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MONOGRAPHIC
MEDICINE
VOLUME II
THE CLINICAL DIAGNOSIS
OF INTERNAL DISEASES
BY
LEWELLYS F. BARKER, M.D. (Ton.), LL.D. (QUEENS; McGiLL)
PROFESSOR OF MEDICINE, JOHNS HOPKINS UNIVERSITY, 1905-1914; PHYSICIAN-IN-
CHIEF, JOHNS HOPKINS HOSPITAL, 1905-1914; PRESIDENT OF ASSOCIATION OF
AMERICAN PHYSICIANS, 1912-1913; PRESIDENT OF AMERICAN NEUROLOGICAL
ASSOCIATION, 1915; PRESIDENT OF NATIONAL COMMITTEE FOR MENTAL
HYGIENE; PROFESSOR OF CLINICAL MEDICINE, JOHNS HOPKINS UNI-
VERSITY; AND VISITING PHYSICIAN, JOHNS HOPKINS HOSPITAL
WITH TEN COLORED PLATES AND TWO HUNDRED AND NINETY
ILLUSTRATIONS IN TEXT
NEW YORK AND LONDON
D. APPLETON AND COMPANY
1917
COPYRIGHT, 1916, BY
D. APPLETON AND COMPANY
Printed in the United States of America
THE CLINICAL DIAGNOSIS
OF INTERNAL DISEASES
GENERAL DIAGNOSIS, INFECTIONS,
RESPIRATORY AND CIRCULATORY
SYSTEMS
BY
LEWELLYS F. BARKER, M.D. (Ton.), LL.D. (QUEENS; McGiLL)
PROFESSOR OF MEDICINE, JOHNS HOPKINS UNIVERSITY, 1905-1914; PHYSICIAN-Itf-
CHIEF, JOHNS HOPKINS HOSPITAL, 1905-1914; PRESIDENT OF ASSOCIATION OF
AMERICAN PHYSICIANS, 1912-1913; PRESIDENT OF AMERICAN NEUROLOGICAL
ASSOCIATION, 1915; PRESIDENT OF NATIONAL COMMITTEE FOR MENTAL
HYGIENE; PROFESSOR OF CLINICAL MEDICINE, JOHNS HOPKINS UNI-
VERSITY; AND VISITING PHYSICIAN, JOHNS HOPKINS HOSPITAL
WITH TEN COLORED PLATES AND TWO HUNDRED AND NINETY
ILLUSTRATIONS IN TEXT
.$1
. <v|
NEW YORK AND LONDON
D. APPLETON AND COMPANY
1917
• COPYRIGHT, 1916, BY
D. APPLETON AND COMPANY
Printed in the United States of America
TO
SIR WILLIAM OSLER, BART.
WITH THE GRATITUDE, ADMIRATION AND AFFECTION OF THE AUTHOR
Preface
In view of the enormous advances made in the sciences formerly
termed auxiliary to medicine, but now recognized as fundamental for all
progress in the healing art, the time would seem ripe for a publication
dealing in a simple, practical way with the clinical diagnosis of internal
diseases.
In the last decade the viewpoint of internists has to a certain extent
been shifted, in that they are now attempting to visualize clearly the
functional pathological processes that are the essence of disease. They are
studying, too, the causes — external and internal — of the deviations from
the normal met with in disease ; and they are no longer content merely with
setting up clinical syndromes", or with attempting to prophesy, during life,
the anatomical lesions that pathologists will find in the bodies of their
patients after death. Control of clinical work by the methods of patho-
logical anatomy and histology will always be highly desirable; but for
the clinical diagnosis of internal diseases today, a knowledge of functional
pathology and of its underlying sciences (biophysics and biochemistry)
is quite as important as a knowledge of pathological anatomy. Indeed,
this substitution of the viewpoint of functional pathology for that of struc-
tural pathology in discussions of the principles and in determining the
practice of inner medicine represents the most radical departure in our
science since Virchow so profoundly influenced it by the introduction of
the conceptions of cellular pathology over fifty years ago.
The growth of the sciences underlying clinical work has been so rapid
and the progress so great that an inner medicine can now be constructed
that is very different in form, methods, and emphasis from the inner
medicine of any previous period — so different, indeed, that of the men
trained in the art and science of diagnosis a few years ago, only those
that have had exceptional opportunities for keeping pace with changes
can find their way in it without a special guide. To provide such an
everyday guide for practitioners, and for students who are now enteriiiL:
upon the study of clinical medicine, this work has heen planned and
written. In it an attempt has been made to present in due proportion
the methods and results of the science of medical diagnosis, in all its
parts. The work has been written from the viewpoint of functional
pathology, as far as this is possible at the present time, but the results
of etiological and pathological-anatomical studies have been also regarded.
viii PREFACE
With our present knowledge, diagnosis should mean not the mere
placing of a patient's malady in a particular group and the assignment
to it of a name, but rather a thorough knowledge of the patient and the
arrival at an understanding of the essence of those deviations from normal
functions that the patient presents. Thus understood, diagnosis involves
(1) the accumulation of data by all possible methods (physical, chemical,
biological, psychical, social, experimental) that can yield information of
importance regarding the patient's body and mind; (2) the drawing of
whatever inferences are justifiable therefrom. To make such a diagnosis
requires much knowledge of both bedside methods of examination and
laboratory technic, and skill acquired by practice in the use of them.
Clinical men have come to realize that they cannot expect the labora-
tory workers in the non-clinical medical sciences to solve clinical problems
for them, for these men have the problems of their own sciences to solve,
and the application of the scientific facts discovered by them, in so far
as they offer a solution of diagnostic and therapeutic difficulties, must be
made by the clinicians themselves. Technical application always involves
new investigations, which fortunately often not only contribute to the
progress of clinical medicine itself but also advance the sciences under-
lying it.
It may be asked whether the present state of inner medicine really
justifies an attempt at description from the viewpoint of functional
pathology. That such a presentation is not easy, and that it must fall
far short of what one would like it to be, must at once be admitted.
Certain parts only of inner medicine have been well worked up on the
functional pathological side; others are as yet almost wholly unex-
plored. At the present time, when there is a seething activity in our
clinics in the application of biochemical and biophysical methods to. diag-
nosis, it can scarcely fail to be helpful to patients and physicians, to
teachers and students, and even to original investigators, to take stock of
what has already been accomplished, to point out the gaps in our knowl-
edge, and to indicate unknown fields that may most profitably be explored.
Eor nothing, perhaps, contributes more to the further progress of an
unevenly developed subject than a clear and concise presentation of its
state at a given time ; the practical value of the results obtained in well-
tilled districts serves as a spur to the cultivation of unbroken ground.
A survey of inner medicine in the light of functional pathology is not
only justifiable at this moment but, for the welfare of our profession, is
urgently demanded.
Naturally it might be asked : Should any one man, in a time like ours,
try to write a textbook of clinical diagnosis that covers the whole field
of inner medicine and its specialties ? Is it not essential that such a
work be written by a large group of specialists, each one contributing the
Chapter bearing upon the particular domain in which he is an expert?
PKEFACE ix
The writer has considered this question very seriously before deciding
to stand as single sponsor for the present work. All will agree that in
the preparation of large systematic treatises, it is desirable that the
single parts be written by special investigators in the several domains.
For the time has long since passed when any one man can be equally
interested, active, and productive in all parts of inner medicine. Each
of the medical specialties requires for its mastery so much experimental
work, so much technical skill, and such a wealth of detail and depth of
special knowledge, that a firm grasp of more than one or two specialties
exceeds the power of a single person. In large treatises, furthermore,
it is not permissible to omit even less important details ; the specialist is
required to discuss theories at length, even those that are of uncertain
value. But the writing of a monograph is an entirely different problem.
In it, there must be a careful selection, a separation of the relatively
important from the less important, the avoidance of unnecessary ballast,
and compression within set limits. Hence it would seem desirable that
a monograph on the diagnosis of internal diseases be produced by
a single writer, provided this writer has had large clinical oppor-
tunities, some years of laboratory training, and has been in close
contact with original workers in the several specialties, always moreover
provided that he has good judgment regarding the needs of students and
general practitioners, a wide acquaintance with home and foreign litera-
ture, and the kind of mind that permits him to sift critically, to balance
evenly, to write concisely and to express himself clearly ; for such a
practical diagnostician, imbued with the scientific spirit, should be able
to prepare a valuable clinical work if the purpose for which it is
designed be kept plainly in view during its production. To a full pos-
session of the ideal qualifications just enumerated the author makes no
claim. None can feel more keenly the shortcomings of the present work.
Should it, however, be adjudged to have met, to some extent, an existing
need, it is hoped that other teachers and practitioners may be kind enough
to call attention to mistakes and omissions, so that their cooperation will
render possible a more adequate presentation of the subject at a later
period. There is one best way to do everything, and the sooner the
"standard methods'7 are found and adopted, everywhere, by single workers,
the greater will be their efficiency.
In the arrangement and presentation of this material, the prac-
tical needs of students and of physicians have been kept foremost
in mind. The idea underlying the plan has been to write the work
in such a way that any one using it, no matter what his special
training, will find in it directions that will, if consistently followed,
permit him to make a complete examination of all parts of the human
body by both the clinical and the laboratory methods now in use, and to
draw from the data thus accumulated all justifiable inferences. The
x PEEFACE
intention has been to lay equal stress upon all the branches of inner medi-
cine, avoiding long-winded discussions and the inclusion of unimportant
material as well as that that is too uncertain and debatable. The infor-
mation given is believed to be full enough to permit a clinician to work
by directly following the text, thus avoiding the necessity and trouble of
using a whole series of special treatises in everyday work. To preserve,
however, the compendious character of the treatise, it has not been thought
desirable to include all the thousand and one methods that are available,
nor to discuss, in detail, the advantages and disadvantages of those that
are described. The student or practitioner who on occasion may desire
fuller information than is here given, or may require to use, for some
special research, methods not sufficiently practical to justify their inclu-
sion in this work, will find appended to the several sections bibliographic
references in which the additional information may be found. In select-
ing these references I have been influenced by (1) the historical impor-
tance of the articles, (2) American work, and (3) the recency of the
contributions. It will be noticed that a number of methods usually found
in textbooks of diagnosis are missing; on careful consideration, methods
that have been judged to be antiquated or that have been perpetuated by
reason of false piety, have been omitted. Additional brevity in the text
has been made possible by the introduction of many explanatory charts,
tables and illustrations.
The author desires to express his thanks to the many friends who
have aided him in gaining the experience upon which the work is pri-
marily based and in the preparation and arrangement of the abundant
material composing it. His thanks are especially due to his colleagues
of the medical and surgical staffs of the Johns Hopkins Hospital, to the
Resident Physicians of the same hospital from 1905 to 1915 (including
Drs. E. I. Cole, C. P. Emerson, B. A. Cohoe, T. E. Boggs, F. J. Sladen
and P. W. Clough), and to the men in charge of the several laboratories
of the medical clinic during the period (including A. D. Hirschf elder,
R. S. Morris, W. L. Moss, C. Voegtlin, C. G. Guthrie, C. E. Austrian,
G. S. Bond, W. A. Baetjer, A. W. Sellards, E. H. Major, S. E. Miller,
A. L. Bloomfield, and E. W. Bridgman). Dr. M. C. Pincoifs has care-
fully revised the section on the urine and has been helpful in many other
ways in the preparation of the volume. Mr. Max Broedel has given
valuable advice regarding the illustration of the volumes, and Mr. W. C.
Shepard and Misses Flora L. Schaefer and Dorothea Pennington have
made most of the original drawings. Miss Daisy P. Tousey and Miss
Dick have aided in the preparation of the temperature charts of the sec-
tion on infectious diseases; Drs. D. K. McLean and Y. P. W. Syden-
stricker, and Drs. Mildred Clark and Mary A. Hodge have helped in the
preparation of legends for the illustrations; while Miss Blogg and her
associates in the Johns Hopkins Hospital Library, Miss Noyes and her
PKEFACE xi
associates in the Library of the Medical and Chirurgical Faculty, and
Miss R. Y. Halsey have verified the accuracy of the many references to
the bibliography. To his faithful secretaries, Miss B. O. Humpton and
Miss Jane Humpton, the thanks of the writer are due for their pains-
taking work on the manuscript ; to the former, he is indebted also for the
preparation of the index. For permission to use cliches, photographs of
interesting cases, roentgenograms, etc., thanks are due to many publishers
of medical works and to the authors of books and of articles in journals.
In each instance acknowledgment has been made in the legend accom-
panying the figure. Especial thanks are due to Dr. F. R. Smith, who
has been good enough to read a part of the proof sheets, and whose valuable
suggestions have contributed to accuracy and clearness.
It is a pleasure to acknowledge, too, the liberality and cooperation of
the publishers, who have shown a sympathetic appreciation of the new
needs of such a work, and have given their consent to a number of ex-
pensive innovations. To their representative, Dr. J. R. Broome, the
writer is particularly under obligations for kind help in many ways.
In conclusion, it may be mentioned that the writing of this monograph
was begun before the outbreak of the great world war. It was the desire of
the author from the beginning, while attempting adequately to present
the results of American work, to value properly, also, the researches of
clinicians in all countries. Since the outbreak of the war the writing
has been continued precisely in the spirit in which it was begun, and in
the bibliography cited every effort has been made to avoid any one-sided
or prejudiced consideration of the literature. Medicine is not a national
subject ; it is and must ever continue to be an international science. Every
physician who has the real progress of medicine at heart should at all
times, and despite all, see to it that he does all in his power to keep the
bonds of scientific brotherhood unbroken.
LEWEKLYS F. BARKER.
1035 K Calvert St.,
BALTIMORE, MD.
Contents
Part I. General Plan for the Clinical Study of a Patient
PAGE
A. Introduction 1
B. The Clinical History ......... 7
1. The Anamnesis 7
(a) The Present Illness 8
(b) The Previous History of the Patient ... 9
(c) The Family History 10
2. The Present State of the Patient (Status praesens) . . 10
(a) The General Condition of the Patient ... 11
i. Gait and Attitude . . . . . . 11
ii. Position of the Patient in Bed ... 11
iii. Height, Weight, and Build .... 12
iv. Mental State 13
v. Body Temperature 14
vi. Skin and Visible Mucous Membranes . . 14
vii. Collateral Circulations ....... 17
viii. Edema 18
ix. The Lymph Glands 19
(b) The Condition of Special Regions and Systems . 19
i. Examination According to Regions . . 19
ii. Examination According to Systems ,. . 20
iii. Combined Plan of History Taking . . 21
3. Catamnesis 23
4. Epicrisis 24
0. General Remarks on Diagnostic Methods 25
Part II. Examination with the Rontgen Rays
(Rontgenoscopy, Rontgenography)
A. Varieties of Apparatus for the Production of Rontgen Rays . 27
• 1. Rontgen Apparatus Utilizing Direct Current with Inductor 28
(a) The Interrupter 29
(b) The Rheostat
(c) Single-impulse Apparatus ... 29
XLV CONTENTS
PAGE
2. Rontgen Apparatus Utilizing the Alternating Current
with High Tension Rectifying Switch . . 30
(a) The Step-up Transformer 30
(b) The High Tension Rectifying Switch ... 31
(c) Advantages of the Rectifying Switch Apparatus . 32
B. The X-ray Examining Room 33
C. Rontgen Tubes 34
1. Structure of a Rontgen Tube ...... 34
2. The Rontgen Tube in Action 35
(a) The Focus of the Cathode Rays . ' . . . 35
(b) The Normal Radiation 36
(c) Glass Rays and How to Stop Them Out ... 36
(d) Coolers of the Anticathode 36
(e) Soft and Hard Rontgen Tubes . . . . 36
(f) Inverse Discharge with the Inductor Apparatus . 38
3. Regeneration of Rontgen Tubes . . . . . . 39
4. Care of Rontgen Tubes 39
D. Origin, Nature, and Properties of Rontgen Rays ... 40
1. Cathode Rays 40
2. Nature of Rontgen Rays 41
3. Properties of Rontgen Rays 42
(a) Penetrability of the Rays 42
(b) Propagation of the Rays . . . . . .42
(c) Secondary Radiation 42
(d) Excitation of Fluorescence 43
(e) Chemical Effects of Rontgen Rays .... 43
(f) Biological Effects of Rontgen Rays ... 43
E. Qualitative and Quantitative Measurements in Rontgenology 44
1. Measurements of Hardness 44
(a) Walter's Penetrometer ...... 44
(b) Wehnelt's Cryptoradiorneter 45
(c) Christen's Absolute Hardness Measurer, or So-called
"Half-value Layer" 45
2. Measurements of the Intensity of the High Tension
Current 47
3. Measurements of the Quantity of Rontgen Radiation
(Dosage of X-rays; Radiometry; Quantimetry) 47
(a) Holzknecht's Modification of the Sabouraud-Noire '
Radiometer 47
(b) lonto-quantimeter of Szillard 48
(c) Quantirneter of Kienbock 49
CONTENTS xv
PAGE}
F. Central Projection and Parallel Projection (Ortho-projection) 50
1. Divergent Rays and Central Projection . . . . 50
2. Parallel Rajs and Ortho-projection (Orthodiagraphy) . 50
3. Telerontgenography and Telerontgenoscopy . . . 51
4. Diaphragms .......... 52
G. Photographic Technic in Rb'ntgenography .... 52
H. Clinical Application of the Rontgen Rays . . . . 53
1. Technic of Rontgenoscopy . . . . . . .53
(a) Fluorescent Screens 53
(b) Vertical and Horizontal Rontgenoscopy . . . 55
(c) On Certain Details of Rontgenoscopy . . 55
2. Technic of Rontgenography 57
(a) Maintenance of the Patient in Correct Position . 57
(b) Compression Apparatus 58
(c) Hardness of Tubes Used in Rontgenography . . 58
(d) Exposure Time 58
(e) Intensifying Screens 60
(f ) Special Clinical Applications of Rontgenography . 60
(g) Stereoscopic Rontgenography 60
(h) Cinematographic Rontgenography .... 63
Part HI. Exploratory Puncture and Examination of
the Fluids Obtained
A. The Technic of Exploratory Puncture 67
1. Exploratory Puncture of the Pleural Cavity ... 67
2. Exploratory Puncture of the Pericardial Cavity . . 70
3. Exploratory Puncture of the Peritoneal Cavity . . 71
4. Exploratory Puncture of the Subarachnoid Space (Lum-
bar Puncture) 72
5. Exploratory . Puncture of the Skull Cavity (Neisser and
Pollak) . . . . . . . . -77
B. Physical and Chemical Examination of Punctates . . > . 78
1. Eluids from the Pleural, Pericardial and Peritoneal
Cavities 78
(a) Appearance of Punctates . . . . . .78
(b) Odor of Punctates 78
(c) Specific Gravity of Punctates 79
(d) Protein Content of Punctates 79
(e) Freezing Point (Molecular Concentration of Punc-
tates) 80
xvi CONTENTS
2. Cerebrospinal Fluid .
(a) Physical and Chemical Properties of Normal Cere-
brospinal Fluid . . . .... 81
(b) Physical and Chemical Properties of the Cerebro-
spinal Fluid in Pathological States . . . 81
i. Total Protein Content 81
ii. Globulin Content . . . . . . 81
iii. Content in Plydrophile Colloids that will Pre-
vent Precipitation of Other Instable Colloids
(e. g., Gold-sol) by Salt Solution . . 83
0. Bacteriological, Serological, and Cytodiagnostic Methods of
Examining Punctates 86
1. Eacteriodiagnostic Methods 86
2. Immunodiagnostic Methods 87
3. Cytodiagnostic Methods . . . . . . . 88
(a) Cytodiagnosis of Pleural, Pericardial and Perito-
neal Fluids 88
i. Cytodiagnosis of Exudates in Acute Infections 89
ii. Cytodiagnosis of Exudates Due to Tuberculous
Infections 89
iii. Cytodiagnosis of Transudates . . . . 90
iv. Cytodiagnosis of Effusions Associated with
Neoplasms 90
(b) Cytodiagnosis of the Cerebrospinal Fluid . . 91
i. Counting and Differential Counting in Stained
Smears 91
ii. Hemocytometer Methods of Enumeration of
the Cells in the Cerebrospinal Fluid . . 91
Part IV. Diagnosis of the Infectious Diseases and of the
Diseases Due to External Physical Causes
Section I. General Diagnosis of Infectious Diseases
A. General Facts Regarding Infection, Infectious Processes and
the Methods of Studying Them . . . . . . 95
1. Definition of Infection 95
2. Infectious Agents and Their Specificity . . . . 97
3. Mechanisms of Aggression of the Infectious Agents .• 98
(a) Sources of the Infectious Agents . . . . 98
i. How the Germs of Disease Leave the Bodies
of the Sick 98
CONTENTS xvii
i ii. How the Germs of Disease Maintain Their
Existence Outside the Bodies of the Sick . 99
iii. How the Germs of Disease Gain Entrance
to the Body (Portals of Entry) . . . 100
(b) Distribution of Microbes Within the Body After
Entrance 101
(c) The Poisons (Toxins) Produced by the Microbes,
and Their Action 101
(d) The Course of an Infectious Process . . .104
(e) The Virulence of the Microbes .... 104
4. Mechanisms of Defense of the Human or Animal Body . 105
(a) On Immunity in General .105
(b) Natural Immunity or Resistance .... 106
i. Antibacterial Resistance .... 106
ii. Antitoxic Resistance 107
(c) Acquired Immunity . 108
i. Antibodies to the Antigens . . . . 109
ii. Theories of Antibody Formation . . .110
iii. Antitoxins Ill
iv. Bacteriolysins and Hemolysins . . . 112
v. Opsonins 118
vi. Precipitins ... . 119
vii. Agglutinins 121
viii. Antiferments 122
(d) Anaphylaxis; Hypersusceptibility ; Allergy . . 122
i. History and Definition 122
ii. Characteristics of Allergy, and Symptoms of
Anaphylactic Reactions . . . .125
iii. Anti-anaphylaxis 129
iv. Theories of Allergy 130
B. The Body Temperature . 131
1. Heat Regulation 131
2. Measuring the Body Temperature (Thermometry) . . 132
3. Normal Temperature of the Human Body . . . 133
4. Fever • .134
(a) Febrile Temperatures
(b) Different Types of Fever .
i. Continued Fever (Febris continua) . . 135
ii. Remittent Fever (Febris remittens) . . 135
iii. Intermittent Fever (Febris intermittens) . 135
iv. Recurrent Fever (Febris recurrens) . 136
(c) Stages of the Febrile Course ..... 136
xviii CONTENTS
PAGE
C. Clinical Application of Bacteriological Methods . . . 137
1. Collection of Material for Bacteriological Examination . 137
2. Kinds of Bacteria Often Found . . . . . 139
3. Microscopic Examinations for Bacteria .... 140
(a) Examination of Dried, Fixed, and Stained Smears 140
(b) Examination of Unstained Fresh Preparations . 141
(c) Examination of Hanging Drop . '. . . 141
4. Methods of Staining Bacteria and Parasites . . . 142
(a) General Stains 142
i. Alkaline Methylene Blue (Loeffler) . . 142
ii. Carbol-fuchsin (Ziehl-Neelsen) . . . 142
iii. Anilin Water Gentian Violet (Ehrlich) . 142
iv. Wilson's and Giemsa's Stain (Methylene
Azure and Eosin) 142
(b) Special Stains 142
i. Gram's Stain 142
ii. Stains for Tubercle Bacilli and Other Acid-
fast Bacilli 143
iii. Stains for Treponema pallidum . . . 144
iv. Stains for Capsules 145
v. Stains for Spores 145
vi. Stains for Flagella 146
5. Bacterial Cultures for Clinical Diagnosis .... 146
6. Animal Inoculations, and Virulence Tests .... 149
D. Clinical Applications of Immunological Methods . . . 150
1. Tests for Agglutinins 150
(a) The Widal Reaction 151
2. Tests for Lysins (Bacteriolysins ; Hemolysins) . . 153
(a) Pfeiffer's Experiment 153
(b) Complement-fixation Tests . . . .154
i. Wassermann Reaction (Wa. R.) . . . 156
ii. Complement-fixation Test for Differentiation
of Human from Animal Blood (Gengou-
Moreschi Phenomenon) . . . .167
iii. Complement-fixation in the Diagnosis of
Echinococcus 167
iv. Complement-fixation in the Diagnosis of
Gonococcal Infections . . . . .167
3. Tests for Precipitins 170
(a) Precipitin Test for Human Blood . . . .170
(b) Precipitin Test for Meningococcal Infection . . 171
4. Tests for Immune Opsonins (Bacteriotropins) . . . 171
CONTENTS xix
PAQH
5. Tests for Ergins 171
(a) Tuberculin Tests 172
i. Subcutaneous Tuberculin Reaction (Koch) . 172
ii. Cutaneous Tuberculin Reaction (von Pirquet) 173
iii. Conjunctival Tuberculin Test, or Ophthalmo-
reaction (Calmette; Wolff-Eisner) . . 174
(b) Epiphanin Reaction (Weichardt) .... 176
(c) 'Meiostagmin Reaction (Ascoli) .... 176
(d) Potassium-iodid-starch Method for Measuring the
Excitation of Catalyser Action by Proteotoxic
Substances (Weichardt and Kelber) . . . 176
(e) Luetin Test (Noguchi) 177
(f) Typhoprotein Conjunctival Test, or Typhoid-oph-
thalmo-reaction ( Chantemesse ; Austrian) . 178
(g) Anaphylactic Test for Protein (Pfeiffer) - . 179
Section II. Special Diagnosis of the Infectious Diseases
I. VEGETABLE MICROORGANISMS . . . . . . . 180
A. Diseases Due to Cocci . .183
1. Diseases Due to Streptococci 183
(a) Streptococcal Septicemia ...... 185
(b) Endocarditis lenta (Subacute Infectious Endocar-
ditis) 186
(c) Erysipelas . . . 187
(d) Streptococcal Puerperal Sepsis .... 189
(e) Streptococcal Sinus Thrombosis (Otogenous Sepsis) 189
(f) Streptococcal Angina 190
(g) Acute Rheumatic Eever 191
2. Diseases Due to Staphylococci 197
(a) Staphylococcal Septicemia 197
(b) Acute Osteomyelitis 198
(c) Eurunculosis . . . 199
3. Diseases Due to Pneumococci . . . . .199
(a) Croupous Pneumonia (Lobar Pneumonia) . . 202
(b) Pneumococcus Septicemia
4. Diseases Due to Gonococci .......
(a) Gonococcal Inflammations of the Urogenital Organs 203
(b) Gonococcal Conjunctivitis (Ophthalmia neonato-
rum) . . . . . . •
(c) Gonococcal Endocarditis (Endocarditis gonorrheica)
(d) Gonococcal Polyarthritis (Gonorrheal Rheumatism)
(e) Gonococcal Iritis . . . . • • 205
xx CONTENTS
PAGE
5. Diseases Due to Meningococci 205
(a) Epidemic Cerebrospinal Meningitis . . . 206
(b)% Meningococcal Arthritis . . . . . .209
(c) Meningococcal Sepsis 209
6. Diseases Due to Micrococcus melitensis . . . .211
(a) Undulant Fever . . . . . . .212
B. Diseases Due to Bacilli .213
1. Diseases Due to the Pneumobacillus (Friedlander) . .213
2. Diseases Due to the Scleroma Bacillus . . . .213
(a) Rhinoscleroma 213
3. Diseases Due to the Anthrax Bacillus ... . .214
.(a) Human Anthrax . 214
4. Diseases Due to the Bacillus of Malignant Edema . .215
5. Diseases Due to the Gas Bacillus (Welch and ISTuttall) . 215
(a) Gas Gangrene (Hospital Gangrene) . . . 215
6. Diseases Due to the Tetanus Bacillus . . . .216
(a) Human Tetanus .... . . . 216
7. Diseases Due to the Influenza Bacillus . . . .219
(a) Influenza (La Grippe) 219
8. Diseases Due to the Bacillus of Bordet and Gengou . . 221
(a) Whooping-cough 222
9. Diseases Due to the Plague Bacillus 225
(a) Plague 225
10. Diseases Due to the Typhoid Bacillus .... 228
(a) Typhoid Fever (Typhus abdominalis) . . . 229
(b) Gastro-enteritis Due to Bacillus typhosus (Gastro-
enteritis typhosa) 243
11. Diseases Due to B. paratyphosus 248
(a) Gastro-enteritis paratyphosa B. (Cholera nostras
paratyphosa) 248
(b) Paratyphus abdominalis B 248
(c) Gastro-enteritis paratyphosa A. and Paratyphus
abdominalis A 249
(d) Typhus manschuricus 249
12. Diseases Due to the Colon Bacillus . . . . .251
(a) Local Infections . . . . . . . 251
(b) Coli-sepsis 251
13. Diseases Due to the Dysentery Bacillus . . . .252
(a) Bacillary Dysentery (Epidemic Dysentery) . . 252
14. Diseases Due to the Bacillus of Ducrey . . . .254
(a) Soft Chancre (Ulcus molle) . , . . .254
CONTENTS xxi
PAQH
15. Diseases Due to the Diphtheria Bacillus .... 254
(a) Pharyngeal Diphtheria 256
(b) Nasal Diphtheria . . . . . 257
(c) Laryngeal Diphtheria 257
(d) Cutaneous 'Diphtheria 257
(e) Vulval Diphtheria 257
(f) Conjunctival Diphtheria 257
16. Diseases Due to the Bacillus pyocyaneus .... 261
17. Diseases Due to the Bacillus mallei ..... 261
(a) Glanders and Farcy . 262
18. Diseases Due to the Tubercle Bacillus .... 263
(a) Pulmonary Tuberculosis 265
i. Acute Phthisis 266
ii. Chronic Ulcer ative Phthisis . . . . 266
iii. Chronic Fibroid Phthisis .... 268
(b) Lymphadenoid Tuberculosis . . . . 269
(c) Tuberculosis of the Serous Membranes . . .270
(d) Tuberculosis of the Joints 270
i. Tuberculosis of the Hip-joint . . . .270
ii. Tuberculosis of the Knee-joint . . . 271
(e) Tuberculosis of the Bones (Caries) . . . 271
i. Spondylitis tuberculosa (Caries of the Spine) 272
(f) Tuberculosis of the Skin . . . . . .273
i. Lupus vulgaris . . . . . . . 273
ii. Scrofuloderma 274
iii. Ulcer ative Miliary Tuberculosis of the Skin . 274
iv. Lichen scrofulosum 274
(g) Tuberculosis of the Urogenital System . . . 275
(h) Tuberculosis of the Meninges (Meningitis tubercu-
losa) .276
(i) Acute General Miliary Tuberculosis . . .277
i. General Remarks on the Early Diagnosis of
Pulmonary Tuberculosis in Adults . . 280
ii. General Remarks on the Early Diagnosis of
Tuberculosis in Children . . . .283
19. Diseases Due to the Leprosy Bacillus . 292
(a) Human Leprosy (Lepra) .
i. Lepra nodosa (Lepra tuberosa) . . . 294
ii. Lepra nervorum ... . 294
iii. Lepra mixta 295
20. Diseases Due to the Cholera Bacillus . ...
(a) Asiatic Cholera . • 297
21. Diseases Due to the Bacillus of Milk Sickness .
(a) Milk Sickness . . .
xxii CONTENTS
PAGB
22. Diseases Due to the Bacillus proteus vulgaris , . . 300
23» Diseases Due to the Bacillus typhi-exanthematici . . 300
(a) Typhus Fever 300
0. Diseases Due to the Coarser Fungi (The Mycoses) . . . 306
1. Mycoses Due to Hyphomycetes 307
(a) Human Aspergillosis 308
(b) Human Mucor-mycoses 309
(c) Human Achorion-mycosis or Favus .... 309
(d) Human Mycoses Due to Tricophyton tonsurans . 310
i. Superficial Ringworm (Trichophytia super-
ficialis) 310
ii. Eczematous Ringworm (Epidermophytia cru-
ris) 310
lii. Barber's Itch or Ringworm of the Hairy
Scalp and Beard (Trichophytia tonsurans
capillatii) 310
iv. Parasitic Sycosis (Trichophytia profunda) . 311
v. Ringworm of the Kails (Trichophytia un-
guium) 311
(e) Human Microsporon Mycoses 311
i. Pityriasis versicolor 311
(f) Erythrasma (Baerensprung) . . . . .312
2. Mycoses Due to Yeasts and Yeastlike Fungi . . . 312
(a) Blastomycosis and Coccidioidal Granuloma . . 314
i. Blastomycetic Dermatitis and Systemic Blasto-
mycosis 314
ii. Coccidioidal Granuloma 317
(b) Diseases Due to Thrush Fungi . . . .319
i. Thrush 319
3. Mycoses Due to Sporotrichum and Related Fungi . . 322
(a) Sporotrichosis (Schenck's Disease) . . . 322
(b) Other Mycoses Resembling Schenck's Sporotrichosis 325
4. Mycoses Due to the Different Varieties of Streptothrix . 325
(a) Typical Actinomycosis in Human Beings . . 326
(b) Mycetoma (Madura Foot) 328
(c)* Pseudo-actinomycoses or Streptotrichomycoses . 329
(d) Discomyces Mycoses 330
CONTENTS xxiii
PAGE
II. DISEASES DUE TO ANIMAT, MICROORGANISMS (PROTOZOA) . 331
A. Diseases Due to Pathogenic Rhizopoda 332
1. Human Amebiasis 332
(a) Amebic Dysentery . . . . . . . 332
(b) Amebic Abscess of the Liver ..... 333
(c) Amebic Pyorrhea 334
B. Diseases Due to Pathogenic Mastigophora, or Flagellata . . 335
1. Diseases Due to Pathogenic Trypanosomidae (Human
Trypanosomiasis) 336
(a) Congo Trypanosome Fever and Sleeping Sickness . 338
(b) Rhodesian Trypanosomiasis (Kaodzera) . . 339
(c) Brazilian Trypanosomiasis (Chagas' Disease; Thy-
roiditis parasitaria ; Careotrypanosis) . . 339
2. Diseases Due to Varieties of Leishmania (Human Leish-
maniasis) 342
(a) Kala-azar 343
(b) Infantile Kala-azar or Infantile Leishmaniasis . 344
(c) Cutaneous Leishmaniasis or Oriental Sore . . 344
3. Human Malaria . . 346
(a) Tertian Malaria 349
(b) Quartan Malaria .349
(c) Estivo-autumnal Malaria 350
4. Relapsing Fever '. 365
5. Syphilis, or Lues . . 368
(a) Acquired Syphilis . 369
(b) Congenital Syphilis 375
6. Yaws or Frambesia 379
7. Granuloma venereum 380
8. Gangosa '381
9. Verruga peruviana 381
10. Oroya Fever 382
C. Diseases Due to Pathogenic Sporozoa . ...
III. DISEASES DUE TO FILTRABLE OR "UI/TRAMICROSCOPIO"
VIRUSES 382
A. Diseases Due to Pasteur's Virus .
1. Rabies .....
B. Diseases Due to Reed, Carroll and Agramonte's Virus . . 389
1. Yellow Fever - 389.
xxiv CONTENTS
PAGE
C. Diseases Due to Ashburn and Craig's Virus . . . .391
1. Dengue Fever . . 391
D. Diseases Due to Flexner and Noguchi's Filtrable and Culti-
vable Virus (Flexneria noguchii) 392
1. Heine-Medin Disease 392
E. Diseases Due to Other Filtrable Viruses . . . . . 404
1. Foot and Mouth Disease 404
2. Pappataci Fever . . . 405
3. Transmissible Sarcoma . 405
IV. DISEASES DUE TO UNKNOWN INFECTIOUS AGENTS . . . 407
A. The Acute Exanthemata 407
1. Scarlet Fever (Scarlatina) 407
2. Measles 412
3. Eubeola 4X7
4. Duke's Fourth Disease 418
5. Chickenpox 419
6. Smallpox (Variola, Ger. Blattern, Fr. Petite verole) . 421
(a) Variola discreta 427
(b) Variola confluens . 431
(c) Varioloid 431
(d) Variola sine eruptione . . . . . .432
(e) Variola hemorrhagica 432
(f) Purpura variolosa 432
(g) Variola inoculata 433
7. Vaccinia (Cowpox and Vaccination) 435
8. Sweating Sickness 441
9. Rocky Mountain Spotted Fever 441
B. Non-exanthematous Diseases . 442
1. Mumps 442
Section III. Special Diagnosis of the Diseases Due to External
Physical Causes
A. Diseases Due to Heat (The Caloric Diseases) .... 445
B. Diseases Due to Exposure to Cold 448
1. Local Effects of Cold 448
2. Death from Freezing 448
3. Cold as a Predisposing Factor 449
G, Piseases Due to Electrical Injuries ... . . . . ,
CONTENTS xxv
D. Diseases Due to Injuries from Rontgen Rays and from Radium 451
1. Rontgen-injury of the Skin . . 452
2. Chronic Dermatitis among Rontgenologists . . .452
3. Rontgen-injury of the Sex Glands 453
4. Rontgen-injury of Other Organs 453
E. Diseases Due to Alterations in Atmospheric Pressure . . 454
1. Caisson Disease . . 455
2. Divers' Disease . 456
3. Air-pressure Diseases among Balloonists and Aviators . 456
4. Mountain Disease (Acosta's Diaease) .... 456
P. Diseases Due to Unaccustomed Movements, or to Alterations
of the Direction of the Movements of the Body (Sea-sick-
ness, Car-sickness, Kinetoses) 458
Part V. Diagnosis of Diseases of the Respiratory
Apparatus
Section I. Methods of Examination
A. Examination of the Nose and the Paranasal Sinuses . . 462
1. Anterior Rhinoscopy . 462
2. Posterior Rhinoscopy and Pharyngoscopy .... 464
3. Sinusoscopy 465
4. Palpation of the Nose and Nasopharynx . . . .465
5. Transillumination of the Paranasal Sinuses . . . 466
6. Rontgenography of the Paranasal Sinuses .... 466
7. Sounding the Maxillary Sinus 469
B. Examination of the Larynx, Trachea and Larger Bronchi . 470
1. External Examination of the Larynx and Trachea . .470
(a) Inspection of the Larynx and Trachea Externally . 470
(b) Palpation of the Larynx and Trachea . . . 470
(c) Percussion of the Larynx . . . . .471
(d) Auscultation of the Larynx and Trachea . . 471
2. Internal Examination of the Larynx (Laryngoscopy) . 472
(a) Direct Laryngoscopy
i. Autoscopy of Kirstein . 472
ii. Direct Laryngoscopy with Hay's Pharyngo-
scope • 473
xxv/ CONTENTS
PAOB
(b) Indirect Laryngoscopy 474
i. General View, and View of the Anterior Parts
of the Larynx 474
ii. View of the Posterior Wall of the Larynx . 475
iii. Lateral View of the Interior of the Larynx . 475
3. Bronchoscopy 476
C. Examination of the Lungs and the Pleurae .... 478
1. Inspection of the Thorax in Relation to Diseases of the
Lungs and Pleura 479
(a) Forms of Thorax 479
i. Thorax paralyticus or Flat Chest . . . 479
ii. Barrel-shaped or Emphysematous Thorax . 480
iii. Normal Thorax 481
(b) Asymmetry of the Thorax in Relation to Diseases
of the Lungs and Pleura . . . .481
i. Pathological Expansion of One-half of the
Thorax 481
ii. Unilateral Contraction of the Thorax . .481
2. Inspection of the Respiratory Movements .... 482
(a) The Diaphragm Phenomenon (Litten's Sign) . 483
(b) Frequency and Rhythm of the Respirations . . 483
i. Cheyne-Stokes Breathing 484
ii. Dyspnea 485
3. Determination of the Volume of the Inspired and Ex-
pired Air (Spirometry) . . . . .488
4. Thoracography or Pneumography 490
5. Palpation of the Thorax Over the Lungs and Pleurae . 494
6. Mensuration of the Thorax 495
7. Percussion Over the Lungs and Pleurae . . . .495
(a) The Intensity and the Quality of the Sounds Pro-
duced on Percussion . . . .500
i. The Loudness of the Percussion Sounds . 501
ii. The Fullness of the Percussion Sounds . . 501
iii. The Pitch of the Percussion Sounds . . 501
iv. The Clang Content, or Timbre, of Percussion
Sounds 502
(b) The Feeling of Resistance on Percussion ' . . 504
(c) Topographical Percussion of the Lungs . . . 505
(d) Comparative Percussion of the Lungs . . . 509
i. Dullness and Flatness on Percussion . .510
ii. Pathological Tympanitic Sounds on Percus-
sion over the Lungs . .. .. ., ,.511,
CONTENTS xxvii
PAGE)
iii. Variations in the Pitch of Tympanitic Percus-
sion Sounds 512
iv. Metallic Sounds Over the Lungs . . . 513
8. Auscultation of the Lungs 513
(a) Auscultation of the Voice Sounds Over the Thorax 514
i. Origin of the Voice Sounds . . . 514
ii. Changes in the Voice Sounds After Their
Formation . . . . . . .515
iii. Voice Sounds Audible Over the Thorax in
Healthy Persons 515
iv. Coughing Sounds and Crying Sounds . . 515
v. Abnormalities of the Voice Sounds Audible
Over the Thorax 516
(b) Auscultation of the Breath Sounds Over the Thorax 517
i. Vesicular Breathing 517
ii. Bronchial Breathing 519
iii. Mixed Breathing; Bronchovesicular Breath-
ing, and Indefinite Respiration . . . 521
iv. Accessory or Adventitious Respiratory Sounds
Audible in Disease 521
9. Relation of Physical Signs to Conditions in the Lung and
Pleura 526
10. Examination of Sputum . . . . . .526
(a) Sources of Sputum 526
(b) Varieties of Sputum 528
(c) Color of Sputum 530
(d) Odor of Sputum . 530
(e) Consistence of Sputum
(f) Protein Content of Sputum 530
(g) Amount of Sputum ... .531
(h) Larger Particles or Masses in the Sputum Recog-
nizable by the Naked Eye . .531
(i) Microscopic Study of the Sputum . . 534
i. Cells in the Sputum
ii. Elastic Fibers in the Sputum .
iii. Crystals in the Sputum . . . 536
iv. Parasites as Seen in Fresh Sputum . 537
v. Bacteria and Parasites as Seen in Stained
Specimens of the Sputum
11. Cough •
xxviii CONTENTS
PAGE
12. Examinations of .the Lungs, Pleurae and Diaphragm by
Means of Rontgen Rays . ; . . .542
(a) Rontgenoscopy of the Lungs . . . 542
(b) Rontgenography of the Lungs 542
(c) Appearances of the Thorax, Lungs, Pleurae, Dia-
phragm, etc., on X-ray Examination . . .543
Section II. Special Diagnosis of the More Important Diseases of
the Respiratory System
A. Diagnosis of the Principal Diseases of the Nose . . . 548
1. Inflammatory Diseases of the Nose (Rhinitis) . . . 550
(a) Acute Rhinitis 550
i. Acute Catarrhal Rhinitis .... 550
ii. Acute Purulent Rhinitis . . . . .551
iii. Acute Pseudomembranous Rhinitis . . 551
iv. Hay Fever 552
(b) Chronic Rhinitis ...."... 554
i. Chronic Nasal Catarrh . . . . . 554
ii. Chronic Purulent Rhinitis . . . .554
iii. Chronic Atrophic Rhinitis . . . .555
(c) Specific Inflammations of the Nose . . . .556
i. Nasal Tuberculosis 556
ii. Nasal Syphilis 556
2. Epistaxis 557
3. Foreign Bodies and Parasites in the Nose . . 557
4. Tumors of the Nose; Nasal Polypi 558
5. Deflections and Distortions of the Nasal Septum . . 559
6. Nasal Hydrorrhea; Rhinorrhea 560
B. Diagnoses of the Diseases of the Paranasal Sinuses . . .560
1. General Remarks on the Diagnosis and Differential Diag-
nosis of Inflammatory Diseases of the Paranasal
Sinuses . 560
2. Maxillary Sinusitis 565
3. Frontal Sinusitis 567
4. Ethmoidal Sinusitis . . . . . . . . 569
5. Sphenoidal Sinusitis 570
6. Mastoiditis 572
C. Diagnosis of Diseases of the Larynx 574
1. Inflammatory Diseases of the Larynx .... 575
(a) Acute Laryngitis 575
i. Acute Catarrhal Laryngitis . . . .575
ii. Acute Pseudomembranous Laryngitis . . 576
CONTENTS
XXIX
PAGE
(b) Chronic Laryngeal Catarrh 576
(c) Specific Inflammations of the Larynx . . . 577
i. Tuberculosis 577
ii. Syphilitic Laryngitis . . . . .578
iii. Typhoidal Laryngitis . . . . .579
2. Circulatory Diseases of the Larynx 579
(a) Edema of the Glottis . ..'-.. . . . 579
3. Paralytic Diseases of the Larynx 580
(a) Paralyses of the Laryngeal Muscles . . . 580
4. Neoplasms of the Larynx 583
(a) Polyps of the Larynx 584
(b) Papilloma of the Larynx 584
(c) Carcinoma of the Larynx 584
(d) Other Tumors of the Larynx . . . . 585
5. Stenosis of the Larynx . . . . . . . . 585
D. Diagnosis of the Principal Diseases of the Trachea and Bronchi 586
1. Inflammations of the Trachea and Bronchi . . . 580
(a) Acute Catarrhal Tracheobronchitis . . . .586
(b) Acute Diffuse Bronchial Catarrh . . . 587
(c) Acute Eibrinous Bronchitis . . . . .588
(d) Chronic Bronchitis . 589
(e) Bronchial Asthma 590
2. Dilations of the' Bronchi 593
3. Stenosis of the Trachea and of the Bronchi . . . 596
E. Diagnosis of the Principal Diseases of the Lungs , . .596
1. Inflammatory Pneumopathies or Pneumonias . . . 597
I. THE PARENCHYMATOUS PNEUMONIAS . . . 597
(a) Genuine Lobar Pneumonia .... 597
(b) Bronchopneumonia ..... 607
(c) Metastatic (Embolic) Pneumonia . . 610
(d) Abscess of the Lung 610
(e) Gangrene of the Lung 611
II. THE INTERSTITIAL PNEUMONIAS .... 613
III. THE SPECIFIC INFLAMMATORY PNEUMOPATHIES . 613
(a) Pulmonary Tuberculosis . . . .613
i. Ordinary Chronic Forms of Pulmonary
Tuberculosis . . . .617
ii. Acute Forms of Pulmonary Tubercu-
losis 617
(b) Syphilis of the Lung .
