,
482 ; conditions of life, 485 ; definition,
482; diagnosis, 511; "febrile," 500;
heredity In, 483 ; hysterical, 500 ; patho-
logy, 492 ; prognosis, 512 ; race and
climate, 484 ; sex in, 483 ; symptoms,
INDEX
1051
481, 497 ; toxic causes, 489 ; treatment,
513
Chlorosis and mitral stenosis, 1034 ; and
renal dropsy, 688 ; diagnosis from per-
nicious anaemia, 535 ; specific gravity of
Wood in, 429
Chorea, acute endocarditis in, 862 ; mitral
regurgitation in, 993 ; specific gravity of
Wood in, 429
Circulatory system, diseases of, 389
Circulatory system, in chlorosis, 500 ; in
leuoocythaemia, 657 ; in pernicious anaemia,
527 ; in phthisis, 214
Cirrhosis of the liver, as cause of ascites, 678 ;
specific gravity of blood in, 429
Cirrhosis, pulmonary, see Pneumonia, chronic,
149 ; diagnosis from chronic phtliisis, 153
Climate, in asthma, 304 ; in phthisis, 156,
233
Clubbing of fingers, in congenital morbus
cordis, 723 ; in empyema, 364
Coagulation-time of blood, determination of,
451 ; method of Brodie and BusseU, 453 ;
of Wright, 452
•Compensation in mitral regurgitation, 975
" Complementary emphysema, " 337
Complexion in chlorosis, 498
Compressed-air bath for emphysema, 282
Congenital syphilis and pulmonary tuber-
culosis, 313
Congenital wry-neck, 559
Constipation in chlorosis, 489, 499 ; treat-
ment, 516
Coronary arteries, embolism o^ 899 ; throm-
bosis of, 900
Coronary arteries in disease of the myo-
cardium, 888
Cough, as cause of emphysemei, 265 ; in
aortic regurgitation, 951 ; in bronchi-
ectasis, 69, 73 ; in chronic pulmonary
tuberculosis, 192 ; treatment of, 234 ; in
pleurisy, 350 ; in syphilitic disease of the
lungs, 329
Creasote treatment for bronchiectasis, 84
Cyanosis in congenital malformation of the
heart, 721
Death, sudden, after paracentesis thoracis,
377
Deformity of chest after empyema, 362 ;
treatment, 377
Dehydration by diet, in dropsy, 690
Dextro-cardia, 712
Diabetes, as cause of dropsy, 680 ; specific
gravity of blood in, 429
Diaphragm, displacement o^ in pleurisy, 354
Diarrhcea and scurvy, 598 ; in phthisis, 216 ;
treatment of, 240 ; in pleurisy, 351
Diastolic shock or concussion, in pericardial
adhesion, 792
Diet, bearing of, on chlorosis, 496, 517 ; in
asthma, 305 ; in dropsy, 690 ; in infantile
scurvy, 614, 619 ; in scurvy, 590, 603
Digestive system in chlorosis, 499 ; in pur-
pura, 574 ; in splenic anaemia, 543
Digitalis in aortic insufficiency, 960 ; in
mitral iusufliciency, 989 ; in mitral steno-
sis, 1032
Dilatation of left ventricle as cause of mitral
iusufliciency, 995
Diverticula of the pericardium, 729
Dropsy, 666 ; bibliography, 693 ; cardiac,
683 ; causes, 680 ; constituents of liquid,
668 ; diabetic, 673, 689 ; general, 679 ;
general pathology, 666 ; local, 677 ; of
venous obstruction, 669, 674 ; renal, 672,
685 ; treatment, 689 ; various forms, 674 ;
see also (Edema
Dropsy, and pleurisy, 363 ; and scurvy, 598 ;
in leucooythaemia, 658 ; in mitral iu-
sufliciency, 987 ; treatment of, 992 ; in
mitral stenosis, 1028 ; general, in peri-
cardial adhesion, 788
Drugs, in aortic regurgitation, 959 ; in
asthma, 305 ; in mitral insufficiency, 990
Ductus arteriosus, stenosis at, 707 ; prema-
ture closure, 710
Duroziez, sign of, 941
"Dusty-lung disease," see Pneumoconiosis
242
Dysentery, specific gravity of blood in, 429
Dyspepsia, as cause of chlorosis, 485 ; in
phthisis, 215 ; treatment of, 239
Dysphagia, in acute pericarditis, 751
Dyspnoea, in aortic regurgitation, 951 ; in
aortic stenosis, 933 ; in bronchiectasis, 73 ;
in large-lunged emphysema, 274 ; in peri-
cardial adhesion, 787 ; in pernicious
anaemia, 528 ; in phthisis, 198, 225 ;
treatment of, 234 ; in pleurisy, 350 ; in
pneumoconiosis, 246 ; in pneumothorax,
381 ; in syphilitic disease of the lungs, 329
Bak, affections of, in leucooythaemia, 646
Ectopia cordis, 712
Efiusion in acute pericarditis, 740 ; effect on