(c) Other Specific Inflammations of the Lung . 633
xxx CONTENTS
PAGE
2. Pneumopathies Characterized by Alterations of the Alve-
olar Lumen 634
(a) Atelectasis 634
(b) Vesicular Emphysema of the Lungs . . . 636
3. Pneumopathies of Circulatory Origin .... 638
(a) Chronic Passive Congestion of the Lungs and Stasis
Bronchitis 63S
(b) Pulmonary Hemorrhage and Hemoptysis . . 639
(c) Pulmonary Embolism; Hemorrhagic Infarction of
the Lung; Thrombosis ..... 640
i. Embolism of the Pulmonary Artery or of One
of its Eight or Left Branches ... 640
ii. Embolism of a Medium-sized Branch of the
Pulmonary Artery Causing Infarction of
the Lung .641
iii. Embolism of the Smaller Branches of the Pul-
monary Artery 642
iv. Thrombosis of the Pulmonary Artery or of its
Branches 643
(d) Edema of the Lungs 644
4. Pneumopathies Due to Foreign Bodies and Parasites . 645
(a) The Pneumonoconioses 645
(b) Parasites of the Lungs 647
5. Neoplastic Pneumopathies 648
F. Diagnosis of the Principal Diseases of the Pleura . . . 653
1. Inflammations of the Pleura (Pleuritis, Pleurisy) . . 653
(a) Dry or Plastic Pleurisy 654
(b) Pleurisy with Effusion ...... 655
i. Pleurisy with Serous or Serofibrinous Effusion 655
ii. Pleurisy with Serohemorrhagic Effusion . 661
iii. Pleurisy with Purulent Exudate . . . 661
iv. Pleurisy with Putrid Exudate . . . .664
(c) Pleural Thickening 664
2. Circulatory Disturbances Involving the Pleura . . . 673
(a) Hydrothorax 673
(b) Hemothorax 674
(c) Chylothorax 674
3. Gas in the Pleural Cavity; Pneumothorax . . . 675
4. Tumors of the Pleura 680
5. Parasites of Pleura 682
COJSTTElsrTS xxxi
PAGB
G. Diagnosis of the Principal Diseases of the Mediastinum . .682
1. Displacements of the Mediastinum through Pressure or
Traction 684
(a) Total Displacements . 684
(b) Partial Displacements 684
2. Space-occupying Processes in the Mediastinum . . . 684
(a) Rontgenography of the Mediastinum . . . 687
(b) Varieties of Mediastinal Tumors . . . . 689
(c) Diagnosis of Mediastinal Tumors .... 690
3. Diseases Involving the Lymph Spaces of the Mediastinum 692
(a) Acute Mediastinitis and Mediastinal Abscess . . 692
(b) Chronic Mediastinitis . . . . . .693
(c) Mediastinal Hemorrhage 693
(d) Mediastinal Emphysema 693
Part VI. Diagnosis of Diseases of the Circulatory
Apparatus (Clinical Angiology)
Section I. Methods of Determining the Condition of the Circulatory System
A. Introduction ... 695
B. Examination of the Position and Size of the Heart and of Its
Several Chambers - 700
1. Position and Size of the Normal Heart .... TOO
2. Methods of Determining the Position and Size of the Heart 701
(a) The Determination of the Position of the Apex
Beat of the Heart . . . . . .702
(b) Determination of the Areas of Cardiac Dullness by
Percussion
i. The Area of Absolute (or Superficial) Cardiac
Dullness ... •
ii. The Area of Eelative (or Deep) Cardiac
Dullness .... .705
(c) Determination of the Size and Position of the Heart
by Means of Rontgen Rays .
i. Simple Rontgenoscopy
ii. Orthodiagraphy
iii. Telerontgenography . . . • .716.
xxxii CONTENTS
i
PAGE
C. Cardiovascular Acoustics ; Normal and Abnormal Sounds Over
the Heart and Vessels 717
1. The Heart Sounds 717
(a) Normal Heart Sounds 717
(b) Origin of the Normal Heart Sounds . . . 717
(c) Auscultation Sites 719
(d) Rhythm and Accentuation of the Heart Sounds . 720
(e) Identification of the Heart Sounds .... 720
(f) Graphic Registration of the Heart Sounds . .721
(g) Detection of Alterations in the Intensity of the
Heart Sounds 722
i. Enfeeblement of the First Sound . . . 722
ii. Accentuation of the First Sound . . . 722
iii. Enfeeblement of the Second Sound . .723
iv. Accentuation of the Second Sound . . .• 723
(h) Detection of Changes in the Number of the Heart
Sounds 724
i. Splittings and Doublings of the Heart Sounds
(2/4 Rhythm) 724
ii. Triple or Gallop Rhythms (3/4 Time) .. . 725
2. Heart Murmurs 727
(a) Introduction 727
(b) Analysis of the Features Presented by Heart
Murmurs 728
i. The Time of Heart Murmurs .... 728
ii. The Topography of Heart Murmurs . . 729
iii. The Direction and Propagation of Heart
Murmurs 730
iv. The Intensity of Heart Murmurs . . .734
v. The Pitch, or Tonality, of Heart Murmurs . 735
vi. The Quality, or Timbre, of Heart Murmurs . 736
(c) Physical Explanation of the Origin of Heart Mur-
murs 730
(d) Significance of Heart Murmurs .... 736
i. Organic Intracardiac Murmurs . . . 737
ii. Inorganic Intracardiac Murmurs . . . 737
3. Extracardiac (or Exocardial) Murmurs . . . . - 740
(a) Pericardial Friction Sounds 740
(b) Pleuropericardial Friction Sounds .... 741
(c) Cardiorespiratory Murmurs 741
(d) Precordial Crackling of Mediastinal Emphysema . 742
(e) Splashing and Water-wheel Sounds .... 742
CONTENTS xxxiii
PAGE
4. Auscultation of the Blood Vessels 743
(a) Auscultation of the Arteries ..... 743
(b) Auscultation of the Right Jugular Vein . . 744
D. Methods of Examining the Movements of the Heart and Blood
Vessels ...... 745
1. Inspection of the Movements of the Heart and Blood
Vessels 745
2. Palpation of the Movements of the Heart and Blood
Vessels 746
3. Instruments for Mechanical Registration of Movements of
the Circulatory Apparatus 746
(a) The Sphygmograph 747
i. James Mackenzie's Improved Ink-polygraph . 747
ii. Jaquet's Cardiosphygmograph . . . 74S
iii. Hirschfelder's Modification of the Erlanger
Apparatus 748
iv. Other Sphygmographs 750
(h) The Plethysmograph ; Volume-pulse . . . 751
(c) The Tachograph; Velocity-pulse .... 751
(d) Rontgenoscopy and Cinematography of the Move-
ments of the Heart and the Aorta . . .753
(e) The Electrocardiograph . . . . . 753
E. Analysis of the Movements of the Heart and Vessels as Studied
Clinically . .758
1. The Apex-beat of the Heart . . . . . . 758
(a) The Extent of the Apex-beat 758
(b) The Strength of the Apex-beat .... 759
(c) The Resistance of the Apex-beat to Compression . 759
(d) The Exact Eorm of the Apex-beat, as Revealed in
the Cardiogram 759
(e) The Rate and Rhythm of the Apex-beat . . 762
2. Precordial Movements Other than the Apex-beat . . 763
(a) Wavelike Movements in the Precordium . . . 763
(b) Retractions at the Base and Apex .... 764
(c) Pulsations Over the Aorta and the Pulmonary
Artery .764
(d) Shocks Due to Valve Closure ... .765
.(e) Certain Thrills, the Palpatory Equivalent of Some
Kinds of Murmurs 766
(f) Pericardial Friction Fremitus . . . 767
3. Broadbent's Sign and Other Pulsations in the Back . 767
xxxiv CONTENTS
4. Abdominal Pulsations ...... « 767
(a) Epigastric Pulsation ....... 767
(b) Hepatic Pulsations ....... 768
5. Pulse in Arteries, Veins and Capillaries . . . .769
Value of Studies of the Pulse ..... 769
Arterial Pulse ...... . . 770
i. Palpation of the Arterial Pulse . . . 770
ii. Graphic Registration of the Arterial Pulse
(Sphygmography) ..... 773
(c) Venous Pulse ........ 776
i. Inspection and Palpation of the Venous Pulse 776
ii. Graphic Registration of the Venous Pulse . 777
1. Physiological Venous Pulse (Normal
Phlebogram) ..... 778
2. Abnormal Eorms of Venous Pulse . . 779
P. Electrocardiograms ......... 782
1. The Electrocardiogram of a Normal Heart . . .782
2. Clinical Value of Electrocardiography ..... 783
3. Physiological Variations of the Electrocardiogram . . 783
4. -The Electrocardiogram in Pathological States . . . 787
5. The Electrocardiogram in Experimental Physiology . 788
G. Measurements of Blood Pressure (Sphygmomanometry or
Tonometry of the Blood Vessels ...... 790
1. Introduction ...... .... 790
2. Instruments for Determination of Arterial Blood Pressure 792
(a) The Cuff for Compressing the Arm . . .793
(b) Manometers for Measuring the Pressure within the
Cuff ......... 794
(c) Instruments for Graphic Registration of Blood
Pressure ....... .796
(d) Oscillatory Instruments ...... 797
(e) Selection of an Instrument for Measuring Blood
Pressure ........ 797
3. Determination of the Maximal (Systolic) Arterial Pres-
sure ......... 798
(a) Palpatory Method ....... 798
(b) Oscillatory and Auscultatory Methods . . .799
4. Determination of the Minimal Diastolic Arterial Pressure 799
(a). Palpatory Method (Janeway) ..... 799
(b) Oscillatory Method (von Recklinghausen; Erlanger) 800
(c) Auscultatory Method (Korotkow) . . . .801
CONTENTS xxxv
PAGE
5. The Arterial Blood Pressure under Normal Conditions . 803
(a) Variations under Physiological Conditions . . 804
6. The Blood Pressure in Pathological States . . . 806
(a) Chronic Arterial Hypertension .... 806
(b) Acute and Chronic Arterial Hypotension . . 808
7. The Absolute Sphygmogram (Sahli) 809
8. Determination of Venous Blood Pressure . . . .811
(a) Method of Hooker and Eyster (1908) . . .811
(b) Method of Moritz and von Tabora (1909-10) . 811
(c) Method of A. A. Howell (1912) .... 812
9. The Normal Blood Pressure in the Veins . . . .812
10. The Venous Blood Pressure in Pathological States . . 812
H. Determination of the Functional Capacity of the Heart . . 813
Section II. Diagnosis of the Special Diseases of the Heart and BBood Vessels
A. Clinical Disorders of the Heart Beat ..... 820
1. Introduction 820
2. Classification of the Cardiac Arhythmias .... 821
3. Common Examples of Cardiac Arhythmia . . . 826
4. Sinus Irregularities 827
(a) Phasic Variations in Rate 827
(b) Dropped Beats 828
5. Arhythmias Dependent upon Abnormal Premature Im-
pulses Arising in the Heart . . . • 829
(a) Extra-systolic Arhythmias 829
i. Ventricular Extrasystoles . . .829
ii. Atrial (or Auricular) Extrasystoles . . 83i
iii. Nodal Extrasystoles
(b) Paroxysmal Tachycardias
(c) Atrial (or Auricular) Fibrillation .
(d) Atrial (or Auricular) Flutter .
6. Changes in Contractile Force of the Heart
(a) Pulsus alternans
7. Disturbances in Conduction in the Heart (Heart Block) .
(a) Atrioventricular Block
i. Delayed Conduction .
ii. Partial Block .
iii. Complete Block
(b) Interventricular Block
xxxvi CONTENTS
rAGB
B. Circulatory Insufficiency .859
1. Chronic Circulatory Insufficiency 859
2. Acute Circulatory Insufficiency 866
C. Reparative and Adaptive Processes in the Heart . . . 867
1. Hypertrophies of the Heart 868
(a) Hypertrophy of the Left Ventricle . . .. .868
(b) Hypertrophy of the Eight Ventricle ... 869
(c) Atrial Hypertrophy ....... 869
2. Dilatation of the Heart (Failure of Tonicity) . . . 870
D. The Inflammatory Cardiopathies . . . . . . 871
1. Endocarditis 871
(a) Acute Endocarditis 872
(b) Subacute Infective Endocarditis . . . .875
(c) Chronic Endocarditis 877
2. Myocarditis 877
3. Pericarditis 879
E. Non-inflammatory Diseases of the Pericardium . . . 885
F. Valvular Disease of the Heart 886
1. Aortic Stenosis 889
2. Aortic Insufficiency 890
3. Mitral Stenosis . .891
4. Mitral Insufficiency 893
5. Pulmonary Stenosis 893
6. Pulmonary Insufficiency 894
7. Tricuspid Stenosis . . . . . . . .894
8. Tricuspid Insufficiency 895
G. Congenital Diseases of the Heart 895
H. The Chronic Toxic-degenerative Cardiopathies . . . .898
1. The Atherosclerotic Cardiopathy (Cardiopathia atheroscle-
rotica) 899
2. The Eatty Cardiopathy or Heart of Obesity (Cardiopathia
adipositatis) 899
3. The Nephropathic Cardiopathy (Cardiopathia nephro-
pathicorum) 900
4. The Thyreotoxic Cardiopathy (Cardiopathia thyreotoxica) 901
5. Other Forms of Chronic Cardiopathy .... 901
CONTENTS xxxvii
J.
Angina pectoris ....
PAGE
901
K.
Diseases of the Arteries
904
1. Atherosclerosis or Arteriosclerosis .....
904
2. Syphilis of the Arteries (Arteritis syphilitica) .
3. Aneurisms
909
912
(a) Aneurism of the Thoracic Aorta ....
(b) Diagnosis of Aortic Aneurism
(c) Aneurism of the Abdominal Aorta ....
(d) Diagnosis of Aneurisms of the Pulmonary Artery .
(e) Arteriovenous Aneurisms
4. Thrombosis and Embolism
913
914
916
916
917
919
5. Thrombo-angeitis obliterans
6. Peri-arteritis nodosa . . .
920
920
L.
Diseases of the Veins .
921
1. Phlebitis and Thrombophlebitis
921
922
3. Phlebosclerosis
923
LIST OF COLORED PLATES
PACING
PAGE
PLATE I ........ . ....... .86
Fig. 1. — Tuberculous Meningitis — Carbolfuchsin Methylene Blue.
Fig. 2. — Diplococcus pneumoniae in Meningitis — Gram Stain.
Fig. 3. — Meningococcus or Diplococcus meningitidis ( Weichselbaum) in
Cells in Cerebrospinal Fluid.
PLATE II ................. 164
Drawing to Illustrate Wassermann Reaction.
PLATE III ................ 184
Fig. 1. — Conradi-Drigalski Plate.
Fig. 2. — Differentiation of Streptococci on Blood-agar Plate.
Fig. 3. — Pus with Streptococci.
Fig. 4. — Quantitative Gradation of the Cutaneous Reaction after von
Pirquet.
PLATE IV ................ 256
Fig. 1. — Smear from Nasal Secretion in Leprosy.
Fig. 2. — Smear from Sputum in Primary Plague-pneumonia.
Fig. 3. — Cholera Bacillus, Pure Culture Stained w.ith Carbolfuchsin.
Fig. 4. — Bacillus diphtheriae — 36-Hour Pure Culture.
Fig. 5. — Bacillus diphtheriae — Pure Culture — Neisser's Stain.
PLATE V ................ .348
Fig. 1. — Parasites of Tertian Fever.
Fig. 2. — Parasites of Quartan Fever.
Fig. 3. — Parasites of Estivo-autumnal Fever.
PLATE VI ........ ........ 350
Fig. 1. — Tertian Schizontes Showing Schiifner's Stippling of the Red Cells.
Fig. 2. — Large Tropical Ring Forms Stained with Maurer's Modification,
of the Romanowski Stain Showing Pernicious Spots. Small and
Medium Size Tropical Ring Forms; Beginning Segmentation.
PLATE VII ........ ...... . 368
F4g. 1.— Treponema pallidum in Section Through Tissue in Hereditary.
Lues.
Fig. 2. — Primary Lesion or "Hard Chancre" of Syphilis in. the Suleus
retroglandularis,
Fig. 3.— Mucous Patches on the Under Surface of the Tongue. Secondary
Syphilis.
Fig. 4. — Tertiary Syphilis. Perforation of Hard and Soft Palate. De-
struction of Uvula. Radial Scar on Posterior Wall of Pharynx.
Healed Lesion.
xxxix
LIST OF COLOEED PLATES
, PAGE
PLATE VIII 384
Fig. 1. — Spirochaete of Relapsing Fever in the Blood.
Fig. 2. — Kala-azar. .Heavily-infected Macrophage from a Splenic Film.
Leishman Stain.
Fig. 3. — Trypanosoma gambiense.
Fig. 4. — Negri Bodies.
PLATE IX . 536
Fig. 1. — Actinomyees with Spores.
Fig. 2. — Actinomyces from the Sputum — Unstained.
Fig. 3. — Cells in the Sputum.
PLATE X 538
Fig. 1. — Smear from Pneumonic Sputum, Stained with Dilute* Carbol-
fuchsin.
Fig. 2. — Bacillus influenzae from Nasal Secretion. Fuchsin Stain.
Fig. 3. — Micrococcus catarrhalis. Gram-fuchsin Stain.
Fig. 4. — Tubercle Bacilli. Stained with Fuchsin and Methylene Blue.
LIST OF ILLUSTRATIONS
FIQ. PAGE
1. — The Male Skeleton 12
2. — The Female Skeleton 13
3. — Supernumerary Nipples 14
4. — Obstruction of the Inferior Vena cava 18
5. — Induction Coil Apparatus . . . .28
6. — Apex High Tension Generator 29
7. — Interrupterless Apparatus. Alternating-current Machine .... 30
8. — Interrupterless Apparatus. Direct-current Machine 31
9. — Wiring for Alternating-current Generator . 32
10. — Wiring for Direct-current Generator 32
11. — Diagram of a Rontgen Tube .35
12. — Water-cooled Tungsten Target Tube 37
13. — The Benoist Penetrometer 44
14. — Wehnelt's Penetrometer 45
15. — Comparative Scale for Penetrometers or Hardness Measurers .... 46
16. — Sabouraud and Loire's Radiometer 48
17. — Holzknecht's Radiometer for Direct Reading of X-ray Dosage .... 48
18. — Kienboeck's Quantitimeter ; 49
19. — Comparative Scale of Quantitimeters . . .50
20. — Ordinary and Orthogonal Projection 51
21. — Lead-protected Rontgenoscope 54
22. — Astral Screen for Fluoroscopy 54
23.— Coolidge X-ray Tube 56
24. — Different Positions for Transillumination on Rontgenoscopy .... 57
25. — Compressor for Use in X-ray Work 58
26.— X-ray Expometer 60
27. — Wheatstone Stereoscope 61
28. — Rb'ntgenoscopic Examination on Stereoscopic Table 62
29. — Record Syringe for Exploratory Puncture . . * 68
30. — Thoracentesis Outfit 70
31. — Trocar for Lumbar Puncture Showing the Stylet in Place and Withdrawn . 72
32. — Apparatus for Lumbar Puncture 73
33. — Lumbar Puncture 73
34. — Selection of Point for Lumbar Puncture just above the Line Joining the
Iliac Crests 74
35. — Lumbar Puncture in the Adult 74
36. — Manometer to be Used in Lumbar Puncture 74
37. — Diagram Showing Numerical Values Assigned to Colors and a Reaction in
the "Luetic Zone" 84
•38. — Reaction in Meningitis 85
39. — Characteristic Curve of General Paresis 85
40. — Receptor of the First Order Ill
41. — Diagram Illustrating How Bactericidal Power (B. P.) May be Raised by
the Addition of Complement in a Very Severe Case of Typhoid Fever . . 113
42. — Schematic Representation of the Process of Hemolysis . . , . .114
43. — Schematic Representation of Complement Fixation and Hemolysis . . ,116
xlii LIST OF ILLUSTKATIONS
FIG.
44. — Effects of Horse-serum in Man .
45.— Double Reaction after Reinjection of Horse-serum in Man .
46. Illustration Showing Large Inflated Lungs Obtained from a Typical Fatal
Case of Horse-serum Anaphylaxis in a Guinea-pig . 125
47. — Anergy — Anti-anaphylaxis
48. Diagram Showing Mechanism of Heat Regulation Under Different Conditions 131
49. — Easy Method of Translating Degrees Centigrade Into Degrees Fahrenheit
and vice versa
50. Suction Apparatus for Collecting Blood for the Wassermann Reaction . .139
51. — India Ink Preparation from a Luetic Papule 145
52. — Widal Reaction . . 151.
53. — Arrangement of Test Tubes for the Gonococcal Complement-Fixation Test . 168
54 —Chart Illustrating a Characteristic Tuberculin Reaction .
55. — Course of Benign Infection of Man with Tuberculosis 173
56. — Purpura in Septicemia 184
57. — Streptococcus Sepsis: Endocarditis ulcerosa 185
58.— Chart of Erysipelas 187
59.— Swollen Glands of the Neck in Septic Sore Throat . .., . . . .190
60. — Temperature Chart of Epidemic Cerebrospinal Meningitis .... 206
01. — Epidemic Cerebrospinal Meningitis — Retraction of the Neck .
62. — Epidemic Cerebrospinal Meningitis 207
G3— Brudzinski's "Identical Reflex" or "Frog Sign" in Meningitis . . . .208
64. — Brudzinski's "Contralatoral Reflex" in Meningitis 208
65._Tetanus Bacilli — Nail Forms 216
66. — Chart of Influenza 220
67.— Pulex irritans
68.— Map for 1907 Showing Typhoid Cases Distributed Evenly Throughout a City 228
69. — Map for 1906 Showing a Typical Milk Epidemic of Typhoid ... 229
70. — Spring in a Brickyard Where Typhoid Fever Developed 230
71. — Chart Showing the Typical Seasonal Rise in Cases of Typhoid Fever, during
July, August, and September . 231
72.— Temperature Chart of Typhoid Fever 232
73.— Typhoid Fever. Initial Staircaselike Rise 233
74. — Typhoid Fever. Amphibolous Stage. Two Hour Chart 234
75. — Chart Showing Loss of Weight in Typhoid Fever Despite a Food Intake
Averaging 2,600 Calories per Day 235
76. — Chart Showing that Weight Equilibrium Can be Maintained by the High
Calory Diet in Typhoid Fever 236
77. — Chart Showing Typhoid Relapses 237
78. — Cellular Infiltration of Heart Muscle in Typhoid Fever 238
79.— Chart Showing Typhoid Perforation 240
80. — Results of Typhoid Inoculation 242
81. — Chart Showing Pulmonary Tuberculosis 267
82.— Caries of Spine 272
83. — Tuberculous Meningitis 276
84. — Middle and Distal Phalanges of a Normal Finger Compared with Those
of a Case of Leprosy 295
85. — Tube Showing Growth of Bacillus typhi-exanthematici on Serum Glucose
Agar 301
86. — Bacillus typhi-exanthematici 302
87.— Pediculi 302
88. — Typhus Fever 303
89. — Microsporon furfur from a Scraping in Pityriasis versicolor . . . .311
90. — Sediment from Tissue Disintegrated in 50 per cent. Alcohol' . . . . 314
91. — Skin Lesions in a Case of Blastomycosis . . ... . . . 315
92. — Characteristic Lesions of Cutaneous Blastomyeosis . ..... 316
93.— Thrush Fungus 320
94.— Qidium..ajbicans. ., ., ., . . . . . . ., . . . . 321
LIST OF ILLUSTRATIONS xliii
FIG. PAGE
95. — Sporotrichosis beurmanni, Smear from Lesion 323
96. — Sporotrichosis 323
97. — Sporotrichotic Gumma. Multiple Fistula 324
98. — Glossina palpalis 337
99. — Oriental Sore 344
100. — Cycle of Development of the Malarial Parasites 347
101. — Mosquitoes 348
102. — Chart of Tertian Malaria 351
103.— Two-Hourly Chart of Tertian Malaria . . .352
104. — Two-Hourly Chart. Double Tertian Malaria 353
105. — Chart of Quartan Malaria 354
106. — Two-Hourly Chart Quartan Malaria 355
107. — Chart of Malarial Fever, Estivo-autumnal Tertian 356
108. — Chart of Estivo-autumnal Malaria 357
109. — Chart of Quotidian Malaria 358
HO. — Temperature Chart of Malarial Fever 359
111. — Chart of Malaria quartana 360
Ilia. — Chart of Malaria tropica 360
lllb. — Chart of Malaria tertiana 361
lllc. — Chart of Malaria quotidiana 361
112. — Spirochetes of Relapsing Fever from Blood of a Rat 365
113. — Ornithodorus moubata 365
114. — Chart of Relapsing Fever 366
115. — Chart Showing Course of a Case of Relapsing Fever of Panama . . . 367
116. — Chart Showing Course of a Case of Relapsing Fever of Europe . . . 367
117. — Treponema pallidum from a Ten-Day-Old Pure Culture in a Horse-Serum-
Agar-Tissue Medium 369
118.— Rupia syphilitica 370
119. — Scaling Syphilid of Palms. Conditions of Palms Two Weeks After Treat-
ment With "606" 372
120. — Scaling Philid of Palms. Duration of Infection, Three Years . . . 373
121. — Alopecia syphilitica 373
122. — Twins with Hereditary Syphilis 375
123.— Hutchinson's Teeth in Hereditary Lues 376
124. — Culture of the Ehrlich Rat Sarcoma . . . . . • . . . .406
125.— Chart of Scarlet Fever 409
126.— Chart of Measles .... 414
127. — Diagram Showing the Maxhr.nl Incubr.tion Period (21 Days) of a Small
Epidemic of German Measles 417
128. — Four Small Vaccine Bodies Situated in the Cytoplasm of Epithelial Cells
Situated at a Distance from the Nucleus 423
129. — Exanthem of Smallpox . 426
130. — Chart of Variola 428
131, — Effects of Cowpox Vaccimi'.'on in Man Watched from Day to Day . . 438
132. — Electric Light on Metal Head-band 462
133. — Bivalve Nasal Speculum 463
134. — Patient in Position for Rontgenography of tl.e IV.ranasal Sinuses . . . 467
135. — Diagram Illustrating the Projection of the Rays 467
136. — Rb'ntgenogram of Normal Paranasal Sinuses in the Adult 468
137. — Diagrammatic Key to Preceding Figure 469
138. — Hay's Pharyngoscope 472
139. — Schmuckert's Electric Pharyngoscope 473
140. — Indirect Laryngoscopic View of the Larynx 475
141. — Diagram of Anterior Surface of the Chest 478
142. — Diagram of Posterior Surface of the Chest 479
143.— Funnel Chest in a Man with Expiratory Type of Thorax 480
144. — Normal Pneumographic Tracing or Pneumogram 490
145. — Pneumogram in Pneumonia 491
xliv LIST OF ILLUSTKATIOJSrS
Fid. PAGE
146. — Pneumogram in Emphysema with Bronchiectasis 492
147. — Pneumogram in Chronic Circulatory Insufficiency 492
148. — Pneumogram from Patient with Ascites 493
149. — Pneumogram Illustrating Paradoxical Breathing in a Patient Suffering
from Severe Renal Disease 493
150. — Topography of the Thoracic and Upper Abdominal Viscera .... 49U
151. — Topography of the Viscera Viewed from Behind 497
152. — Topography of the Thoracic and Upper Abdominal Viscera Viewed from
Left Side 498
153. — Goldscheider's Orthopercussion 499
154. — Percussion with the Orthoplessimeter 499
155. — Normal Percussion Boundaries of the Lungs, Liver, Spleen, and Traube's
Space on the Anterior Surface of the Body 506
156. — Percussion Boundaries of the Lung, Liver, Spleen, and Traube's Space on
the Left Side 507
157.— Fibrin Cast 532
158. — Curschmann's Spirals 533
159. — Charcot-Leyden Crystals — 100/1 537
160. — Egg of Paragonimus 540
161. — Diagram Illustrating the Mode of Making a Rontgenogram of the Apices
of the Lungs and the Superior Aperture of the Thorax .... 544
162. — Transverse Section Above the Base of the Skull Seen from Above . . . 561
163. — Diagram Showing the Relations of the Paranasal Sinuses to Hiatus semilu-
naris 562
164. — Rontgenogram in Influenzal Inflammation of Antrum 5(56
165. — Rontgenogram Showing Clouding of Sinuses in Sinusitis 568
166. — Method of Showing Right and Left Sphenoidal Sinuses 571
167. — Rontgenogram of Mastoid Disease 573
168. — Diagrammatic Representation of the Position of the Vocal Cords in Different
Forms of Laryngeal Paralysis 581
169. — Diagrammatic Chart Representing Relation of Temperature in Pneumonic
Crisis 600
170. — Regions of the Thorax Over Which Percussion and Auscultation Should Be
Carried Out Systematically in Confirming Diagnosis of Tuberculosis 618
171. — Pulmonary Tuberculosis 621
172. — Tuberculosis (X-ray) 622
173. — Generalized Tuberculosis of the Lungs (X-ray) 623
174. — Artificial Pneumothorax (X-ray) 624
175.— Tumor of Lung (X-ray) 650
176. — Intrathoracic Tumor; Probably a Teratoma (X-ray) 651
177. — Areas in Which Pain and Hyperalgesia Were Present in a Case of Diaphrag-
matic Pleurisy '. 654
178. — Greece's Sign — Aortic Aneurism 658
179. — Pleurisy and Empyema 662
180. — Artificial Pneumothorax with Pleural Adhesions 678
181. — Collateral Circulation Between the Superior and Inferior Vena cava in a
Case of Mediastinal Tumor 685
182. — Large Vascular Sarcoma of Posterior Mediastinum 688
183. — Diagram of the Heart of the Eel 696
184. — Diagram of the Mammalian Heart for Comparison with the Heart of the Eel 696
185.— Steplike Line of.Kroenig 705
186. — Normal Percussion Areas of Liver and Heart 706
187. — Relative and Absolute Cardiac Dullness with Enlarged Right Ventricle and
Auricle 707
188. — Absolute and Relative Cardiac Dullness with Enlarged Left Ventricle . . 707
189. — Normal Cardiovascular Stripe on Rontgenoscopy 709
190. — Cardiovascular Shadow As Seen on Ventrodorsal Sagital Transillumination,
Schematic 710
LIST OF ILLUSTKATIONS xlv
PAGE
191. — Frontal Transillumination of Thorax, Schematic ...... 710
192. — Thorax in Oblique Transillumination ..... ... . 710
193. — Abnormal Forms of Cardiovascular Stripe on Rontgenoscopy . 711
194. — Abnormal Forms of Cardiovascular Stripe (continued) .... 712
195. — Schematic Representation of Orthodiagraph in Cross-section . 713
196. — Sagittal Orthodiagram . ...... .... 715
197. — Frontal Orthodiagram ............. 713
198.— Orthodiagram of the Heart, Lung Area, and Diaphragm of a Normal Man . 714
199. — Orthodiagram of a Normal Heart ......... 715
200. — Diagram Showing Position of the Valves and Areas of the Heart . 719
201. — Length of Pauses Between the Heart Sounds in Seconds ..... 720
202. — First, Second and Third Heart Sounds as Graphically Recorded by Method
of Einthoven and Geluk ... ........ 721
203.— Diagram Showing the Relation of the More Common Simple Murmurs to
Events of the Cardiac Cycle ........ 729
204. — Division of the Precordial Area Into Zones and Regions .... 730
205. — Distribution of Heart Murmurs in a Man, Age 36 ...... 731
206. — Distribution of Heart Murmurs in a Man, Age 33 ...... 732
207. — Areas in Which Heart Murmurs Were Audible in Acute Rheumatic Fever
with Mitral Insufficiency and Mitral Stenosis ..:... 733
208. — Instrument Recording Two Simultaneous Tracings Only . . . . 747
209. — Jaquet Cardiosphygmograph ........... 74g
210. — Erlanger Apparatus for Determining Maximal and Minimal Pressure, with
Hirschf elder Polygraph Attachment ........ 749
211.— New Portable Polygraph ............ 750
212. — Distribution of Cardiac Electricity on the Surface of the. Body . . . 753
213. — Small Electrocardiograph, Edelmann Model ........ 754
214. — Large Electrocardiograph, Cambridge Model .... . . . 755
215. — Williams-Hindle Electrocardiographic Outfit . . . . . . . 756
215a. — Williams-Hindle Electrocardiographic Outfit ....... 756
215b. — Williams-Hindle Electrocardiographic Outfit ....... 757
216. — Cardiogram, Phlebogram and Arteriogram in a Person Presenting a Third
Heart Sound .............. 760
217. — Carotid Arteriogram (Lower Tracing) with Cardiogram (Upper Tracing)
for Comparison ............. 773
218. — Diagram Showing Various Forms of Arterial Pulse Curve Encountered
Clinically ............... 774
219. — Diagram Showing Shaded Portion of the Cardiac Cycle Corresponding to
Ventricular Systole . . .......... 777
220. — Simultaneous Tracings of the Carotid and Venous Pulses ..... 778
221. — Phlebogram from a Patient Suffering from Paralysis of the Right Atrium . 780
222. — Phlebogram in a Case of Tricuspid Insufficiency with Cardiogram for Com-
parison ............... 780
223. — Normal Electrocardiograms Obtained by Photographing the Movements of a
Sensitive Galvanometer ............ 783
224. — New Nicholson Sphygmomanometer . . . . . . . . . 794
225. — Janeway Sphygmomanometer ........... 795
226. — New Oliver Sphygmomanometer .......... 795
227. — Tycos Sphygmomanometer ............ 796
228. — Faught's Blood Pressure Apparatus . ....... 796
229. — Uskoff's Blood Pressure Apparatus ......... 797
230. — Determination of Maximal and Minimal Pressure by Erlanger's Apparatus . 800
231. — Auscultatory Method of Determining Minimal Blood Pressure . . . 800
232. — Gallavardin's Diagrammatic Representation of the Auscultatory Phases . 801
233. — Gallavardin's Diagram Illustrating the Relationship Between the Oscillatory
and Auscultatory Phenomena .......... 602
234.— A Bracelet Stethoscope ............ 803
235. — Chart Showing Course of Blood Pressure in Radial Artery . . . .810
xlvi LIST OF ILLUSTKATIONS
FIQ. PAGE
236.— Chart Showing Absolute Sphygmograms and Pulse Tracings from Two Per-
sons 810
237. — Apparatus of Hooker and Eyster for Determining the Venous Pressure . 811
238. — Phlebogram and Arteriogram in the Youthful Type of Irregularity . . 827
239. — Phlebogram and Arteriogram in Pulsus irregularis respiratorius . . 827
240. — Electrocardiogram in Sinus Arhythmia. Respiratory Form .... 828
241. — Electrocardiogram of Dropped Beats 828
242. — Diagram of Disturbance Produced by a Ventricular Extrasystole . . . 829
243. — Ventricular Extrasystoles 830
244. — Ventricular Extrasystoles 830
245. — Electrocardiograms of Ventricular Extrasystoles 831
246. — Diagrammatic Representation of an Atrial Extrasystole 832
247. — Extrasystole Arising in the Atrium or Auricle 833
248. — Atrial Extrasystole 833
249. — Electrocardiograms of Atrial, or Auricular Extrasystole 834
250. — Diagram Showing Nodal Extrasystole 834
251. — Electrocardiogram of Extrasystole Arising at Point Somewhere Between
the Auricles and Ventricles 835
252. — Pulsus bigeminus 835
253. — Paroxysmal Tachycardia. Tracing Taken During Attack 838
254. — Paroxysmal Tachycardia. Tracing Taken After Attack 838
255. — Electrocardiogram in Paroxysmal Tachycardia, Atrial or Auricular Type . 839
256. — Electrocardiogram in Paroxysmal Tachycardia, Ventricular Type . . . 839
257. — Diagram of Atrial Fibrillation 840
258. — Phlebogram and Arteriogram in Pulsus irregularis perpetuus with Atrial
Paralysis 840
259. — Electrocardiograms in Atrial Fibrillation and Flutter 841
260. — Diagram of Atrial and Ventricular Beats in Atrial Flutter .... 844
261. — Diagram of Pulsus alternans Due to Disturbance of Cardiac Contractility . 846
262. — Jugular Phlebogram and Brachial Arteriogram in Paroxysmal Tachy-
cardia with Ventricular Venous Pulse 846
263. — Delayed Conductivity 848
264. — Remarkable Delay in Conduction Time with Beginning Heart Block . . 849
265. — Diagram of 2:1 Heart Block 849
266. — Beginning Heart Block 850
267. — Tracing from the Right Jugular and Brachial During a Period of Partial
Block 851
268. — Tracing from the Right Jugular and Brachial in a Case of Partial Vagus
Block 851
269. — Chart of Heart Block Showing Complete Dissociation Between the Con-
tractions of the Auricles and those of the Ventricles 852
270. — Chart Showing Jugular Phlebogram and Radial Arteriogram in a Case of
Complete Heart Block 852
271. — Electrocardiogram in Complete Heart Block 853
272. — Electrocardiogram from a Patient with a Lesion of One Branch of the
Bundle of His • ... 854
273.— Wall of Left Ventricle 855
274. — Electrocardiograms in Hypertrophy of Left Ventricle . . . . . 868
275. — Electrocardiogram in Hypertrophy of the Atria (or Auricles) . . . 870
276. — Erythema multiforme with Chorea, Mitral Insufficiency and Stenosis and
Chronic Tonsillitis " 873
277. — Frontal Section Through a Pericardial Exudate 880
278. — Diagram Showing Factors that May Affect the Cardiohepatic Angles . . 881
278a. — Diagram Showing Factors that May Affect the Cardiohepatic Angles . . 882
279. — Case of Pericarditic Pseudocirrhosis 883
280. — Distribution and Character of the Murmur Due to a Patent Interventric-
ular Septum 896
281. — Ectopia cordis, Secondary to Malformation of the Sternum . 897
LIST OF ILLTJSTKATIOKS xlvii
282. — Shaded Area Showing the Distribution of the Cutaneous Hyperalgesia
After the First Attack of Angina Pectoris 902
283. — After Repeated Attacks of Angina Pectoris the Pain and Hyperalgesia Ex-
tended to the Regions Shaded Here 902
284. — Chart of Blood Pressure Curve Showing Crises of Hypertension . . . 903
285. — Marked Peripheral Arteriosclerosis; Erachial Artery 905
286. — Treponema pallidum from the Wall of an Aneurism 913
287. — Unusually Large Aortic Aneurism 912
288. — Large Thoracic Aneurism. (X-ray) . . 915
289. — Aneurism of Descending Portion of Arch of Aorta. (X-ray) . . . .916
290. — Diagram of Case of Latent Cancer of Stomach with Multiple Thrombi in
the Veins . 922
Part I
General Plan for the Clinical Study
of a Patient
A. Introduction
In no part of medicine has greater progress been made during the
last decade than in clinical diagnosis. The careful control of clinical
studies at the end of the nineteenth century by means of pathological
anatomy and histology prepared the way for what we are now witnessing,
namely, a great development of internal medicine as influenced by patho-
logical physiology. The application of physical, chemical and biological
methods to the study of disease during life is what chiefly characterizes
medicine at the beginning of the twentieth century.