action of the heart, 745 ; on heart and
great vessels, 742 ; on heart sounds, 766 ;
on neighbouring structures, 745 ; on peri-
cardium, 741 ; on shape of chest, 758 ; on
the impulse and apex beat, 759 ; mode of
collection, 743 ; position of heart in, 743
Effusions in pleurisy, absorption of, 359 ;
chylous, 357 ; haemorrhagic, 357 ; kinds
of, 356 ; liquid, 352 ; purulent, 356, 365 ;
serous, 349, 356
Elastic tissue in sputum of phthisis, 194
Electric currents of high pressure, injuries
by, 855 ; bibliography, 860 ; cause of
death, 858 ; morbid anatomy, 859 ; treat-
ment, 859
Emaciation in phthisis, 200, 225 ; in
syphilitic disease of the lungs, 330
Embolism, after paracentesis thoracis, 377 ;
in infective endocarditis, 878, 880 ; in
mitral stenosis, 1013 ; of coronary
I052
SYSTEM OF MEDICINE
arteries, 899 ; pulmonary, in phthisis,
214
Emotion as cause of chlorosis, 486
Emphysema of the lungs, 263 ; acute vesi-
cular, 272 ; symptoms of, 279 ; biblio-
graphy, 286 ; diagnosis from pneumo-
thorax, 383 ; etiology, 267 ; hypotheses,
264 ; in phthisis, 181 ; interlobular or
interstitial, 285 ; large-lunged form, 269 ;
diagnosis of, 279 ; symptoms of, 274 ;
lesions, 272 ; local or compensatory, 271 ;
symptoms of, 278 ; morbid anatomy, 269 ;
pathogeny, 264 ; physical examination,
275 ; prognosis, 280 ; small-lunged form,
271 ; symptoms of, 278 ; treatment, 280 ;
varieties, 269
Empyema, 360 ; diagnosis from bronchiec-
tasis, 77 ; in advanced phthisis, 238 ;
incurable, 361 ; loculated, 357, 361 ;
pulsating, 358 ; rupture of, 360 ; treat-
ment, 374
Empyema after pneumonia, 124 ; diagnosis
from broncho -pneumonia in children,
147 ; from pulmonary cirrhosis, 154 ; in
children, 145
Endocarditis, acute simple, 860 ; age in,
865 ; bibliography, 875 ; causation, 861 ;
complications, 870 ; course and termina-
tion, 871 ; diagnosis, 871 ; fcetal, 865 ;
idiopathic, 865 ; physical signs, 868 ;
prognosis, 873 ; symptoms, 868 ; treat-
ment, 873
Endocarditis, foetal, as cause of cardiac
malformation, 713
Endocarditis, infective, 876 ; bibliograpliy,
885 ; complications, 881 ; diagnosis, 882 ;
pathological anatomy, 876 ; prognosis,
884 ; symptoms, 878 j treatment, 884 ;
types, 878
Enteric fever, diagnosis from infective endo-
carditis, 882 ; from pneumonia, 148
Epistaxis in mitral stenosis, 1027
Epithelioid lining of blood-vessels in clotting
of blood, 404
"Epithelioma" of the lung in congenital
syphilis, 312
Erythrocytes, 413 ; nucleated, 415
Ether bronchitis, 7
Exhaustion as cause of slow pulse, 835
Expectoration, in bronchiectasis, 73 ; in
large-lunged emphysema, 274 ; in phthisis,
225 ; treatment of, 235 ; in pleurisy, 350;
in syphilitic disease of the lungs, 330 ;
serous, after paracentesis, 351, 376
Expiration, mechanically aided, in suffoca-
tive bronchitis, 40
Eye, aifections of, in leucocytheemia, 646,
660
Fainting, 838
Fatly heart, 887, 893
Fibrin-ferment in clotting of blood, 403
" Fibroid phthisis," 163
Fibrosis in phthisis pulmonalis, 182
Films, examination of blood, 41 1
Fingers, clubbing of, in cirrhosis of the lung,
152 ; in congenital morbus cordis, 723 ;
in empyema, 364 ; in phthisis, 202
"First rib sign" in acute pericarditis,
758
Fistula in ano in phthisis, 217
Foramen ovale in congenital malformation
of the heart, 699 ; development of, 715 ;
premature closure, 710
" Funnel " form of mitral stenosis, 1008
Ganorene of the bronchi, 60 ; of the lungs
in scurvy, 598 ; in phthisis, 184 ; in
pleurisy, 362
Garlic in treatment of bronchiectasis, 82
Gas of pneumothorax, 380
Gastric ulcer, specific gravity of blood in,
429
Gastro - intestinal system in pernicious
anaemia, 528
Generative organs in chlorosis, 486
Genito-urinary system in chlorosis, 509
Glands in phthisis, 186, 211
Globulinuria, paroxysmal, and haemoglobi-
nuria, 631
Gout and acute endocarditis, 864.