There is such a wealth of new methods and the data that can be
accumulated regarding a single patient are so numerous, that one who
begins to work in internal medicine, unless carefully and judiciously led,
may easily become confused and find difficulty in deciding what is rel-
atively important and what relatively unimportant in a given instance.
An experienced clinician gradually learns to select from the multitude
of phenomena presented to him in a given case the characteristic and
essential features of that higher reality, a "clinical picture," much as an
artist on viewing nature selects and combines, for his purposes, the ele-
ments necessary for his work of art.
The science and art of internal medicine are always leading to the construction
of new clinical pictures. A student is fortunate when, in his early work, he is
privileged to observe the clinical pictures constructed by masters of internal medi-
cine, either as demonstrated to him as living patients, or as vividly reported for
him so that he may visualize the picture by reading the records of observation left
by such masters. But there is no royal road to clinical knowledge and experience;
the novice must learn the technic of the clinical art, beginning with the simplest
methods of analysis, practicing one method after another, at the bedside and in
the laboratory, and continuing his practice under instruction, until he attains to
skill. He must not expect in his earlier analytical studies to be able to judge of
the proportionate value of the individual data obtained by analysis. Only after
considerable experience dare he hope to be able properly to synthesize the data
1
2 PLAN" FOE CLINICAL STUDY OF PATIENT
and to compose a clinical picture in which the interest will center in the most im-
portant facts, with all the accessory facts duly subordinated. Native capacity for
clinical work is essential to the highest success. In the study of pictorial art nearly
everyone can learn to paint pictures by long study and training, but not everyone
can become a Velasquez; similarly, any person of average intelligence can learn
the technic of studying patients, but it is not given to many to compose clinical
pictures as did Sydenham and Graves, or Laennec and Trousseau, or Friedreich
and Kussmaul, or Flint, Janeway, and Fitz, to mention only some of the greater
internists no longer living.
References
1. Systems and Ilandboolcs of Medicine
Allbutt (Sir T. C.) & Rolleston (H. D.). A system of medicine, by many writers. Edited
by Thomas Clifford Allbutt and Humphrey Davy Rolleston. 9 vols.
London, 1906-1911, Macmillan & Co. S°.
Gilbert (A.} & Thoinot (L.). Nouveau Traite de Medccine et de Therapeutique. 40 fasc.
Paris, 1908-1913, J. B. Bailliere & fds.
Mohr (L.) & Staehelin (R.). Handbuch der inneren Medizin, bearb. von L. Bach, J.
Baer [et al.}. Hrsg. von L. Mohr & R. Staehelin. 6 v. Berlin, 1911-
1914, J. Springer. 8°.
Nothnagel (H.). Specielle Pathologic und Therapie. Ilrsg. von Hermann Nothnagel
unter Mitwirkunff von M. Bernhardt, 0. Binswangcr [et al.}. lift. 1-17.
8°. Wien, 1896-1904.
Osier (Sir William) & McCrae (Thomas). Modern medicine, its theory and practice in
original contributions by American and foreign authors. 2 ed. Phila-
delphia, 1915, Lea & Febiger. 5 vols. 8°.
2. Textbooks of General Practice
Anders (J. M.). A text-book of the practice of medicine. 6th ed., revised. Roy. 8°. Phila-
delphia, New York & London, 1903.
Bovaird (David), Jr. Internal medicine. Philadelphia & London, 1912, J. B. Lippincott
Co. 635 p., 7 pi. 8°.
Debove (G. M.) & Sallard (A.). Precis de pathologic interne. 2e ed. 2 vols. Paris,
1913, J. Lamarre & Cie. 952, 1044 P> 8°.
Dieulafoy (G.). A text-book of medicine. Authorized English transl. from the 15th ed.
of " Manuel de pathologic interne" by V. E. Collins andj. A.Liebmann.
2 vols. London, 1910, Bailliere, Tindall & Cox. 2081 p. 4°. Also:
New York & London, 1911, D. Appleton & Co. 1045, 1036 p. 4°.
Edwards (Arthur JR.). A treatise on the principles and practice of medicine. 2d ed.
Philadelphia & New York, 1909, Lea & Febiger. 1257 p. 8°.
von Mering (Joseph) Frhr. Lehrbuch der inneren Medizin, bearbeitet von D. Gerhardt [et
al.]. Hrsg. von L. Krehl. 7. Aufl. Jena, 1911 , G. Fischer. 1298 p.,
8 pi. 4°>
Monro (Thomas Kirkpatrick). Manual of medicine. 3d ed. London, 1911, Bailliere.
Tindall & Cox. 1045 p. . 8°.
Osier (Sir William). The principles and practice of medicine. 8th ed., revised with the
assistance of Thomas McCrae. New York & London, 1912, D. Appleton
& Co. 1250 p. Roy. 8°.
von Strumpell (Adolf). A text-book of medicine. 4th ed. Transl. from the 17th Ger. ed.
by H.F. Vickery and P. C. Knapp. 2 vols. New York & London, 19119
D. Appleton & Co. 831, 800 p. 8°.
INTBODUCTION 3
von Striimpell (Adolf}. Lehrbuch der speziellen Pathologic und Therapie der inneren
Krankheiten. 18. Aufl. 2 v. Leipzig, 1912, F. C. W. Vogel 762 v ,
3 pL; 880 p., 3 pi. 4°.
Taylor (Frederick). The practice of medicine. 9th ed. London. 1911, J. & A. Churchill
1137 p., 8 pi. 8°.
Tyson (/.) & Fussell (M. H.). The practice of medicine, with special reference to diagnosis
and treatment. 6th ed. Philadelphia, 1914, P. Blakiston's Son & Co
1211 p. 8°.
3. Textbooks of General Medical Diagnosis
Anders (James Meschter} & Boston (Leonard Napoleon). A text-book of medical
diagnosis. Philadelphia & London, 1911, W. B. Saunders Co. 1195 p
25 pi. Roy. 8°.
Brugsch (Theodor} & Schittenhelm (Alfred). Lehrbuch klinischer Untersuchungs-
methoden. 2. Aufl. Berlin & Wien, 1911, Urban & Schwarzenberg.
727 p., 11 pi. 4°.
Butler (G. R.). The diagnostics of internal medicine. 3d ed. New York & London, 1909,
D. Appleton & Co. 1193 p. 8°.
Eulenburg (A.),Kolle (W.) & Weintraud (W.) . Lehrbuch der klinischen Untersuchungs-
methoden und ihrer Anwendung auf die specielle drztliche Diagnostic.
Berlin & Wien, 1905, Urban & Schwarzenberg. 2 v. 1707 p., 4 pi. 4°.
Greene (C. L.). Medical diagnosis. 3d ed. Philadelphia, 1910, P. Blakiston's Son & Co.
744 P- 8°.
Hare (H. A.}. Diagnosis in the office and at the bedside; the use of symptoms and physical
signs in the diagnosis of disease. 7th ed. Philadelphia & New York,
Lea & Febiger. 547 p. 8°.
Hutchison (R.) & Rainy (H.). Clinical methods; a guide to the practical study of medi-
cine. London, Paris cfc Melbourne, 1897. 16°.
Krause (Paul). Lehrbuch der klinischen Diagnostik innerer Krankheiten mil besondere^
Jlcrucksichtigung der Untersuchungsmethoden. Ed. by P. Krause. 2.
Aufl. Jena, 1913, G. Fischer. 1050 p., 3 pi. 4°.
Morrow (A. S.). Diagnostic and therapeutic technic. Philadelphia & London, 1911, W.
B. Saunders Co. 775 p. 8°.
Musser (J. H.). A practical treatise on medical diagnosis. 6th ed., revised by J. H. Musser,
Jr. Philadelphia & New York, 1913, Lea & Febiger. 793 p. 8°.
Paviot (Jean-M.). Precis dc diagnostic medical et de semeiologie. 2e ed. Paris, 1912,
0. Doin et fits. 1312 p. 8°.
Sahli (Hermann}. A treatise on diagnostic methods of examination. Edited iviih additions
by Nathaniel Bowditch Potter. 2d ed. Philadelphia & London, 1911,
W. B. Saunders Co. 1229 p., 11 pi. 4°.
Seifert (O.) & Muller (F.). Taschenbuch der medizinsch-klinischen Diagnostik. 16.
Aufl. Wiesbaden, 1913, J. F. Bergmann. 378 p. 8°.
Sergent (E.) [et al.]. Technique clinique medicate et semeiologie elementaires. Paris,
1913, A. Maloine. 773 p. 8°.
Simon (Charles E.) A manual of clinical diagnosis. 7th ed. Philadelphia & New
York, 1911, Lea & Febiger. 778 p., 25 pi. Roy. 8°.
Wilson (James Cornelius}. A handbook of medical diagnosis. 3d ed. Philadelphia &
London 1911, J. B. Lippincott Co. 1461 p., 14 pi. Roy. 8°.
4. Textbooks of Physical Diagnosis
Anders (H. 5.). Physical diagnosis, with case examples of the inductive method. New
York & London, 1907, D. Appleton & Co. tf5 p. 8°.
4 PLAN FOE CLINICAL STUDY OF PATIENT
Cabot (Richard Clark). Physical diagnosis. 5th ed. New York, 1912, W. Wood &
Co. 540 p., 5 pi. Roy. 8°.
Da Costa (John Chalmers). Principles and practise of physical diagnosis. 2d ed.
Philadelphia & London, 1911, W. B. Saunders Co. 357 p. 8°.
Flint (A.). A manual of auscultation and percussion. Embracing the physical diagnosis of
diseases of the lungs and heart and of thoracic aneurysm, and of other
parts .' 6th ed., revised by Haven Emerson. Philadelphia & New York,
1912, Lea & Febiger. 361 p. 12°.
Gee (S.). Auscultation and percussion, together with other methods of physcial examination
of the chest. 6th ed. London, 1908, H. Frowde. 327 p. 8°.
Gerhardt (C.). Lehrbuch der Auskultation und Perkussion, mil bes. Beriicksicht. der Be-
sichtigung, Betastung und Messung der Brust und des Unterleibes zu
diagnost. Zwecken. 6. Aufl. Tubingen, 1900, H. Laupp. 381 p. 8°.
5. Laboratory Methods of Diagnosis
Abderhalden (E.). Handbuch der biochemischen Arbeitsmethoden. 7 v. Berlin, 1912-1914.
Bard (Louis). Precis des examens de laboratoire employes en clinique. 2e ed. Paris,
1911 , Masson & Cie. 792 p. 8°.
Brugsch (T.) & Schittenhelm (A.). Technik der speziellen klinischen Untersuchungs-
methoden. 2 vol. Berlin & Wien, 1914, Urban & Schwarzenberg.
1078 p., 1 pi.
Emerson (Charles Phillips). Clinical diagnosis. 4th ed. Philadelphia & London
1913, J. B. Lippencott Co. 735 p., 5 pi. Roy. 8°.
Faught (Francis Ashley}. Essentials of laboratory diagnosis. 3d ed. Philadelphia,
1911, F. A. Davis Co. 350 p., 11 pi. 8°.
French (Herbert [Stanley]). Medical laboratory methods and tests. 3d ed. London.
1912, Balliere, Tindall & Cox. 210 p. 12°.
Guiart (Jules) & Grimbert (Leon-Louis). Precis de diagnostic chimique, microscopique
et parasitologique. 3e ed. Paris, 1912, J. Lamarre & Cie. 1062 p. 8°.
von Jaksch (R.). Clinical diagnosis; the bacteriological, chemical and microscopical evi-
dences of disease. 5th ed., edited by A. E. Garrod. London, 1905, C.
Griffin & Co. 628 p. 8°. Also, J. B. Lippincott Co., Philadelphia &
London.
Lenhartz (H.) Manual of clinical microscopy and chemistry. Transl. from the Jtfh Ger.
ed., with notes and additions, by Henry T. Brooks. Philadelphia, 1904,
F. A. Davis Co. 435 p. 8°.
Mikroskopie und Chemie am Krankenbett. Fur Studierende und Aerzte.
6. Aufl. Berlin, 1910, J. Springer. 417 p. 8°.
Morris (Roger S.). Clinical laboratory methods; a manual of technique and morphology.
New York & London, 1913, D. Appleton & Co. 363 p. 8°.
Reale (E.). Manuale di chimica clinica. Milano, 1914. 1+78 p.
Simon (Charles E.}. A manual of clinical diagnosis by means of laboratory methods. 8th
ed. Philadelphia & New York, 1914, Lea & Febiger. 809 p. 8°.
Stitt (E. R.). Practical bacteriology, blood work and animal parasitology, including bac-
teriological keys, zoological tables and explanatory clinical notes. 3d ed.
Philadelphia, P. Blakiston's Son & Co., 1913. 408 p., 4 pi.
Webster (Ralph Waldo}. Diagnostic methods, chemical, bacteriological and microscopical.
4th ed. Philadelphia, 1914, P. Blakiston's Son & Co. 774 P-
Williams (Byron G. R.) & Williams (Edwin Gordon Culbertson). Laboratory
methods, with special reference to the needs of the general practitioner.
With an introduction by Victor C. Vaughan. St. Louis, 1912, C. V.
Mosby Co. 204 p. Roy. 8°.
Wood (Francis Carter). Chemical and microscopical diagnosis. 3d ed. New York &
London, 1911, D. Appleton & Co. 815 p., 9 pi. Roy. 8°.
nSTTKODUCTION 5
6. Tropical Medicine
Castellani (A.) & Chalmers (A. /.)• Manual of tropical medicine. 2d ed. New York,
1913, W. Wood & Co. 1747 p. 8°. Also, London, 1913, Bailliere,
Tindall & Cox.
Grail & Clarague. Traite de pathologie exotique. Paris, 1913.
Lambart (H. C.}. A practical handbook of the tropical diseases of Asia and Africa. Lon-
don, 1914, C. Griffin & Co. 339 p. 8°.
Manson (Sir P.)» Tropical diseases, a manual of the diseases of warm climates. Jfiln, ed.
London, 1907, Cassell & Co., Ltd. 896 p. 12°. Also, W. Wood &
Co., New York.
Mense (C.). Handbuch der Tropenkrankheiten. 3 v. Leipzig, 1905-06, J. A. Barth,
854, 472, 818 p. 8°.
Rogers (L.) Fevers in the tropics; their clinical and microscopical differentiation, including
the Milroy lectures on kald-azar. 2d ed. London, 1910, H. Frowde,
428 p. 4°-
Scheube (B.). Die Krankheiten der warmen Lander. 4- Aufl. Jena, 1910, G. Fischer,
1072 p. 8°.
Stitt (E. /£.)• The diagnostics and treatment of tropical diseases. Philadelphia, P. Blak-
iston's Son & Co., 1914. 421 p. 8°.
Ziemann (H.). Gesundheitsratgeber fur die Tropen. Berlin, 1913, D. Reimer. 63 p.
1. History of Medicine
Allbutt (T. C.) & Payne (J. F.). The history of medicine. In Syst. Med., London, All-
butt & Rolleston, 1910, i, 1-45. 8°.
Baas (Johann Hermann). Outlines of the history of medicine and the medical profession.
Transl. by H. E. Handerson. New York, 1889, J. H. Vail. 1173 p. 8°.
Bayle & Thillaye. Biographic medicale par ordre chronologique d'apres Daniel Leclerc,
Eloy, etc. Mise dans un nouvel ordre, revue ei complelee. 2 v. Paris,
1855, A. Delohaye. 560, 950 p. 8°.
Camac (C. N. B.). Epoch-making contributions to medicine, surgery and the allied sciences.
Being reprints of those communications which first conveyed epoch-making
observations to the scientific world, together with biographical sketches of
the observer. Collected by C. N. B. Camac. Philadelphia & London,
1909, W. B. Saunders Co. 44$ P- 8°.
Garrison (Fielding H.}. An introduction to the history of medicine, with medical chron-
ology, bibliographic data, and test questions. Philadelphia & London,
1913, W. B. Sanders Co. 763 p. 8°.
Gross (S. Z>.). History of American medical literature, from 1776 to the present time.
Philadelphia, 1876, Collins. 85 p. 8°.
Haeser (Heinrich). Lehrbuch der Geschichte der Medicin und der epidemischen Krank-
heiten. S.Aufi.,3Bde. Jena, 1875-1882,0. Fischer. 8°.
Hirsch (A.). Handbuch der historisch-geographischen Pathologie. 2. Aufl., 3 Bde. Stutt-
gart, 1881-1886, F. Enke. 8°.
Kelly (Howard A.). Cyclopedia of American medical biography. 2 v. Philadelphia,
1912, W. B. Saunders Co. 424, 545 p. 8°.
Meunier (Leon). Histoire de la medicine depuis ses origines jusqu'd nos jours. Paris,
1911, J. B. Bailliere & fils. 64% p. 8°.
Mumford (James G.}. A narrative of medicine in America. Philadelphia & London,
1903, J. B. Lippincott Co. 508 p. 8°.
Neu burger (Max). History of medicine. Transl by E. Play fair. Vol.1. London, 1910 ',
H. Frowde & Hodder & Stoughton. 404 P- 8°.
6 PLAN FOE CLINICAL STUDY OF PATIENT
Packard (Francis /?.)• The history of medicine in the United States. A collection of facts
and documents relating to the history of medical science in this country,
from the earliest English colonization to the year 1800; with a supple-
mental chapter on the discovery of anesthesia, Philadelphia & London,
1901. J. P. Lippencott Co., 542 p. 8°.
Pagel (Julius L.}. Geschichte der Medicin. Berlin, 1898, S. Karger. 959 p. 8°.
Biographisches Lexicon hervorragender Aerzte des neunzehnten Jahr-
hunderts, mit einer historischen Einleitung. Berlin & Wien, 1901, Urban
& Schwarzenberg. 1983 p. 8°.
Park (Roswell). An epitome of the history of medicine; based upon a course of lectures de-
livered in the University of Buffalo. 2d ed. Philadelphia, New York &
Chicago, 1899. F. A. Davis Co., 570 p. 8°.
Puschmann (Theodor). Handbuch der Geschichte der Medizin. Begrundet von Th.
Puschmarin. Bearbeitct von Arndt, Bartels, Becher [et al.\. Hrsg. von
Max Neuburger und Julius Pagel. Jena, 1903-5. 3 v.
Stephen (Leslie}. Dictionary of national biography. London, 1885-1912. 68 v.
Withington (E. T.). Medical history from the earliest times. A popular history of the
healing art. London, 1894, Scient. Press. 424 p. 8°.
8. Oilier General Reference Books
Adami (J. G.). The principles of pathology. Vol. I: General pathology. 2d ed. Phila-
delphia & New York, 1910, Lea & Febiger. 1027 p. 8°.
Adami (J. G.) & Nicholls (A. G.). The principles of pathology. Vol. II: Systemic
pathology. 2d ed. Philadelphia & New York, 1911, Lea & Febiger.
1160 p. 8°.
Aschoff (L.). Pathologische Anatomie. Ein Lehrbuch fiir Studierende und Aerzte. 3d ed.,
2 vols. Jena, 1913. 1851 p.
Bernard (Claude). Introduction a V etude de la medccine experimentale; avec des notes
critiques par.le R. P. Serlillanges. Paris, 1900. 100 p. 12°.
Bramwell (Byron). Atlas of clinical medicine. 2 v. Edinburgh, 1892-93, T. & A.
Constable. 184, 1^8 P- fol. Ports 1-3 of v. I were issued in 1891.
Cabot (Richard Clarke}. Differential diagnosis. 3d ed., 2 v. Philadelphia & London,
1915, W. B. Saunders Co. 8°.
Caille (A.). Differential diagnosis and treatment of disease. New York & London, 1906,
D. Appleton & Co. 896 p. 8°.
French (Herbert}. Index (an) of differential diagnosis of main symptoms, by various
writers. Edited by Herbert French. Bristol, 1912, J. Wright & Sons.
1029 p. 8°.
Fritsch (G. T.}. DieGestalt des Menschen. MitBenutzung der Werke vonE. Earless und
C. Schmidt. Stuttgart, 1899, P. Neff. 173 p. fol.
Leftwich (R. W.}. An index of symptoms with diagnostic methods. J^ik ed. New York,
1910, W. Wood & Co. 451 p. 12°.
McKisack (Henry Lawrence}. A dictionary of medical diagnosis; a treatise on the signs
and symptoms observed in diseased conditions. 2d ed. London, 1912,
Bailliere, Tindall & Cox. 601 p. 8°.
Oliver (Sir Thomas). Diseases of occupation, from the legislative, social and medical
points of view. London, 1908, Methuen & Co. 44@ P'
de Quervain (F.}. Spezielle chirurgische Diagnostik fiir Studierende und Aerzte. 3d ed.
Leipzig, 1911. F. C. W. Vogel. 730 p., 4 pi. 8°.
Rosenau (M. J.}. Preventive medicine and hygiene. New York & London, 1913, D.
Appleton & Co. 1074 P> 8°.
Vierordt H.}. Anatomische, physiologische und physikalische Daten und Tabellen. Zum
Gebrauche fur Mediziner. 2. Aufl. Jena, 1906, G. Fischer. 622 p. 8°,
THE CLINICAL HISTOKY 7
9. Journals
These include:
American Journal of Medical Sciences, Philadelphia. Archives of Internal Medicine,
Chicago. Journal of the American Medical Association. Journal of Experimental Medicine,
Lancaster. Journal of Infectious Diseases, Chicago. Journal of Medical Research, Boston.
Ergebnisse der inneren Medizin und Kinder heilkunde, Berlin. Progressive Medicine. A
quarterly digest of advances, discoveries and improvements in the medical and surgical sciences,
Philadelphia. Quarterly Journal of Medicine, Oxford. Southern Medical Journal. Zentral-
blatt fur die gcsammte innere Medizin und ihre Grenzgebiete ( Kongresszentralblatt, Berlin) .
Many other journals, American and foreign, will be referred to in the individual references
throughout the book. For the bibliography of modern medicine the student should consult the
Index Catalogue of the Library of the Surgeon-General's Office (34 vols., 1879-1913), supple-
mented by the monthly " Index Medicus " (1879-1899; 1903-1915}.
B. The Clinical History
In collecting the clinical data, preceding their synthesis to a "clinical
picture/' in an individual case, it is desirable to follow some more or less
systematic plan, for otherwise important points may easily be overlooked.
The results of the clinical analysis are recorded in a so-called Clinical
History.
The clinical history consists of four parts: (1) the anamnesis, (2)
the status praesens, (3) the catamnesis, and (4) the epicrisis.
1. Anamnesis. — This is the account given by the patient and his
friends of the life of the patient previous to the time of examination.
2. Status praesens. — This is the record of the objective examination of
the patient by the physician, with the aid of physical, chemical, and
biological (including psychological) methods.
3. Catamnesis. — This is the subsequent history of the patient, includ-
ing notes on the course of the disease, the kind of treatment used, and
the results thereof.
4. Epicrisis. — This is the physician's final judgment upon the case,
with discussion of all the findings. It is especially valuable for science
in instances in which the clinical history has been controlled by surgical
operation, or, in case of death, by autopsy.
1. The Anamnesis
The taking of a proper anamnesis is not easy. It requires, if it is to
be well taken, a large experience, and a wide familiarity with the phe-
nomena of disease; in the absence of these, it is scarcely possible, by
inquiry, to obtain a correct idea of the previous history of the disease, and
of the subjective symptoms from which the patient suffers. An experi-
enced clinician insists, when possible, on taking the anamnesis himself,
especially in obscure cases. He can much more safely delegate the making
of a physical examination to a less experienced man, than deprive him-
8 PLAN FOE CLINICAL STUDY OF PATIENT
self of the knowledge gained through personally obtaining the anamnestic
data.
Here, as everywhere, however, one has to learn by doing, and in acquir-
ing skill it is well, at any rate for beginners, to follow a definite plan,
asking certain questions, in every case, in serial sequence. Later on, it
may be permissible to take "short cuts." An experienced consultant will
sometimes secure a better anamnesis in five or ten minutes than the fourth
year student can secure in an hour, but the briefer route dare not be'
followed by the tyro. And even the most skillful and experienced will
overlook important items if he deviate too far from a well-ordered plan,
or remain satisfied with too brief a questionaire.
In taking the anamnesis, the physician tries to get as exact a descrip-
tion of the abnormal sensations and feelings of the patient as possible,
their duration, and the order in which they appeared. In recording these,
it is important to distinguish between the actual feelings and sensations
of the patient, and the interpretations or explanations he gives of them.
A layman's diagnosis, while often interesting, is not what -is most helpful
to the physician. When a patient is asked how he suffers, he replies most
often with a "diagnosis," saying that he has "rheumatism," or "catarrh
of the stomach," or "heart disease." AYhile the physician will, for the
moment, patiently listen to such a statement, he should at once ask the
patient why he thinks he has the trouble he mentions, and will put down
as the complaint of the patient, not the latter's diagnosis, but (1) any ob-
jective changes the sick person has noted himself and (2) the subjective
symptoms upon which the layman's diagnosis is based.
(a) The Present Illness
After recording the name, age, occupation, and residence of the pa-
tient, the date on which he is first seen, and the chief complaints for
which he seeks medical help, it is well to ask particular questions about
the present illness, when and how it began, whether it developed sud-
denly or insidiously, how it progressed, and any treatment followed before
consulting the physician. Inquiry is made as to loss of weight or strength,
as to capacity for work, or, if the patient be in bed, as to the time when
}ie had to go to bed.
It is well to ask the patient, also, what he believes caused his illness,
knowing, when the question is asked, that the sick man may be wrong
Jn his belief. In this part of the anamnesis, important data regarding
(1) a preceding trauma, (2) physical or mental overexertion, (3) dietetic
errors, (4) exposure to cold and wet or (5) exposure to infection, may
be obtained. If the patient suffer from an infectious disease, the pos-
sibilities of contagion from other cases in the home, in the neighborhood,
in the school, or elsewhere, should be gone into.
THE CLINICAL HISTOEY 9
After the patient has described, voluntarily, his main symptoms, it
is well to inquire systematically regarding various subjective symptoms
referable to different parts of the body. Among these may be mentioned
pain (location, character, duration, time of appearance, things which
influence it, etc.), headache (position, accompaniments, frequency), dizzi-
ness, ringing in the ears or tinnitus, appetite, nausea or vomiting, state
of digestion, constipation or diarrhea, presence or absence of hemorrhoids,
cough, sputum, dyspnea, palpitation, retrosternal pain, swelling of the
ankles, micturition, nocturia, the sexual functions, sleep, memory, con-
centration of attention, depression, power of decision, fears, feelings of
unreality, etc.
In framing the questions, one keeps in mind the commoner subjective
symptoms associated with the different bodily systems (respiratory system,
circulatory system, digestive system, urogenital system, locomotor system,
nervous system, metabolic system, endocrine glands). A symptom referred
to a definite organ may depend upon a distant, or a general, rather than
upon a local, cause ; thus, the complaint of dyspnea need not indicate a pri-
mary disease of the lungs or of the respiratory passages, but may be due
to intoxication of the nervous system from renal disease, to anemia, or to
some other cause. Similarly, a fast pulse (tachycardia) may not indicate
a primary disease of the heart, but may depend upon an intoxication of
the sympathetic nervous system due to disease of the thyroid gland (as
in Graves's disease). When the subjective symptoms point with consid-
erable certainty to some one of the several systems of the body, the
investigation may be supplemented by a whole list of questions directed
especially toward the condition of the system under suspicion.
(b) The Previous History of the Patient
After gathering the important data regarding the present illness, the
earlier history of the patient may conveniently be gone into, especially
with regard to (1) diseases of childhood, (2) post-childhood diseases,
(3) the general bodily functions and the sexual life, and (4) the patient's
habits, education and experience.
Among the diseases of childhood concerning which we inquire are
included measles, German measles, diphtheria, scarlet fever, small-pox,
affections of the lymph glands, tonsillitis, adenoids, rickets and convul-
sions.
Of the post-childhood diseases we inquire especially regarding infec-
tions like typhoid, malaria, pneumonia, and pleurisy, and then briefly
record any other serious disease passed through. In "nervous patients,"
we inquire especially regarding earlier periods of strain, of "nervous
breakdown," or of "fainting spells." In men, the existence of a preced-
ing gonorrheal, luetic, or other venereal infection should always be asked
10 PLAN FOE CLINICAL STUDY OF PATIENT
about, and if such an infection has existed, full details regarding it, and
the treatment followed, should be recorded.
The general bodily functions and the sexual life should be inquired
into, the latter to a variable extent in different cases. Here the tact and
common sense of the physician must guide him as to how much question-
ing is necessary and will be helpful. Any unnecessary investigation of
sexual matters is to be deprecated, but the physician must not shrink from
any inquiry which may be of importance for the patient's welfare. In
women, we inquire regarding menstruation, pregnancies, puerperal states,
interrupted pregnancies, children born dead, etc. In men, we inquire
regarding sexual power (potentia), sexual desire (libido), and, if
necessary, regarding sexual excesses or abnormalities. Inquiry regarding
venereal disease has already been referred to.
In inquiring into the habits, education, and experience of a patient it
is necessary to know something of his social state (luxury, poverty) and
of his mode of life (muscular and mental activities). Any possible
injuries associated with his occupation should be considered. The use
of stimulants, and especially any abuse of these, should be investigated
(tea and coffee, tobacco, alcohol).
(c) The Family History
We next study the evidence regarding the nature of the germ plasm
of the patient as judged of by the results of inquiries concerning his
ancestors and his children, for we can get information regarding heredity
only through data regarding either the antecedents (direct or collateral)
or the descendants of the patient. We ask whether the father and mother
are living, or, if dead, the age and cause of death, and what diseases they
suffered from during their lifetime. Similar inquiries are made regard-
ing the sibs (sisters and brothers), and the children of the patient. In
some instances, further inquiries regarding the family history (uncles,
aunts, cousins, nephews and nieces, etc.) may be desirable. Should the
disease from which the patient suffers be one in which heredity is
believed to play a part (diabetes, gout, alcoholism, nervous and mental
diseases, lues, tuberculosis, endocrinopathies, hemophilia, etc.), it may
be well to construct a family tree, using squares to represent the males
and circles to represent the females, indicating, by some special shading,
the persons in whom the disease appeared.
2. The Present State of the Patient (Status praesens)
After taking the anamnesis, the physician makes a record of his own
objective examination of the patient, of the state in which he finds him
(status praesens). It is customary to describe (1) the general condition
THE CLINICAL HISTOEY 11
of the patient (attitude and gait, if up and about; position assumed, if
lying in bed ; state of nutrition ; strength ; general appearance and habitus ;
facial expression; speech; condition of skin; visible mucous membranes,
and superficial blood vessels) ; and (2) the results of examination of the
various organs and organ-systems of the body. This latter portion of
the record may be made in either one of two ways. Some prefer to
classify the findings under headings corresponding to the individual sys-
tems (circulatory, respiratory, digestive, nervous, urogenital, etc.) ; others
like to classify the findings according to the regions which are most con-
veniently examined in succession (head, neck, thorax, abdomen, extremi-
ties), and, afterwards, the results of various laboratory tests are appended.
For systematic analysis and description in a text-book, the former method
offers especial advantages ; but in practical application at the bedside, the
latter method is the easier to follow.
(a) The General Condition of the Patient
i. Gait and Attitude
If the patient be up and about, we can form some idea of the state of
his muscles, his nervous system, and especially his organs of equilibrium,
from the position he assumes and the way he walks/ The experienced
physician can also, from the first glance at the patient, gather data which
help him to "size up" the individual — to "place him" — physically, psy-
chically, and socially. Occupation, study, and social surroundings leave
their stamp upon the individual. The greater the physician's knowledge of
the world, and the wider his experience among all classes of human beings,
the more acute will he be, other things being equal, in his discernment at
the first encounter with the patient. Insight into human nature, tact,
sympathy, and good judgment are the qualities in the physician, which
at the first meeting help to gain access to the patient's personality and to
inspire his confidence.
The different forms of abnormal gait and attitude are described in
the section on examination of the nervous system.
ii. Position of the Patient in Bed
The patient usually assumes the position which is most comfortable
for him. If an unusual position is maintained, the reason for it should
be sought ; it may be the only position possible for the patient.
To a certain extent the breathing of a patient determines his posture
in bed ; the more marked the shortness of breath, the less possible is the
recumbent posture. A patient may be compelled to sit up in bed in order
to breathe (orthopnea). The details of the various postures assumed by
patients have been made the object of an especial study by Ebstein (q. v.).
PLAN FOE CLINICAL STUDY OF PATIENT
Reference
Ebstein (E.). Ueber Lage und Lagerung von Krariken in diagnostischer und therapeu*
tischer Beziehung. Ergebn. d. inn. Med. u. Kinderh., Berlin, 1912,
viii, 379-453.
iii. Height, Weight and Build
It is well to record the patient's exact height in cubic centimeters, to
estimate from this, by one of the formulae available (see chapter on
Obesity), what his ideal weight would be, and to place beside this his
actual weight as determined by the scales. A note should be made also
as to the bony framework (strong; delicate), the musculature (well devel-
1 23
Fig. 1. — The Male Skeleton, 1 — Anterior View ; 2 — Posterior View ; 3 — Lateral View.
oped; feeble), and the amount of subcutaneous fat. In connection with
the bony framework, the "span" or distance between the tips of the fingers
of the two hands when the arms are stretched out horizontally from the
shoulders, and also the form of the thorax (normal, paralytic, pyriform,
emphysematous, rickety, pigeon-breast, funnel-chest, etc.) should be noted.
The general habitus of the patient should be recorded (habitus asthenicus,
habitus phthisicus, habitus apoplecticus, etc.). In abnormal cases, besides
THE CLINICAL HISTOEY
13
the measurements of the epigastric angle, the so-called Lenhoff index may
be determined — that is, the distance from the episternal notch to the
symphysis pubis, multiplied by 100, divided by the minimal circumference
of the abdomen. In normal women, in the recumbent position, this index
2 13
Fig. 2. — The Female Skeleton, 1 — Anterior View ; 2 — Posterior View ; 3 — Lateral View.
averages 75. In men it is generally less than 75. A higher index (over
80) is met with in individuals with general visceroptosis (asthenia uni-
versalis congenita).
A note should be made of any anomalies of development (e. g., super-
numerary fingers or toes; supernumerary nipples), or of any "stigmata of
degeneration" visible.
iv. Mental State
At the very beginning of the objective examination, a note is made
of the general mental state of the patient, whether he is conscious or
unconscious, restless or delirious, and whether the state be one of apathy,
14
PLAN FOR CLINICAL STUDY OF PATIENT
of stupor, of drowsiness (sopor) or of deep unconsciousness (coma). One
notes whether the speech is normal or abnormal (hesitation, stuttering,
syllable stumbling, dysarthria, asphasia, aphonia). One's first impres-
sions regarding the memory of the patient for recent events, and his mood
(depression, euphoria) should also be recorded. These first impressions
may give clues for the course of a precise psychiatric examination to be
made later,
v. Body Temperature
This is taken by means of a clinical thermometer, either by mouth,
by axilla, or by rectum (see Diagnosis of Infectious Diseases), and the
result recorded in a tem-
perature chart, on which
the number of respira-
tions and the pulse rate
per minute, the number
of stools per day, and
the amount of urine (in
cubic cent i meters) void-
ed each 24 hours, may
also be noted.
vi. Skin and Visible Mu-
cous Membranes
The color, thickness
and transparency of the
skin are observed. An
abnormal pallor may
point to anemia, or at
any rate to the necessity
for a blood examina-
tion. After some expe-
rience one learns to dis-
tinguish between the pallor due to secondary anemias (following hemor-
rhages or wasting diseases) or to the pseudo-anemias (oligemia, etc.), and
the peculiar waxy color of the skin seen in chlorosis (transparent yellowish
white or alabaster white), or lemon-yellow tint or straw-yellow tint seen
in the Addison-Biermer type of hemolytic anemia. Pallor is not always
due to anemia, but may be due to a pseudo-anemia, in which there is an
abnormally small supply of blood in the vessels of the skin (collapse,
tobacco poisoning, mitral stenosis, syncope, aortic insufficiency).
An abnormally red skin, due to dilatation of the vessels, may be tran-
sient (blushing, emotional excitement), or more permanent, as in fever.
Fig. 3. — Supernumerary Nipples, when Present, Other Stig-
mata of Degeneration Should Be Looked For. (Medical
Clinic, J. H. II.)
THE CLINICAL HISTOBY 15
alcoholic intoxication, polycythemia rubra, or congestions of the head due
to disturbances of sympathetic innervation.
Sometimes the skin looks bluish red, or cyanotic. When the whole
skin assumes this color (general cyanosis) the cause may lie in general
venous stasis, due to faulty action of the right ventricle (myocardial
insufficiency; congenital heart disease), or to interference with the gas
interchange in the lungs (dyspnea from various causes, emphysema, etc.),
or, again, to polyglobulia.
A local cyanosis depends usually upon local obstruction (pressure,
thrombosis) to venous outflow, or it may be secondary to hindrance to the
arterial flow in the periphery, in which event the skin over the cyanotic
part feels cold. In the latter case, the danger of gangrene should always
be kept in mind. Among the forms of local cyanosis, or asphyxiation,
may be mentioned: (1) that occurring in the fingers or toes in Kaynaud's
disease, and (2) that due to crises of arterial constriction in arteriosclerosis.