Graves' disease and chlorosis, 491 ; dia-
gnosis from tachycardia, 830 ; mitral
insufficiency in, 1004 ; treatment of, 1005
Gravity, force of, influence on heart, 478
Gumma in syphilitic disease of the lungs,
313, 316, 319
Gums in infantile scurvy, 607 ; in scurvy,
593
HiBMATOIDIN, 460
Hsematnria, diagnosis from hsemoglobinuria,
622 ; in infantile scurvy, 607
Hsemooytometer, of Gowers, 442 ; of Thoma-
Zeiss, 444
Haemoglobin, 460 ; absorption spectra of,
455 ; clinical examination of, 432 ; func-
tion, 399
Hsemoglobinometer, of Gowers, 437 ; of
Oliver, 432 ; of von Fleischl, 439
Hsemoglobinuria, 621 ; bibliography, 634 ;
causation, 621 ; urine in, 622 ; infantile,
626 ; morbid anatomy, 625 ; paroxysmal,
627 ; pathology, 624 ; specific gravity of
blood in, 429 ; toxic, 624 ; treatment,
633 ; urine in, 622
Haemolysis, 401 ; in pernicious anaemia,
532
Haemo-perioardium, 800
Haemophilia, 548 ; bibliography, 555 ;
diagnosis, 553 ; etiology, 549 ; heredity
in, 549 ; morbid anatomy, 552 ; pro-
droma, 550 ; prognosis, 553 ; sex in, 553 ;
symptoms, 549 ; treatment, 554
Haemoptysis after paracentesis, 376 ; in
bronchiectasis, 74 ; in large-lunged em-
INDEX
I0S3
physema, 275 ; in mitral stenosis, 1027 ;
in phthisis, 196 ; treatment of, 236
Haemorrhage, as cause of chlorosis, 487 ;
from pleuritic membranes, after paracen-
tesis, 376 ; in pernicious ansemia, 528, 533
Haemorrhage, umbilical, in new-born children,
550 ; diagnosis from haemophilia, 553 ;
spontaneous, 561
Hemorrhages in infective endocarditis, 881,
883 ; in leucocythaemia, 646, 658 ; in
purpura, 574 ; in splenic anaemia, 543
Haemorrhages in new-born children, 556 ;
bibliography, 567 ; cephalhaeraatoma,
556 ; clinical features, 558, 560, 566 ;
etiology, 557, 563, 566 ; from female
genitals, 562 ; gastvo - intestinal, 561 ;
haematoma of the sterno-mastoid, 559 ;
idiopathic cases, 560 ; into abdominal and
thoracic viscera, 560 ; intritcranial, 557 ;
morbid anatomy, 558, 562 ; spontaneous,
560 ; subcutaneous ecohymoses, 562 ;
traumatic, 556
Hair in phthisis, 201
Hay fever, 286 ; treatment, 307
Heart, aneurysm of, 899 ; atrophy of, 901
Heart, bifid apex, 712
Heart, congenital malformation of, 697 ;
anomalous septa, 711 ; atresia or stenosis
of the aorta, 706 ; bibliography, 726 ;
defects in septa, 698, 717 ; differential
diagnosis, 724 ; duration of life, 724 ;
irregularities in number and form of
valves, 710 ; misplacements of the heart,
712 ; premature closure, or patency of
fcetal passages, 710 ; stenosis or atresia of
the pulmonary artery, 703, 718 ; symptoms
and physical signs, 721 ; transposition or
malposition of aorta and pulmonary artery,
708, 720 ; treatment, 725
Heart, degeneration, hyaline, 887 ; degenera-
tion, pigmentary, 901 ; deterioration in
chlorosis, 497, 501 ; development, 714 ;
dilatation after pleurisy, 363 ; displace-
ment in phthisis, 207 ; displacement in
pleurisy, 354
Heait disease and phthisis, 164
Heart, diseases of, 695
Heart, fatty, 887, 889 ; repair, 887, 890 ;
symptoms and signs, 891 ; treatment, 892
Heart, fibroid infiltration of, 895 ; causes,
895 ; diagnosis, 898 ; pathology, 896 ;
symptoms and signs, 897 ; treatment, 999
Heart, functional disorders o^ 807 ; biblio-
graphy, 840 ; bradycardia, 833 ; cardiac
asthenia, 820 ; irritable heart, 821 ;
murmurs, 816 ; neurotic element in, 823 ;
palpitation, 816 ; rate, 812 ; rhythm,
813 ; syncope, 839 ; tachycardia, 824 ;
tone, 810 ; weak heart, 818
Heart in aortic regurgitation, 942 ; in
chronic pericarditis, 783 ; in emphysema
of the lungs, 273 ; in leucocythaemia,
645 ; in mitral stenosis, 1013
Heart, mass movements of, 468 ; filling of,
468 ; influence of force of gravity on,
478 ; peripheral resistance to, 474 ; worlt
of, 470
Heart, mechanical strain of, 841 ; causation,
849 ; muscular exercise, 844 ; soldier's
heart, 851 ; stress, 843
Heart pressure, intra-auricular, 468 ; intra-
ventricular, 469
Heart, valvular disease of, as cause of
general dropsy, 680 ; various diseases of,