When the skin becomes yellow, due to the deposit in it of bile pigment,
the sclerae of the eye beneath the conjunctivae will also be seen to be
yellow. Such a discoloration, known as jaundice, or icterus, follows upon
the entrance of bile into the general circulation (see Diseases of the
Liver).
A peculiar bronzed appearance of the skin is met with in that remark-
able disease of the suprarenal glands known as Addison's disease. The
bronzing affects mostly the exposed parts of the body and those areas that
are normally more or less pigmented (face, neck, waist, breasts, linea alba,
axillae, perineum), as well as those that are exposed to the pressure of
the clothing. The bronzing may affect the mucous membrane of the mouth,
and, in white people, this is of diagnostic importance; "blue gums" in
the negro may not represent any abnormality. The fingernails do not
become pigmented in Addison's disease.
Another form of bronzing, usually not so dark as that seen in Addi-
son's disease, is the brown discoloration met with in hemochromatosis
(q. v.) and in the so-called "bronze diabetes," which so often accompanies
its later stages. If a bit of the skin be excised for histological study,
characteristic changes are found.
Local pigmentations in the skin follow upon local irritation of various
sorts, especially in people of dark complexion ; thus, after sunburn,
exposure to the x-ray, the application of plasters or of heat, areas of
pigmentation appear. Similarly, after skin lesions (eruptions, ulcers,
herpes), the skin becomes pigmented. Pigmentation, associated with
scratch-marks and filth of the skin, is common in pediculosis (morbus
vagabondi). Sometimes, in pediculosis pubis, small blue spots (taches
bleuatres; maculae caeruleae) appear on the abdomen and on the thighs.
In pregnancy, the normal pigment deposits of the body are increased
in amount (Moasma uterinum). In Graves's disease, in chronic tuber-
16 PLAN FOE CLINICAL STUDY OF PATIENT
culosis, and in chronic lues, a general yellowish, or brownish, pigmenta-
tion of the skin is not uncommon.
Peculiar pigmentations of the skin may follow the use of drugs ; thus,
patients suffering from gastric ulcer or from tabes, for which silver nitrate
has been taken over long periods, may exhibit a general, dirty gray, or
bluish gray pigmentation of the skin known as argyria. If arsenic be taken
for over three months at a time a general darkening of the skin not infre-
quently occurs (arsenical melanosis).
The skin varies in its thickness and in its moisture. A thick, dry,
harsh skin is met with in myxedema ; a thin, moist, transparent skin is
common in Graves's disease. A fishlike, scaly skin is known as iclitliyosis.
The moisture of the skin depends largely upon the secretion of sweat,
which is under the control of the autonomic nervous system ; thus, very
abundant sweating (hyperhydrosis) is common in vagotonic states, while
dryness of the skin (hypohydrosis) is common in sympathicotonic states.
Sweats are common in the course of various infectious diseases (acute
rheumatic fever, pulmonary tuberculosis, sepsis, malaria). After pro-
fuse sweating, it is common to find on the skin of the trunk numerous
vesicles (miliaria crystallina) , the size of a pin's head or smaller, which
look like minute dewdrops. They are little retention cysts, due to tem-
porary obstruction of the sweat glands. Sometimes the sweat is colored
and stains the clothing; thus, in infections with the Bacillus pyocyaneus,
the sweat may be greenish blue; in jaundice, it may be yellow. Red
sweat, or so-called bloody sweat, has been shown to be due to the presence
of the Bacillus prodigiosus.
Cutaneous eruptions (macular, papular, vesicular, etc.), or exanthems,
should always be carefully studied ; thus, rose spots upon the abdomen or
back may be helpful in the diagnosis of typhoid fever. An early acquaint-
ance with the eruption in the acute exanthematous diseases (scarlet fever,
measles, chicken-pox, small-pox, etc.) is desirable, in order that humiliat-
ing mistakes may be avoided. The copper-tint common to luetic eruptions
is very characteristic, and once observed, is easily recognizable.
If hemorrhages are present in the skin, their form, size and distribu-
tion should be noted. Minute, punctiform hemorrhages are spoken of as
petechiae; larger hemorrhages are referred to as eccliymoses, or blood-
extravasations. Petechiae should not be confused with minute naevi or
telangiectases; when the latter are multiple they are sometimes associated
with recurring epistaxis (Osier).
Petechiae may be due to insect bites, to septic emboli of the cutaneous
vessels, or to hemorrhages dependent upon diseases associated with the
so-called hemorrhagic diathesis.
The presence of ulcers, scars, or bed-sores, and their size, location,
and cause (when ascertainable), should be recorded.
THE CLINICAL HISTOEY 17
References
Besnier (E.}, Brocq (L.) & Jacquet (L.). La pratique dermatologique. Paris, 1900-
1901, 2 v.roy. 8°, Masson et Cie.
Bulkley (L. /).)• On the relations of diseases of the skin to internal disorders. With ob-
servations on diet, hygiene and general therapeutics. New York, 1906,
Rebman Co. 190 p. 8°.
Crocker (H. R.). Diseases of the skin; their description, pathology, diagnosis and treatment,
with special reference to the skin eruptions of children, and an analysis of
fifteen thousand cases of skin disease. 3d ed. Philadelphia, 1903, P.
Blakiston's Son & Co. 1466 p. 8°.
Darter (/.). Precis de dermatologie. Paris, 1909, Masson & Cie. 721 p. 8°.
Duhring (L. A.}. Cutaneous medicine: a systematic treatise of the diseases of the skin.
Philadelphia, 1895-98, J. B. Lippincott Co. 494 p. 8°.
Gaucher (E.). Maladies de la Peau. Paris, 1909, J. B. Bailliere & fils. 516 p. 8°.
[Nouv. Traite de Med. de Therap., XIV.}
Hewetson (/.). Note on the Significance of laches bleudtres. Johns Hopkins Hasp. Bull.,
1894, V, 19.
Lesser (E.}. Lehrbuch der Haut- und Geschlechtskrankheiten. 13th. ed. Berlin, 1914, J.
Springer. 658 p., 31 pi.
Osier (W.}. On a family form of recurring epistaxis, associated with multiple telangiectases
of the skin and mucous membranes. Johns Hopkins Hosp. Bull., Bal-
timore, 1901, xii, 333-337.
Pusey (W. A.}. The principles and practice of dermatology. 2d ed. New York & Lon-
don, 1911, D. Appleton & Co. 1079 p., 5 pi.
Riecke (E.). Hygiene der Haut, Haare und Nagel im gesunden und kranken Zustande.
2. Aufi. Stuttgart, 1913, E. H. Moritz. 219 p. 8°.
Sabouraud (.R.)* Elementary manual of regional topographical dermatology. Engl. Trans.
by C. F. Marshall. London & New York, The Rebman Co., 1906.
Stelwagon (H. TF.). Treatise on diseases of the skin. 7th ed. Philadelphia & London,
1914, W. B. Saunders Co. 1250 p. 8°
vii. Collateral Circulations
The existence of dilated blood vessels in any part of the body should be
mentioned, if found; thus, varicose veins of the leg, varicocele, and col-
lateral circulations should be looked for.
In obstruction of the portal vein, developing gradually (as in cirrhosis
of the liver, or in lues hepatis), the blood from the portal domain finds
its way into the venae cavae by three roundabout routes :
1. Through the anastomoses of the superior gastric veins with the
esophageal veins to the vena azygos, accounting for esophageal varix and
the hematemesis so common in cirrhosis hepatis;
2. Through the anastomoses of the inferior mesenteric veins with the
hemorrhoidal veins (accounting for the anal hemorrhoids so common in
cirrhosis hepatis and in chronic constipation) ;
3. Through the parumbilical veins (a) to the internal mammary veins
and superior cava, above, and (b) to the inferior epigastric veins and the
femoral and iliac veins and the inferior cava, below, thus accounting for
those large tortuous "central veins" radiating out from the umbilicus and
known as the caput medusae often seen in cirrhosis hepatis.
18 PLAN POK CLINICAL STUDY OF PATIENT
In obstruction of the inferior vena cava, from abnormal pressure of
any sort in the abdomen, it is the lateral veins of the abdominal wall that
are dilated in the formation of the collateral circulation, rather than the
central veins mentioned above as concerned after portal obstruction. Here,
also, the venous outflow from
the lower extremities is inter-
fered with (cyanosis; edema).
In cirrhosis hepatis, with as-
cites, there may be obstruction
both of the portal circulation
and of the circulation through
the inferior vena cava.
Pulsating subcutaneous ar-
teries on the trunk may be ob-
served in instances of congenital
narrowing of the aorta.
Reference
Pleasant* (J. H.}. Obstruction of the
inferior vena cava,
with a report of eigh-
teen cases. Johns
Hopkins Hosp. Rep.,
Baltimore, 1911, xvi,
363-548.
viii. Edema
In edema of the skin and of
the subcutaneous tissue, there is
an increased amount of fluid in
the tissues; the part is swollen,
tense, and, sometimes, glistening
and pale. In non-inflammatory
edema, the part is not painful.
Fig. 4. — Obstruction of the Inferior Vena cava. rm j 'vu J.-L
(Mod. Clinic, J.H. II., after J. Hall Pleasants.) When pressed Upon With the
finger, a depression remains
for some time after the pressure has been removed. In edema of the
extremities, the normal contours disappear. In fresh edema, the skin is
easily indented with the finger-tip, but when the edema has lasted a long
time this grows ever more difficult (boggy edema; tough edema).
When edema exists, its cause should always be sought. While in all
cases edema arises through disturbance of the relation between the for-
mation of lymph and the outflow of lymph from the tissues, this disturb-
ance can arise from several different causes. It may be due :
1. To venous stasis (stasis edema), then occurring first in the depend-
THE CLINICAL HISTOKY 19
ent parts of the body, the ankles on standing, the hack and hips when in
the recumbent posture;
2. To the injury of the blood vessels of the skin occurring in acute
nephritis (nephritic edema), then appearing, usually, first in the face, and
especially in the loose subcutaneous tissue of the eyelids ; 1
3. To various inflammations and intoxications in which no evidence
of cardiac or renal disease exists (cachectic, toxic and inflammatory ede-
mas), as, for instance, in the course of malignant neoplasms or the severe
anemias, or in aserum disease" ;
4. To abnormal autonomic innervations (angioneurotic edema, or
Quincke's edema), as in transitory edema of the upper lip, the parts about
one eye, etc.
ix. The Lymph Glands
In healthy individuals, the lymph glands are scarcely palpable, but
in pathological states they may become enlarged, either all over the body,
or (and this fact is very important for diagnosis) in the regions closest
to some diseased part or organ. When enlarged, they can be felt as round
or bean-shaped lumps, singly or in groups, in the subcutaneous tissue.
One should ascertain whether or not they are soft or hard, tender or
painless on pressure, discrete or matted together and adherent. It is
well, in every case, to palpate systematically the principal accessible
lymph-gland areas (epitrochlear, preauricular, submaxillary, retrocer-
vical, jugular, supraclavicular, infraclavicular, axillary, paramamillary,
thoracic, abdominal, inguinal, popliteal). If there is general enlarge-
ment of all the glands, one thinks of some general infectious or toxic
process (syphilis, tuberculosis, Hodgkin's disease, infectious polyarthritis,
leukemia, aleukemic lymphadenosis, etc.). If there is swelling of certain
groups only, one looks for local infections in the regions drained by the
particular group concerned (tuberculosis, pyogenic infections, plague,
local arthritis, chancres, eczemas), or for some neoplasm metastasizing in
the glands (carcinoma). (A fuller account of the diseases affecting the
lymph glands will be found in Part VII.)
(b) The Condition of Special Regions and Systems
The further course of the objective examination of the patient will
depend, for its order, upon which of the two plans already mentioned —
(1) that of regions and (2) that of organ-systems — is adopted.
i. Examination According to Regions
Those who prefer, on account of convenience, to examine the body by
regions, irrespective of the systems of organs in each region, will, after
1 The edema occurring in contracted kidney is rarely a nephritic edema in the
sense mentioned, but is most often a stasis edema due to myocardial insufficiency.
20 PLAN FOE CLINICAL STUDY OF PATIENT
making notes on the general state of the body, examine systematically and
record their findings in the following regions:
1. Head (skull, face, eyes, ears, nose, lips, mouth cavity, tongue,
throat).
2. Neck (form, thyroid, lymph glands, skin, vessels, larynx, esoph-
agus, cervical spine).
3. Thorax (inspection, palpation, percussion, auscultation, mensu-
ration).
4. Abdomen (inspection, palpation, percussion, auscultation, mensu-
ration).
5. Extremities (condition of skin, bones, joints and muscles; motil-
ity, sensibility, reflexes, etc.).
6. Laboratory examinations (urine, sputum, stomach juice, feces,
blood, cerebrospinal fluid, x-ray examinations, etc.).
ii. Examination According to Systems
Those who follow the second plan, and make their examinations more
strictly according to the individual organ-systems, independent of the
body regions, will group their findings, say, under the following headings :
1. Osseous system (skull, spine, thorax; pelvis, extremities).
2. Skin and subcutaneous tissue (color, elasticity, turgor, moisture,
edema, exanthems, pigmentations, striae, scars, collateral circulations).
3. Muscular system (atrophy, hypertrophy, electrical examination).
• 4. Joints (mobility, swelling, pain, x-rays).
5. Lymph glands (enlargements, consistence, etc.).
6. Circulatory apparatus (pulse and pulse-tracings, blood pressure,
inspection, palpation, percussion and auscultation of heart, functional
tests, rontgenoscopy, telerb'ntgenography, electrocardiography).
7. Respiratory apparatus (thorax anomalies; respiration; inspection;
palpation, percussion and auscultation of lungs ; sputum ; nose ; paranasal
sinuses; larynx; transillumination ; rontgenoscopy; rb'ntgenography).
8. Digestive apparatus (mouth, tongue, pharynx, esophagus, stomach,
intestine, liver, pancreas, spleen, functional tests of secretion and motil-
ity, rontgenoscopy and rontgenography).
9. Urogenital apparatus and urine (kidneys, bladder, genitals, urine).
10. Blood and blood-building organs (hemoglobin, enumeration of
formed elements, fresh blood slide, dried and stained smears, parasites,
bacteriological and serological examinations).
11. Nervous system and sense-organs (mental state, common sensibil-
ity, organs of special sense, motility, coordination, reflexes, autonomic
functions, speech, identification, praxia).
12. Metabolic functions and endocrine glands,
THE CLINICAL HISTOKY 21
13. Evidences of infection, immunity, and anaphylaxis.
Most clinicians come to some compromise between Plan I and Plan II.
It is rarely that either plan is strictly followed.
iii. Combined Plan of History Taking
The following schedule is one found convenient by the author for his
&
own clinical records.
7. Anamnesis
1. Preliminary Data: Name in full; age; state; occupation; home
address; date of examination; chief complaint.
2. History of Present Illness.
A. Date and mode of onset; possible causes (intoxication, infec-
tion, physical or psychic trauma, occupation injury, dietetic
errors, exposure to cold or wet, exposure to contagion) ; course
from beginning to time of consultation; treatment followed
hitherto.
B. Epitome of symptoms existing at time of consultation (pains;
headache; dizziness; visual or auditory disturbances; cough;
sputum; dyspnea; palpitation; appetite; nausea or vomiting;
eructations; constipation or diarrhea; hemorrhoids; sweats;
sleep; urine; nocturnal micturition; changes in body-weight;
menstruation; libido; potentia; nervous or mental symptoms).
3. Previous History of Patient.
A. Diseases that the patient has earlier had.
(a) Diseases of childhood: measles, scarlet fever, diphtheria,
"scrofula," congenital lues, etc.
(b) Post-childhood diseases: infections (typhoid, pneumonia,
acute rheumatic fever, tonsillitis, gonorrhea, lues) ; dis-
eases of various systems (circulatory, nervous, etc.) ;
surgical operations.
B. Remarks on the general bodily functions (inclusive of the
sexual) in earlier life; respiratory; circulatory; digestive;
urogenital ; nervous.
In women: menstruation; births; puerperal periods; miscar-
riages; chlorosis.
In men : libido ; potentia ; sexual excesses ; pollutions.
C. Habits, Education, Experience:
(a) Work; exercise; rest; diversion.
(b) Food (amount; variety; time of meals; mastication).
(c) Alcohol (beer; wine; whiskey; cocktails, etc.).
22 FLAK FOR CLINICAL STUDY OF PATIENT
(d) Tobacco (cigars; cigarettes; pipes; chewing tobacco;
snuff).
(e) Tea and coffee.
(f) Drugs (trional; veronal, cocain; morphin; heroin; coca
cola; bromoseltzer, etc.).
(g) Education (time; places; character).
(h) Experience (occupation; travel; social life, etc.).
4. Family History.
(A) Age if living, or at time of death, of (1) parents, (2) sibs
(sisters and brothers), and (3) children. Health of each.
(B) Instances among near, or distant, relatives of diseases in
which either heredity, or contact, may play a role (tubercu-
losis; syphilis; nervous and mental diseases; alcoholism;
metabolic disturbances; endocrinopathies ; neoplasms).
II. Status praesens
1. General Points.
A. Gait; attitude; posture.
B. Height; weight; build (habitus); nutrition; musculature.
C. Mental state.
D. Skin: Color (pallor, rubor, cyanosis), thickness, transparency,
moisture, eruptions, edema, pigmentations, scars, striae, dilated
veins, pulsating arteries.
E. Body-temperature. Striking phenomena ("snap-shot" diagnosis).
F. Lymph glands; bones; joints; muscles.
G. Radial pulse on both sides; blood pressure,
2. Regional Examination.
HEAD. Form of skull; facial expression; conjunctivae ; eye move-
ments; pupils; ears (tophi); hearing; sense of smell; nasal
obstruction; lips; tongue; teeth; gums; throat; facial and lingual
movements; speech.
NECK. Length and breadth ; thyroid ; larynx ; trachea ; tracheal tug ;
esophagus ; blood vessels ; lymph glands ; cervical spine ; cervical
ribs.
THORAX. Form ; epigastric angle; depressions or bulgings; dilated
veins ; breasts.
LUNGS.
Inspection. Respiratory movements: number; type (costal, ab-
dominal, dyspneic, orthopneic, depth, symmetry) ; Litten's
sign.
Palpation. Respiratory movements; vocal fremitus; friction
fremitus.
THE CLINICAL HISTOEY 23
Percussion. Lung limits; comparative percussion of two lungs.
Auscultation. Breath sounds ; voice sounds ; pleural sounds.
HEART AND AORTA.
Inspection. Heart base ; abnormal pulsations ; apex beat.
Palpation. Apex beat ; other pulsations ; shocks ; thrills.
Percussion. Superficial and deep cardiac dullness ; retrosternal
dullness.
Auscultation. Heart sounds; aneurysmal bruit; pericardial
sounds.
ABDOMEN AND PELVIS.
Inspection. Form (retraction, distension) ; position of umbilicus;
changes during respiration ; tumors or other bulgings ; col-
lateral circulations; visible peristalsis; hernias; strength of
Mm. recti.
Palpation. Rigidity; local or general tenderness; hernial sites;
tumor masses; stomach; intestine (small; appendix; cecum ;
transverse colon; sigmoid) ; spleen; liver; pancreas; kidneys;
suprapubic region; inguinal regions; rectal examination;
vaginal examination ; genitals.
Percussion. Ascites ; meteorism ; stomach ; liver ; spleen ; bladder ;
uterus; tumor masses.
Auscultation. Friction sounds; aneurysmal bruits.
NERVOUS SYSTEM.
Sensory. Cutaneous and deep sensibility; stereognosis ; sight;
hearing ;' taste ; smell.
Motor. Muscular power ; finer movements ; coordination ; tonus.
Reflexes. Pupils; knee-jerks; ankle-jerks; periosteal radial;
biceps and triceps jerks; plantar and abdominal reflexes;
sphincters.
Autonomic. Vasomotors; secretory; trophic (sweat-glands, nails,
hair, skin, etc.)
Psychic. Orientation; memory; calculation; attention; halluci-
nations; delusions; mood, etc.
LABORATORY TESTS (Routine). Urine; blood; sputum (if any);
Wassermann.
LABORATORY TESTS (// indicated). Stomach juice; feces; cerebro-
spinal fluid ; x-ray examinations ; tuberculin tests ; metabolic
studies; electrocardiogram, etc.
3. Catamnesis
If the clinician is to profit by his experience, it is essential that he
keep careful records of the history of his patients after they are first seen
and examined, including the subsequent examinations made from time to
24 PLAN FOR CLINICAL STUDY OF PATIENT
time, with observations upon the course followed by the disease, the kinds
of therapy used, and their effects. Many hospital histories are fairly
complete as far as anamnesis and status praesens are concerned, but are
woefully lacking as regards the catamnesis; the same defect is too often
true of the records kept by physicians in their private practice.
4. Epicrisis
Every practitioner of medicine should feel it his duty to contribute,
whenever possible, to the advance of medical knowledge. He should be
on the lookout for cases that can be of interest for science, and should
see to it that such cases are thoroughly studied, and the results given to
his fellow practitioners. Even if he be too busy to undertake the scien-
tific studies himself, he should, when he recognizes suitable opportunity,
call the attention of scientific workers to the case, and at least give them
the opportunity of investigation.
In the epicrisis, the final judgment upon a case is recorded, with dis-
cussion of the meaning of the symptoms and signs. When an operation
has been performed, or, in case of death, when an autopsy has been done,
the findings are correlated as far as possible with the observations made
before operation or before autopsy.
It would be well if every practitioner would go over his list of patients
from time to time and attempt an epicrisis in each one. He will often
be surprised at what he finds, and his clinical judgment should be greatly
improved if he will follow the practice.
References
Futcher (Thomas Barnes). Outlines of physical diagnosis of the circulatory and respira-
tory systems. Prepared by John Gardner Murray. Baltimore, 1913,
Students Book Store, 179 p. 8°.
Mackenzie (James). Symptoms and their interpretation. New York, 1914, P.B. Hoeber,
304 P.
McKisack (H. L.). Systematic-case taking. A practical guide to the examination and
recording of medical cases. New York, 1914, P. B. Hoeber. 166 p.
von Strumpell (Adolf). Kurzer Leitfaden fur die klinische Krankenuntersuchung. Fur
die Praktikanten der Klinik. 5. Aufl. Leipzig, 1900, F. C. W. Vogel.
40 p. 16°.
Wandel (O.). Anamnese und Allgemeinstatus. In:Lehrb. d. klin. Diagnostik (P. Krause).
2d ed. Jena, 1913, G. Fischer. 2-40.
Wilson (Gordon). A lecture on history taking. Baltimore, 1914, Meyer & Thalheimer. 13 p.
Woolley (Paul G.). The clinical history in outline. St. Louis, 1914, C. V. Mosby Co.
53 p. 8\
GENEKAL KEMAEKS ON DIAGNOSTIC METHODS 25
C. General Remarks on Diagnostic Methods
The time-honored methods of physical examination — inspection, pal-
pation, percussion, auscultation, mensuration — are still the most impor-
tant diagnostic methods. To them have been added in recent years a
large number of other methods — physical, chemical and biological — and
many of these have now become indispensable for the diagnostician.
All methods of physical examination depend upon the utilization of
the sense-organs of the examiner (sight, hearing, touch, temperature
sense, taste, smell). The experienced clinician can make an extensive
examination with his unaided sense-organs, but, as the science of medi-
cine grows, the sense-organs of the examiner have to be aided by an
increasing number of methods devised to extend these observing powers.
Thus, through the help of the microscope (with or without the aid of
selective dyes), the ophthalmoscope, the, laryngoscope, the bronchoscope, the
gastroscope, the sigmoidoscope, the cystoscope, the spectroscope, the
colorimeter, the polar imeter, the refractometer, etc., the eye gains access
to fields invisible without these accessories.
Through the stethoscope the ear can be made to hear sounds which
would otherwise escape it; by means of the electrophonograph, sound
vibrations at present inaccessible, even to the aided ear, can be registered
and interpreted by the eye. Our impressions of the temperature of a
patient gained through our own temperature sense are crude and inaccu-
rate compared with the exact information yielded by the clinical ther-
mometer. The palpation of the pulse by the fingers will tell much con-
cerning the rhythm and the blood pressure, but instrumental methods of
examination (sphygmograph, sphygmomanometer, electrocardiograph)
permit of still more accurate analysis, and a comparison of the results
obtained by the unaided sense-organs with those obtained by instrumental
methods through a certain period of time greatly increases the knowledge
obtainable by the former.
No hard and fast line can be drawn between clinical and laboratory
methods. The use of our sense-organs (naked and aided) is common to
both. Whether a given test shall be performed at the bedside, or in the
laboratory, is merely a matter of convenience. There is no fundamental
difference, in principle, in the two methods employed. One-sided views,
however, are apt to prevail among men who work only at the bedside and
who never make examinations in laboratories separated from the patient.
The same is true of men whose circumstances confine them to laboratory
studies and who do not come into contact with patients at the bedside.
To prevent narrowness of view, it is desirable, either that one and the
same man shall make both clinical and laboratory examinations, or that
the ;men making bedside examinations predominantly shall be kept in
26 PLAN FOE CLINICAL STUDY OF PATIENT
close and intimate relations with, the men who are making laboratory
tests predominantly. It is difficult for one whose work limits him largely
to bedside examinations properly to value results of laboratory tests, unless
he has had at least some first-hand experience with the laboratory tests
themselves. Similarly, the judgment of the man whose work is pre-
dominantly in the laboratory will be better if he has had at least some
training in the clinical methods of examination, and at least some expe-
rience* in the course of disease as studied at the bedside. There is,
undoubtedly, real difficulty at the present time, on account of the division
of labor and the specialization of activity that the extension of the
methods of clinical diagnosis has made necessary, in correlating all the
results of examination that can be accumulated, and in arriving at a
proper judgment regarding the condition of the patient as a whole.
Upon a proper synthesis of the results, and upon the estimate formed of
the relative importance of the various deviations from the normal, depends
the therapy to be instituted. In this time of unprecedented specialism,
there is greater need than ever for the all-around internist with sound
judgment. The beginner, introduced to a great variety of specialistic
methods, can scarcely avoid, at first, a feeling of bewilderment ; do his
best, he is likely to "lose sight of the wood on account of the trees." For
this reason it is desirable that the young internist should work for a con-
siderable period in close contact with, and under the direction of, clini-
cians of long experience; while perfecting himself in the technic of the
single methods of examination, he will gradually learn, through the
example of his more experienced seniors, how best to synthesize, and how
adequately to value, the results of the physical, chemical, and biological
investigations of the patients he studies.
References
Barker (L. JF.). Methods in medicine. Bost. M. & S. J., 1905, cliii, 319-327; The science
of medicine and medical practice. Johns Hopkins Univ. Circ., Bait.,
1906, xxv, 8-18; and On the cultivation of the clinical sciences of diag-
nosis and therapy. Science, N. Y., 1913, n. s., xxxvii, 731-738.
Hastings (T. W.). Reciprocal relations of the clinic and the laboratory in medicine. J.
Am. Med. Ass., Chicago, 1913, Ixi, 651-655.
Miiller (F.). Der Ausbau der klinischen Untersuchungsmethoden. Ztschr. f. arztl. Fort-
bild., Jena, 1906, Hi, 433.
Osier (Sir William). Internal medicine as a vocation. In: Aequanimitas and Other
Essays (Osier). Philadelphia, 1904, 137-152.
Pratt (J. H.). The method of science in clinical training. Bost. Med. & Surg. J., 1912,
clxvi, 835-842.
Thayer (W. S.). On the importance of fundamental methods of physical examination in
the practice of medicine. Southern Med. J., Mobile, 1914, vii, 933-942.
Part II
Examinations with Rontgen Rays
(Rontgenoscopy; Rontgenography)
The Rontgen rays penetrate different parts of the body with varying
degrees of facility; for the different tissues vary in their absorption of
the rays, the air-filled lungs, for example, absorbing very few of the rays,
the heart on the contrary absorbing them to a greater, the bones to a still
greater, degree. It is accordingly possible, by means of photographic
plates or of a fluorescent screen, to register, graphically, shadow pictures
of the organs and tissues, corresponding to the differences in the penetra-
bility of the parts by the rays.
A. Varieties of Apparatus for the Production
of Rontgen Rays
Two fundamentally different kinds of Rontgen-ray apparatus are now
available for rontgenological work :
1. An induction-coil apparatus with high-tension direct current and
interrupter; and
2. A non-induction, interrupterless apparatus, with alternating cur-
rent, step-up transformer, and high-tension rectifying switch that sends
a unidirectional current into the x-ray tube.
Both of these apparatus can be used with either a direct or an alter-
nating current; thus, for the inductor apparatus, an alternating current
can first be converted into the direct current required; and for the non-
induction, rectifying switch apparatus, a direct current can be converted,
by means of an inverted rotary converter, into the alternating current
required.
Coolidge has recently reported experiments that indicate that before
long we may expect very definite improvements in the apparatus for pro-
ducing Rontgen rays.
27
28
EXAMINATIONS WITH RONTGEN RAYS
1. Rontgen Apparatus Utilizing Direct Current with
Inductor
In this apparatus, an interrupter breaks up the high-tension direct
current into single impulses, which arrive in the primary coil of the
induction apparatus. On closure of the current, a magnetic field is
formed, which disappears again when the current is opened. In the
secondary coil, an impulse is induced every time the primary current is
opened, and also when it is closed. For the x-ray tube, however, use is
made only of the induced current that arises on opening the circuit.
A pulsating unidirectional current of sufficient intensity and tension is
obtained in the secondary circuit by an ingenious arrangement, through
Fig. 5. — Induction Coil Apparatus. (By courtesy of the Scheidel- Western X-ray Coil Co.)
YAKIETIES OF APPAKATUS FOR PRODUCTION 29
which, the opening current is made sudden and intense and the closing
current as much as possible suppressed (condenser, jump-spark, or, better,
"valve-tubes" that permit the current to pass through in one direc-
tion only).
(a) The Interrupter
The interrupter determines the rhythmical closure and opening of
the primary circuit. Several varieties of interrupter are in use, the best
ones being (1) a mercury centrifugal interrupter, in which contact with
mercury closes, and contact with petroleum or alcohol opens, the circuit,
and (2) a gas interrupter, in one variety of which, (a) the "apex inter-
rupter," the current is made by contact with mercury, but broken by a
gaseous dielectric (illuminating gas), and in another type, (b) Wehnelt's
"electrolytic interrupter," gas is
generated around a platinum elec-
trode in quantity sufficient to inter-
rupt the current.
(6) The Rheostat
A rheostat is intercalated in
the primary circuit to regulate the
intensity of the current by alter-
ing the resistance.
(c) Single Impulse Apparatus
The "single impulse Rontgen
apparatus" is a modification of
the inductor apparatus above de-
scribed, especially adapted for "in-
stantaneous rb'ntgenography," the
single "flash" lasting about 1/200
second. With this instrument,
moving organs, like the heart,
lungs, diaphragm, stomach, intes-
tine, larynx on swallowing, etc.,
can be sharply outlined. It is use-
/? l i -i • • Fig. 6. — Apex High tension Generator. Model
ful, also, in making x-ray examma- fnSt (Byp courtessy of the Kny-Scheerer Co.)
tions in young children, in the in-
sane, and in Parkinson's disease (tremor). The same machine can be
adapted also for general work not requiring instantaneous exposures. This
"single impulse" apparatus has contributed much to rontgen-cinematog-
raphy.
30
EXAMINATIONS WITH RONTGEN RAYS
2. Rontgen Apparatus Utilizing the Alternating Current
with High-Tension Rectifying Switch
This apparatus does away with the inductor and the interrupter
entirely, and is fast displacing the apparatus above described for general
x-ray work. Though it makes use of an alternating current (Snook's
A. C. Machine), a form of the apparatus is made that will supply the
alternating current required from a direct current by means of an inverted
rotary converter (as in Snook's D. C. Machine).
Fig. 7. — Interrupter-less Apparatus. Alternating-current Machine.
(By courtesy of the Snook-Rontgen Mfg. Co.).
(a) The Step-Up Transformer
A step-up transformer raises the voltage to very high tension. By
means of a switch, the ratio of transformation may be changed through
the "taps" provided in the primary winding of the transformer; as a
result of this adjustment, the transformer secondary voltage varies from
VAEIETIES OF APPARATUS FOR PRODUCTION 31
70,000 to 120,000 volts. A rheostat in the primary circuit of the trans-
former regulates the current output.
(5) The High-Tension Rectifying Switch
The high-tension alternating current delivered by the transformer is
carried through a high-tension rectifying switch, which changes it to a
Fig. 8. — Interrupterless Apparatus. Direct-current Machine.
(By courtesy of the Snook-Rontgen Mfg. Co.).
unidirectional current, suitable for use in x-ray tubes. In the A. C.
machine, a synchronous motor drives the high-tension rectifier; in the
D. C. machine, the rectifying switch is mechanically attached to the shaft
of the inverted rotary converter and is thereby maintained in synchronism
with the alternating current delivered by the converter.
When one has a choice, it is best to use an alternating current (220
volts, single phase, 60 cycles) as a source, and the A. C. machine. In buy-
ing a machine, it is necessary to know (1) what kind of current is avail-
able, (2) the voltage, and if the available supply be an alternating current,
(3) the frequency, and the number of phases.
32
EXAMINATIONS WITH EONTGEN EAYS
(c) Advantages of the Rectify ing -Switch Apparatus
With this kind of Rontgen apparatus there are several distinct advan-
tages, aside from its noiselessnesSj and its simplicity.
1. Inverse discharge is absolutely excluded.
2. Since there is no external magnetic field (a closed magnetic current circuit
transformer being used, and the magnetic flux being confined to the iron of the
Fig. 9. — Wiring for Alternating-current Genera-
tor (Interrupterless Transformer Appa-
ratus). (By courtesy of the Kelley-Koett
Mfg. Co.)
Fig. 10. — Wiring for Direct-current Generator
(Interrupterless Transformer Apparatus).
(By courtesy of the Kelley-Koett Mfg. Co.)
THE X-KAY EXAMINING-EOOM 33
transformer) , there is no enlargement of the focus spot, such as an external magnetic
field mav cause through its influence upon the cathode stream; when transformers
with open magnetic circuits and induction coils are used, the focus spot of the
tube wanders, and, dancing around on the target, results in blurring of the
rontgenogram.
3. Very short exposures are possible, for the x-ray tube can be furnished with
all the energy it can take unimpaired, and this energy-capacity of the machine is
unassociated with any inverse-discharge; in the inductor apparatus, if the capacity
is increased beyond a certain point, the "inverse discharge" becomes too strong for
the x-ray tube, though with the "single-impulse" modification of the inductor-
apparatus admirable instantaneous exposures are obtainable (see above).
4. The x-ray tubes are protected wonderfully and will last much longer than
with the inductor apparatus ; this is accounted for by the absence of "inverse," and
by the lessened "digging" of the target.
5. The current measurements are absolutely reliable, and one can be quite sure
just what x-ray effect is obtainable with a given tube and a given adjustment ; with
the inductor apparatus, there are so many variable factors that no equivalent
certainty is possible.
6. The mixture of x-rajTs given out by tubes used with this machine is very
rich in "soft rays" ; an extraordinary richness of detail in the rontgenograms.
especially of soft parts like the lung tissue, is attainable. Very much softer tubes
can be used than with a coil apparatus.
7. By means of a "triple reel" attachment, the operator can control and measure
the tube-vacuum from his position at the switch table; there is no danger of ruining
tubes by "arcing" at the regulator.
8. An especially designed fluoroscopic attachment permits the operator to use
a tube for the maximum length of time with a minimum of heating and of drop
in vacuum. By simply moving a switch, a change to a heavy current for radio-
graphic work can be made immediately.
9. For general rdntgenography and rontgenoscopy and for surface therapy, this
form- of apparatus is by far the best ; for deep therapy, especially for intensive
therapy in the depth, the inductor apparatus is said to be better. When one has
both inductor apparatus and rectifying-switch apparatus at one's disposal, the
former may be used for depth therapy and for fluoroscopic work, the latter for
all other x-ray work. Great advances in deep therapy have resulted from the
introduction of the Coolidge tube.
B. The X-Ray Examining-Room
Now that rontgenoscopy or fluoroscopy (transillumination by x-rays;
view on fluorescent screen) has become so helpful in medical diagnosis,
and rontgenography (use of photographic plates) is indispensable, in
both medicine and surgery, an x-ray examining-room should certainly be
available in every town, and many individual practitioners are installing
outfits of their own.
A commodious room that can be made absolutely dark is necessary,
and the examiner should, for rontgenoscopy, adapt his eyes to the dark
for five or ten minutes before making his examination.
In order tbat there may be a little light in the room between ront-
34 EXAMINATIONS WITH RONTGEN KAYS
genoscopic examinations, a weak green light placed close to the ceiling
can be used and is the best. One can install a four-candle power, green-
colored bulb, mounted in an "indirect" fixture ; it should have a pendant,
or a switch-control, operable from the position occupied by the examiner.
The room should be well ventilated, by light-tight methods through
the doors and windows; electric fans are objectionable as they cause too
much draught for an undressed patient.
The walls of the room should be painted a dull bluish gray, or a light
gray containing a little red ; they should not be black or dark red.
The -floor should be of hard wood (parquet), not of linoleum, cement,
or tiles.
Nearby, a convenient photographic dark room should be provided; it
should be kept dry, clean, and orderly, and should have a supply of
running water, a sink, a work-table with shelves, and red and white light,
or Caldwell's ruby light. It should be properly warmed in winter.
In order to protect the examiner and the patient from harmful effects
of the rays the x-ray tubes are nowadays provided with protective lead-
glass shields (50 per cent. lead). In addition, a lead screen, 3J ft. wide
and 44 ft. high, with a foot of transparent lead-glass above it, affords
additional protection. Protective gloves and lead-glass spectacles are also
available.
While most x-ray examinations are made of persons who can sit
up or stand up, it is sometimes important to have an x-ray photograph
or a fluoroscopic examination made of a patient so sick that he must keep
the recumbent position. Movable x-ray tables have been constructed with
the x-ray tube underneath ; with such a table, the very sick pneumonia
patient can, if deemed necessary, be photographed.
C. Rontgen Tubes
1. Structure of a Rontjjen Tube
The x-ray tubes, used for the production of Rontgen rays, consist of
spherical flasks in which a high-grade vacuum is produced by means of
a mercury pump and heat; these flasks are provided with several attach-
ments for special purposes.
Each tube contains three mirrors: (1) an anode mirror, connected
with the positive pole of the high-tension current deliverer, this mirror
being replaced in the newer instruments by a rod — the "anode rod"; (2)
a cathode mirror (concave), connected with the negative pole of the cur-
rent deliverer; and (3) an anticathode mirror, or target, consisting usu-
ally of platinum (iridium, tungsten, or tantalium), placed opposite the
KONTGEN TUBES
35
cathode mirror at an angle of 45° to the axis of the tube. Outside the
tube, the anode and the anticathode are united by a conductor.
2. The Rdntgen Tube in Action
When the tube is in action, particles are driven off from the cathode
(the so-called cathode-rays, visible in the form of a fine blue bundle) and
strike upon the anticathode mirror or target, being roughly "focused"
H
A — Anode.
B- -Assistant Anode.
C— Cathode.
D — Regulating
Chamber.
F — Regulating Ad-
juster.
G — Hemisphere.
H — Connection
Wire.
I — Assistant Anode
Cap.
K — Anode Cap.
L — Cathode Cap.
M — 'Cathode Stream.
N— Focal Point.
Fig. 11. — Diagram of a Rontgen Tube. (By courtesy of the Scheidel-Western X-ray Coil Co.)
upon it through the concavity of the cathode mirror.. They give rise,
on striking the target, to the Rontgen rays, or x-rays, which pass off in
all directions toward the half of the tube faced by the target (Fig. 11).
(a) The Focus of the Cathode-Rays
A "sharp" focus of the cathode stream favors the clearness of rb'nt-
genograms; but for rontgenoscopy and for therapeutic use of the rays,
it is better to have the focus less sharp, since the anticathode plate tends
to become very hot, and, on longer use, will burn through or be badly
"dug out" if the cathode stream is too sharply focused.
36 EXAMINATIONS WITH EONTGEN EAYS
(b) The Normal Radiation
The greatest Eontgen energy is possessed by what is known as the
normal radiation. By this is meant the pyramid of x-rays emerging from
the anticathode at approximately an angle of 90° to the bundle of
cathode-rays.
(c) Glass-Rays and How to Stop Them Out
When an x-ray tube is working -right, about one-half of the tube is
brightly illuminated, while the other half remains darker, the junction
between the two halves lying in the plane of the anticathode mirror.
The illuminated half has a soft yellowish green fluorescent look due to
the fact that not all the cathode-rays striking the target are transformed
into x-rays ; part of them are reflected and thus hit the glass wall of the
x-ray tube, where they are converted into x-rays, at the same time causing
fluorescence of the glass of the tube and warming of the glass. The
x-rays thus produced are known as glass-rays, to distinguish them from
the x-rays originating at the anticathode. These glass-rays, since they
proceed from a widespread surface, are very diffuse in their distribution,
and so are prone to cause blurring of the x-ray shadows. In order to avoid
this blurring, as many of them as possible are cut off by means of a
diaphragm interposed between the x-ray tube and the organ to be photo-
graphed, the diaphragm being placed as close to the x-ray tube as possible.