as causes of general dropsy, 680
Heart wall, syphilitic disease of, 904
Hemiplegia in pleurisy, 364
Hepatisation, chronic lobar, 150 ; pneu-
■ monia, stages of, 109 ; site of, 110, 132
Heredity in chlorosis, 483 ; in haemophilia,
549 ; in phthisis, 171
Herpes labialis in pneumonia, 93, 134
Hip disease, specific gravity of blood in
429
Hyaline leucocytes, 417
Hydatid cyst, diagnosis from pleurisy, 369
Hydrsemia as cause of dropsy, 689
Hydrarthrosis in scurvy, 598
Hydrocephalus, chronic, 674 ; treatment,
676
Hydropericardium, 798; bibliography, 806;
clinical history, 799 ; treatment, 800
Hydropneumopericardium, 802
Hydrops pericardii, 798
Hydrothorax in scurvy, 598
Hypoleuoocytosis, 420
Hypoplasia in chlorosis, 487
Impulse in pericardial adhesion, 790
Infarcts in acute endocarditis, 870 ; in in-
fective endocarditis, 880
Infection, septic, of whole body, in pleurisy,
351
Infectious diseases as cause of aortic disease,
908
Interlobular or interstitial emphysema, 285
Interstitial pneumonia in congenital syphilis,
312
Intestinal parasites, anaemias due to, dia-
gnosis from pernicious anaemia, 535
Intestinal system in leucocythaemia, 657
Intestines in mitral insufficiency, 974 ; in
phthisis, 216 ; treatment of, 239
Intrapleural tension, 335 ; bibliography,
346 ; in empyema, 346 ; in pneumothorax,
339, 380 ; in serous effusion, 343
Intratracheal injection for bronchiectasis, 83
Iron in treatment of chlorosis, 513
Jaundice and haemorrhages in new-bom
children, 5P5
Joints, affection of, in haemophilia, 552 ;
treatment, 555
KrDNET disease as cause of dropsy, 680
I0S4
SYSTEM OF MEDICINE
Kidneys in emphysema of the Inngs, 274 ;
in leuoocythsemia, 644 ; in mitral in-
sufficiency, 974 ; renal lesions in phthisisj
219 ; treatment of, 241
L&BDACEOUS disease as cause of dropsyi 680,
688 ; diie to emphysema, 364 ; of kidneys
in phthisis, 219
Laryngeal tuberculosis in phthisis, 210 ;
treatment, 238
Leucocytes, 401, 415 ; in chronic leuco-
cythtemia, 654 ; in spleno-mednHary leuco-
cythsemia, 637
Leucocythsemia, 635 ; acute form, 654 ;
bibliography, 665 ; chronic form, 652 ;
conditions of occurrence, 648 ; diagnosis,
661 ; diagnosis from scurvy, 601 ;
hereditary influences, 649 ; introduc-
tory, 635 ; lymphatic form, 639, 650 ;
morbid anatomy, 640 ; nature and etio-
logy, 650 ; pathological anatomy, 637 ;
pathological chemistry, 646 ; prognosis,
662 ; remoter causes, 649 ; specific gravity
of blood in, 429 ; spleno-meduUary form,
637, 650 ; symptoms, 652 ; the blood,
637 ; treatment, 663 ; varieties, 636
Leucocytosis, 418 ; diagnosis from leuoo-
cythsemia, 661 ; inflammatory, 420 ; in
prognosis, 423 ; in the new-bom, 418 ;
of cachexia and of malignant diseases,
421 ; of certain infections, 420 ; of
digestion, 419 ; of pregnancy, 419 ;
pathological, 419 ; physiological, 418 ;
post-hsemorrhagic, 422 ; "terminal," 422 ;
toxic, 420
Leucolysis, 422
Leukaemia, see Leucocythsemia, 635
Liver, in emphysema of the lungs, 273 ; in
infective endocarditis, 881 ; in leuco-
cythsemia, 643, 657 ; in mitral insufficiency,
973 ; in pericardial adhesion, 788 ; in
phthisis, 217 ; in splenic anaemia, 543,
•545
Lung, collapse of, in pleurisy, 362, 367 ;
cirrhosis of, 71 ; hypertrophy of, 181
Lungs, disease of, as cause of general dropsy,
680
Lungs, elasticity of, 335 ; in pneumonia,
338 ; in pneumothorax, 337
Lungs, in leucocythaemia, 645 ; in mitral
insufficiency, 973; in mitral stenosis, 1011
Lungs, over-distension of, in emphysema,
266 ; lesions in emphysema, 272 ; normal
anatonjy of a pulmonary lobule, 268
Lungs, tubercle of, in pleurisy, 348, 362
Lymphadenoma, diagnosis from leuco-
cythiemia, 661 ; specific gravity of blood
in, 429
Lymphaemia, 635
Lymphatic glands in leuoocythsemia, 642,
655
Lymphatic pump," the, 343
Lymphocytes, 417
Lymphocythsemia, 636
Lymphodermia pemiciosa in leucocythsemia,
659
Maoeoctth^mia, 414
Malarial fever and asthma, 294
Malignant tumour of the Jung, diagnosis
from pleurisy, 369.