(d) Coolers of the Anticathode
Various forms of cooling apparatus are used to prevent melting of
the metal of the anticathode (water-cooled tubes, metal-cooled tubes, air-
cooled tubes).
(e) Soft and Hard Rontgen Tubes
As has been said, the Eontgen rays have different degrees of penetra-
bility, according to the velocity of the cathodal x-rays producing them,
this velocity in turn depending upon the grade of vacuum in the x-ray
tube; the higher the grade of vacuum, the greater the average pene-
trability, or hardness, of the Eontgen radiation. The reason for this lies
in the fact that a higher tension of the electric current fed to the tube is
needed to overcome the internal resistance of the tube when a high-grade
vacuum exists, and this high tension gives the cathode-rays a greater
velocity.
Since the x-rays are always produced by single high-tension impulses,
it is probable that the radiation is never homogeneous, but consists of a
mixture of rays of the most different penetrating capacity, the composi-
EONTGEN TUBES
37
tion of the mixture depending upon the discharge curve of each single
impulse of the current sent into the tube. The form of the discharge in
the rectifying-switch apparatus is such that the number of rays of variable
hardness given off, especially of soft rays, is large. This is a real advan-
tage, since the parts of the body of variable absorption capacity are much
better differentiated on the fluorescent screen or in the photographic plate
when the soft rays are abundant. With the older forms of inductor
apparatus it was impossible to get good pictures of soft parts. The intro-
duction of the rectifying-switch apparatus has led to enormous improve-
ments in the detail of the negatives.
Fig. 12. — Water-cooled Tungsten Target Tube. (By courtesy of the Kelley-Koet Mfg. Co.)
It is, accordingly, customary to divide Rontgen radiations into (1)
very soft, (2) soft, (3) medium, (4) hard, and (5) very hard radiations.
Anyone who works with x-ray tubes soon learns to distinguish the kind
of radiation being sent off by a tube from its appearance in action.
In very hard tubes, streaks of light fly through the air outside the tube,
between the attachment of the anticathode, the tension of the current
required for such a tube being so high that the current passes more easily
through the air than through the tube.
In the hard tubes, so-called "hardness-spots" -of bright light appear in
the tube, and the glass neck of the tube near the cathode mirror becomes
strongly illuminated. Great care must be taken in using hard tubes, for
there is always danger that the glass wall of the tube may be perforated,
in which case air will enter and ruin the tube.
38 EXAMINATIONS WITH RONTGEN RAYS
In a medium-soft tube, one half of the spherical flask is brightly illu-
minated; the other half is much darker, the plane dividing these two
halves heing that of the surface of the target. The illuminated half of
the tube presents a soft yellowish green fluorescence, due to the fact that
some of the cathode-rays, striking the target, instead of being transformed
like the majority into Rontgen rays, are reflected from it, so as to strike
the glass wall of the tubes where they are converted into Rontgen rays,
the glass-rays described above.
In a very soft tube, the whole tube is illuminated except the dark
cathodal space, and the blue bundle of cathode-rays is easily visible.
(f) Inverse Discharge with the Inductor Apparatus
In using the inductor apparatus, one of the most troublesome difficul-
ties is that of inverse discharge, the current passing the wrong way
through the tube. Such inverse discharge can often be prevented, on using
a new tube, by placing a resistance coil, or a fuse, in a glass tube in
the connection between the anode and the anticathode outside the x-ray
tube. After a few weeks' use, the connection can be made directly to the
anticathode if desired.
When inverse discharge occurs through a tube, dust may come off the
metal of the anticathode ; after the tube has been removed and this metallic
dust has cooled, much of the gas in the tube will become united to the
glass walls, and this will make the tube very much harder than it was
before. Or, the vacuum of the tube may become "unstable," being very
hard one minute and very soft the next, swinging to and fro between the
two extremes like a pendulum.
In older tubes used with the inductor apparatus, a grayish black layer
on the walls can be seen, due to metallic dust from inverse discharge. The
violet discoloration of the glass wall of old tubes is entirely different in
origin, depending, as has already been said, on the separation of colloidal
manganese from the glass.
Fortunately, all inverse discharge is avoided by the use of the rectify-
ing-switch form of Rontgen apparatus described, and a soft tube can be
used for a very long time without growing hard.
It is important that tubes should be exposed to exactly the electrical
tension that is best suited to them. If a tube grow softer, it is a sign
that it has been given too heavy a burden; if it tend quickly to become
hard, it is a sign that it has not been sufficiently burdened.
Since tubes gradually become harder with time owing to the diminu-
tion of their gas-content (absorption by metallic dust, accumulation on
the glass walls), it is well to make use of them according to their degree
of hardness; thus, the young, soft, tubes (low grade vacuum) should be
used for photographing thinner parts of the body, like the hands and feet,
KONTGEST TUBES 39
while the older, harder, tubes should be used for photographing thicker
parts (heart, kidney, hip-joint, etc.).
3. Regeneration of Rontgen Tubes
As tubes grow older and become harder, it may be necessary to
increase the gas-content a little. This may be brought about by any one
of several methods of regenerating the tubes ( (1) osmo-regeneration of
Villard, in which a palladium tube is heated and a little hydrogen enters
the tube through the metal;1 (2) carbon-regeneration, in which gas is
driven out of carbon into the tube; (3) condenser-regeneration, for espe-
cially hard tubes (Gundelach) ; (4) air-regeneration, in which a little air
is allowed to enter the x-ray tube through a porous plate — especially use-
ful for fluoroscopic tubes).
4. Care of Rontgen Tubes
Each particular brand of tube requires special care, and full instruc-
tions should be obtained from the maker regarding the treatment of the
tube. Certain general rules, however, which I epitomize from the article
by Janus and Schittenhelm, should be kept in mind :
1. No opportunity for grounding of the high-tension current should be permitted.
2. For each tube there is an optimal current, and care should be taken not to
feed the tube with a stronger, or a feebler, current than this optimal strength.
3. New tubes, or so-called young tubes, should be very cautiously used at first,
with avoidance of too strong a current and of the passage of the current through
the tube for a long period. In a few weeks a tube can be "trained," or "educated,"
so that it will stand longer exposures and stronger currents. Sometimes a new
tube may be hard; if so, it should not be treated as though it were a tube that
has become hard through age, but should be subjected to a regenerative process
until it is soft, and then slowly "educated" to its maximal performance.
4. If a tube does not respond in the way expected, no attempt should be made
to force it to do so by increasing the burden thrown upon it. Sometimes, in
winter, simply warming a tube for a few hours before use will make it more
responsive.
5. X-ray tubes should be kept absolutely clean, protected from dust, and the
exterior of the tube should never be touched with the fingers.
6. When selecting tubes it is well to buy a few of the best makes, and to learn
thoroughly how to use the tube chosen. It is a mistake to experiment with a whole
series of different varieties of tubes, since each make demands special treatment.
If one has from four to six good tubes of different degrees of hardness, he should
keep them, when well "trained," for the particular purposes for which they are
most adapted. It is, as a rule, a mistake to use one and the same tube for different
purposes. Much expense will be avoided if this precaution is observed.
1 Holzknecht's modification of this form of regeneration is preferred by the
Vienna school.
40 EXAMINATIONS WITH KOJSTTGEN KAYS
7. One should form the habit of testing a tube every time before use; its hard-
ness should be measured, and its behavior under a definite strength of current
(milliamperemeter) and voltage determined. If, when the tube is in use, the
intensity of the current, as shown by the milliamperemeter, increases, the tube is
becoming softer; one should at once lessen the burden thrown on the tube, or it
will soon become too soft. If, on the contrary, the intensity of the current decreases
(milliamperemeter), the tube is becoming harder and a heavier burden should be
thrown upon the tube, though this is less important than when the tube is becom-
ing too soft. The worker has himself to blame when tubes become softer; the
softening is due either to his throwing the wrong burden upon the tube, or to the
youth of the tube.
8. In order to avoid using the tube any longer than is absolutely necessary,
thorough preparation of the apparatus, and of the patient, should precede the turn-
ing on of the current. With a burden of 25 milliamperes or more for a single
second, a young tube may be completely ruined.
D. Origin, Nature, and Properties of
Rontgen Rays
In order to understand the origin of the x-rays and their nature it
is necessary tu begin with a description of the so-called cathode-rays.
1. Cathode-Rays
In a vacuum tube like an x-ray tube, the electrode through which the
electric current, when passing through, leaves the tube containing the
rarefied gas is known as the cathode. From the surface of this cathode,
during the passage of the current, little particles known as electrons,
charged with negative electricity, are driven with tremendous velocity.
These electrons are extremely minute, probably not larger than 1/200
part of a hydrogen atom. When this cathode stream of electrons passes
through the rarefied gas of the tube, the gas in the tube becomes illumi-
nated, only the immediate neighborhood of the cathode remaining dark,
forming the so-called dark cathodal space, the region poorest in electrons.
The greater the rarefaction of the gas in the tube, the larger the area of
the dark cathodal space, and the greater the velocity of the electrons in
the cathodal stream. In a high-grade vacuum, the velocity may reach
almost that of light (300,000 km. per second).
The electrons are emitted in a straight line, perpendicular to the sur-
face of the cathode which ejects them. In the x-ray tube, the mass of the
electrons in this cathodal stream form a bundle of rays — the cathode-rays
— possessing peculiar properties :
ORIGIN, NATURE AND PROPERTIES 41
1.. They make glass, upon which they impinge, give off light, the
color of the light (sometimes green,- sometimes blue) varying with the
chemical constitution of the glass.
2. They go off perpendicular to the plane of the cathode, heing unin-
fluenced by the shape or position of the anode. When a concave cathodal
surface is used, the rays converge more or less toward a focus, though the
focus is not a precise one, owing to deflection of some of the rays through
magnetic or electric forces, especially in the inductor apparatus (q. v.).
This deflection, however, can be largely avoided by the use of the recti-
fying-switch apparatus. The higher the grade of vacuum and the higher
the tension of the current delivered to the tube, the less the deflection of
the rays.
3. The cathode-rays heat the object they strike, enormously, so that
arrangements for cooling the target, which they strike, are necessary.
4. Cathode-rays can cause chemical changes; a photographic plate
inclosed within an x-ray tube is affected more or less as it is by light.
5. Bodies struck by cathode-rays become charged with negative
electricity.
6. Cathode-rays do not penetrate the glass wall of an x-ray tube, but
are absorbed by it, the glass becoming illuminated and heated during the
absorption.
7. Most important of all, when the cathode-rays strike an object, besides
the development of heat, another transformation of energy takes place, in
that, from the place struck, another kind of ray is emitted: namely, the
Rontgen rays, or x-rays, discovered by Rontgen of Wurzburg in 1895.
These Rontgen rays are of several different sorts, their character depend-
ing upon the velocity of the cathode-rays producing them. Thus, cathode-
rays of greater velocity, in tubes with high-grade vacuum, yield hard
Rontgen rays capable of great penetration, while cathode-rays of slower
velocity, produced in x-ray tubes containing more gas, yield soft Rontgen
rays, of less penetrability.
2. Nature of the Rontgen Rays
The nature of these rays is still under discussion. According to the
view dominant at present, they consist of pulses in the ether, not unlike
light rays. They are believed to be electromagnetic waves of very small
wave-length; in other words, ultraviolet light rays of wave-length still
smaller than those of the ultraviolet rays hitherto known. It is supposed
that the smallest observed light wave is at least a thousand times longer
than the greatest wave-length of a soft Rontgen ray, the hard Rontgen rays
consisting of still shorter waves,
42 EXAMINATIONS WITH RONTGEN EAYS
3. Properties of Rontgen Rays
(a) Penetrability of the Rays
The x-rays are capable of penetrating chemical substances in inverse
proportion to their atomic weight; the greater the atomic weight, the
greater the absorption of the rays by the substance. In bodies of complex
composition, like the organs of the human body, the rays are absorbed in.
very different degree by different parts. This accounts for the shadows
visible upon the fluorescent screen, and for the variable effects upon the
photographic plate in rontgenography.
The penetrability of the Rontgen rays varies, according as they are
soft or hard; that is, according to the velocity of the cathode-rays pro-
ducing them.
(6) Propagation of the Rays
The Rontgen rays are propagated in straight lines, but in all direc-
tions in space. As far as is known, they do not undergo refraction, nor
can they be deflected from their course; in this they resemble light rays,
and differ from cathode-rays. It is possible that some of the x-rays,
namely, those with the longest waves, can be bent by means of the crystals
of certain minerals. Investigations of this point are now being made.
Unlike cathode-rays, the Rontgen rays cannot be deflected either by
magnetic or by electric forces.
(c) Secondary Radiation
Bodies struck by Rontgen rays give off secondary rays which have
properties quite similar to the Rontgen rays giving rise to them. The
greater the penetrability of the Rontgen rays, the greater also the pene-
trability of the secondary rays to which they give rise. It is asserted that
chemical substances of high atomic weight give off a soft secondary radia-
tion. Such a secondary radiation is usually given off by large bodies and
is therefore diffuse.
The reason why it is not possible to get sharply circumscribed margins
to organs in x-ray pictures is due to the blurring effect of the diffuse sec-
ondary radiation. When a certain thickness of the body has been passed
through by the x-rays, the diffuse secondary radiation becomes so great as
to exceed in its effects those of the x-rays themselves, and a sharp picture
can no longer be obtained. And if x-rays of higher penetrability are used,
the secondary radiation becomes all the stronger and the result is worse.
It should, therefore, be borne in mind that on working with the x-rays on
the human body, we are not dealing with a pure absorption of the x-rays,
but with absorption and a simultaneous transformation of the rays.
ORIGIN", NATURE AND PROPERTIES 43
(d) Excitation of Fluorescence
Rontgen rays, like cathode-rays, are capable of exciting definite chem-
ical substances, like calcium tungstate, barium platinum-cyanur, zinc-
blend, etc., to fluorescence. Utilization of this fact is made in rontgen-
oscopy, where the fluorescent screen is used ; a further application is the
intensifying screen in rontgenography.
The fluorescence varies in color, according to the chemical compound
excited. The illumination of the screen will, in some instances, continue
after the current has been cut off (so-called "phosphorescence" seen in
certain intensifying screens).
(e) Chemical Effects of Rontgen Rays
Rontgen rays act upon photographic emulsion in the same way as the
light of the ultraviolet spectrum (visible and invisible). The bromid of
silver is decomposed in the photographic plate. Upon this property, ront-
genography depends.
Advantage is taken of this fact also in the invention of a method of
measuring Rontgen energy quantitatively, in the so-called quantimeter of
Kienbock.
Still other chemical processes occur, under the influence of Rontgen
rays, and have been utilized for measurements of Rontgen energy, as, for
example, the formation of calomel from a mixture of corrosive sublimate
and ammonium oxalate (Schwarz), or of iodin from a solution of iodoform
(Freund), or the change of color from a green to a brownish yellow in
barium platinum-cyanur (radiometer of Sabouraud-Noire).
An interesting chemical effect of the x-rays is often seen, in older
x-ray tubes, in the glass opposite the anticathode; a bluish violet discolor-
ation appears, due to the separation of collodial manganese from the other
constituents of the glass.
The Rontgen rays are capable of ionizing gases so that they can con-
duct electricity. This fact is taken advantage of in the making of meas-
uring instruments, for example, in the ionto-quantimeter of Szillard.
(/) Biological Effects of Rontgen Rays
The Rontgen rays can destroy living cells. Certain cells are much
more susceptible to their influence than others. Therapeutically, advan-
tage has been taken of this fact (1) to destroy the cells of the lymphade-
noid and the myeloid leukopoietic tissues in the leukemias, (2) to render
individuals sterile for eugenic, or other, reasons by killing the germina-
tive parts of the sex glands, and (3) to destroy the smooth muscle cells of
large uterine myomata, a procedure which bids fair to lessen the work of
the operative gynecologist.
44 EXAMINATIONS WITH EONTGEN BAYS
Unfortunately, repeated and prolonged exposures to the x-rays may
sometimes excite the tissues of the skin to carcinomatous proliferation.
Many a rontgenologist of the earlier days has already paid, or is now
paying, the price of our then ignorance of how to protect the operator from
the rays.
E. Qualitative and Quantitative Measure-
ments in Rontgenology
It is astonishing how many rontgenologists work in a haphazard way,
never resorting to accurate methods of measurement, though they now
have at their disposal a group of methods which permit them to work pre-
cisely. It is true that an experienced rontgenologist may make fewer
errors without measurements, than a tyro will make with a complete set
of measuring instruments ; but, other things being equal, the worker who
constantly controls his apparatus quantitatively, calling to his aid the dif-
ferent forms of measuring apparatus, will be far more successful and will
progress more rapidly in scientific rontgenology than he who eschews these
methods. It is probably true that most of the failures in x-ray work, most
of the time and material sacrificed, and, too, most of the harm done to
patients, has been due either to a complete neglect to measure the degree of
hardness of the radiation and its amount or to attempts at measurement by
unskilled persons.
1. Measurements of Hardness
Among the many "hardness measurers" now available, those of Walter,
of Wehnelt, and of Christen are perhaps the best known. Other hardness
measurers or penetrometers are those of Benoist, of
Beez, and of Bauer.
(a) Walter's Penetrometer
This consists of a lead disk, 2 mm. thick and about
20 cm. in diameter, containing 8 round openings, each
measuring 6 mm. in diameter ; each of these openings
contains a sheet of platinum, varying in thickness
(0.005; 0.01; 0.02; 0.04; 0.08; 0.16; 0.32; 0.64
of the Kny- mm). In front of the disk is a fluorescent screen
(lead-glass, coated with barium platinum-cyanur).
On testing an x-ray tube, the number of circles visible increases with
the penetrating power of the rays being tested; thus, a tube which illumi-
QUALITATIVE MEASUREMENTS 45
nates six circles is said to have a hardness of 6 on the Walter scale ; one
illuminating four circles has a hardness of 4 Walter-units, etc.
(6) Wehnelt's Crypt or adiometer
This instrument is known as a Precision Cryptoradiometer. It con-
tains an arrangement by which a wedge of aluminium can be shoved past
an opening in a protective plate, and its illumination compared with that
of an opening filled by a silver plate 0.11 mm. thick. The wedge is
shoved along until the two areas present the same illumination. The
hands and face of the observer are protected by a lead plate. By means of
an attached "cryptoscope," the
test can be made outside the dark
room.
A simpler form of the Weh-
nelt apparatus has been devised,
the reading of which depends up-
on an optical illusion. It is fas-
tened behind the fluorescent
screen. Behind the silver plate
the screen fluoresces of course
evenly, but the eye seems to per-
ceive an unequal illumination.
A pair of clear areas and a pair
of dark areas lie diagonal to one Fig> ^.-weh^it's Penetrometer.
another. The point at which
these four areas meet gives the hardness of the radiation, which can
be read off on a perforated copper scale on the fluorescent screen. This
instrument is very convenient, since fairly accurate readings can be made
with it at a glance. With the aid of the cryptoscope, this simple form
also can be used outside the dark room.
(c) Christen' s Absolute Hardness Measurer, or So- Called
"Half -Value Layer"
By using this instrument, the attempt is made to do away with arbi-
trary values and to establish an absolute unit of measurement, the so-called
"half-value layer" ; that is, the thickness of a layer of water which will
absorb half of the radiation striking it, the other half passing through.
As a matter of fact, water itself is not used, but, instead of it, a solid
substance (bakelit), which has the same absorption capacity as water. The
general make-up of the instrument resembles Wehnelt's Cryptoradiometer,
but instead of Wehnelt's aluminium wedge, we have, in Christen's instru-
ment, an echelon, or staircaselike, graduation of the wedge, the individual
46
EXAMINATIONS WITH BONTGEN EAYS
steps of the staircase being composed of the substance having the same
absorptive power as water.
The illumination of a portion of the wedge is compared with that of an
evenly perforated metal sieve. The latter yields a fluorescence illumina-
tion corresponding to "half-value" since the areas of the transverse section
of all the sieve openings is equal to half the area of the transverse section
of the whole sieve surface. By removing the sieve some distance from the
fluorescent screen, the single fine openings in the sieve are not projected,
but, instead, there is a homogeneous illumination of medium grade.
This absolute "half-value layer" represents a real advance in hardness
measurement. With it, we can get a better idea of the penetrability of the
x-rays than is possible by any other method; thus, for example, if the
half -value layer, as measured, amounts to 0.6 cm., we know immediately
h/ehneltscale
Half value layer
Benokt scale
Walter scale
Benoist-Watter
1
2
3
/
5 C
' 7
6
9
10
11
12
13 J4\
ai
(2 (J.
5
0,4
a
(If, 0,7
Of OjJ
i
i
V
1C,
& 2
\ 1
# 3
1
i
:» 4
5
6
7 (
9
10
um
I 1
i ;
4
,
Jf
6
8
9
/
2
3
4
5
6
Fig. 15. — Comparative Scale for Penetrometers or Hardness Measurers.
that, at a depth of 0.6 cm., half of the radiation concerned is still active,
and that at double this depth, i. e., at 1.2 cm., a quarter of the radiation is
still active; at triple the depth (1.8 cm.) only a ninth, and so on. As Janus
and Schittenhelm point out, this kind of measurement is especially valu-
able in therapeutic applications of the x-rays to the deeper tissues, for, if
one knows the half-value layer and the dose of radiation, he is accurately
informed as to the amount of radiation reaching to definite depths.
A special modification of the half-value measurer for photographic
registration has been devised. In it, the echelon wedge is made in the
form of a circle. The apparatus is laid on a photographic plate; a
fly-wheel, run by clock-work, rotates, exposing the different parts of the
wedge. The plate is then developed and fixed, and the hardness read off.
This apparatus is especially helpful in scientific researches on the Rontgen
rays.
QUALITATIVE MEASUREMENTS 47
2. Measurements of the Intensity of the High-Tension
Current
In order to know the intensity of the current entering an x-ray tube,
and, from it, to estimate the burden we are throwing upon the tube, a
milliamperemeter can be intercalated in the high-tension circuit. It is
desirable to use a large milliamperemeter, the scale of which can be seen,
at a distance of 10 or 15 feet, in a darkened room. Since, for different
purposes, different amounts of burden are thrown upon the tube, it is
necessary that the milliamperemeter be provided with a wide range of
measurement possibilities ; thus, it may sometimes be desired to measure
currents of low intensity say 0-5 milliamperes, as in rontgenoscopy and
in therapeutic applications of the x-rays, whereas, for rontgenography,
stronger currents are used, for some tubes, 0-25 milliamperes, for other
tubes, especially for instantaneous rontgenography, 0-50 milliamperes.
The intensity of the radiation sent out from the tube is approximately
proportional to the intensity of the current flowing through the tube; in
other words, if the intensity of the current be 10 milliamperes, the x-ray
effect will be about double that with a 5 milliampere current during the
same time. It must be borne in mind, of course, that with currents of
stronger intensity, the hardness of the tubes increases to a certain extent ;
in other words, a current of double strength will yield a little more than a
double x-ray effect.
The milliamperemeter should be protected by a small condenser, placed
parallel to it in the circuit ; otherwise oscillating discharges may give rise
to false readings. When the inductor apparatus is used, one may be
deceived by readings affected by inverse discharge. This is avoided
entirely in the modern form of x-ray apparatus, in which alternating cur-
rent and rectifying switch are used.
3. Measurements of the Quantity of Rontgen Radiation
(Dosage of X-Eay ; Radiometry; Quantimetry}
In therapeutic applications of the x-rays, it is essential to know the
quantity of radiation that is being applied; otherwise x-ray burns of the
skin, or wholly unexpected and sometimes dangerous x-ray effects on the
organs, will be obtained. A number of radiometers, or quantimeters, have
been introduced. Among these, the best types are : (1) Holzknecht's modi-
fication of Sabouraud and Loire's radiometer, (2) Szillard's ionto-quanti-
meter, and (3) Kienbock's quantimeter.
(a) Holzknecht's Modification of the Sabouraud-Noire Radiometer
In the original French instrument, circular disks 7 mm. in diameter,
made of potassium platinum-cyanur, of yellowish green color, were
48
EXAMINATIONS WITH EONTGEN EAYS
exposed at half of the focus-skin distance to the radiation ; under radiation,
the color changes gradually to reddish brown. This discoloration is com-
pared in diffuse daylight with the discoloration which corresponds to an
"erythema dose/' that is, to that dose of Rontgen radiation that causes
slight inflammation of the skin and falling out of the hair.
Certain precautions must be observed :
1. The exposure should be made in dim daylight only, owing to the
fact that the pastilles are discolored by bright light; after the exposure,
the comparison with standard color
should be quickly made.
2. The stock of pastilles should
be kept in a cool place, since heat dis-
colors them.
3. Discoloration from the heat of
the x-ray tube is avoided by placing
the disks at least 2 cm. distant from
the glass wall of the x-ray tube.
4. In making the test, the pas-
tilles must be exposed to the same
pyramid of rays as is used in the
therapeutic treatment.
Fig. 16. — Sabouraud and NolrSs Radio-
meter.' (By courtesy of the Schei-
del- Western X-ray Coil Co.)
Fig. 17. — Holzknecht's Radiometer for
Direct Reading of X-ray Dosage.
(By courtesy of V. Mueller & Co.)
With the original instrument, only the maximal dose could be meas-
ured; with Holzknecht's modification, this objection is overcome, in that
the discoloration of the exposed pastille is compared with the color of a
fresh pastille which is shoved along beneath a strip of celluloid of increas-
ing redness until the two colors are alike ; on an adjoining scale, the "dose"
can be read off.
(6) lonto-Quantimeter of Szillard
This is an application of the fact that x-rays ionize air. The instru-
ment consists of an ionization chamber, which is laid upon the area of
QUALITATIVE MEASUREMENTS
49
the body that is to be exposed. The instrument is wound up by turning a
crank on one side until the indicator stands at zero. There is an adjust-
ment by which the opening of the ionization chamber can be enlarged or
diminished to compensate for variable grades of "hardness" of the radi-
ation. Radiation is then begun and the advance of the indicator on the
scale is observed. As soon as the dosage desired has been reached, the cur-
rent is turned off.
(c) Quantitimeter of Kienbock
A small strip of photographic gas-light paper is inclosed in black paper,
placed upon the surface of the body to be treated, and the exposure begun,
the x-ray tube receiving a current of definite intensity (milliamperes), and
the hardness of the tube having previously been measured. After a certain
definite time-exposure, the gas-light paper is developed and fixed, and the
blackening compared with that of a standard scale that permits one to
read off the dose directly. The difference between this amount and the
dosage decided upon is now known, and, as a control, a second strip of gas-
light paper is exposed, while the remainder of the dose is given. This
second strip is subsequently developed and fixed ; its amount added to the
amount indicated by the first strip, should correspond to the exact dosage
determined upon beforehand.
Fig. 18.— Kienboeck's Quantitimeter.
(By courtesy of the Scheidel-Western X-ray Coil Co.)
I would call attention to the value of this method as a protection of the
rontgenologist in medicolegal cases. If the strips of paper as developed
are kept on file, they may form valuable evidence if the rontgenologist
should be wrongly accused and subjected to lawsuit.
50 EXAMINATIONS WITH EONTGE1ST KAYS
SCALE OF QUANTITY.
Holzknecht
Units
Chromo-Radiometer
1
1.5
3
4
S
6
7-8
14
20-22
H
Sabouraud-Noir4
Radiometer
B
Tint
Bordier
Chromo-Radiometer
0
0-1
1
MI
II
III
IV
Tint
Kienboeck
Units
Quantitimeter.
2
3
6
8
10
12
14-16
28
40-44
M
Schwartz
Precipitation Radiometer
1
2
3.5
Kaloms
Fig. 19. — Comparative Scales of Quantitimoters.
(By courtesy of the Scheldel-Western X-ray Coll Co.),
F. Central Projection and Parallel
Projection
1. Divergent Rays and Central Projection
When the Rontgen rays start out from the tube, the stream is only a few
millimeters in diameter at the target, but the rays diverge, and an organ of
the body placed between the tube and a fluorescent screen (or photographic
plate) will appear in the picture in central projection, enlarged, owing to
the divergence of the rays. The closer the plate or screen to the organ,
the less the enlargement; this is why, on looking at the heart, the fluores-
cent screen is held over the heart in front, rather than behind.
2. Parallel Rays and Ortho-Projection
( Ortliodiagraphy)
In order to determine the exact size of an organ by means of the x-rays,
an apparatus known as the orthodiagraph was devised by Moritz, and
later improved by Groedel. It has been especially useful in studies of the
heart.
By this method, a complete parallel projection is made possible ; it per-
mits of an exact reproduction of the outlines of the heart, in natural size.
This parallel projection is achieved by means of an apparatus which makes
the x-ray tube movable, so that a very small bundle of the rays, from the
CEOTKAL AND PAKALLEL PKOJECTION
51
anticathode, can be made to move in all directions in a plane ; the bundle of
rays in the different situations follows lines which are parallel to one
another. Thus the bundle can be made to move around the margin of the
organ under observation (parallel projection) ; the x-ray tube and the
marker, for recording the outline on the fluorescent screen, move as a single
piece, being firmly united with one another. At many points, along the
outline of an organ (first the right margin of the heart, then the left mar-
gin, then the diaphragm, the lung margins, and the lower edges of the
1
1
h
1
\ 1
1
1 '
1
1 \
I
1 !
^ \
'N
V \
, ^ y >
| i
1
I
1
^
1
^
^
1
^
i
^
^
|
1
1
1
1
1
1
1
,
}
i
^m
BBB
"__
Fig. 20.— Ordinary and Orthogonal Projection. (After T. Brugsch and A. Schittenhelm.)
•
clavicles), a mark is made on paper by pressing on a rubber ball, and these
marks are later united by lines to form the aorthodiagram." With more
recent apparatus (e. g., Snook's vertical fluoroscope), the orthodiagraphic
image is traced on tracing-glass with a grease pencil, the simultaneous
movement of the tube and the tracing-pointer being accomplished by a set
of large heavy metal parallelograms.
The orthodiagrams obtained over the normal heart and over patholog-
ical hearts are described in the section dealing with the diagnosis of circu-
latory diseases.
3. Teleront^eno^raphy and Telerontjjenoscopy
Eecently, it has been found possible to replace orthodiagraphy by the
so-called telerontgenography. By rontgenographing the patient at a dis-
tance of 2 meters from the x-ray tube, with a very short exposure (1/10-
52 EXAMINATIONS WITH EONTGEN EAYS
1/8 second) , a rontgenogram is obtained in which the heart is of almost
natural size (Kohler), the error not exceeding 2 mm. for either margin of
the heart. At this distance from the tube, practically a parallel projection
is obtained, and the error no greater than with orthodiagraphy. If de-
sired, the same principle can be used for fluoroscopic examination of the
heart (making a drawing on the lead-glass of the fluorescent screen) ; for
this purpose a drawing-stand, permitting of movement in two directions,
is a great convenience.
Telerontgenograms taken with the single impulse apparatus are said
to yield very sharp pictures of the outlines of the heart as all blurring
from pupation is absent.
4. Diaphragms
In order to prevent blurring of the shadows by the glass-rays (q. v.)
and by the secondary radiation (q. v.), it is necessary to use diaphragms,
or, better still, tubes, through the openings 'of which the more central pyra-
mid of rays is made to pass ; in this way, sharper pictures, richer in con-
trast, are obtained. This helps especially in getting details of a lung
apex, or of a kidney.
G. Photographic Technic in Rontgenography
A few practical points in the photographic technic may be mentioned.
It is best to use dry plates (bromid of silver), especially prepared for x-ray
work (thicker film of emulsion). Plates of several sizes are required (8 x 10;
10x12; 11x14; 14x17).
It is false economy to use the cheaper varieties of plates.
Just before use, a plate may be placed in a black envelope, to protect it from
the perspiration of the patient.
Each plate should be numbered by means of a rontgenographic "plate marker";
when helpful, the right side, or left side, should be marked (kidney). The plates
should not be too old.
For rontgenography of the teeth, celluloid dental films, 1^4" x 1%", can be
purchased; they come in small envelopes of black paper, ready for use in the
mouth.
For developing the negatives in the dark room, a slow developer, capable of
developing through the whole layer of emulsion to the glass, without fogging, is
recommended; either a glycin-developer, or a metol-hydrochinon developer will
be found satisfactory.
After development, the plates are fixed, being left in the fixing-bath twice as
long as is necessary wholly to dissolve the bromid of silver; the time amounts to
at least six or eight minutes. The plates are then washed thoroughly, in running
water, for at least an hour, or in non-running water, changed four or five times, for
at least two hours. Unless the fixing and washing is thorough, yellow spots will
later appear on the negatives.
CLINICAL APPLICATION 53
H. Clinical Applications of the Rontgen
Rays
The shadow pictures obtainable, due to differences in absorption power
of the different tissues of the body, are of the greatest help in clinical
diagnosis. With Dr. F. H. Baetjer, the rontgenologist at the clinic in
which I work, and with his associate, Dr. Waters, I have had manifold
opportunity to observe the rontgenologicaj. shadow-pictures in all kinds of
clinical conditions, and have come to rely upon rontgenoscopy and rontgen-
ography as two of the most important aids in present-day clinical diagnosis*
In the thorax, the cardivascular stripe can be studied as well as the
lung areas, the esophagus, and the mediastinal structures ; tumors, pleural
effusions, etc., can also easily be made out.
In the abdomen, by the introduction of contrast substances like barium
sulphate into the gastro-intestinal tract, or thorium into the urinary tract,
the form, position, and motility, of these organs can be accurately studied.
Fistulse can be filled with bismuth paste before study. Sometimes it is
helpful to blow air into the intestine or into the bladder, before taking an
x-ray photograph. The orthopedists have found help from oxygen injec-
tions into the joint cavities, before making the x-ray picture, in the differ-
entiation of some forms of arthritis.
For some purposes, observation on the fluorescent screen (rontgenos-
copy) is of greater value. In other cases, x-ray photographs (rb'ntgenog-
raphy) are more helpful. Thus, in the examination of the thoracic organs,
and of the gastro-intestinal tract, rontgenoscopy is for most purposes best,
though, for finer changes in the lungs, and for permanent records of
momentary conditions in the abdomen, rontgenography is essential. In
bone work and in genito-urinary work, rontgenography is more valuable
than rontgenoscopy.
1. Technic of Rontgenoscopy
In rontgenoscopy the x-rays from the tube pass through the body and
excite the fluorescent screen, held on the other side, into fluorescence.
The parts that most completely absorb the rays appear, therefore, as
shadows upon this screen.
(a) Fluorescent Screens
These consist of frames, containing a plate coated with a fluorescent
substance, usually barium platinum-cyanur in fine crystals, imbedded in
cellulose. The smaller the crystals, the sharper (though darker) the pic-
54
EXAMINATIONS WITH KONTGEN KAYS
"astral screen" (Kup-
It gives results fully
tures obtainable. By thickening the layer of the fluorescent substance,
greater brilliance is obtainable, though the price is increased. Since the
brilliance of the fluorescence de-
pends upon the water of crystal-
lization in the crystals, care must
be taken not to drive off any of
this crystallization water (by
heat, pressure, scratching, etc.).
A less expensive screen is the
so-called
precht).
equal to the platinum screen, and
is not so easily spoiled.
To protect the examiner, the
screen is covered with lead-glass,
and if the screen is held in the
hands, these should be protected
by lead flanges, or the examiner
may wear protective gloves. In
the newer vertical fluoroscopes,
the frame on the operator's side
carries a 17" x 17" screen, cov-
ered with a special lead-glass,
which stops all the direct rays
that fall upon the screen. The
Pig. 21. — Lead-protected Rontgenoscope. (By .
courtesy of the Scheidel-Western X-ray Operator IS protected further
Co11 Co-) from secondary radiation, by
curtains of special material hung around the patient. Automatic
protection is also afforded
by mechanical devices
that prevent too great a
relative motion between
the tube and the screen.
Larger screens are also
now in use— 18" x 24",
24" x 30", 30" x 40", 40"
x 50". For most purposes,
the smaller screen is suffi-
cient. To make permanent
records of the rontgenos-
copic view, one can draw
Fig. 22. — Astral Screen for Fluoroscopy.
(By courtesy of the Kny-Scheerer Co.)
visible contours on the lead-glass surface with a grease pencil. After the ex-
amination is over, this outline is copied by means of tracing paper. The
lead-glass plate is then rubbed dry and is- ready for another examination.
CLINICAL APPLICATIONS 55
(b) Vertical and Horizontal Rontgenoscopy
In most cases, the vertical fluoroscope is used, the patient standing, and
the examiner sitting in front of him on an adjustable stool. Feeble
patients may, when necessary, be steadied by a canvas band and two ver-
tical rods by which they are held close to the screen. Children, even
sucklings, can be fluoroscoped in the upright position by fastening them in
a "baby's stand" (Grosser).
In the horizontal fluoroscope, the tube-case is placed under the examin-
ing table. Many varieties are available ( Trochoscope ; Universal Exam-
ining Table, etc.).
In simple rontgenoscopic outfits, tube stands, with lead-shields, are
used, but, in the more expensive outfits, the tubes are held in tube holders
inside a tube-box. *
(c) On Certain Details of Rontgenoscopy
On account of the long exposure in fluoroscopy, special water-cooled
tubes, or, better still, tubes fanned by cool air, are desirable.
If the inductor apparatus be used, the interrupter frequency should not
exceed 30 or at most 40 per second. With the alternating current and
rectifying-switch apparatus one uses the lowest number of impulses of
which the machine permits.
The degree of hardness of the tube varies for different kinds of exam-
inations. For rontgenoscopy of the lungs, a tube with a hardness of 8
Wehnelt nuits (half-value layer 1 cm. ; 7 Walter units) ; for rontgenoscopy
of the cardiovascular stripe, or of the gastro-intestinal canal, a harder tube
is desirable (not less than 9 Wehnelt units; 1.2 cm. half-value layer; 7 or
8 Walter units). It is best to keep tubes of these strengths available, using
the one strength for examining the lungs, and the other for the stomach
and intestines. Used in this way, the tubes will last longer.
As to the strength of the current employed, 2-3 milliamperes will be
sufficient with the inductor apparatus, 3-5 milliamperes with the alternat-
ing current and rectifying-switch apparatus.
The Coolidge tube is especially valuable for rontgenoscopy since the
penetrability of the rays can be varied at will while the tube is in action.
The direction of the transillumination is varied according to the object
in view. The following are the main directions :
1. Sagittal direction.
(a) Dorsoventral (tube behind ; fluorescent screen in front).
(b) Ventrodorsal (tube in front ; screen behind).
2. Frontal direction; that is, from side to side.
(a) Dextrosinistral (tube on right side; screen on left).
(b) Sinistrodextral (tube on left; screen on right).
56
EXAMINATIONS WITH EONTGEN KAYS
Fig. 23.— The Coolidge X-ray Tube, Operating In Connection with a Current Generating Unit
for Heating the Cathode Spiral. The Amperemeter Indicates the Amount of Current
Passing Through the Cathode Spiral of the Coolidge Tube. (By courtesy of the Kny-
Scheerer Co.)
3. First oblique diameter (fencing position).
(a) Dorsoventral (tube, posterolateral on the left; screen, antero-
lateral on the right).
(h) Ventrodorsal (tube, anterolateral, on the right; screen, pos-
terolateral on the left).
4. Second oblique direction.
(a) Dorsoventral (tube, posterolateral on the right; screen, antero-
lateral on the left).
(b) Ventrodorsal (tube, anterolateral on the right; screen, pos-
terolateral on the left).
The examiner should remain at least 5 or 10 minutes in the dark room,
until his eyes are perfectly adapted to the darkness, before making the
examination.
The application of rontgenoscopic methods to the thorax, heart, great
vessels, trachea, lungs, diaphragm, esophagus, stomach, intestines, liver,
and spleen will be referred to under the diagnosis of diseases of these
several organs.
CLINICAL APPLICATIONS
57
2. Technic of Rontjjenojjraphy
Here a photographic plate takes the place of the fluorescent screen;
after exposure, it is developed, fixed, washed, dried, and examined in a
good illuminating box.
(a) Maintenance of the Patient in Correct Position
It is essential that the patient do not move during the exposure. For-
tunately, with the alternating current and rectifying-switch apparatus,
very short exposures are possible, and, with the single-impulse inductor
apparatus, exposures of only 1/200 of a second suffice. Still, even with
instantaneous exposures, it is necessary that the part shall stand in pre-
cisely correct relation to the pyramid of x-rays on the one hand, and to the
photographic plate on the other; thus, whether the patient be standing,
sitting, or lying, during the exposure, the exact position of the patient, and
the maintenance of this, are of great importance. Supports of various
sorts help to keep the patient in the correct position.
1.— Sagittal dorso-
ventral transillu-
mination.