Marriage and phthisis, 229
Marrow of bone in leuoocythsemia, 641, 656 ;
in pernicious anaemia, 531, 533
Mediastinitis, chronic, 783
Mediastino- pericarditis, 747 ; indurative,
783
Mediastinum, displacement of, in pleurisy,
353
Megaloblasts, 415
Melaena neonatorum, 561 ; spurious, 564
" Melalgia " in phthisis, 221
Meningitis in phthisis, 221
Menstruation in phthisis, 161, 220
Mesentery, retraction of, in phthisis, 218
Mesocardia, 712
Microcythsemia, 414
Milk-spots, 729, 746
Mitral insufficiency, 968 ; Ijibliography,
1006 ; clinical groups of, 983 ; estimation
of degree, 980 ; from anasmia, 1002 ; in
chorea, 993 ; in Graves' disease and
allied afl'eotions, 1004 ; morbid anatomy,
968 ; due to dilatation of left ventricle,
995 ; from rheumatic endocarditis,
968, 983 ; treatment, 986, 988, 996,
1003
Mitral stenosis, 1007 ; age in, 1008 ; as
cause of dropsy, 683 ; due to rheumatism,
1025 ; in chronic renal disease and arterio-
sclerosis, 1035 ; associated with disorders
of nutrition, 1034 ; with nervous symp-
toms, 1032 ; bibliography, 1038 ; cardio-
graphic evidence, 1021 ; clinical gioups,
1025 ; diagnosis and signs, 1016 ; morbid
anatomy, 1007 ; sex in, 1028 ; some
difficulties in diagnosis, 1024 ; sphygmo-
graphic evidence, 1023 ; treatment, 1029,
1035, 1037 ; working of the heart in,
1013
Mitral valve, diseases of, 968 ; bibliography,
1006, 1038 ; insufficiency, 968 ; stenosis,
1007
Mitral valve, rapture o^ producing in-
sufficiency, 969
Moisture, influence on phthisis, 157
Morbus caeruleus, 697, 721
Murmurs in chlorosis, causation of, 506 ;
aortic, 506 ; apical, 506 ; cardio-arterial,
503 ; pericardial, 755 ; pulmonary, 504 ;
figs., 505 ; venous, 501
Muscular affections in chlorosis, 499
Muscular effort as cause of emphysema of the
lungs, 265
Muscular exercise in treatment of mitral
in.sufficieuoy, 998
INDEX
1055
Muscular strain as cause of aortic disease,
912
Muscular system in mechanical strain of the
heart, 846
Myelsemia, 636
Myelocytes, 417
Myocarditis in acute endocarditis, 870
Myocarditis, interstitial, 895, 903 ; paren-
chymatous, 904 ; puruleut, 904 ; syphi-
litic, 904
Myocardium, diseases of, 885 ; bibliography,
906 ; changes in, in mitral regurgitation,
975 ; cloudy swelling, 887 ; growths,
906 ; impairment, arising from functional
strain, 901 ; due to senile changes, 901 ;
of inflammatory origin, 903 ; parasites,
906 ; secondary to altered blood-supply,
888 ; secondary to general blood condi-
tions, 886 ; tumours, 906
Myomalacia cordis in leucocythsemia, 645
Myxoedema, specilic gravity of blood in, 429
Nbphkitis, in pleurisy, 363 ; specific gravity
of blood in, 429
Nervo-musoular system in chlorosis, 510
Nervous shock as cause of aoi'tio disease,
914
Nervous system, in acute pericarditis, 752 ;
in aortic regurgitation, 950 ; in leuco-
cythaemia, 660 ; in mitral stenosis, 1032 ;
in pernicious anaemia, 529 ; in phthisis,
221 ; treatment of, 241 ; in pneumonia,
96
Neuralgias in chlorosis, 510
New-born children, hsemorrhagio disease of,
560
Night-blindness in scurvy, 596
" Nummular sputum " in phthisis, 193
Nutrition in aortic regurgitation, 951
Occupation in treatment of phthisis, 229
(Edema, in chlorosis, 508 ; in pernicious
anaemia, 526 ; see. also Dropsy, 666
Oligsemia, 483
Oligocythaemia, 414 ; in pernicious anaemia,
627
Optic neuritis in chlorosis, 510
Osseous system in phthisis, 221
Oxyhaemoglobin, absorption spectra of, 455
Oxyphil leucocytes, 416
Pain, in acute pericarditis, 748 ; in aortic
regurgitation, 949 ; in aortic stenosis,
933 ; in pericardial adhesion, 787 ; in
pleurisy, 350
Palpitation in pericardial adhesion, 787
Paracentesis in pleurisy, 372 ; dangers of,
376 ; in pneumothorax, 385 ; pericardii,
775
Parasites of the myocardium, 906
Peliosis rheumatica, 577
Peribronchitis, 1
Pericardial adhesions and thickening, 780 ;
exo-pericardial, 782 ; pericardial, 780 ;
fibrosis, 781
Pericardial effusion, chronic, 779
Pericardial friction, 754
Pericardial murmur or friction sound, 755 ;
tests for, 756
Pericarditis, acute fibrinous and sero-fib-
rinous, 732 ; absorption, 746 ; adhesions,
747 ; age and sex in rheumatic, 733 ;
associated with miscellaneous general
diseases and blood-states, 737 ; associated
with new growths, 737 ; bacteriology,
738 ; bibliography, 806 ; clinical histoi-y,
748 ; course and termination, 769 ; dia-
gnosis, 770 ; discussion of symptoms, 748 ;
disorders of cardiac action in, 750 ; dry
form, 740 ; effects of change of posture,