2. — Sagittal ventro- 3. — Frontal dextro- 4. — Frontal
dorsal transillu- sinistral transil- trodextral trans-
mination. lumination. illumination.
5.— First oblique di-
rection.
6. — Second oblique 7. — Third oblique 8. — Fourth oblique,
direction. direction. direction.
Fig. 24.-. ./Different Positions for Transillumination on Rontgenoscopy s
after T. Brugsch and A. Schlttenhelm. )
58
EXAMINATIONS WITH KONTGEN KAYS
Fig. 25. — Compressor for Use In X-ray Work (Gurt).
(6) Compression Apparatus
In making x-ray photographs of the kidneys, and sometimes of other
parts, especially in stout individuals, it is helpful to use an Alb ers-Scho en-
berg compression apparatus, so as to lessen the body thickness ; at the same
time the x-rays are passed through a ring, or a tube, in order to avoid sec-
ondary radiation as much
as possible.
More recently, the
Gurt compressor, consist-
ing of a broad band, pulled
tightly across the body by
means of a pulley and lev-
er, permits of strong com-
pression, without causing
, ™^ ^v pain. Under the band,
©I ^1 >v an air bag, or a cushion,
may, if desired, be placed,
in order to produce strong
local pressure, for exam-
ple, over one kidney.
, It is common, nowa-
days, to combine some
form of diaphragm, or tube, with the compression apparatus (e. g., Lam-
bertz's stand, Robinson's compression tube).
(c) Hardness of Tubes Used in Rontgenography
For rb'ntgenography, x-ray tubes of medium hardness (8-9 Wehnelt
units ; 1.2 cm. half-value layer ; 7 Walter units) are employed, though for
taking a hand, a foot, or the lungs, a somewhat softer tube will be used
(6-7 Wehnelt units) ; while for photographing a kidney, harder tubes
(7-7.5-8-9 Wehnelt units) are best. Still harder tubes are employed
when photographing the passage of a bismuth meal through the stomach
and intestine (9.5 Wehnelt units). With the rectifying-switch apparatus,
softer tubes can be used with a higher intensity of current than is possible
with the inductor apparatus; this accounts for the excellent results now
being obtained in ordinary x-ray work. Indeed, on the average, one can
use, with the rectifying-switch apparatus, a tube, softer by 1—2 Wehnelt
units, than the tube required with the inductor apparatus.
(d) Exposure Time
This varies greatly, according to the end in view. Thus, time exposures
last ten seconds, or a little longer, with a current of 2-3 milliamperes ;
quick exposures, last J-10 ^seconds, with # current intensity of 10-30-40
CLINICAL APPLICATIONS
milliamperes. Instantaneous exposures, with the strongest currents
that the tube will bear, last from 1/20-1 second in the slower instances,
and 1/50-1/200 in the quickest exposures in which a single impulse is
used. When making instantaneous exposures, an intensifying screen is
usually placed over the dry photographic plate,
It is convenient to keep in mind the rule that, with all exposition-times,
the product (milliamperes of current X time in seconds) is about the same.
One can, therefore, easily calculate the milliamperage that should be
employed with a given exposition time.
The following table, prepared by Janus and Schittenhelm, shows at a
glance the exposition-time used for photographing the various parts of the
body by means of the x-rays :
Synoptical Table of Exposition-Values for Different Parts of the Body
(Janus and Schittenhelm)
Part of body of a medium
sized adult (say 1,68
m. high; 70 kg. weight)
Focus-plate
Distance
HARDNESS OF TUBE IN WEHNELT UNITS
7
8
9
6
7
8
Without Intensify-
ing Screen
With Intensifying
Screen
Exposition-value
= milliamperes x seconds
Head, from in front
Head, from side
Tube-diaphragm, or
60 cm
350
250
100
50
240
140
180
120
50
200
150
400
200
130
130
80
100
'30
120
90
250
500
250
'so
250
30
10
100
75
40
120
70
35
20
70
45
60
40
15
*60
150
150
120
45
150
15
6
60
40
20
70
40
20
'46
25
35
25
8
50
35
80
180
80
70
25
80
10
4
35
25
15
40
25
'25
15
20
"5
25
25
50
120
50
'is
50
5
2
20
15
10
Tube-diaphragm, or
60 cm
Eyes and nose, lateral. . .
Cervical spine
Thoracic spine
Thorax. . .
Tube
160
80
Tube
Tube or 60 cm
60 cm
Thorax, lateral
Sternum ....
60 cm
Tube
200
80
Heart and lungs
Heart (distant view)
60 cm
2 m
Shoulder
Tube
Lumbar spine. .
Tube . . .
Lumbar spine, lateral . . .
Sacrum and coccyx.
Tube
Tube
400
350
140
400
50
15
180
140
70
Renal, or vesical, stone . .
Stomach and intestine. . .
Pelvis, or hip-joint
Arm
Tube...
550
'so
25
60 cm. . .
Tube or 60 cm
Tub^
Hand
Tube
Thigh or knee, from in
front
Tube
Leg or knee, from side. .
Foot
Tube
Tube
100
The hardness of the tube most suitable for the various views is indicated by bold-face type.
The items given in the table hold only for work done with the best photographic appa-
ratus made for rontgenographic purposes.
The exposition-time can also be very well determined by means of a slide-rule (Fig. 25).
60 EXAMINATIONS WITH RONTGE1ST BAYS
To use the above table of exposition-values, Janus and Schittenhelm
give the following example : Let us suppose that it is desired to take a
photograph of the stomach, for which a tube hardness of 9 Wehnelt units
is best. On testing the tube, it is found that it stands well a current of 8
milliamperes. From the table, one sees that the exposition-value in milli-
amperes seconds is 80. If we divide this exposition-value (80) by the
number of milliamperes (8), we see that the exposition-time necessary
THE PEABODY- WINTER"* RAY EXPO METER
For Correctly Timing RadiograpMc Exposure!
DISTANCE OP ANODE FROM PLATE IN INCHES
U t< 11 II 1C 1> H !t !l,-'!0 •
* * r ' i 'i '1 J. I J Jin I HI IAIJJ-AUUU
'MltXi'A'WPERES Of- CUHWENT PASSING Tn»OUCM TUBE
Pig. 26.— The X-ray Expomcter. (By courtesy of the Kny-Scheoror Mfg. Co.)
(without intensifying screen) is 10 seconds. If, on the other hand, the
instrument permits of a current of strong intensity, say 40 milliamperes,
only 2 seconds exposure time will be required.
When using the intensifying screen, it is to be kept in mind that a
tube, which has been measured with a current of 2-3 milliamperes, will be
harder by about ^-1 Wehnelt units when a current of greater intensity (10
milliamperes and more) is passed through it.
(e) Intensifying Screens
An intensifying screen consists of a layer of calcium tungstate, which
is laid over the photographic plate, in an especially constructed holder, or
"kassette." Such a screen will shorten 'the exposure-time to 1/5, or even
1/30, of the ordinary time.
00 Special Clinical Applications of Rontgenography
The special methods of applying rontgenography to the paranasal sin-
uses, the skull, the teeth, the lungs, the bronchial glands, mediastinal
growths, esophagus, gastro-intestinal tract, gall stones, renal stones, vesical
stones, bones and joints will be referred to under the diagnois of diseases
of these parts.
(g) Stereoscopic Rontgenography
For the study of lesions in the lung (tubercles, cavities, pneumo-
thorax), and for the study of the exact position of stones in the kidney, or
CLINICAL APPLICATIONS
61
ureter, stereoscopic views are very helpful. In the clinic in which I work,
Drs. Dunham and Boardman have made a large series of stereoscopic
x-rays of the lungs. Another series, made by the rontgenologist to the
hospital, Dr. F. H. Baetjer, in a number of normal people, has been
controlled carefully by physical examinations made by Dr. Louis Hamman.
We now have stereoscopic rontgenograms made as a routine in the clinic in
the more interesting cases of intrathoracic lesion.
Fig. 27. — The Wheatstone Stereoscope. (By courtesy of the Rontgen Mfg. Co.)
These stereoscopic plates are indeed very instructive,' and should be
made in all cases where the diagnosis is difficult by ordinary methods. Two
plates are exposed, without movement of the part photographed during, or
between, the two exposures. The source of the x-rays for one plate must
be 2^ inches away from the position of the source for the second plate (cor-
responding to the average distance between the centers of the two eyes). By
62
EXAMINATIONS WITH EONTGEN EAYS
an ingenious arrangement, the x-ray tube is, therefore, moved 2J inches
between the two exposures, and the center of this line of movement is placed
perpendicularly over the center of the plate. This movement of the source
is accomplished by an automatic tube-shifting device. The vertical dis-
tance from the focus of the tube to the plate should be 14 inches plus the
thickness of the object. The position of the vertical line, drawn from the
focus-spot of the tube to the plate, is different for each of the two plates
Pig. 28. — Rontgenoscopic Examination on Stereoscopic Table.
(By courtesy of Scheidel- Western X-ray Coil Co.)
because of the movement of the tube between exposures. The foot of the
vertical line, at the point where it rest on the plate, is called the "foot-
point" (Eijkmann). . The operator marks the location of the "foot-
points" on his finished plates ; when viewing them, later, in the Wheatstone
CLINICAL APPLICATIONS 63
stereoscope, lie places them in the illuminating box, glass side out, and with
the "foot-points" toward the back of the boxes. In viewing the plates in
the stereoscope, the eyes of the observer must optically replace the focus-
spots of the tube, in order to get correct impressions of depth without
distortion.
Various plate-changing devices are used; these must support the object
while the plates are being changed. Among them may be mentioned (1) the
non-automatic stereoscopic plate-changer; (2) the automatic stereoscopic
tunnel plate-changer. The latter shifts the plates in less than one second.
With the rectifying-switch form of apparatus, it is easy to make a pair
of 14" x 17" chest plates in three seconds. The pulling of a cord releases
the spring that shifts the plates.
In making stereoscopic rontgenograms of the kidneys, it is very con-
venient to have a stereographic table with automatic shifting apparatus and
compression rings. Such tables are provided, also, with an inclined plane
for frontal-sinus work.
(h) Cinematographic Rontgenography
Attempts have been made to prepare cinematographic films of moving
organs in the body, photographed by the x-ray; thus, the shadows on a
fluorescent screen have been directly photographed by an ordinary cinema-
tographic apparatus, but unfortunately the yellow light of the fluorescent-
screen has very slight photographic effect. Cinematographic photographs
have, however, been taken by this method of the internal organs of dogs
and monkeys, the number of reproduction-pictures per second being
exactly the same as the number of photographs taken.
Other workers, by means of a rapid plate-changing machine, have
taken x-ray photographs on single plates, the x-ray tubes being excited
synchronously with the change of plates, by means of the single-impulse
apparatus. Thus far, it has not been possible to take more than 4 or 5
photographs per second by this method. Since to produce cinematographic
effects, it is necessary to reproduce 15-18 pictures per second, these inves-
tigators have copied the picture from each single plate three or four times
on the film, thus making the so-called pseudo-cinematographic film from the
kino-series plates (Groedel; Rosen thai). Groedel of Nauheim has taken a
kino-series simultaneously with electrocardiograms on which were marked,
electrically, the times of the taking of the single rontgenograms.
References
1. General Works
Albers-Schonberg (H. E.) u. Walter (B. G. H. L.}. Die Rontgentechnik. 3. Aufl.
Hamburg, 1910.
Albert- Weil (Ernest). Elements de radiologie; diagnostic et therapeutique par les rayons
X. Paris, 1914, F. Alcan. 502 p.
64 EXAMINATIONS WITH RONTGEN EAYS
Arthur (David) & Muir (John). A manual of practical x-ray work. London, 1909 , Reb-
man, Ltd. 256 p. 8°.
Bythell (W. J. S.) & Barclay (A. E.). X-ray diagnosis and treatment. London, 1912,
H. Frowde. 159 p. 8°.
Christie (A. C.). A manual of x-ray technic. Philadelphia & London [1913], J. B. Lip-
pincott Co. 112 p. 8°.
Dessauer (F.) & Wiesner (B.). Leitfaden des Rontgenverfahrens. Unter Mitarbeit von
A. Blencke, Hildebrand, A. Hoffa, A. Hoffmann, Guido Holzknecht,
herausgegeben von Friedrich Dessauer und B. Wiesner. Leipzig, 1908,
O. Nemnich. 344 P> 8°>
Gillet (/.). Die ambulatorische Ronlgentechnik in Krieg und Frieden. Stuttgart, 1909,
F. Enke. 175 p.
Gocht (H.). Handbuch der Rontgenlehre zum Gebrauche fur Mediziner. 4th ed. Stutt-
gart, 1914, F. Enke. 494 p.
Groedel (F. M.). Atlas und Grundriss der Rontgendiagnostik in der inneren Medizin.
Miinchen, 1904.
Harrass (P.). Vorbereitung zum Arbeiten im Rontgenlaboratorium. Stuttgart, 1909, F.
Enke. 116 p.
Janus (F.). Rontgenologische Methodik. In: Brugsch (T.) & Schittenhelm (A.}, Technik
der speziellen klinischen Untersuchungsmethoden, Bd. i, 156-284. Ber-
lin u. Wien, 1914.
Kaye (G. W. C.). X-rays: an introduction to the study of Rontgen rays. London, 1914.
272 p. 8°.
Knox (.R.)» Radiography, x-ray therapeutics and radium therapy. New York, 1915,
Macmillan Co. 406 p. 4°.
Krause (P.)« Die Rontgenuntersuchung innerer und Nervenkrankheiten. In: P. Krause's
Klinische Diagnostik. 2d ed. Jena, 1913, G. Fischer. 838-912.
Morton (E. R.). Textbook of radiology. New York, 1915, E. B. Treat & Co. 220 p.
Munk (F.). Grundriss der gesamten Rontgendiagnostik innerer Krankheiten fur Arzte und
Studierende. Leipzig, 1914, G. Thieme. 263 p. 8°.
Rieder (Hermann) & Rosenthal (Josef). Lehrbuch der Rontgenkunde. Unter Mit-
wirkung von A. Cieszynski, H. Dietlen [etc.]. Bd. I. Leipzig, 1913, J.
A. Earth. 612 p.
Tousey (Sinclair). Medical electricity and rontgen rays, with chapters on phototherapy
and radium. Philadelphia & London, 1910, W. B. Saunders Co. Ill 6 p.
Walsh (I).). The Rontgen rays in medical work. Pt. I : The electrical apparatus, by H.
Lewis Jones. Pt. II: Medical and surgical, by the author. 4th ed.
New York, 1907, W. Wood & Co. 461 p. 8°.
Williams (F. H.). The Rontgen rays in medicine and surgery as an aid in diagnosis and as
a therapeutic agent. 3d ed. New York & London, 1903, Macmillan Co.
757 p. 8°.
2. Examinations of Special Domains
Arnsperger (H. E. R.). Die Rontgenuntersuchungen der Brustorgane und ihre Ergebnisse
fur Physiologie und Pathologic. Leipzig, 1909, F. C. W. Vogel. 263 p.
8°.
Die Rontgenuntersuchung des Magen-Darmkanales und ihre Ergebnisse
fiir Physiologie und Pathologic. Leipzig, 1912, F. C. W. Vogel. 80 p.
Assmann (H.). Erfahrungen ueber die Rontgenuntersuchung der Lungen unter besonderer
Beriicksichtigung anatomischer Kontrollen. Arb. a. d. med. Klin,
zu Leipzig, Jena, 1914. 167 p., 14 pi-
Case (J. T.). The x-ray examination of the alimentary tract. [Photo-stereoroentgenograms.]
Troy, 1915, The Southworth Co.
Cotton (W.}. An apparatus for x-ray localization. Brit. M. J., London, 1915, i, 464-
CLINICAL APPLICATIONS 65
Dieck (W.). Anatomie und Pathologic derZahne und Kiefer im Rontgenbilde mil besonderer
Beriicksichtigung der Aufnahmetechnik. Hamburg, 1911, L. Grafe &
Silleur. 92 p.
Groedel (F. A/.). Die Orthorontgenographie. Munich, 1908, J. F. Lehmann. 79 p.
Die Technik der Rontgenkinematographie. Deutsche med. Wchnschr.,
Leipzig u. Berlin, 1909, xxxv, 434~435.
Die Rontgendiagnostik der Herz- und Gefdsserkrankungen. Berlin,
1912, H. Meusser. 196 p.
Hoffman (F. A.}. Atlas der Anatomie des Mediastinums im Rontgenbilde. Leipzig, 1909,
W. KlinkhardL 16 p. Obi.
Holzknecht (G.). Die rontgenologische Diagnostik der Erkrankungen der Brusteingeweide.
Hamburg, 1901, Grafe & Silleur. 229 p.
Krause (P.) & Friedrich (O.). Beitrdge zur Rontgendiagnostik von Lungenkranken.
Ztschr. f. med. Elektrol u. Rontgenk., Leipzig, 1908, x, 16; 65.
Lippo- Cramer. Die Rontgenographie in ihrem photographischen Teil. Halle, 1909. In:
Enzyldopadie d. Photogr.
Schuller (Artur). Rontgen-Diagnostik der Erkrankungen des Kopfs. Wien u. Leipzig,
1912, A. Holder. 226 p., 5 pi. 4°.
Wetterer (Josef}. Handbuch der Rontgentherapie nebst Anhang; Die radioaktiven Sub-
slanzen in der Therapie. 2d ed. Leipzig, 1913, Otto Nemnich. 41 1
p., 13 pi.
[See also references to x-ray work under methods of examination of the different
organs of the body.]
3. Oilier References
Alwens. Neuere Fortschritte in der Rontgentechnik und -diagnostik. Munchen. med.
Wchnschr., 1913, Ix, 2682-2685, 2740-2741.
Bordier (H.). Action biochimique des radiations et en particulier des radiations de Ront-
gen. Arch, d'electr. med., Paris, 1913, xxi, 289-314.
Carman (R. D.}. Medical roentgenology as a specialty. J. Missouri M. Ass., St. Louis,
1910-11, vii, 121-123.
The diagraphoscope. St. Louis, M. Rev., 1911, n. s. v, 198-200.
X-ray localization of foreign bodies. J. Missouri M. Ass., St. Louis,
1910-11, vii, 214-217.
Case (J. T.). A word of caution concerning palpation under the fluorescent screen. Med.
Rec., New York, 1914, Ixxxv, 1059-1061.
Cumberbatch (E. P.}. Fatal leucopenia following x-ray treatment. Arch. Rontgen Ray,
Detroit, 1913, xviii, 187-189.
Dessauer (F.). Instantaneous radiography in less than one-hundredth second; a new method
of radiography. Med. Rec., New York, 1909, Ixxv, 890-892.
Lasst sich die y-Strahlung des Radiums kiinstlich in Rontgenrohren her-
stellen? Munchen. med. Wchnschr., 1914, Ixi, 989-990.
Radium. Mesothorium und harte X-Strahlung und die Grundlagen ihrer
medizinischen Anwendung mil einem Beitr. a. d. Konigl. Instil, f.
exper. Therap. (Dir. Exzellenz Ehrlich). Leipzig, 1914, Otto Nemnich.
156 p.
Forssell (G.). Die Bedeutung der Rontgentherapie fur die innere Medizin. Wien. klin.
Wchnschr., 1914, xxvii, 221-227.
Fraenkel (E.) & Budde (W.). Histologische, cytologische und serologische Untersuch-
ungen bei rontgenbestrahlten Meerschweinchen. Fortschr. a. d. Geb. d.
Rontgenstrahl., Hamburg, 1913, xx, 355-363.
Hansemann (D. v.). Ueber Verdnderungen derGewebe und der Geschwulste nach Strahlen-
behandlung. Berl. klin. Wchnschr., 1914, U, 1064-1065.
Kaestle (C.), Rieder (H.) & Rosenthal (P. J.). The biorontgenography of the internal
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66 EXAMINATIONS WITH KONTGEN EAYS
Kahn (/'.). Physikalische, chemische und biologische Eigenschaften von Thorium X.
Strahlentherapie, Berlin u. Wien, 1913, ii, 480-488; Hi, 94-103.
Lazarus- Bar low (W. S.}. Die Wirkung radioaktiver Substanzen und deren Strahlen auf
normales und pathologisches Gewebe. Strahlentherapie, Berlin u. Wien,
1913, Hi, 365-378.
Lipliawsky (Semjou) & Lung wit z (Hans). Die Radioelemente in der Heilkunde; Hand-
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Laboralorium fur tierexperimentelle Rontgenuntersuchungen. Beschrei-
bung des Rontgenlaboratoriums in der ersten medizinischen Klinik
Munchen. Fortschr. a. d. Geb. d. Ronlgenstrahl., Hamb., 1914, xxii,
38-43.
Newcomet (William Stell). Radium and radiotherapy. Philadelphia & New York,
1914, Lea & Febiger. 345 p.
Pfahler (G. E.}. The present status of the Rontgen rays in the diagnosis and treatment of
disease. Internal. Clin., Phila., 1914, 24th s., ii, 66-92.
Present-day danger of rontgen-ray burns and how to prevent them. J. Am.
M. Ass., Chicago, 1914, Ixii, 189-191.
Pohl (/?.)• Ueber die Natur der Rontgenstrahlen. Strahlentherapie, Berlin u. Wien, Orig.,
1914, iv, 552-569.
Rontgen (W. C.). Ueber eine neue Art von Strahlen. Sitzungsb. d. phys.-med. Gesellsch.
zu Wurzb., 1895, 132-141.
On a new kind of ray. Science, New York & Lancaster, Pa., 1896,
n. s. Hi, 227-231.
Rutherford (E.). Radio-active substances and their relations. New York, 1913, G. P.
Putnam's Sons. 706 p. 8°.
Steinhaus (/.)• L' action des rayons X sur les tissus neoplasiques comparativement a celle
sur les tissus normaux. J. med. de Bruxelles, 1913, xviii, 351-354.
Warthin (A. S.). Ueber die in kukaemischen Geweben durch Rontgenbestrahlung her-
vorgerufenen Verdnderungen. Strahlentherapie, Berlin u. Wien, Orig.,
1914, iv, 722-727.
Williams (F. H.}. A study of the adaptation of the X-rays to medical practice and some
of their uses. Med. & Surg. Rep., Bost. City Hosp., 1897, 8 s., 134-191.
An outline of the clinical uses of the fluoroscope. Med. Communicat.
Mass. M. Soc., Bost., 1898, xvii, 859-873.
Zueblin (E.}. The present status of radioactive therapy in medicine. Md. Med. J., Balti-
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4. Journals on Rontgenology
These include: Archives d1 electricite medicale, experimental et clinique, Bordeaux.
Archives of the Rontgen Ray (Rebman Co.), New York & London. American Journal of
Rontgenology. Editor: P. M. Hickey, M.D., Detroit. The American Rontgen Ray Society.
Annales d'electrobiologie, d' electrotherapie et d'electrodiagnostic, Paris. Fortschritte auf dem
Gebiete der Rontgenstrahlen. Herausgeber: Prof. Albers-Schonberg, Hamburg. Journal de
radiologie et d'electrologie. Radium in Biologie und Heilkunde. Monatsschrift fur biologisch-
therapeutische, Leipzig. Radium, Pittsburgh. Rontgen-Taschenbuch (Rontgenkalender) .
Leipzig. Editor: E. Sommer. Leipzig, 1908-1914, i-vi, Otto Nemnich. Strahlentherapie.
Berlin u. Wien. Zeitschrift fur Rontgenkunde und Radiumforschung. Herausgeber: Dr.
Paul Krause, Leipzig. Zeitschrift fur medizinische Elektrologie und Rontgenkunde. Leipzig.
Part III
Exploratory Puncture and Exami-
nation of the Fluids Obtained
In this chapter we shall consider :
(A) The technic of exploratory puncture of the pleural cavity,
pericardial cavity, peritoneal cavity and the subarachnoid space ; and other
exploratory punctures (liver, spleen, kidneys, joints, etc.) less commonly
made;
(B) The examination by chemical and physical methods of the fluids
obtained ; and
(C) The examination by bacteriological, serological and cytodiagnostic
methods of the fluids obtained.
A. The Technic of Exploratory Puncture
1. Exploratory Puncture of the Pleural Cavity
If we suspect the presence of fluid in the pleural cavity, and desire to
inform ourselves, definitely, as to this point, we resort to exploratory punc-
ture; we introduce a sterile needle into the pleural sac, and, if fluid is
obtained, we investigate its nature.
Physicians are often too dilatory in resorting to the needle for differ-
ential diagnosis. Information regarding the pathological state and its
etiology can often be more promptly and definitely obtained by exploratory
puncture than in any other way, and the results may be highly important
for therapy. At the same time, the clinician should not put in a needle
before he has made a thorough examination by the ordinary physical
methods. A careful physical examination will give the indication for the
exploratory puncture if it exist, and will do much to prevent an unneces-
sary or a "dry tap." The most skilled physical examiner will occasionally
be in doubt in making the differential diagnosis between pleural effusion,
67
68
EXAMINATION OF THE FLUIDS OBTAINED
pleural thickening, and infiltration of the lung. Here the results of punc-
ture are usually decisive.
In suspected empyema, one may have to puncture at several points
before finding the pus. It is hetter to make one or two fruitless punctures
than to overlook something important through neglect to use the needle.
Syringe for Pleural Exploration. — A syringe with glass cylinder, per-
mitting one immediately to see any fluid removed, is required. The most
satisfactory syringe, in my experience, is the Record syr-
inge, with metal piston exactly fitted to the cylinder
(Fig. 29). It comes in a metal case, which can be
used as a sterilizing vessel. The piston should be re-,
moved from the syringe during sterilization, in order
not to break the glass cylinder. The hollow needle
should be sharp, at least 6 cm. in length, and
should have a lumen large enough to permit
of the passage of thick pus.
Preparation of the Part. — The part to be
punctured is scrubbed with soap and water,
dried with a sterile towel, and swabbed witli
tincture of iodin to render the skin aseptic.
When possible, it is best to have the pa-
tient sit up, but if lie be too ill for this, he
may lie upon his side, near the edge of the
bed. The arm of the side to be tapped may
be pulled up by an assistant, or the patient
may himself hold his hand on top of his head.
Technic of Puncture. — Having chosen the intercostal space to be punc-
tured, the physician presses the tip of the index finger of his left hand
firmly in this space, »o as to press the ribs still further apart. The syringe
is held in the right hand while the needle is introduced perpendicular to
the skin surface, close to the upper margin of the rib beneath the space to
be punctured, so as to avoid the intercostal artery which runs along the
lower margin of the rib above. With care, the needle should not strike a
rib, but if the examiner meet with this mishap owing to a very narrow
intercostal space, he must draw the needle back and try again. In the
back, the thickness of the chest wall is considerable, and the tyro may be
surprised at the distance to which it is necessary to push a needle (4-6 cm.)
before the pleural cavity is entered. Usually one can feel distinctly when
the tip of the needle passes through the parietal pleura into the fluid. On
pulling the piston back a little, the fluid will then be seen to enter the
syringe, and, if desired, the syringe may be filled with fluid before with-
drawing. If, however, no fluid appear, the needle may not be far enough
in, or it may have been pushed too far, and have penetrated the lung. By
keeping a vacuum in the syringe and pushing the needle a little further in,
Fig.
29. — Record Syringe
Exploratory Puncture.
for
TECKNTC OF EXPLORATORY PUNCTURE 69
or withdrawing it a little, the fluid will be obtained if any be present in
the pleural cavity in the region punctured. A thickened pleura may cause
a greatly increased sense of resistance when the needle reaches it. Some-
times fluid will be found beyond such a thickened pleura.
If the lung be penetrated, a little blood may enter the syringe. Usually
puncture of the lung is entirely harmless, and in pneumonia, where it is
desirable for serotherapeutic reasons quickly to establish the type of pneu-
mococcus causing the inflammation, lung puncture may be resorted to for
the purpose if suitable sputum be unavailable (R. I. Cole).
If a dry tap result when the physical examination points strongly to
pleural exudate, the needle should be removed and examined to make sure
(1) that it is not plugged, and (2) that it possesses good suction power; if
the needle be found to be working properly, the puncture should be repeated
in an adjacent region. A dry tap is occasionally due to flocculi of fibrin in
the fluid.
Site of Pleural Puncture. — In choosing the spot for puncture, the clini-
cian will be guided by the physical signs, and, especially, by the presence of
flatness. If there be a flat area at the base, the puncture will be made
somewhere between the upper border of flatness and the level of the dia-
phragm; since it is important not to injure the latter, it is a good rule not
to puncture at a level lower than that of the normal limit of the lung
(upper margin of the 7th rib in the right mammillary line; upper margin
of the 8th rib in the mid-axilla ; upper margin of the 9th rib in the scapular
line).
If interlobar empyema on the right side be suspected, a puncture in
the fourth space in the right axilla, is the site of predilection. The
chest wall is especially thin in the axilla. On the left side, on account of
the position of the heart, it is a safe rule not to puncture in front of the
anterior axillary line. When fluid is free in the pleural cavity, puncture
in the scapular line is best; but, when the exudate is encapsulated, one
chooses, when practicable, the center of the area of flatness.
Removal of Large Amounts of Fluid from the Pleural Cavity. — For
this purpose an aspirator (Fig. 30) attached to a pleural trocar is best.
A pleural trocar consists of a cannula with a lumen of 2-4 mm.,
armed with a sharp pyramidal stylet, which can be withdrawn after punc-
turing the pleural sac so as to let the fluid run through a lateral tube
into the aspirating chamber, while at the same time no air can enter the
pleural cavity. The fluid should be drawn off slowly, at least 20 minutes
being allowed for 1 liter, and it is unwise to remove more than a liter, or a
liter and a half, at a time. To prevent coughing, the aspiration should be
preceded by the injection of a sixth of a grain of morphin.
If a patient begins to cough during aspiration, the withdrawal of fluid
should be stopped for a moment ; if the coughing persists, and especially if
it becomes at all violent, the procedure should be interrupted by removal of
70
EXAMINATIONS OF THE FLUIDS OBTAINED
the needle, (1) owing to the danger of injuring the lung; and (2) on
account of the danger of inducing so-called albuminous expectoration by
withdrawal of too much fluid; in the latter, the patient coughs up large
quantities of frothy serum (danger of asphyxiation).
Fig. 30. — Thoracentesis Outfit. (After P. Krause, "Lehrb. d. klin. Diagnostik d. inner. Krank-
heiten," published by G. E'ischer, Jena.)
If pus is present in the pleural cavity, removal by aspiration is insuffi-
cient, except perhaps in young children. Instead of aspiration, the pus
cavity should be drained by incision, ' and in most cases, to insure free
drainage, a portion of a rib should be excised.
2. Exploratory Puncture ol the Pericardial Cavity
This is resorted to when the presence of fluid in the pericardial cavity
is suspected, and especially when the size of the exudate, or the course of
the disease, makes removal of the fluid for therapeutic reasons seem advis-
able. The actual exploratory puncture determines the presence or absence
of fluid, and, when fluid is present, its nature.
The skin is rendered aseptic with soap and water and with tincture of
iodin, and the puncture is made with a Record syringe, as in the case of
pleural puncture (vide supra).
TECHETC OF EXPLOKATOKT PUNCTURE 71
In diseases ordinarily accompanied only by a serous or serohemorrhagic
exudate, the determination of the nature of the fluid by puncture may not
be important; but, in septic processes, the differentiation of a purulent
exudate from a serous exudate in the pericardial cavity may be life-
saving.
Having introduced the point of the needle well under the skin and
then having withdrawn the piston so as to create a vacuum in the syringe,
one pushes the needle slowly in until the fluid is reached and a drop or two
begins to appear in the syringe. If the accumulation of fluid be consider-
able, the needle may be introduced in the 5th or 6th intercostal space, just
lateral from the mammillary line, at a point beneath which there is abso-
lute dullness but no pleural friction or cardiac pulsation. The needle should
be directed obliquely inward and to the right, toward the apex of the
heart. With this precaution, the heart will usually be avoided, but should
the needle touch the apex of the heart, no harm is done as a rule.
If the accumulation of fluid in the pericardial sac be small, one may
puncture in the 5th or 6th space on the left side, medial from the mammil-
lary line, at the most lateral region of absolute dullness.
If the effusion be large, the needle may be introduced in the left costo-
xiphoid angle, and be passed upward and backward, close to the costal
margin.
3. Exploratory Puncture of the Peritoneal Cavity
If fluid be suspected in the abdominal cavity (ascites; inflammatory
exudate), the physical examination may reveal shifting dullness in the
flank, or, if the quantity be large, a fluctuation wave. When desirable to
examine some of the fluid for diagnostic purposes, or if, for therapeutic
reasons, the fluid should be drained off, we resort to abdominal tapping
(paracentesis abdommis). The patient sits up in bed, most conveniently
on the edge of the bed, the back being well supported by pillows or by an
assistant. The skin is rendered aseptic (soap and water; tincture of
iodin). Before tapping, one should make sure that the bladder is empty,
passing a catheter if there be doubt.
The needle, or the trocar, is introduced in an area over which there is
flatness or percussion, preferably in the middle line, a little below the
umbilicus, or in the lower left quadrant at about the junction of the middle
and lateral third of the line drawn from the umbilicus to the anterior
superior iliac spine (avoidance of arteria epigastrica at the margin of the
rectus abdominis). If a trocar be used, the puncture is made with the
stylet in. When the peritoneal cavity has been entered, the stylet is with-
drawn and the fluid allowed to flow out.
If a large quantity of fluid is to be removed, it is well to surround the
72
EXAMINATIONS OF THE FLUIDS OBTAINED
abdomen with a long bandage, slit at each end, so that pressure can be
exerted upon the abdominal cavity as the fluid is withdrawn ; otherwise,
the lowering of the abdominal pressure during evacuation may lead to
dilatation of the splanchnic blood vessels and cause cerebral anemia and
collapse.
After the tapping, the puncture wound is covered by a small pad of
gauze held in place by a atrip of adhesive.
4. Exploratory Puncture of the Subarachnoid Space
(Lumbar Puncture)
This procedure, introduced in 1891 by Quincke, permits us to secure
the liquor cerebrospinalis from the subarachnoid space for clinical study.
This cerebrospinal fluid occupies the space
between the pia mater and the arachnoid.
The subarachnoid space is in communica-
tion, normally, with the ventricle of the
brain through the foramen of Magendie
and the lateral apertures of the fourth
ventricle.
Lumbar puncture is of the greatest
importance in the diagnosis of the differ-
ent forms of meningitis and of luetic af-
fections of the central nervous system.
Lumbar puncture and lumbar injection
are now important procedures in the
therapy of meningitis, of tabes, and of
dementia paralytica.
Technic. — A hollow needle, 7-9 cm.
long, with a caliber of 0.6-1.2 mm. (or
19-20 Standard gauge), armed with a
steel stylet is the instrument used. To
the outer end of the needle, a calibrated
glass tube, 30 cm. long, can be connected
by rubber tubing, for the determination
of the pressure exerted by the fluid.
Two sterile test tubes closed with sterile
cotton, should be in readiness for the re-
ception of the fluid.
Special instruments for measuring
the pressure have been devised by Kroenig
Fig. 3i.-Trocar for Lumbar Punc- and by Kausch, but the simple instru-
ture Showing the Stylet in Place, . i ^ M a • /« •
a^d Withdrawn. mentarium above described is sufficient.
TECHNIC OF EXPLOKATOKY PUNCTUKE
73
(6)
Fig. 32. — Apparatus for Lumbar Puncture: (a)Kronig's Apparatus, (6) Kausch's Apparatus.
(From P. Krause, "Lehrb. d. klin. Diagnostik d. inner. Krankheiten," published by G.
Fischer, Jena.)
The puncture may be done with the patient either in the sitting posi-
tion, or in the lateral posture, lying on the left side, with the head and
shoulders bent forward
and the knees drawn up
toward the chin, so as to
increase the width of the
intervertebral spaces.
The skin over the
lumbar spine is thor-
oughly disinfected with
soap and water, subli-
mate, alcohol and ether,
or, perhaps better, with
tincture of iodin. The
hands of the physician
and his instruments are
of course rendered asep-
tic before making the
puncture.
The needle may be
iii ,1 Fig. 33. — Lumbar Puncture. Introduction of the Needle
introduced between the WhpT, thft pfttlQn|. is in the Sitting Position,
74 EXAMINATIONS OF THE FLUIDS OBTAINED
second and third, the third and fourth, or the fourth and fifth lumbar ver-
tebrae. In the majority of cases, it is easiest to puncture between the
third and fourth lumbar
vertebrae. If one draws a
line between the highest
points of the two iliac
crests, this line will pass
through the spinous proc-
ess of the fourth lumbar
vertebra. The space above
this spine is the one usu-
ally chosen for puncture.
In children, the needle
should be introduced ex-
actly in the middle line,
and should be directed al-
most straight forward, or
a trifle upward; in the
child, the needle passes 2
or 3 cm. into the depth be-
fore the subarachnoid
space is reached.
In the adult, puncture
in the middle line is the
best routine procedure; it
is sometimes easier how-
ever to introduce the nee-
dle at a point about 1 cm. lateral from the middle line at a level correspond-
ing to the junction of the middle and
lower thirds of the spinous process of
the third lumbar vertebra. The needle
is directed forward and medialward, so
as to reach the meninges at about the
middle line. In this way, the tough
interspinous ligament is avoided. In
the adult, the meninges lie 5-6 cm.
from the surface; the needle must,
therefore, be introduced for a distance
of 6-7 cm. before the subarachnoid
space is reached. After passing
through the rather tough intervening
tissue, the sudden letting up of the resistance announces the entrance of
the point of the needle into the subarachnoid space.
Since the spinal cord does not pass below the level of the second lumbar
Fig. 34. — Selection of Point for Lumbar Puncture just
above the Line Joining the Iliac Crests (in the 4th
Lumbar Interspace) and Slightly Lateral from the
Middle Line.
Fig. 35. — Lumbar Puncture, in the
Adult. Note the Passage of the
Needle Through the Soft Parts and
the Interlaminar Space. The
Needle has been Inserted Somewhat
Lateral from the Median Line.
TECHNIC OF EXPLORATORY PUNCTURE
75
vertebra, it cannot be injured by lumbar puncture. One might, of course,
strike one of the nerves of the cauda equina, but this rarely occurs.
If the point of the needle be misdirected, it may strike against bone;
in this event it should be withdrawn a little, and the needle directed a little
more downward, as it is usually the bone above the space which is struck.
After the needle has reached the space, the stylet is withdrawn and the
cerebrospinal fluid appears, usually drop by drop. To measure the pres-
sure, the sterile glass and rubber tubing are immediately applied after
withdrawal of the mandrin.
If the pressure is not to be measured, the fluid may be collected directly
in two sterile test tubes, say 2 c.c. in each.
Now and then, blood-tinged fluid is obtained. Occasionally, this is due
to hemorrhage into the subarachnoid space that has occurred before the
puncture, but, as a rule, it is due to injury of a minute vessel at the time of
puncture. This contamination of the fluid by blood is a regrettable occur-
rence, since it interferes with cytodi-
agnosis, and may necessitate another
puncture later on.
After a sufficient amount (2-10 c.c.
for diagnostic purposes) has been col-
lected, the needle is quickly with-
drawn, a small wad of sterile gauze
applied over the puncture, and held
in place with a strip of adhesive.
Measurement of the Pressure. —
If no calibrated glass tube be at hand
for measuring the pressure, a piece of
plain tubing (small bore !)
may be used, and the
height of the fluid measured
with an ordinary tape.
Fig. 36. — Manometer to be Used in Lumbar Puncture. The Scale gives the Absolute Value in
mm., the Pressure Measured is Twice the Reading. (After E. Neisser, "Handbuch d.
Neurol.," published by J. Springer, Berlin.)
The pressure of the cerebrospinal fluid under normal conditions corre-
sponds to 40-100 mm. of water when the patient is in the recumbent posi-
tion and breathing quietly. Before reading the pressure, one should wait
until the patient is entirely quiet, since movements increase the pressure.
76 EXAMINATIONS OF THE FLUIDS OBTAINED
Any pressure above 150 mm. is pathological. In meningitis, and in
hydrocephalus, the pressure may be very high, 200-400 mm. or more.
Sometimes the fluid is not under pressure at all. It should be remembered
that, in the sitting position, the pressure may be twice as high as in the
recumbent posture. Slight oscillations of pressure (as much as 20 mm.)
may be noticeable ; these are probably due to the pulsations of the arteries
at the base of the brain, and to respiration.
Effects of Lumbar Puncture. — After lumbar puncture, it is not uncom-
mon for patients to suffer from severe headache for periods varying from a
few hours to a week (meningeal irritation). This is usually more severe
in persons with normal spinal fluid than in those with inflammatory
fluids — and is often aggravated by withdrawal of large amounts of fluid.
In a few cases, sudden death has followed lumbar puncture. Most of
these deaths have been in cases of tumor cerebri, a few of them in menin-
gitis, or in cerebral apoplexy.
To avoid the dangers of lumbar puncture, and to minimize the subsequent
headache, certain rules should be strictly followed:
1. When possible, the puncture should be made in the lateral recumbent posi-
tion rather than in the sitting position.
2. The patient should be kept in bed, flat on his back, with the head low, for
at least 12 to 24 hours after the puncture.
3. Only small amounts of fluid should be removed except in cases of meningitis.
4. Great caution should be observed if puncture be done in cases of tumor
cerebri, where the pressure is increased.
5. One may be tempted to do lumbar puncture in dispensary or office prac-
tice among ambulant patients, but this is, whenever possible, to be avoided.
For the headache that sometimes follows lumbar puncture, a little
pyramidon, aspirin or phenacetin, with, or without, a half grain of codein,
will give some relief. Rest in the completely recumbent posture is imper-
ative. The patient can be assured that the headache will certainly pass off
in a few days, though I have often seen it last a week. Recently, it has
been discovered that a glass of water, taken hourly, for several hours
before and after lumbar puncture will often prevent the "lumbar-punc-
ture headache."
Skilfully performed, lumbar puncture, as a rule, causes but little pain,
though, in highly neurotic patients, gas anesthesia may be necessary. In
apprehensive patients, an ethyl chlorid spray robs the actual puncture of
much of its accompanying pain.
I have been struck with the little inconvenience experienced on lumbar
puncture by patients who suffer from tabes or from dementia paralytica.
It would seem as though such persons were almost anesthetic to lumbar
puncture.
TECHNIC OF EXPLOEATOEY POTTCTUEE 77
5. Exploratory Puncture of the Skull Cavity
(Neisser and Pollak)
This method, considerably used in Germany, has not become popular in Amer-
ica. Here, we prefer exploratory puncture, after exposing the meninges by surgi-
cal operation like that used for decompression of the brain (Gushing). In Ger-
many, the method is employed in suspected cerebral abscess, in hydrocephalus, and,
sometimes, in cases of tumor, or of cerebral hemorrhage. I regard it as an
unnecessary and unjustifiable procedure.
6. Other Exploratory Punctures
Puncture of the liver may be necessary in the diagnosis of hepatic
abscess,, or of echinococcus cyst (see Part VIII). As a rule, however, an
exploratory laparotomy is better.
Puncture of the spleen was formerly much used in the diagnosis of
malaria. It is rarely necessary, however, and is not devoid of danger.
In the tropics, splenic puncture is often undertaken for the diagnosis of
kala-azar (see Part IV).
Puncture of the kidney is sometimes undertaken for the purpose of
studying the contents of a cyst or an abscess. It is rare, however, that
renal puncture is advisable (see Part X).
Puncture of a joint-cavity is sometimes undertaken for cytodiagnostic
or bacteriodi agnostic reasons, sometimes as a therapeutic measure. It
should be aseptically done, with a medium sized needle.
Puncture of a lymph gland may be necessary in the diagnosis of
sleeping-sickness. Or a bubo may be punctured with bacteriodiagnostie
intent (Bacillus of Ducrey; Treponema pallidum; Bacillus pestis).
References
1. General
Allard (/?.). Die Lumbalpunktion. Ergebn. d. inn. Med. u. Kinderh., Berl., 1909, iiit
100-139.
Blechmann (G.). Les epanchements du pericarde. La ponction epigastrique de Marfan.
Ann. d. med. et chirurg. infant., Par., 1913, xvii, 417-423.
Lommel (F.). Lehre von Punktionen und klinische Zytologie. In: Lahrb. d. klin. Diag-
nostik (P. Krause), 2d ed., Jena, 1913, G. Fischer, 458-470.
Marfan (A.-B.}. Le diagnostic des epanchements pericardiques et la ponction epigastrique
du pericarde. Semaine med., Par., 1913, xxxiii, 4^9-476.
Naunyn (#.). Kurzer Leitfaden fur die Function der Pleura- und Peritonealergusse.
Sfrasburg, 1889, K. J. Trubner. 26 p. 8°.
Neisser (E.). Lumbalpunktion und Hirnpunktion. In: Hdb. d. N enrol. (Lewandowsky),
Berl., 1910f i, 1173-1215.
78 EXAMINATIONS OF THE FLUIDS OBTAINED
Plaut (F.), Rehtn (O.) & Schottmuller (H.}. Leitfaden zur Untersuchung der Cerebro-
spinalflussigkeit. Jena, 1913, G. Fischer. 150 p., 21 pi.
Quincke (H.). Die diagnostische und therapeutische Bedeutung der Lumbalpunktion.
Deutsche med. Wchnschr., Leipz. u. BerL, 1905, xxxi, 1825-1829,
1869-1872.
Tice (F.}. Paracentesis thorads. Internal. Clin., Philadelphia, 1911, 21 s., Hi, 75-84.
2. Complications
Allen (H. W.). Albuminous expectoration following thoracentesis, with report of a case.
Johns Hopkins Hosp. Bull., Bait., 1903, xiv, 18-21.
Canfield (R. B.). Some conditions associated with the loss of cerebrospinal fluid. Ann.
Otol., Rhinol. and Laryngol., 1913, xxii, 604-622.
Dayton (H.}. Fatal pneumothorax following exploratory puncture. Am. J. M. Sc., Phila.
& N. Y., 1912, cxliv, 241-245.
Minet (/.). La mort subite suite de ponction lumbaire. J. de med., Par., 1914, xxxiv,
812-313.
Riesman (D.). Albuminous expectoration following thoracocentesis. Am. J. M. Sc.t
Phila., 1902, cxxiii, 620-630.
B. Physical and Chemical Examination of
Punctates
1. Fluids from the Pleural, Pericardial and
Peritoneal Cavities
These may owe their origin to mechanical factors (transudates) or to
inflammations of the corresponding serous membranes (exudates).
In studying punctates, we pay attention to (a) the appearance, (b) the
odor, (c) the specific gravity, (d) the quantity of protein, and (e) (in
some cases) the freezing point (molecular concentration).
(a) Appearance of Punctates
We notice whether the punctate is clear and yellowish (serous), or tur-
bid, owing to the presence of cells or fibrin. Sometimes the fluid looks
milky, due to the presence of emulsified fat (chylous effusion), or to finely
divided insoluble protein or lecithin (pseudo-chylous effusion). A hemor-
rhagic punctate can be recognized by its red color. It is of great impor-
tance, indicating, as a rule, either tuberculous or carcinomatous disease,
though it may sometimes depend upon a general hemorrhagic diathesis.
(b) Odor of Punctates
This should be noted especially in purulent punctates, particularly if a
complicating gangrenous process be suspected.
PHYSICAL, CHEMICAL PUNCTATES 19
(c) Specific Gravity of Punctates
The specific gravity of the fluid, as determined by an aerometer, is of
importance in distinguishing transudates from exduates. Most aerom-
eters are calibrated for fluids having a temperature of 15—17° C. Since
punctates often coagulate at these low temperatures, it is advantageous to
use an aerometer calibrated for a temperature of 36° C. (Englander), and
to make the determination immediately after the withdrawal, using a
graduate previously warmed to a temperature of 36° C. in a water-bath.
If an ordinary aerometer (standardized for 15° C.) is used when the
fluid is warm, the readings may be corrected by adding 0,001 for every 3°
of temperature above 15° C.
Inflammatory exudates from the pleural cavity often have a specific
gravity of 1018-1020, from the peritoneal cavity sometimes having a
specific gravity as high as 1030. Pleural transudates, on the other hand,
usually have a lower specific gravity (1010-1015). In ascites, especially
in the form accompanying cachectic or hydremic states, the specific gravity
of the transudate may fall as low as 1005.
The specific gravity depends upon the quantity of substances in solu-
tion, and, chiefly, upon the amount of protein dissolved.
(d) Protein Content of Punctates
This can be roughly determined by Tsuchiya's modification of Esbach's
method for the urine, diluting the fluid so that the reading in the Esbach
tube will be less than 4, that is, so that the albumin content of the dilu-
tion shall be less than 0.4 per cent. We acidify the dilution slightly with
acetic acid, and perform the test in the ordinary way (see Urine). The
reading is made after 24 hours ; if we multiply this by the dilution, the
result is the number of grams of coagulable protein per liter of punctate.
A simple, rougher method still of estimating the amount consists in
observing the precipitate caused by a few drops of nitric acid added to the
punctate in a test tube. Thus, in inflammations, in tuberculosis, or in carci-
noma of the pleura, the precipitate will consist of thick heavy masses of
protein that quickly fall to the bottom of the tube, while in transudates
due to myocardial insufficiency, the precipitate, still large, is looser and
less heavy, and in purely hydremic transudates, there may be only a
marked opalescence, or small swimming flocculi (Runeberg).
For more exact determinations of the protein content, the total nitro-
gen in grams per cent is determined by Kjeldahl's method ; then the non-
protein nitrogen is determined in grams per cent and subtracted from the
total N; by multiplying the nitrogen value thus obtained by 6.25, we have
the content in coagulable protein. The method is fully described by R. S.
Morris, who has made careful studies of the incoagulable nitrogen in punc-
tates. Morris finds that in most punctates, the non-protein 1ST is below 0.07
80 EXAMINATIONS OF THE FLUIDS OBTAINED
grams per cent. Values between 0.07 and 0.09 are of doubtful signifi-
cance, but when the non-protein N exceeds 0.09 grams per cent, the proba-
bility is strong that the fluid is neoplastic in origin (ca"ncer; sarcoma).
The protein content can also be determined by the gravimetric method:
1. Pour 10 c.c. of the punctate into 100 c.c. of boiling 1 per cent salt solution
(feebly acidulated with acetic acid), and filter through a weighed filter.
2. Wash the coagulated protein on the filter with feebly acidulated water, and
afterwards with alcohol and ether, and dry to constant weight at 100° C.
3. Subtract the weight of the filter and we have the protein content in 10 c.c.
of the punctate; multiplying by 100, we have the protein content per liter.
In general, a high protein content (above 40-60 g. per liter) speaks for
p.n exudate and low protein content (below 30 g. per liter) for a transu-
date ; in stasis transudates the protein content varies between 10 and 30 g.
per liter ; in pure hydremic transudates it may fall as low as 1-3-5 g. per
liter.
Bivalta's Test for Distinguishing Exudates and Transudates. — This is of some
importance, since, in inflammatory exudates, the reaction is constantly positive,
while in non-inflammatory effusions the test is entirely, or almost entirely, negative.
The test depends upon the presence in inflammatory exudates of a protein
substance which is precipitated by acetic acid in the cold. In a glass graduate, or
in a narrow beaker, one places 200 c.c. of distilled water and adds 2 drops of
glacial acetic acid ; to this feebly acidulated water a drop of the punctate is allowed
to fall from a glass rod. If the substance on which the test depends be present, a
gray cloud resembling tobacco smoke appears around the drop as it falls to the
bottom. If only a minute quantity of the substance be present (as in transudates),
this turbidity appears very slowly, and is much feebler. The nature of the sub-
stance concerned is in dispute (euglobulin and pseudo-globulin, globulin, or
mucin?). Other methods of applying the test have been used by Runeberg, Umber,
and Staehelin.
(e) Freezing -Point (Molecular Concentration of Punctates)
Cryoscopy applied to punctates is of but little clinical value, though it
may sometimes be of interest to the scientific investigator. The method
employed is that used in examining urine (q. v.).
References
Gerhartz (H.). Chemie der Transudate und Exudate. In: Handb. d. Biochemie (Oppen-
heimer), Jena, 1909, ii, Abt. ii, 187 et seq.
Javal (A.). 1} 'albumins-diagnostic des epanchemenls pleuraux et peritoneaux. J. de
Physiol. et de Path. Gen., Par., 1914, xvi, 223-237.
Miller (J. L.). Transudates and exudates, with report on 75 fluids. Am. Med., Phila.,
1904, viii, 835-843.
Morris (R. S.}. The incoagulable nitrogen of puncture fluids, with special reference to
cancer. A preliminary note. Arch. Int. Med., Chicago, 1911, viii,
457-462.
Runeberg (J. W.). Von der diagnostichen Bedeutung des Eiweissgehaltes in pathologischen
Trans- und Exudaten. Berl. klin. Wchnschr., 1897, xxxiv, 710-713.
PHYSICAL, CHEMICAL PUNCTATES , 81
Staefielin (/£.). Ueber den durch Essigsdure fdllbaren Eiweisskorper der Exudate und des
Urins. Munchen. med. Wchnschr., 1902, xlix, 1413-1415.
Umber (F.). Zurn Studium der Eiweisskorper in Exudaten. Ztschr. /. klin. Med. Berl.,
1903, xMii, 364-388.
2. Cerebrospinal Fluids
(a) Physical and Chemical Properties of Normal Cerebrospinal Fluid
The normal Cerebrospinal fluid is as clear as water, colorless, feebly
alkaline, specific gravity 1008-1013, and with a protein content varying
between 0.02 and 0.05 per cent. The sodium chlorid content varies nor-
mally between 0.55 and 0.8 per cent, tfte sugar content (determined with
Haines's solution) between 0.06 and 0.09 per cent. The sugar disappears
quickly on exposure to the air; it is supposed to be glucose (Kafka). The
normal fluid contains a minute amount of cholin. The freezing-point is
about the same as that of blood (—0.56 C.).
(6) Physical and Chemical Properties of the Cerebrospinal Fluid
in Pathological States
In pathological conditions, the fluid may undergo important chemical
and physical changes, though these are far less significant for diagnosis than
the changes demonstrable by the methods of cytodiagnosis and of immu-
nodiagnosis.
i. The Total Protein Content
The amount of albumin is increased in meningitis both in the acute, and in
the chronic, forms. The total protein content can be approximately estimated
by Tsuchiya's modification of Esbach's method, or, simply, by the heat and nitric
acid test, more accurately by Kjeldahl's method or by the gravimetric method.
ii. The Globulin Content
Much more important for diagnosis, however, than the mere determina-
tion of the total protein content is the estimation of the content in globulin
by methods introduced in 1903 in the French clinics (Widal, Sicard and
Ravaut; Guillain and Parant) and subsequently improved by various
workers. At first, the globulin was precipitated by magnesium sulphate,
but later ammonium sulphate was found to be a more delicate precipitating
agent. Among the methods now employed are those recommended (1) by
Nonne and Apelt, (2) by Noguchi, (3) by Ross and Jones, and (4) by
Pandy.
Nonne and Apelt Modification of the French Method. — Mix equal volumes of
Cerebrospinal fluid and of a neutral solution of Merck's ammonium sulphate (sat-
urated with heat, filtered and cooled). This precipitates the globulin-nucleoalbunrin
82 EXAMINATIONS OF THE FLUIDS OBTAINED
fraction within three minutes, and the precipitate is designated by Nonne and
Apelt as Phase I, while the coagulable protein present other than globulin, obtained
by boiling the nitrate from the preceding, is known as Phase II.
Both globulin and serum albumin are present in normal fluid in minute amounts ;
in pathological states, an increase in globulin goes approximately parallel to the
total protein increase. The degree of increase, however, is more easily estimated
for the globulin than for the total protein.
Normally, the globulin precipitate (Phase I) is seen only as a trace of opal-
escence. In such cases, Phase I is designated as negative. In the increased globulin
reaction of pathological states we meet with several grades of globulin content,
from (1) a trace of opalescence (normal), through (2) feeble opalescence, (3)
opalescence, to (4) outspoken turbidity (Phase I, positive).
Phase I is never positive in functional diseases of the central nervous system.
Even in lues, Phase I is negative unless the nervous system is involved. The
method is strongly corroborative of th« cytodiagnostic methods and of the Wasser-
mann test in lues cerebrospinalis, in tabes, and in dementia paralytica.
In lues cerebrospinalis, Phase I is positive in the cerebrospinal fluid along with
lymphocytosis of this fluid, though the Wassermann reaction in the fluid is usually
negative, while the Wassermann reaction of the blood is positive (80 per cent of
the cases). In general paresis, all four reactions are positive. An additional aid
in distinguishing between lues cerebrospinalis and dementia paralytica lies in the
colloidal gold test (see below).
Noguchi's Butyric Acid Test. — This is an excellent test for increased
globulin, as those who have used it will testify.
1. Place 0.1 c.c. of cerebrospinal fluid in a test tube; add 0.5 c.c. of a solu-
tion of chemically pure butyric acid (10 per cent) in a solution of pure sodium
chlorid (0.9 per cent) ; boil briefly over the flame of Bunsen burner.
2. Now add quickly 0.1 c.c. of N/l sodium hydroxid; boil again for a few
seconds.
If the globulin-content be increased, a coarsely granular, sometimes
flocculent, precipitate will appear. It becomes visible, as a rule, within 10
or 20 minutes, but should none be visible at the time, the test tube is set
aside for 3 hours, after which it is again looked at.
In normal cerebrospinal fluid, there is only a slight, even, opalescence ;
coarser precipitates never form, even if the fluid be allowed to stand for
several hours after the test has been made. Simon Flexner has found the
reaction very helpful in his experimental studies of cerebrospinal fluid.
If the character of the reaction be doubtful, a second test should be
made, using 0.2 c.c. of fluid instead of 0.1 c.c.
Ross and Jones's Modification of the French Method. — This very deli-
cate method is a favorite one with the assistants in the clinic. The same
solution of ammonium sulphate is used as in the Nonne-Apelt method de-
scribed above.
1. Place 2 c.c. of the solution of neutral ammonium sulphate in a test tube.
2. Incline the tube, and, with a pipet, allow 1 c.c. of c.s. fluid to run gently
down upon the surface of the fluid in the tube, without mixing the fluids.
3. At the end of 3 minutes,, examine the line of contact of the two fluids on
PHYSICAL, CHEMICAL PUNCTATES 83
indirect illumination, holding the tube against a dark background, with the eye
at right angles to the source of light. A thin, grayish-white ring constitutes a
positive reaction.
4. At the end of half an hour, observe the ring again; when the reaction is
positive, a cobweb-like appearance is visible on the surface of the ring.
Tandy's Test. — Pandy's test has not received the attention it deserves.
None of the other reactions used to reveal an excess of globulin is so
simple in execution, or so quickly decisive in its results.
1. The reagent consists of a saturated aqueous solution of carbolic acid; ten
parts of pure crystals are added to 100 parts of hot distilled water; the mixture
is kept at room temperature for 3-4 days, during which time it should be fre-
quently shaken. At the end of this time the clear supernatant fluid is drawn off
into another bottle.
2. To approximately 1 c.c. of this solution is added one drop of the spinal
fluid.
3. Normally no change occurs, or at the most, an extremely faint opalescence;
with a fluid abnormal in its protein content, there develops instantly at the point
of contact, a bluish-white cloud often resembling a ring of smoke, which gradu-
ally settles to the bottom of the tube.
iii. The Content in Hydrophile Colloids that will Prevent the Precipitation of
Other Instable Colloids (e. «M Gold Sol) by Salt Solution
Since the fundamental researches of Wolfgang Pauli upon the stability
of colloids when exposed to thermal, chemical, and electrical influences,
special methods have begun to be devised for demonstrating slight altera-
tions in the stability of colloids. Among these are (1) II. Schade's "trans-
parency for print" test, and (2) K. Zsigmondy's Gold Number method-
The latter has already been applied clinically by Lange, Sippy, Sydney
Miller, and others.
The Colloidal Gold Test, or Gold Number Method (Zsigmondy; Lange).— The
principle is as follows: A colloidal solution that just hinders the precipitation
of a gold sol (10 cm. prepared in a definite way) by 1 c.c. of 2N/1 solution NaCl
is said to have a gold number — 1. The color of the colloidal solution of gold in
the gold sol is red ; as the gold begins to be precipitated, the color changes to blue.
The gold number of a protein is the number of milligrams of that
protein that will protect 5 c.c. of colloidal gold against 0.5 c.c. of 10
per cent ]STaCl.
The gold number is very different for the different hydrophile colloids ; thus the
number of milligrams of colloid necessary to protect vary from 0.005-0.01 gelatin,
to 0.01 casein, 0.06-0.3 egg albumin, 10-20 dextrin, 10 sodium stearate (at 60° C.),
0.001 sodium stearate (at boiling point), and 0.4-1 sodium oleate (Zsigmondy).
In the cerebrospinal fluid, we deal with a mixture of hydrophile colloids.
The gold sol is prepared by adding to 1,000 c.c. of freshly, and doubly, dis-
tilled water, 10 c.c. of 1 per cent solution of gold chlorid and 10 c.c. of 2 per cent
KOH. Boil over a Bunsen burner. Extinguish the flame, and then add quickly
(in several portions), shaking thoroughly while adding, 10 0,0, of a 1 per cent
84
EXAMINATIONS OF THE FLUIDS OBTAINED
solution of formol (obtained by mixing 1 c.c. of commercial concentrated for-
maldehyd solution with 100 c.c. distilled water).
The gold sol should present a purple-red tone, and should be perfectly clear
and transparent and remain free from sediment on long standing. In preparing-
the solution, and in carrying out the test, the greatest cleanliness must be observed.
Ten small test tubes are placed side by side in a test tube rack. In the first
one is placed 1.8 c.c. of a 0.4 per cent solution of NaCl, and the amounts in each
successive test tube increased successively by 1 c.c. of salt solution. To the first
test tube is added 0.2 c.c. of the cerebrospinal fluid to be examined. From the mix-
ture in the first tube one takes 1 c.c. and puts it into the second tube, and, after
mixing, takes 1 c.c. from the second tube and places it in the third, and so on until
one gets dilutions as high as 1:5,120. After these dilutions have been pre-
pared, 5 c.c. of the gold sol are quickly poured into each tube and allowed to
stand for a few hours, after which the reaction may be read off. A test tube with
pure 0.4 per cent NaCl solution and 5 c.c. gold sol is used as a control; in this
tube, the color must remain unchanged; otherwise the solution dare not be used.
Precipitates, and change of color, occur in various dilutions, according as the
case is normal, or one of cerebrospinal lues, of tabes, of dementia paralytica, of
meningitis, etc. It is customary to record the results in the form of curves.
It is too soon as yet to speak, finally, regarding the value of this gold sol test,
but the studies of B. W. Sippy of Chicago, of Grulle and Moody in congenital
lues, and of Sydney Miller of Baltimore, indicate that it may be of some value in
the differentiation, especially of the different forms of luetic and para-luetic in-
fections of the central nervous system.
[As this volume goes to press, a new article has appeared, in which
Miller, Brush, Hammers and Felton describe (1) important modifica-
tions of the method of preparation of the colloidal gold reagent and (2)
the criteria for judging the reaction ; those who desire to use the method
should consult this paper, the reference to which is given below.]
Pit unions of
C.S. fluid
0
o
^
<o
<=t
o
f
CD
sO
§
ro
j_
0
^3-
o
o
CO
c^
1
§
<x
0
G^
Lp
g
§
r_>
5
Colorless
4
Vole or
Graii-Blue
3
"Blue
r-
-n
£
Lilac or
Purple
f
A
1
"Red-Blue
/
\
0
"Red
/
/
\
\
Fig. 37. — Diagram Showing Numerical Values Assigned to Colors, and a Reaction in the
"Luetic Zone." (After Miller and Levy.)
PHYSICAL, CHEMICAL PUNCTATES
85
Pi lu [Ions of
GLS. Fluid
o
O
ex
_L
O
^3-
o
CO
1
O
^0
0
G^
fO
J
0
^t
£
§
G^
J_
O
L8
cv
1
O
CM
LO
1
J
5
Colorless
4
Pale or
Graq-Blue
-*
3
Blue
/
A
2
Lilac or
Pupple
/
\
1
Red-Blue
/
\
\
0
Red
0—
— •—
J
7
\
V
— e
Fig. 38. — The Reaction in Meningitis. (After Mil'.er and Levy.)
References
Bigelow (O. P.). Cytology of cerebrospinil fluid. . Cleveland M. /., 1915, xiv, 196-205.
Donald (/£.)• ^ method of estimating numerically and qualitatively ihz cells in permanent
preparations of cerebrospinal fluid, with notes on the cell-count of speci-
mens. Folia haematol., Berlin, 1913, xvii, 139-163.
Geissler (W.). Ueber Blut in der Spinalflussiglteit. Munch, med. Wchnschr., 1913, Ix,
121-124.
Henderson (D. K.) & Muirhead ( W.}. The differentiation of the cells in the cerebrospinal
fluid by Alzheimer's method. Rev. Neurol. & Psychiat., Edinburgh,
1913, xi, 195-205.
PiluHons OP
C.S.fluid
o
?
0
T
o
CO
<o
vO
o
ca
KD
o
'=^f
o
1
o
i
2
LO
cu
o
G^
LP-
S
J
5
Colorless
4
T^le or
Graq-Blue
\
\
5
Blue
s
\
2
Lilac or
Purple
\
1
Red-Blue
\
0
Red
s
V
•
— •
Fig. 3D. — The Characteristic Curve of General Paresis. (After Miller and Levy.)
86 EXAMINATIONS OF THE FLUIDS OBTAINED
Kirchheim & Schroder. Ueber Meningismus bei Infektionskrankheiten. Deutsches
Arch. f. klin. Med., Leipzig, 1911, cm, 218-234.
Rons (E. P.). Clinical studies of the cerebro-spinal fluid, with special reference to pressure,
protein-content and the number and character of the cells. Am. J. M. Sc
Philadelphia, 1907, cxxxiii, 567-582.
Szecsi (5.)- Neue Beitrdge zur Cytologie des Liquor cerebrospinalis ; uber Art und Her-
kunfl derZellen. Zlschr.f. d. ges. Neurol. u. Psychiat., Berlin u. Leipzig,
1911, vi, 537-588.
[NOTE. — For other references on C. S. fluid, see end of Part IV.]
C. Bacteriological, Serological, and Cyto-
diagnostic Methods of Examining
Punctates
1. Bacteriodiagnostic Methods
The methods described for making smear preparations, cultures on
blood agar, and animal inoculations in the section on Infectious Diseases
and on the Blood are applicable to the study of puncture fluids.
Tubercle Bacilli. — In fluids from the serous cavities and from the sub-
arachnoid space, it is often desirable to search especially for tubercle ba-
cilli. Formerly, exudates were subjected to artificial digestion (inoscopy)
for this purpose. At present, we rely rather upon the antiformin method,
in which the thick exudate or a sediment obtained on standing or on cen-
trifugalization is mixed with 20-50 per cent antiformin, later centrifugal-
ized and the sediment stained for tubercle bacilli.
In tuberculous meningitis, the cerebrospinal fluid collected in a sterile
test tube may be allowed to stand for from 12 to 24 hours in the ice-box ; at
the end of that time, the delicate, filmy clot that forms may be spread
out upon a glass slide, slowly dried in the air, fixed by passing through the
flame three times, and then stained by the carbol-fuchsin method, in the
ordinary way, for tubercle bacilli ( J. Hemenway).
In chronic cases of serous-membrane tuberculosis, or of tuberculous
meningitis, inoculation of guinea-pigs with 5-10 c.c. of the fluid may be
employed for diagnostic purposes; it is best to inject the aseptically col-
lected suspected fluid directly into the peritoneal cavity. At the end of
three weeks, the animal may be killed, and the lesions may be examined
histologically.
Other Parasites. — In the fluid obtained by lumbar puncture, smears of
the sediment may be stained (besides for tubercle bacilli), for meningo-
cocci, for pneumococci, for influenza bacilli, etc., and in the tropics, where
sleeping-sickness is suspected, for trypanosomes. In rare instances, it may
be possible to find the Treponema pallidum.
PLATE I
Fig. 1. — Tuberculous Meningitis — Carbolfuchsin
Methylene Blue. (After N. v. Jagic u. H. K.
Barrenschen, "Atlas u. Grund. d. Klin. d. Mikros-
kopie," published by M. Perles, Wien.)
_
Fig. 2. — Diplococcus pneumoniae in Meningitis
— Gram Stain. (After F. Plaut, O. Rehm
u. H. Schottmuller, "Leitfaden zur Unter-
such. d. Cerebrospinalfliissigkeit," published
by G. Fischer, Jena.)
Fig. 3. — Meningococcus or Diplococ
cus meningitidis (Weichselbaum)
in Cells in the Cerebrospinal
Fluid. Stained with Methylene
Blue. (After F. Plaut, O. Rehra
u. H. Schottmuller, "Leitfaden zur
ITntersuch. d. Cerebrospinalfliis-
sigkeit," published by G. Fischer,
Jena.)
BACTEBIOLOGICAL, SEKOLOGICAL PUNCTATES 87
References
Hemenway (/.)• The constant presence of tubercle bacilli in the cerebrospinal fluid of
tuberculous meningitis; with observations on the cerebrospinal fluid in
other forms of meningitis. Am. J. Dis. Child., Chicago, 1911, i, 37-41-
Nichols (H. J.) & Hough (W. H.}. Demonstration of the spirochaeta paUida in the cere-
brospinal fluid. From a patient with nervous relapse following the use
of salvarsan. J. Am. M. Ass., Chicago, 1913, Ix, 108-110.
2. Immunodiagnostic Methods
The most important of these for practical clinical purposes is the
Wassermann reaction as applied to the cerebrospinad fluid. When the re-
action is positive, we have the proof not only that the patient has had syphi-
lis at some previous time, hut that we have to deal, in the case before us,
with some syphilogenous disease of the central nervous system (cerebrospi-
nal lues ; dementia paralytica ; tabes) . In dementia paralytic*, the reaction
is so constantly positive that a negative result almost rules out the disease.
It is positive in 85-90 per cent of the cases if 0.2 c.c. of fluid is used, and in
100 per cent if 1.0 c.c. is used. In tabes the reaction is, in 90-95 per cent
of the cases negative with 0.2 c.c. of fluid, but positive in nearly 100 per
cent of the cases if 1.0 c.c. is used. In cerebrospinal lues, the reaction is also
nearly always positive with 1.0 c.c., but negative in 90 per cent of the cases
with only 0.2 c.c. of fluid. The reaction is usually positive in the blood
serum in cerebrospinal lues and in dementia paralytica, but often negative
in tabes.
The Wassermann reaction as applied to the fluid, when either positive
or negative, should be accompanied by the results (1) of a Wassermann
test applied to the blood serum; (2) of a test for globulin in the cerebro-
spinal fluid, and (3) of a cell count of the cerebrospinal fluid, in order that
the best judgment possible can be formed regarding the underlying
condition.
The technic of the Wassermann reaction is fully described in Part IV.
References
Barker (B. /.). The enzymes of fibrinous exudates; the effect of one enzyme upon another.
J. Exper. M., Lancaster, Pa., 1908, x, 666-672.
Cabot (Richard Clarke). The serum diagnosis of disease. New York, 1899, W. Wood
&Co. 154 p. 8°.
Dochez (A. JR.). Proteolytic enzymes and anti-enzymes of normal and pathological cere-
brospinal fluids. J. Exper. M., Lancaster, Pa., & N. Y., 1909, xi,
718-742.
Kaplan (D. M.) & Casamajor (Louis}. The neuroserological findings in tabes, general
paresis, cerebrospinal syphilis, and other nervous and mental diseases.
Arch. Int. Med., Chicago, 1912, ix, 262-272.
Serology of nervous diseases. Philadelphia & London, 1914, W. B.
Saunders Co. 346 p. 8°.
88 EXAMINATIONS OF THE FLUIDS OBTAINED
Lade (F.). Anwendung der Hermann-Perutzschen Reaktion bei der Priifung von Lum-
balpunktaten. Munch, med. Wchnschr., 1313, Ix, 590-591.
Liverato (S.) & Crossonini (E.). Untersuchungen uber die tuberkulosen Exudate beim
Menschen in ihren Beziehungen zur Immunitdt. Centralbl. f. Bakteriol.
(etc.), 1. AbL, Jena, 1911, Orig., 139-147.
Major (R. H.} & Nobel (E.). The glycyl-tryptophan reaction in meningitis. Arch. Int.
Med., Chicago, 1914, xiv, 883-387.
Marshall (H. T.) & Morgenroth (/.). Ueber Anticomplemente und Antiamboceptoren
normaler Sera und pathologischer Exudate. Ztschr. f. klin. Med.,
Berl, 1902, xlvii, 279-301.
Mutter (P. T.}. Serodiagnostic methods. Transl. from the 3d Ger. ed. by R. C. Whitman.
Philadelphia & London, 1913, J. B. LippincottCo. 146 p. 8°.
Noguchi (Hideo}. Serum diagnosis of syphilis and luetin reaction, together with the butyric
test for syphilis. 3d ed. Philadelphia & London, 1912, J. B. Lippincott
Co. 320 p. 8°.
Opie (E. L.). Enzymes and anti-enzymes of inflammatory exudates. J. Exper. Med., New
York, 1905, mi, 316-334.
The enzymes in phagocytic celkof inflammatory exudates. J.Expcr. Med.,
New York, 1906, viii, 410-436.
Opie (E. L.) & Barker (B. /.). Enzymes of tuberculous exudaics. J. Exper. Med., Lan-
caster, Pa., & N. Y., 1909, xi, 686-694.
Plaut (F.}. The Wassermann sero-diagnosis of syphilis in its application to psychiatry.
New York, 1911, Jour. Nerv. & Ment. Dis. Pub. Co. 188 p. 8°.
Umber (F.). Ueber autolytische Vorgdnge in Exudaten. Miinchen. med. Wchnschr.,
1902, xlix, 1169-1171.
Wile (U. J.) & Stokes (J. H.}. Further studies on the spinal fluid with reference to the in-
volvement of the nervous system in early syphilis. J. Am. M. Ass.,
Chicago, 1915, Ixiv, 1465-1470.
Wolff-Eisner (Alfred). Clinical immunity and sero-diagnosis. Transl. by Ray W.
Matson. London, 1911, Baillicre, Tindall & Cox. 198 p. 8°.
3. Cytodiagnostic Methods
(a) Cytodiagnosis of Pleural, Pericardial, and Peritoneal Fluids
From the cytodiagnostic standpoint, four main types of these fluids are
distinguishable: (i) exudates in acute infections of the serous membranes,
(ii) exudates in tuberculous serositis, (iii) transudates, and (iv) effu-
sions associated with neoplasms.
It is well to examine (1) a fresh unstained droplet of the sediment, and
(2) dried and stained smears of the sediment. If the fluid be purulent,
smears may be made directly from it ; if it be clear, or turbid, it should be
centrifugalized immediately after it is obtained, before clotting has taken
place, or, if this be inconvenient, after treatment with an equal volume of
solution of sodium fluorid (1 per cent), or a solution of sodium citrate
(1.5 per cent) in physiological salt solution, when it may be kept without
clotting and be sedimented, or centrifugalized, any time within the next 1 2
to 24 hours. Smears of the sediment are spread upon glass slides, air-
dried, fixed and stained like blood-smears (see Examination of the Blood).
BACTERIOLOGICAL, SEROLOGICAL PUNCTATES 89
Unless the spinal fluid is purulent it is well to use some albumen-fixative
on the slide before applying the stain. Otherwise it is common to wash
the entire smear off. As a stain, we may use Jenner's, Wilson's, Giemsa's,
or hematoxylin and eosin.
i. Cytodiagncsis of Exudates in Acute Infections
In the different forms of acute infectious serositis (pleuritis, pericar-
ditis, peritonitis), aside from the demonstration in the stained smears> of
the pyogenic microorganisms (streptococcus, staphylococcus, pneumococ-
cus, etc.) concerned, one can often be fairly sure of the nature of the
process by the large number of polymorphonuclear neutrophiles present.
Occasionally, however, a primary tuberculous pleuritis may be ushered in
by a temporary polynucleosis ; but the degenerative changes that occur i:i
the polymorplionuclear leukocytes representing the main contingent of cells
in the exudate often suffice to differentiate the two groups of pleuritides.
Thus the degenerative change in the pyogenic infections consists in a swell-
ing and clearing up of the cell and of its nucleus, while in acute tubercu-
lous pleuritis with polynucleosis, the cells are shrunken, and the nuclei
pyknotic and fragmented (Koeniger).
In a few cases, large numbers of eosinophils have been met with in
pleural exudates. Ordinarily, the eosinophils do not make up more than
1-4 per cent of the count, but in so-called upleural eosinophilia," as many
as 10-70 per cent of the cells may be eosinophils. The etiology appears to
be variable.
When the cyto]ogical formula is lymphocytic, and not polymorphonu-
clear, it speaks strongly against an infection due to pyogenic micro-
organisms.
ii. Cytodiagnosis in Exudates Due to Tuberculous Infections
In tuberculous serositis, whether involving the pleura, the pericardium, or
the peritoneum, there is often an outspoken lymphocytosis demonstrable in
the fluid ("lymphocytic formula"). This may or may not be accompanied by
the presence of red blood corpuscles. When the latter are present, also, the
finding speaks strongly for a tuberculous etiology. In the beginning of an
acute tuberculous pleuritis, a temporary polymorphonuclear leukocytosis
may be demonstrable in the fluid. Even in outspoken lymphocytosis
there may also be many polynuclears present, though the number is exceeded
by that of the lymphocytes. But "tuberculous polynucleosis'' can usually
be distinguished from the polymorphonuclear formula in pyogenic infec-
tions by the behavior of the cells and their nuclei (see above).
In the more chronic forms of pleuritis, a lymphocytosis may be met
with, not only in tuberculosis, but also in sarcoma of the pleura, and in
luetic pleuritis. In the sarcomatous cases, however, many endothelial cells
90 EXAMINATIONS OF THE FLUIDS OBTAINED
accompany the lymphocytes ; in luetic pleuritis, the Wassermann reaction is
positive.
In instances in which polymorphonuclear cells predominate, the pres-
ence of a large number of lymphocytes (1/3 of the total count or more)
and of red hlood corpuscles should make one suspect a tuberculous etiology,
especially if endothelial cells be absent, or present in only small numbers.
The study of the cells in exudates from tuberculous peritonitis yields
findings resembling those in tuberculous pleuritis. There is always an out-
spoken leukocytosis, but the exudate differs from a pleural exudate in that
there are, in addition, many large mononuclear cells and often many poly-
morphonuclears present. Endothelial cells may also be present in larger
numbers than in the tuberculous pleural exudates. These endothelial cells
are large cells with round or oval nucleus and a relatively large amount of
protoplasm. The nuclei stain relatively feebly.
iii. Cytodiagnosis of Transudates
In simple hydrothorax, hydropericardium, and ascites, one finds, on cytodiag-
nosis, a very small number of cells, with preponderance of cells of the endothelial
type, often united in chains or strips — the so-called "placards." Such endothelial
cells may make up from 60-80 per cent of the total cell count. The remaining
cells are chiefly lymphocytes, though, here and there, a polymorphonuclear element
may be met with. Any circumstance that leads to a complicating inflammation
of the serous membrane concerned will change the cell picture (appearance of
polymorphonuclear elements).
iv. Cytodiagnosis of Effusions Associated with Neoplasms
These effusions are often rich in endothelial cells ; occasionally, typical
groups of tumor cells may be found in the fluid. If a minute fragment of
tissue should be obtained, it is important to fix it, embed it, and section it,
and then be guided by the histological picture found in the sections. Great
care, however, must be exercised in asserting that a given cell is a tumor
cell. Of course, if the cells are arranged in groups such as occur in known
tumors, the diagnosis may not be difficult, but when one has to judge from
single cells it is easy to err, though the so-called seal-ring cells with colloidal
content and eccentric nuclei are characteristic, and, as Dock has empha-
sized, the presence of many cells containing nuclei undergoing karyokinetic
division or mitosis, is very suspicious.
It should constantly be kept in mind also that a hemorrhagic effusion is
in the majority of cases either of tuberculous or of neoplastic origin.
References
Bunting (C. H.) The etiology of serofibrinous pleurisy, with reference to cytological diag-
nosis. Johns Hopkins Hosp. Bull., Bait., 1903, xiv, 185-191.
BACTERIOLOGICAL, SEROLOGICAL PUNCTATES 91
Dock (€?.)• Cancer of the stomach in early life and the value of cells in effusions in the
diagnosis of cancer of the serous membranes. Am. J. M. Sc., Phila..
1897, cxiii, 658-668.
Koeniger (JET.). Die zytologische Untersuchungsmethode, ihre Entwicklung und ihre kli-
nische Verwertung an den Ergussen seroser Hohlen. Jena, 1908, G.
Fischer. 116 p.
Mosny (E.) & Portocalis (A.). Polynucleose pleurale acidophile, basophile et mixte. J.
d. physiol. et d. pathol. gen., Par., 1913, xv, 120-130.
Warren (L. F.). The diagnostic value of mitotic figures in the cells of serous exudates.
Arch. Int. Med., Chicago, 1911, viii, 648-658.
(b) Cytodiagnosis of the Cerebrospinal Fluid
Here, the exact number of cells present as ascertained by a given
method of technic is important in differential diagnosis. Two principal
methods are employed :
(i) Counting and differential counting in stained smears, and (ii) the
hemocytometer method of enumeration.
i. Counting and Differential Counting in Stained Smears
To estimate the number of cells in cerebrospinal fluid by this method,
we centrifugalize 2-3 c.c. of the fluid for 45 minutes in a conical test tube,
pour off the supernatant fluid, take up the sediment in a capillary pipet,
mixing the cells well by blowing them gently back from the pipet into the
tube, repeating this several times. A small droplet of the well-mixed sedi-
ment is then placed on a glass slide, spread out cautiously, dried in the air,
fixed and stained. The earlier workers used a methylene blue stain. It is
now customary to stain with Jenner's stain, or with one of the methylene-
azure-and-eosin stains (Wilson's; Hastings's; Giemsa's).