767 ; etiology and pathology, 732 ; from
exhaustion or irritation, 736 ; morbid
anatomy, 738 ; physical signs, 753 ; pro-
gnosis, 772 ; renal, 735 ; rheumatic, 732 ;
secondary to cardiac or aortic disease,
737 ; septic, 737 ; signs connected with
neighbouring structures, 766 ; signs in
stage of effusion, 757 ; stage of absoi-ption,
.768; stages, 738; traumatic and per-
forative, 736 ; treatment, 773
Pericarditis, in pleurisy, 363 ; in scurvy,
598 ; in acute endocarditis, 870 ; in
phthisis, 214
Pericarditis, chronic, 779 ; anatomical char-
acters and efiecl-s, 781 ; bibliography,
806 ; clinical history, 786 ; diagnosis,
796 ; etiology, 780 ; physical signs, 789 ;
prognosis, 797 ; treatment, 797
Pericarditis, suppurative, 776 ; anatomical
characters, 777 ; clinical history, 778 ;
etiology and pathology, 776 ; treatment,
779
Pericardium, adherent, 780 ; blood in, 800 ;
carcinoma of, 805 ; deficiency of, 713,
729 ; diseases of, 726 ; dropsy of, 798 ;
gas in, 801 ; hydatids of, 805 ; morbid
growths, 804 ; tubercle, 804
Pericardium, parasites of, 804 ; bibliography,
806 ; treatment, 805
Pericardium, the normal, 726 ; acute in-
flammation of, 732 ; calcareous deposit in,
731 ; congenital defect in, 729 ; foreign
bodies in, 731 ; morbid conditions, 728 ;
stretching or distension, 729
Peri-endocarditis, 733
Peripneumonia notha, 1, 16
Peritonitis, acute, in leucocythEemia, 657 ;
in pleurisy, 363 ; tuberculous, specific
gravity of blood in, 429
Petechise in purpura, 585
Phlebitis in chlorosis, 509
Phosphaturia in phthisis, 220
Phthisis pulmonalis, 156 ; age in, 160 ;
anomalous localisation of physical signs,
208 ; bibliography, 242 ; complications,
210 ; contagion, 170 ; course, 222 ; dia-
ios6
SYSTEM UF MEDICINE
gnosis, 209 ; diagnosis from bronctiectasis,
77 ; eniphysematous form, 207 ; etiology,
156 ; heredity in, 171 ; histogenesis, 179 ;
house infection in, 169 ; infection, 16S ;
irregular forms, 207 ; laryngeal form,
209 ; mode of extension, 183 ; patho-
logical anatomy, 175 ; physical diagnosis,
202 ; pleuritic form, 207 ; prognosis,
224 ; sex in (tables), 160, 170 ; socio-
logical causes, 158 ; symptomatology,
186 ; treatment, 228
Physiognomy, characteristic of emphysema
of the lungs, 275
Pigmentation, in phthisis, 181 ; in pneumo-
coniosis, 247
Pityriasis tabescentium in phthisis, 201
Plasma, specific gravity of, 428
Pleura, diseases of, 333 ; perforation in
phthisis, 212
Pleural abscess, 357
Pleural cavity, inflammatory effusion in, and
scurvy, 598 ; tension in, 335
Pleurisy, 346 ; age and sex in, 347 ; as-
sociated diseases, 362 ; bacteriology, 347 ;
bibliography, 377 ; course and termina-
tion, 359 ; diagnosis, 367 ; etiology, 347 ;
latent, 349, 352 ; morbid anatomy, 364 ;
pathogeny, 365 ; prognosis, 371 ; signs,
362 ; sudden death in, 371 ; symptoms,
349 ; treatment, 372 ; with and without
effusion, 352
Pleurisy in phthisis, 185, 213 ; treatment
of, 237 ; in acute endocarditis, 870
Pleuro-bronohitis, acute, 25
Pleuro-pericarditis, 747
Pleuro-pneumonic fibrosis, influence of, on
bronchiectasis, 71
Plumbism, chronic, specific gravity of blood
in, 429
Pneumoconiosis, 242 ; bibliography, 256 ;
diagnosis, 253 ; pathology, 246 ; pro-
gnosis and treatment, 255 ; symptoms,
245
Pueumomycosi-, 257
Pneumonia, 91 ; age in, 118, 130, 138 ;
anatomical events, 111 ; bacteriology,
112 ; bibliography, 140 ; clinical course,
94 ; clinical varieties, 108 ; complications
and sequels, 105, 119, 134 ; diagnosis,
103 ; distribution and local prevalence,
117 ; duration, 135 ; etiology, 116 ; his-
tology, 109 ; history, 92, 119 ; morbid
anatomy, 109 ; mortality, 135 ; onset, 92,
131 ; pathology, 114 ; physical signs, 97,
133 ; prognosis, 117 ; sex in, 117, 130 ;
statistics of cases, 130 ; statistics of
double pneumonia, 132 ; termination, 96 ;
treatment, 119
Pneumonia, acute, in pulmonary tuber-
culosis, 180, 213
Pneumonia in scurvy, 598 ; in acute endo-
carditis, 870
Pneumonia, catarrhal, 140 ; anatomy, 141 ;
bibliography, 155 ; clinical symptonjs,
142 ; course, complications, and prognosis,
145 ; diagnosis, 146 ; treatment, 148
Pneumonia, chronic, 149 ; bibliography,
155 ; diagnosis, 153 ; influence on bron-
chiectasis, 70 ; morbid anatomy, 151 ;
prognosis, 154 ; symptoms, 152 ; treat-
ment, 164
Pneumonia, secondary, 107
Pneumonia, white, in congenital syphilis,
312
Pneumonoconiosis, 242 ; as cause of phthisis,
159
Pneumopericardium, 801 ; bibliography,
806 ; diagnosis, 803 ; physical signs, 802 ;
treatment, 804
Pneumothorax, 378 ; bibliography, 386 ;
diagnosis, 383 ; etiology, 378 ; pathology
and morbid anatomy, 379 ; physical signs,
381 ; prognosis, 384 ; proph\ laxis, 386 ;
symptoms, 381 ; treatment, 385
Pneumothorax, after paracentesis, 376 ;
diagnosis from emphysema of tlie lungs,
279 ; in phthisis, 185, 211 ; treatment o^
238
Pneumothorax, elasticity of lungs in, 337 ;
inspiratory and expiratory pressure in,
341 ; intrapleural tension in, 339, 380 ;
with pleural effusion, 362
Poildlooytosis, 415 ; in spleno- medullary
leucocythsemia, 639
Poiseuille's "law" in relation to blood-
pressure, 475
Portal thrombosis as cause of ascites, 678
Pregnancy in phthisis, 162, 220
Pressure, intrapleural, see Intrapleural
tension, 335
Pseudo-tuberculosis, 258
Psoriasis and asthma, 291
Pulmonary artery, atresia or obliteration of,
704 ; irregularities in number and form of
valves, 710 ; stenosis, 703, 718 ; stenosis
at conus arteriosus, 706 ; stenosis at
valves, 706 ; stenosis of the trunk, 705 ;
transposition or malposition, 708, 720
Pulmonary cavities in phthisis, 181
Pulmonary congestion, acute, 104
Pulmonary gangrene, diagnosis from bron-
chiectasis, 77
Pulmonary tissue in bronchiectasis, 60
" Pulmonary tone," 338
Pulmonary tympanites, 338
Pulse, anacrotic and bisferiens, in aortic
stenosis, 930
Pulse in acute pericarditis, 750 ; in aortic
regurgitation, 936 ; retardation of, 939,
965 ; in mitral insufficiency, 982 ; in
phthisis, 201, 225
Pulse in functional disorders of the heart,
811 ; hysterical slow, 835 ; in palpitation,
818 ; in tachycardia, 830 ; intermittent,
81 4 ; in weak heart, 819 ; slow, classes of,
833
INDEX
1057
Pulsua paradoxus, 750 ; in pericardial ad-
hesion, 795
Puncture, exploratory, as means of diagnosis
in pleural effusion, 355
Purpura, 568 ; age and sex in, 573 ; biblio
graphy, 585 ; classifications, 574 ; diag-
nosis, 582 ; diagnosis from leucocythsemia,
662 ; diagnosis from scurvy, 600 ; etiology
and pathology, 568 ; Henoch's, 581
iodic, 580 ; neurotic, 575 (note) ; petechiae,
-585 ; probable causes, 571 ; prognosis,
583 ; purpura hsemorrhagica, 575 ; pur
pura rheumatica, 577 ; purpura simplex,
575 ; symptoms, 573 ; treatment, 584
Pyopericardium, 776
Pyopneu!nopericardium, 802
Pyopneumothorax subphreuicus, diagnosis
from pneumothorax, 384
Pyrexia in infectire endocarditis, 883 ; in
phthisis, 198, 224 ; treatment of, 234 ; in
pleurisy, 349 ; in purpura, 574, 577
QummE as cause of haemoglobinuria, 625
Eaoe, influence on phthisis, 158
Raynaud's disease and hsemoglobinuria, 622
Eed corpuscles, 399, 413 ; nucleated, 415 ;
in spleno-medullary leucocythsemia, 639
Begurgitation, aortic, 936 ; diagnosis, 952 ;
£eart sounds, 943 ; prognosis, 953 ;
" pulmonary, " 945 ; symptoms and signs,
936 ; treatment, 957
Eegurgitation, mitral, consequences of, 975 ;
diagnosis, 976 ; in chorea, 993 ; mechaa-
ism of, 974
Benal disease, chronic, and mitral stenosis,
1035
Benal tuberculosis in phthisis, 219
Eeproductive system in leucocythsemia, 660
Bespiration and the atmosphere in infantile
bronchitis, 47 ; in muscular exercise, 847 ;
"of the tissues," 398
Bespiratory movements in pericardial ad-
hesion, 794
Bespiratory organs, in acute renal dropsy,
687 ; in general dropsy, 681
Bespiratory oscillation, 335 ; in pneumo-
thorax, 341 ; in serous effusion, 345
Bespiratory pressures in mechanical strain
of the heart, 848
Bespiratory system in acute pericarditis,
751, 764 ; in aortic regurgitation, 951 ;
in leucooythaemia, 657
Betina in infective endocarditis, 881, 883 ;
in leucocythsemia, 660
Betinitis leucsemica in leucocythsemia, 646
Eheumatism, acute endocarditis in, 861 ;
acute, as cause of aortic disease, 908
" Scorbutic anaemia," 583
Scurvy, 586 ; bibliography, 603 ; complica-
tions, 598 ; diagnosis, 600 ; distribution,
586 ; etiology, 587 ; general pathology,
VOL. V
■589 ; pathological anatomy, 598 ; pre-
vention, 602 ; prognosis, 601 ; symptoms,
692 ; treatment, 603
Scurvy, infantile, 604 ; bibliography, 620 ;
course, 610 ; diagnosis, 616 ; etiology and
general pathology, 613 ; history, 604 ;
morbid anatomy, 611 ; prognosis, 617 ;
symptoms, 605; treatment, 618
Septa, cardiac ; auricular, absence of, 698 ;
defects in, 699, 717 ; development of, 715 ;
ventricular, absence of, 698 ; defects in,
699, 700, 717 ; developkent of, 716
Septic and pyaemic infection, diagnosis from
infective endocarditis, 882
Shock, specific gravity of blood in, 430
Siderosis, 248
Silicosis, 248
Sinus of Valsalva, aneurysm oi, diagnosis
from simple aortic regurgitation, 940
Skin in infantile bronchitis, 48 ; in leuco-
cythaemia, 659 ; in phthisis, 201
Skodaic resonance, 338
Sneezing, paroxysmal, in asthma, 289
Soldier's heart, 851 ; bibliography, 855 ;
prognosis, 854 ; symptoms and physical
signs, 853
Spectroscopic examination of blood, 454 ;
method, 455
Sphygmographic signs in aortic regurgita-
tion, 952
Spleen in infective endocarditis, 881 ; in
leucooythaemia, 640, 651, 655 ; in mitral
insufficiency, 974 ; in pericardial adhesion,
788 ; in phthisis, 217 ; in splenic anasmia,
543, 545
Splenaemia, 636
Spleno-megalie, primitive, 539
Sputum, see also Expectoration ; bacteriology
of, in putrid bronchitis, 34 ; in bronchiec-
tasis, 73 ; in pleurisy, 350 ; in pneumonia,
95, 134
Staining blood films in microscopic examinst-
tion, 412
Stenosis, aortic, 927 ; causes, 919 ; diagnosis,
933 ; prognosis, 935 ; symptoms and signs,
927
Stenosis, influence of bronchial, on bron-
chiectasis, 71
Stenosis, mitral, 1007 ; see Mitral stenosis
Stemo-mastoid tumour, 559
Stokes-Adams disease, 834
Stomach, in chlorosis, 499 ; in mitral in-
sufficiency, 973 ; in phthisis, 215
Strain, cardiac, 841
Stress, as cause of mechanical strain of tho
heart, 843
Subcutaneous tissues in mitral insufficiency,
974
Sweats in phthisis, 200 ; treatment, 234
Syncope, 838
Syphilis, acute endocarditis in, 864 ; as cause
of aortic disease, 909
Syphilitic disease of the lungs, 311 ; ac-
3y
1058
SYSTEM OF MEDICINE
quired, 315 ; bibliography, 332 ; changes
in bronchial glands and lymphatics of the
lung, 321 ; differentiation from tuber-
culosis, 328 ; fibroid induration, 320 ;
hereditary syphilis, 311; lobular orbronoho-
pneumonia, 319 ; morbid anatomy, 311,
316 ; pathology, 316 ; physical signs, 330 ;
prognosis, 331 ; symptoms, 329 ; treat-
ment, 332
" Syphilitic phthisis," 321
Systolic recession, and retraction in peri-
cardial adhesion, 790
Tabes and aortic disease, 950
"Tabes mesenterica," 218
Tachycardia, 824 ; age and sex in, 830 ;
bibliography, 832 ; diagnosis, 830; morbid
anatomy, 828 ; pathogeny, 828; prognosis,
831 ; treatment, 831
Temperature in acute pericarditis, 761 ; in
infantile bronchitis, 48 ; in leucocythaemia,
659 ; in paroxysmal hasmoglobinuria, 628,
631 ; in pernicious anaemia, 526 ; in
phthisis, 198, 225 ; in pleurisy, 349 ; in
pneumonia, 94, 134 ; in splenic anaemia,
544
Thoracic walls in pericardial adhesion, 791
Thorax in bronchitis, 9
Thrill in aortic- stenosis, 929
Thrombosis in chlorosis, 508 ; of coronary
arteries, 900
Thymus gland in leuoocythsemia, 643
Thyroid gland in leucocythaemia, 656
Tintometer, Lovibond's, 432
Toxaemia as cause of disease of the myo-
cardium, 887
Trachea bronchitis, 4 ; treatment, 36
Traumatism, acute endocarditis in, 864 ; as
cause of aortic disease, 914 ; in causation
of phthisis, 164
Tricuspid stenosis as cause of dropsy, 685
Tmncus arteriosus, deyelopment of, 716
Tubercle bacillus, in sputum of phthisis, 194,
225; inoculation with, 166; invasion of
lungs by, 175 ; mode of extension of
process, 183 ; mode of growth, 165
Tuberculin in treatment of phthisis, 230
Tuberculosis, acute endocarditis in, 864 ; in
mitral stenosis, 1012
Tuberculosis of the lungs, diagnosis from
lobular pneumonia, 146
Tuberculosis of the kidney, specific gravity
of blood in, 429
Tuberculosis, pulmonary, 156 ; see also
phthisis pulmonalis, 156 ; acute, 186 ;
acute miliary, 190 ; broncho-pneumonic
form, 188 ; inherited, 173 ; lobar-pneu-
monic form, 186
Tuberculosis, pulmonary, chronic, 192 ; ex-
pectoration, 193 ; microbes, 194 ; modes
of invasion, 192; symptoms, 192
Tuberculous phthisis, diagnosis from pleurisy,
368
Tumours of the myocardium, 906
Typhoid fever, Widal-Griinbaum method for
diagnosis of, 458
Ulceration, intestinal, in phthisis, 216
Ulceration of cardiac valves, 920
Uraemia, specific gravity of blood in, 429
Urine, in chlorosis, 491, 510 ; in infective
endocarditis, 881 ; in haemoglobinuria,
622 ; leucocythaemia, 669 ; in pericardial
adhesion, 788 ; in pernicious anaemia, 629 ;
in pneumonia,' 94 ; in scurvy, 597
Urogenital system in phthisis, 218
Veins in adherent pericardium, 795
"Ventricle, left, in mitral reflux, 970, 995 ;
in mitral stenosis, 1010 ; filling of, 469
Vomicae, signs of, in phthisis, 181, 205;
diagnosis from pneumothorax, 383
Vomiting in pleurisy, 351
Waseinq out the pleura, dangers o^ 374
Zymotic fevers, acute endocarditis in, 863
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