Using a magnification of 300 diameters, and counting six fields of the
microscope, the average number of cells in each field is then calculated.
The normal fluid should, according to Nissl, contain not more than from 4-8
cells in each microscopic field. If the number be 6-20 cells per field, Nissl speaks
of feebly positive lymphocytosis ; if the number be 20-60 cells per field, of positive
lymphocytosis ; if it exceed 60 per field, he speaks of strongly positive lympho-
cytosis ; as many as 900-1,200 cells per field have been met with in some instances.
Obviously, for the enumeration of the cells in the fluid, such a method
cannot be reliable. It is, however, of great value for the making of a dif-
ferential count of the cells present, and the determination of the relative
numbers (percentages) of the different varieties of cells (lymphocytes,
polymorphonuclears, etc.) in the fluid. For making a differential count, it
is desirable to count a large number of cells, 100-300 if possible.
ii. Hemocytometer Methods ol Enumeration of the Cells in the Cerebrospinal Fluid
This is preferable to Nissl's method, and is the one used in the clinic in
which I work. If it be associated with the study of a stained smear for the
92 EXAMINATIONS OF THE FLUIDS OBTAINED
differential count of the cells, it will be found very satisfactory. The exact
number of cells per cubic millimeter of c. s. fluid is determined, very much
as one counts the leukocytes in a counting-chamber. Either a Biirker
modification of the Thoma-Zeiss cell counter with a Neubauer ruling (see
Part VII) may be used, or, best, the Fuchs-Rosenthal counting-chamber.
Emerson's Method. — Into a "leukocyte pipet" of a hemocytometer,
draw Unna's polychrome methylene blue as far as the mark 0.5 ; then draw
in the fresh cerebrospinal fluid to the mark 11, or, if it be very rich in
cells, to the mark 21. Mix well. Proceed as in counting the white blood
corpuscles.
Rous's Method. — Into the "red corpuscle pipet" of a hemocytometer,
draw a saturated aqueous solution of methyl violet (5 B), as far as 0.4 on
the capillary tube ; then draw in fresh cerebrospinal flu-id, shaking thor-
oughly first to make sure that the cells will be evenly distributed throughout
the fluid. Now mix the stain and the fluid, by holding the pipet horizon-
tally, both ends closed, and shaking for three minutes. The counting-
chamber of the hemocytometer is then filled, and the cells counted, just as
in counting blood. The beginner should be careful not to count red blood
corpuscles, should any be present, as lymphocytes.
Fuchs-Rosenthal Method. — The counting-chamber by this name is
specially designed for the enumeration of cells in the spinal fluid; it is
deeper and offers a larger ruled surface (4 X 4 X 0.2 mm.). Using a
"white cell pipet" one draws in a staining fluid to the mark 1, and spinal
fluid to the mark 11. All the cells in the entire ruled area are counted.
The total number divided by 3 gives the number of cells per c.mm. An
excellent staining-fluid has the following composition: methyl-violet 0.1,
glacial acetic acid 2.0, water to 50.0. This fluid stains the nuclei and makes
a differential count possible at the same time the enumeration is made.
If any hemorrhage has occurred in making the lumbar puncture and blood
becomes mixed with the cerebrospinal fluid, it is best not to attempt a count of the
cells. In such cases, it has been suggested that all the white cells (those of the
fluid -(- those of the blood mixed with the fluid) be counted first; that then
the red cells in the mixture be counted; that finally a red count and a white count
of the patient's blood be made so as to determine the relative number of white and
red cells in his blood; after this, a correction for the blood admixture with the
fluid is made. But the sources of error are so great that I advise strongly against
the use of this method. It is better to do lumbar puncture again later on and to
examine a specimen free from blood.
In normal cerebrospinal fluid, the number of cells per cubic millimeter
is usually less than 6 ; if more than 10 cells per cubic millimeter be found,
the condition is to be regarded as pathological.
In addition to counting the cells, it is always well to make a smear
from the sediment, and to dry, fix and stain this smear in order that the
exact morphology of the cells (S. M. ; P..M. N. ; P. M. E. ; P. M. B. ; endo-
BACTERIOLOGICAL, SEEOLOGICAL PUNCTATES 93
thelial cells; R. B. C.) may be studied and a differential count made (see
above).
In the various forms of meningitis, the cell content of the cerebrospinal
fluid is usually markedly increased. In epidemic cerebrospinal meningitis,
polymorphonuclear cells predominate, though lymphocytes and large endo-
thelial cells (some of them phagocytic) are also present. As the disease
dies down, the polymorphonuclears decrease and the lymphocytes increase
in number. A considerable lymphocytosis may persist for a long time after
recovery.
In purulent meningitis not due to the meningococcus, but caused by
pneumococci, streptococci, etc., the polymorphonuclears dominate the cell-
count in the acute stage, though in convalescence lymphocytes appear.
In tuberculous meningitis, the lymphocytes are usually more numer-
ous than the polymorphonuclear elements, though in some acute forms the
polymorphonuclears may markedly predominate. With sufficient care, in
such exudates, tubercle bacilli can usually be demonstrated.
In the paraluetic or metasyphilitic diseases of the central nervous sys-
tem, there is an outspoken lymphocytosis of the cerebrospinal fluid. A
careful study of smears shows, however, that, along with the lymphocytes,
one may see large mononuclear elements, some polymorphonuclear cells,
eosinophils, and endothelial cells ; in other words, in such cases an actual
pleocytosis exists. Such pleocytosis is found in every cases of dementia
paralytica, though the cell-count may be low during remissions in the dis-
ease. In the majority of cases of tabes, also, a pleocytosis is demonstrable.
In cerebrospinal lues (aside from tabes and dementia paralytica), the
pleocytosis may be marked in meningoencephalitic or meningomyelitic
processes ; but the number of cells may be small in systemic degenerations
of the white matter due to lues, in endarteritis, and in cases in which
only isolated gummata occur (Lommel).
It should be remembered that a pleocytosis in itself does not permit us
to separate luetic from metaluetic diseases of the central nervous system ;
moreover, a certain degree of pleocytosis may be met with in other chronic
diseases of the central nervous system (tumor; hydrocephalus; multiple
sclerosis). In secondary lues with skin lesions the cerebrospinal fluid may
show an outspoken lymphocytosis, often in the absence of any other signs
pointing to involvement of the central nervous system.
References
Bisgaard (A.). Untersuchunqen iibsr die Eiweiss- und StickstoffverhcjiUnisse der Cerebro-
spinaiflussigkeit sowie ilber die Wasserstoffionenkonzentration derselben.
Biochem. Ztschr., Berlin, 1913, Iviii, 1-64.
Dixon (W. E.) & Halliburton (W. Z>.). The cerebrospinal fluid. L Secretion of the fluid.
J. Physiol, Cambridge, 1913, xlvii, 215-242.
94 EXAMINATIONS OF THE FLUIDS OBTAINED
Ellis (A. W. M.) & Swift (H. F.). The cerebrospinal fluid in syphilis. J. Exper. M.,
Lancaster, Pa., 1913, xviii, 162-182.
Fraser (F. R.). A study of the cerebrospinal fluid in acute poliomyelitis. J. Exper. M.,
Lancaster, Pa., 1913, xviii, 242-251.
Frazier (C. H.). The cerebrospinal fluid in health and disease. J. Am. M. Ass., Chicago,
1915, Ixiv, 1119-1124.
Frazier (C. H.} & Peet (M. M.}. Influence of di-iodotyrosine and iodothyrine on the secre-
tion of cerebrospinal fluid. Am. J. PhysioL, Baltimore, 1915, xxxviii,
93-97.
Guillain (G.) & Parant (F.). Sur la presence d'albumines coagulables par la chaleur dans
le liquide cephalo-rachidien des paralytiques spinaux. Rev. neurol,
Par., 1903, xi, 406-411.
Miller (S. R.). The spinal fluid in syphilis. N. Y. State J. M., 1915, November.
Miller (S. R.), Brush (N.), Hammers (J. S.) & Felton (L.). A further study of the
diagnostic value of the colloidal gold reaction, together with a method for the
preparation of the reagent. Johns Hopkins Hosp. Bull., Baltimore, 1915,
xxvi.
Miller (S. R.) & Levy (R. L.). The colloidal gold reaction in the cerebrospinal fluid. Johns
Hopkins Hosp. Bull., Bait., 1914, xxv, 133-140.
Myerson (A.). The albumen content of the spinal fluid in its relation to disease syndromes.
J. Nerv. & Ment. Dis., New York, xli, 154-161.
Noguchi (H.) & Moore (J. W.). The butyric acid test for syphilis in the diagnosis of
metasyphililic and other nervous diseases. J. Exper. Med., Lancaster,
Pa., 1909, xi, 604-613.
Pandy (K.). Ueber eine neue Eiweissprobe fur die Cerebrospinalfliissigkeit. Neurol.
Centralbl., 1910, xxix, 17} 915.
Ross (G. W.} & Jones (E.). On the use of certain new chemical tests in the diagnosis of
general paralysis and tabes. British M. J., Lond., 1909, i, 1111-1113.
Rons (F. P.). Clinical studies of the cerebrospinal fluid, with especial reference to pressure,
protein-content, and the number and character of the cells. Am. J. M.
Sc., Phila. & N. Y., 1907, cxxxiii, 567-682.
Schulz (F. N.} & Zsigmondy (R.). Die Goldzahl und ihre Verwertbarkeit zur Charak-
terisiening von Eiweissstoffen. Beitr. z. chem. Physiol. u. Path., Brnschw.,
1903, Hi, 137-160.
Sippy (B. W.) & Moody (A. M.). The colloidal gold reaction in the diagnosis of syphilitic
and other lesions of the cerebrospinal nervous system. Tr. Ass. Am.
Physicians, Phila., 1913, xxviii, 720-738.
St rouse (S.}. The diagnostic value of the butyric acid test (Noguchi) in the cerebrospinal
fluid. J. Am. M. Ass., Chicago, 1911, M, 1171-1174.
Weed (L. H.}. Studies on cerebrospinal fluid. J. M. Research, Bost., 1913, xxvi, 21-117.
taloztecki (A.). Ueber den Eiweissgehalt der Cerebrospinalflussigkeit. Die Eiweissreak-
tionen in normalen und pathologischen Fallen. Deutsche Ztschr. f. Ner-
venheilk., Leipz., 1913, xlvii and xlviii, 783-815.
Part IV
Diagnosis of the Infectious Diseases
and of the Diseases Due to
External Physical Causes
SECTION" I
GENEEAL DIAGNOSIS OF INFECTIOUS DISEASES
A. General Facts Regarding Infection, In-
fectious Processes and the Methods
of Studying Them
1. Definition of Infection
By this term is meant the invasion of the body by living microorganisms,
which find there conditions permitting of their multiplying and causing
injury to the body, thus giving rise to disease-phenomena. Similar disease-
phenomena sometimes follow intoxications in which no living parasites
enter the body, e. g., after the ingestion of spoiled food (botulismus) ; here
the microorganisms have produced outside the body the poisons that,
when swallowed, give rise to symptoms. Many of the symptoms of diph-
theria and of tetanus can be produced experimentally in susceptible animals
by injection of their sterile toxins, but such toxins, unlike the microor-
ganisms that generate them, are incapable of multiplication, and do not
give rise in the animal to a communicable disease.
The infectious diseases (morbi contagiosi) were formerly subdivided into three
groups :
(a) The contagious diseases proper, which are communicated from one person
to another, either directly, or indirectly by objects (fomites) contaminated
by a so-called "contagium" ;
95
96 DIAGNOSIS OF INFECTIOUS DISEASES
•
(b) The miasmatic diseases, in which the infectious agent ("miasma") enters
the body from the outside, arising either independently of any sick person,
or, if originating in another patient, undergoing some ripening process in
the outside world;
(c) The miasmatic-contagious diseases, in which the infectious agent is sup-
posed to go through two developmental stages before being capable of
causing disease, one stage in a sick person, the other outside.
The artificiality of this classification has become obvious since the causes of
the infectious diseases and the modes of their transmission have been worked out.
References
Abel (R.)» Ueberblick uber die geschichtliche Entwickelung der Lehre von der Infektion,
Immunitat und Prophylaxe. In: Handb. d. pathogen. Mikroorg. (Kolle
& Wassermann.) 2. Aufl. Jena, 1912, i, 1-29.
Bail (O.). Versuch eines natiirlichen Systems der bakteriellen Infektionen. Jahresber. uber
die Ergebn. d. Immunitatsf., 1912, vii, Abt. i, 91-138.
Carnot (P.). Maladies microbiennes en general. Paris, 1912, J. B. Bailliere & fils. 272
p. 8°. [Nouv. Traite de Med. de Therap., I.}
Hektoen (L.). Introduction to the study of infectious diseases. In: Mod. Med. (Osier &
McCrae), Philadelphia & New York, 1913, 2d ed., i, 17-66.
Jochmann (G.). Lehrbuch der Infeklionskrankhei en. Berlin, 1914, J . Springer. 1023 p.
Ker (C. B.}* Infectious diseases. London, 1909, H. Frowde. 555 p. 8°.
Kolmer (John A.}. A practical textbook on infection, immunity and specific therapy, with
special reference to immunological technique. Philadelphia & London,
1915, W. B. Saunders Co. 899 p. 8°.
Kruse (W.}. Allgemeine Mikrobiologie, die Lehre vom Stoff- und Kraflwcchsel der Klein-
wesen, fur Aerzte und Naturfovscher dargcstellt. Leipzig, 1910, F. C. W.
Vogel. 1194 p. 8°.
Muller (P. T.). Vorlesungen uber Infektion und Immunitat. 4. Aufl.. Jena, 1912, G.
Fischer. 478 p. 8°.
Vorlesungen uber allgemeine Epidemiologie. Jena, 1914, G. Fischer. 257 p.
Pasteur (L.). De V extension de la theorie des germes d Vetiologie de quelques maladies com-
munes. Bull. Acad. de Med., Paris, 1880, 2d ser., ix, 435-447. Also:
Compt. rend. Acad. d. sc., Paris, 1880, xc, 1033-1044.
Ritchie (/.)• The general pathology of infection. In: Sys. Med. (Allbutt & Rolleston),
London, 1909. ii, pt. i, 1-198. 8°.
Rostoski (O.)« Infektionskrankheiten. Allgemeiner Teil. In: Handb. d. inn. Med. (Mohr
& Staehelin), Berlin, 1911, i, 1-64.
Rubner (M.), Gruber (M. v.) & Picker (M.). Handbuch der Hygiene. Bd. Hi, Abt. i.
Die Infektionskrankheiten. Leipzig, 1913, S. Hirzel. 853 p.
Simon (C. E.}. An introduction to the study of infection and immunity, including chapters
on serum therapy, vaccine therapy, chemotherapy and serum diagnosis.
Philadelphia & New York, 1913, Lea & Febiger. 352 p. 8°.
Wandel (O.). Diagnostik der acuten Infektionskrankheiten. In: Lerhb. d. klin. Diagnostik
(P. Krause). 2d ed., Jena, 1913, G. Fischer. 41-89.
v. Wassermann (A.} & Keysser (Fr.). Misch- und Sekunddr-infektion. In: Handb. d.
pathogen. Mikroorg. (Kolle & Wassermann.} 2. Aufl. Jena, 1912, i,
Wesen der Infektion. In: Handb. d. pathogen. Mikroorg. (Kolle &
Wassermann.) 2. Aufl. Jena, 1912, i, 555-331.
Zinsser (H.). Infection and resistance; an exposition of the biological phenomena under-
lying the occurrence of infection and the recovery of the animal body from
infectious disease. New York, 1914, The Macmillan Co. 546 p. 8°.
GENERAL FACTS REGARDING INFECTION 97
2. Infectious Agents and Their Specificity
The agents that enter the body from the outside and are the "exciting
causes" of the infectious diseases are minute living parasites (animal or
vegetable), distinguishable from the non-pathogenic saprophytes by their
ability to grow in higher living organisms and to injure such organisms.
The vegetable* parasites belong chiefly to the (a) bacteria or fission-
fungi (Schizomycetes), including the cocci, bacilli, and spirilla, though a
few belong to (b) the Tricliomycetes, including the leptothrix, cladothrix,
and streptothrix forms and to (c) the Blastomycetes (or yeast fungi) and
the Hyphomycetes.
The animal parasites causing infections belong to the protozoa, in-
cluding (1) the Ehizopoda (e.g., amebae), (2) the Flagellata, (e.g.,
trypanosomes), (3) the Sporozoa (e. g., coccidia) and (4) the Infusoria
(e.g., balantidium).
The larger animal parasites like the parasitic worms (Vermes) and
insects (Arthropoda) are not usually regarded as the cause of "infections'"
(due to microorganisms) but rather as the cause of "parasitic invasions."
Certain diseases (poliomyelitis, yellow fever, hydrophobia, etc.) are
due to filtrable viruses, that is, to viruses that are so minute that they
will pass through filters thought to be impermeable to ordinary bacteria;
they are on the border line between the visible and the invisible, i. e., they
are "ultramicroscopic."
Each infectious disease has a specific cause, that is to say, each infec-
tious agent is capable of giving rise to a given disease ; this disease can be
caused by it alone, and the agent is incapable of transformation into one
of another kind.1 For example, the sore throat due to the diphtheria
bacillus is a different disease from the sore throat due to the true strepto-
coccus infection, though in many respects they may resemble one another
clinically; again, a pneumonia due to the pneumococcus differs from a
pneumonia due to Friedlander's bacillus.
Koch's Laws. — To establish beyond question the causal relationship of a given
microorganism to a given disease, Koch required (1) that the suspected germ be
present in all cases of the disease, (2) that its presence in the diseased tissues of
the body be limited to this disease, (3) that it be grown in pure culture, and (4)
that the disease be typically reproduced through inoculation of a healthy individual
with the pure culture.
These requirements have been met for a few of the infectious diseases, notably
for tetanus, diphtheria, pneumonia, and tuberculosis; but, for many of the in-
fectious diseases, the first requirement only has been complied with. The causal
agents in a large number of diseases, undoubtedly infectious in nature, are as yet
1 Recent studies by E. C. Rosenow and by others hint that this specificity may not
be so complete as we have been accustomed to believe. Thus Rosenow believes he
can transform streptococci into pneumococci.
98 DIAGNOSIS OF INFECTIOUS DISEASES
utterly unknown; this is especially true of the exanthemata (smallpox, scarlet
fever, etc.).
For a time, medical men, delighted with their power to isolate the
causes of some of the infectious diseases, were content to direct their ener-
gies largely toward such isolation as a means of diagnosis. More recently,
since the essence of the infectious process has come to be recognized as a
specific reciprocal influence — a kind of warfare — between the infectious
agents on the one hand and the cells of the persons attacked on the
other, interest has centered rather in the mechanisms of'aggression and the
mechanisms of defense of both parasites and hosts (vide infra). For the
study of these mechanisms, the clinics and the experimental laboratories
have employed the most diverse biological, chemical, and physical methods ;
these have led to the development of the elaborate technic which now char-
acterizes the sciences of bacteriology, parasitology, and immunology.
Reference
Kolle (W.)» Spezijizitat der Infektionserreger. In: Handb. d. pathogen. Mikroorg. (Kolle
& Wassermann.) 2. Aufl. Jena, 1912, i, 869-904.
3. Mechanisms of Aggression of the Infectious Agents
(a) Sources of the Infectious Agents
The most important source is undoubtedly the sick man or animal,
whence the germs may pass directly or indirectly to other men or animals
and start new infections. It is, therefore, of the greatest importance to
know (i) how the germs leave the bodies of the sick, (ii) how they main-
tain their existence,- if at all, outside, and (iii) how they gain entrance
into the bodies of other men or animals.
i. How the Germs of Disease Leave the Bodies of the Sick
This varies for the different diseases and their respective infectious
agents. The germs may leave :
1. Through the feces (typhoid, cholera, dysentery).
2. Through the urine (typhoid, Malta fever, bubonic plague, tuber-
culosis, etc.).
3. Through the saliva (hydrophobia).
4. Through the milk (tuberculosis, anthrax).
5. Through the sputum (tuberculosis, pneumonia, diphtheria, strep-
tococcus infections, influenza, plague, etc.), especially
through the spray during speaking, coughing, and sneezing in
the so-called "droplet-infection" (Fliigge).
GENERAL FACTS REGARDING INFECTION 99
6. Through pus and through the secretions of the diseased skin and
mucous membranes (gonorrhea, lues, tuberculosis, meningitis,
poliomyelitis, exanthemata), and, perhaps, by scales of the
skin itself (scarlet fever ?).
7. Through the blood, by means of insect bites, or by transfusion
(malaria, yellow fever, sleeping sickness, relapsing fever,
typhus).
ii. How the Germs of Disease Maintain their Existence Outside the Bodies
of the Sick
Certain germs (e. g., malarial parasites) seem to be incapable of living
outside the body of some animal, except under very special (artificial) con-
ditions. Others are capable of existing for a shorter or longer time in the
outside world under natural conditions, provided they find sufficient nour-
ishment and conditions not too inimical to them (drying; sunlight).
Some germs are not readily killed by drying, and so may be spread
through dust (e. g., tubercle bacillus, pyogenic cocci, tetanus bacilli, an-
thrax spores, etc.) ; others are not viable in air-dried dust (gonococcus, in-
fluenza bacillus, cholera vibrio, plague bacillus).
Some germs can live in water under natural conditions for some time,
even for weeks or months. Much typhoid fever, cholera, amebic dysentery
and bacillary dysentery is due to water-borne infection. Polluted waters
may contaminate oysters or shell fish with typhoid bacilli or with cholera
vibrios. Freezing does not kill the cholera vibrio, so that ice may be a
source of infection.
In soil, though the deeper layers are sterile, certain germs, notably
those of typhoid and cholera, may be viable for some time. Anthrax bacilli
assume the spore form and live for some time in soil. In manured soils,
such as garden earth, tetanus bacilli and gas bacilli may remain viable for
a long period.
Various foodstuffs may harbor pathogenic germs, either through their
direct derivation from diseased animals (tuberculosis, anthrax, Malta
fever), or through contamination on the way to the consumer (milk, meat,
fish, oysters).
Certain healthy human beings and healthy animals may harbor patho-
genic germs and not be ill themselves. These are the so-called healthy
carriers, who play, perhaps, an important part in the spread of typhoid
fever, cholera, diphtheria, influenza, meningitis, poliomyelitis, and plague.
Again, certain pathogenic bacteria are capable of living in the skin
(staphylococci), mouth, and throat (pneumococci ; streptococci), or digestive
tract (B. coli; streptococci) of most healthy human beings; under certain
special conditions these germs may infect the carrier himself. Certain
animals act as mechanical carriers of germs ; thus flies may carry typhoid
bacilli to food or directly to the lips of human beings.
100 DIAGNOSIS OF INFECTIOUS DISEASES
Among the most interesting modes of life of germs outside the bodies of
the sick is life in an intermediate host in which a developmental cycle
necessary for the acquisition of the power to infect is gone through (para-
site of Texas fever in the tick; malarial parasites in the anopheles mos-
quito; virus of yellow fever in the stegomyia mosquito).
iii. How the Germs of Disease Gain Entrance to the Body (Portals of Entry)
In the infectious diseases, the germs enter the body through one or
another opening — the so-called "portals of entry." As long as the epi-
thelium of the skin and of the mucous membranes is absolutely intact,
infection does not occur through them, but should the epithelium be
physically or chemically injured (wounds, heat, poison), germs may pene-
trate, and, multiplying within the tissues, start an infectious process.
Among the portals of entry may be mentioned the skin with its gland
ducts and hair follicles, the conjunctiva, the nose, nasopharynx, and para-
nasal sinuses, the mouth (especially the gums), the tonsils, the bronchi
and pulmonary alveoli, the mucous membrane of the esophagus, stomach,
and, especially, of the intestine (including the bile ducts, pancreatic ducts,
and vermiform appendix), the anus, especially when hemorrhoids or
fissures exist, and the urogenital tract (including the urethra, bladder,
ureters, and renal pelves in both sexes, and the mucous membranes of the
special organs of sex in the male and in the female).
By germinal infection is meant the transmission of infection to the
child by means of the egg cell or the sperm cell of a parent. Syphilis may
be thus transmitted, but placental infection from the mother is probably
more frequent than direct germinal transmission. Intra-uterine (placental)
infection may occur in a number of diseases (e, g., syphilis, typhoid fever,
tuberculosis, smallpox, etc.).
Certain germs can enter through almost any portal, while others never enter the
body except through a single portal. Thus, plague bacilli may enter through the
skin, through the mouth, through the lungs, or through the conjunctiva. But, as
far as we know, the cholera spirillum acts only upon the intestinal mucous mem-
brane ; injected under the skin it does not cause disease except in the rare instances
in which the cholera vibrios wander thence to the intestine. Midway in position
between the organisms which can enter by almost any portal and those limited
in entrance to a single portal, are the germs that, while preferring definite portals,
occasionally enter through others. The bacillus of diphtheria preferably attacks
the mucous membrane of the throat, but occasionally it may attack the nose, the
conjunctiva, or the larynx. It rarely, if ever, attacks an open cutaneous wound.
Similarly, gonococci preferably attack the urethral mucous membrane ; but they
may invade the rectum or the conjunctiva; they do not multiply in cutaneous
wounds.
The number of germs gaining entrance may be of great importance. If
only a few enter they may be quickly overcome before they give rise to evi-
GENEKAL FACTS KEGABDING INFECTION 101
dent signs of disease. In experimental animals, the number necessary to
give rise to a fatal infection is known as the "minimal lethal dose."
Occasionally, more than one infectious process is going on in the body
at the same time. If the two infections arise simultaneously we speak of
mixed infections; if one follows upon the other we speak of a secondary
infection.
Such contemporaneous infections are often important clinically. Many
of the deaths in diphtheria and scarlet fever are due to complicating strep-
tococcus infections. A terminal septic infection in typhoid is not uncom-
mon. The streptococcus and influenzal infections complicating pulmonary
tuberculosis are well-known and much feared.
(b) Distribution of Microbes Within the Body After Entrance
.In certain of the infectious diseases (diphtheria; tetanus), the germs
remain at the portal of entry, or extend along the contiguous surface, with-
out going far into the tissues, and without being disseminated through the
blood or lymph to distant points; these are local infections. The action of
the germs themselves in such instances is purely local, but they often injure
distant parts of the body through the production of soluble poisons, which
are absorbed. Such diseases are often spoken of as intoxication diseases
in contrast with the infectious diseases in the narrower sense in which the
germs reach various distant points of the body by metatasis through the
blood or lymph (e. g., infectious polyarthritis), or on entering the blood
or lymph, multiply there in large numbers, giving rise to septicemia or
bacteriemia (e. g., anthrax).
In some diseases, bacteria may, after a period, cease to multiply, but
some of them may still remain alive in secluded parts of the body (lat611*
infection), and under special circumstances, later on, begin to multiply
again with renewal of disease symptoms. Such latent infections are
especially common in the protozoan invasions (lues, malaria, trypanoso-
miasis), but latency is also met with in bacterial diseases (e. g., erysipelas,
subacute infective endocarditis, chronic polyarthritis, tuberculosis).
Reference
Billings (Frank). Focal infection in relation to systemic disease. In: Forchheimer's Thera-
peiLsis of internal diseases. New York & London, 1914, v, 169-181.
(c) The Poisons (Toxins) Produced by the Microbes,
and Their Action
These are divisible into two groups : ( 1 ) soluble substances which may
be looked upon as metabolic products or secretions of the germs — the
so-called ectotoxins (e. g., the toxins of tetanus and diphtheria), and (2)
poisonous substances contained within the bodies of the bacteria themselves
102 DIAGNOSIS OF INFECTIOUS DISEASES
and set free only when the f acteria are hroken up — the so-called endotoxins
of Pfeiffer (e. g., the poisons derived from the bodies of pneumococci,
tubercle bacilli, typhoid bacilli, cholera vibrios, etc.).
A number of other poisons should be mentioned here. The so-called,
ptomains are substances derived from the nutrient media in which bacteria
grow. They resemble alkaloids and their nature depends upon the indi-
vidual species of microorganism taking part in the process and upon the
nutrient medium invaded (meat, cheese, ice cream, etc.).
The bacterioproteins of Buchner are thermostable proteins derived from
bacterial bodies. These proteins are usually pyogenic in action when
injected under the skin. Those from different bacteria resemble one
another closely. Old tuberculin and mallein are rich in such proteins.
The nature of the so-called aggressins of Bail is still disputed. Bail
believes that bacteria produce aggressins that paralyze phagocytes, since
bacteria injected into animals along with the sterilized exudate produced
by infection with the same bacterium kill more quickly than when the
bacteria are injected without such exudate.
According to an hypothesis of W. II. Welch, bacteria may be stimu-
lated by their host to the production of bacteriogenic antibodies that
exert a specific toxic effect upon the cells of the body of the host — a bac-
teria-protective mechanism on the part of the bacteria to overcome the
bacteria-offensive mechanisms of the body.
Certain other chemical substances produced by the germs in the body
(especially the antigens that give rise to precipitins, agglutinins, opson-
ins, and lysins) will be referred to further on when the phenomena of
immunity are discussed.
Selective Action of Poisons. — The poisonous substances produced by
the germs often exert a selective action upon the various parts of the body.
Certain organs possess an especial affinity for certain poisons. This has
been shown in the test tube, notably for the tetanus toxin, which is avidly
bound by fresh emulsions of cerebral gray matter. Similarly, the laking
poison produced by staphylococci, and known as staphylolysin, is quickly
bound by red blood corpuscles in test tube experiments.
Union of Poisons with Body-Cells. — One difference between suscep-
tible animals and those that are insusceptible to a given infection seems
to consist in the capacity of certain body-cells to unite with the poisons
produced; thus, tetanus toxn injected into susceptible animals disappears
from the blood in from 4-8 minutes. Injected into lizards, the toxin is
demonstrable in the blood for two months, though the lizard shows no
symptoms. It has no cells, apparently, which unite with the toxin. A
scorpion injected in the same way shows no symptoms, though the toxin
quickly disappears from the blood ; in this animal it unites with the liver
cells and can be again extracted from the liver, the extracts producing
typical tetanus in mice.
GEKEKAL FACTS EEGAEDING INFECTION 103
Distribution of Poisons in the Body. — In the distribution of poisons
in the body and their retention in certain organs, physical conditions such
as solubility-relations are in part responsible and chemical affinities also
play a role.
Poisons, while usually disseminated through the blood current or the
lymph stream, may in certain instances follow a wholly different route;
thus, in tetanus, the toxin reaches the central nervous system neither by
way of the blood nor of the lymph, but, entering the motor nerves at the
myoneural junction, travels in a centripetal direction until the central
nervous system is reached.
References
Bail (O.). Untersuchungen uber Typhus- und Choleraimmunitdt. Arch. f. Hyg., Munchen
u. Berlin, 1905, Hi, 272-377.
Untersuchungen uber die Aggressivitdt des Choleravibrio. Arch. f. Hyg.,
Munchen u. Berlin, 1905, liii, 302-328.
Das Problem der bakteriellen Infektion. Folia serolog. [etc.], Leipzig, 1911,
vii, 14, 119, 252.
Das Problem der bakteriellen Infektion. Leipzig, 1911, W. Klinkhardt.
106 p. Roy. 8°.
Besredka (A.). Endotoxines microbiennes. Bull, de Vlnst. Pasteur, Paris, 1914, xii,
145-154; 193-205.
Des endotoxines solubles typhique pesleuse et dysenterique. Ann. de Vlnst.
Pasteur, Paris, 1906, xx, 304-310.
Brieger (L.). Ueber Ptomaine. Berlin, 1885, A. Hirschwald. 80 p. 8°.
Weitere Untersuchungen uber Ptomaine. Berlin, 1885, Hirschwald.
83 p. 8°. -
Buchner (H.). Ueber pyogene Stoffe in der Bakterienzelle. Berl. klin. Wchnschr., 1890,
xxvii, 673-377.
Die Bedeutung der activen loslichen Zellproducte fur den Chemismus der
Zelle. Munchen. med. Wchnschr., 1897, xliv, 299-302.
Gewi,nnung von plasmatischen Zellsaften niederer Pilze. Munchen. med.
Wchnschr., 1897, xliv, 1343.
Ehrlich (P.). Ueber die Constitution des Diphtheriegiftes. Deutsch. med. Wchnschr.,
Leipzig, 1898, xxiv, 597-600.
Glenny (A. T.) & Walpole (G. S.}. Detection and concentration of antigens by ullrafiltra-
tion, pressure dialysis, etc., with special reference to diphtheria and tetanus
toxins. Biochem. J., Cambridge, 1915, ix, 298-308.
Hahn (M.). Immunisirungs- und Heilversuche mit den plasmatischen Zellsaften von Bac-
terien. Munchen. med. Wchnschr., 1897, xliv, 1344-1347.
Madsen (T.). La constitution du poison diphterique. Ann. de Vlnst. Pasteur, Paris,
1899, xiii, 566-580, et 801-832.
Pearce (JR. Af.). Concerning the specificity of the somatogenic cytotoxins. J. Med. Res.,
Boston, 1904, n. s. vii, 1-15. '
Rossle (.R.). Fortschritte der Cylotoxinforschung. Ergebn. d. allg. Pathol. u. AnaL, Wies-
baden, 1910, xiii, 124-252.
Samuely (F.). Tierische Toxine. In: Handb. d. Biochem. (Oppenheimer .) Jena, 1909,
i, 583-598.
Vaughan (V. C.) & Novy (F. G.}. Cellular toxins, or the chemical factors in the causation
of disease. 4th ed. Philadelphia & New York. [1902], Lea Bros. & Co.
495 p. 8°.
Wassermann (A.) & Citron (J.). Zur Frage der Bildung von bakteriellen Angriffsstoffen
im lebenden 'Organismus. Deutsche med. Wchnschr., Leipzig u. Berlin,
1905, xxxi, 1100-0003.
Zinsser (#.). Bacterial Poisons. In: Infection and Resistance (H.Zinsser). New York.
1914. 28-48.
104 DIAGNOSIS OF INFECTIOUS DISEASES
(d) The Course of an Infectious Process
Some little time elapses after the microbes have gained entrance into
the body before the first symptoms of the disease appear. This time is
called the period of incubation. Usually the outspoken symptoms of the
disease are preceded by a brief stage in which there are more or less vague
symptoms (prodromata) . Before recovery from an infection, there may be
one or more periods of exacerbation, often spoken of as a recrudescence or
an intercurrent relapse. Sometimes the infection appears to have been
entirely overcome and convalescence fully established when the patient
and the physician are surprised by a recurrence of the symptoms of the
infection ; such a condition is called a true relapse or recidive.
(e) The Virulence of the Microbes
A microbe is said to be pathogenic, or virulent, when it is a*ble to mul-
tiply in the organism invaded and to produce poisons that injure it. The
degree of virulence varies according to the extent of these two capacities.
Virulent organisms often become avirulent when grown upon artificial
media. Sometimes the virulence can be renewed by passage through sus-
ceptible animals, the virulence increasing on passage from one animal to
another until a maximum is reached, the so-called "fixed virus" of Pasteur.
As the microbes grow more virulent, they acquire increased resistance to
the antibodies produced by the organism invaded, and become less suscep-
tible to phagocytosis. In addition, the microbes may produce substances
(bacteriogenic antibodies) that combat the chemical agents used by the
organism invaded in its defense (Welch).
Despite the increase in virulence of microbes by experimental passage
through susceptible animals, virulence remains at a relatively low level in
nature, and the mortality rates of infectious diseases appear to be falling
rather than rising. A plausible biological explanation has been given by
Theobald Smith, who suggests that many pathogenic microbes are being
reduced to a more parasitic form of life. A microbe, to maintain its exist-
ence, must be able to adapt itself to conditions that allow the invasion of
host after host. In addition, the most susceptible hosts are being gradually
weeded out. The advance toward parasitism on the part of the microbes
and the advance toward less susceptibility on the part of the hosts must be
followed by a decline in virulence and in mortality rates.
Reference
Zinsser (#.)• Infection and the problem of virulence. In: Infection and Resistance (H.
Zinsser). New York, 1914. 1-27.
GENEKAL EACTS KEGAKDING INFECTION 105
4. Mechanisms of Defense of the Human or Animal Body
Though an infected animal supplies a nutrient medium for the growth of
the invading microbe, it possesses manifold mechanisms of defense, which
it makes use of in repelling, or in overcoming, the enemy. When we con-
sider the variability of the Dathogenicity and virulence of the microbes on
the one hand, and the variability in the susceptibility and in the mechan-
isms of defense of the hosts on the other, we can understand why the symp-
toms and course of infections must vary, and how unlikely it is that a given
concrete case under observation will conform in every particular to a
"typical text-book description.77
When a person is protected by natural or artificial means against a
certain infection or intoxication, he is said to be immune. When he is not
so protected he is said to have a disposition for, or to be susceptible to, the
disease.
(a) On Immunity in General
Inborn protective power of the organism against infections is known as
natural resistance or inborn immunity. The protective powers that are
acquired in the course of life are spoken of as acquired immunity. It has
long been known that one attack of certain infectious diseases protects from
subsequent attacks. The acquired immunity here is natural, or sponta-
neous, but in many instances we can produce an immunity at will, by sys-
tematically treating the body with the microbes or their poisons (active
immunization). These harmful substances, known as antigens, give rise
to reactions in the hosts that lead to the production of so-called antibodies
that neutralize or destroy the antigens.
In acquired immunity, the protection may depend upou the chemical
neutralization of pathogenic toxins by specific antitoxins (acquired anti-
toxic immunity). In some instances it may depend upon the acquisition
of the power quickly to destroy the entering microbe (antibacterial or bac-
teriolytic immunity) ; in still other cases the protection may depend upon
the formation of substances that prepare the bacteria for phagocytosis
(phagocytic immunity). Immunity may also be produced by injecting
immune substances derived from artificially immunized animals (passive
immunization).
References
Arrhenius (Svante}. Immunochemistry. New York, The Macmillan Co., 1907. S20 p. 12°.
Bordet (/.). Studies in immunity. Transl. by F. P. Gay. New York, J. Wiley & Son,
1909. 552 p. 8°.
Ehrlich (Paut). Gesammelte Arbeiten uber Immunitdtsforschung. Berlin, 1904. A. Hirsch-
wald. 788 p. 8°.
Kraus (R.) & Levaditi (C.). Handbuch der Technik und Methodik der Immunitdts-
forschung. Jena, G. Fischer. 5 v. 1908-09.
106 DIAGNOSIS OF INFECTIOUS DISEASES
MetschniJcoff (£".). Die Lehre von den Phagocyten und deren experimentelle Grundlagen.
In: Handb. d. pathogen. Mikroorg. (Kolle & Wassermann.} 2. Aufl.
Jena, 1913, ii, 1, 655-731.
Muir OR.). Studies on immunity. London, 1909, H. Frowde. 216 p. 8°.
Pasteur (L.). Chicken cholera. C. R. Acad. Med., Paris, 1880.
Salmon (D. E.} & Smith (T.). On a new method of producing immunity from contagious
diseases. Proc. Biol. Soc., Washington, 1884-86, Hi, 29-33.
Vaughan (V. C.), Vaughan (V. C., Jr.) & Vaughan (J. W.). Protein split-products in
relation to immunity and disease. Philadelphia & New York, 1913, Lea
& Febiger. 505 p. 8°.
Webb (G.), Williams (W. W.) & Barber (M. A.). Immunity production by in'oculation
of increasing numbers of bacteria beginning with one living organism.
J. Med. Res., Boston, 1909, n. s. xv, 1-25.
Welch (W. H.). The Huxley lecture on recent studies of immunity, with special reference
to their bearing on pathology. Johns Hopkins Hospital Bull., Baltimore,
1902, xiii, 285-299.
Wells (H. G.}. The present status of our knowledge of the chemistry of the processes of im-
munity. Arch. Int. Med., Chicago, 1908, i, 262-276.
Zinsser (H.). Immunity. In: Infection and Resistance (H.Zinsser). New York, 1914.
49-103.
(b) Natural Immunity, or Resistance
This may be either antibacterial or antitoxic.
i. Antibacterial Resistance
An antibacterial resistance may depend upon (1) the closure of the
portals of entry, (2) conditions unfavorable to the growth of bacteria after
entrance, or (3) bactericidal powers of the fluids themselves.
Natural bactericidal action of the blood depends upon substances in the
serum (alexins) ; these are thermolabile and resemble ferments in that
they require a certain temperature, a slightly alkaline or neutral reaction,
and a certain salt content, to exert their bactericidal effects. The serum
can be made inactive by heating thirty to sixty minutes at 55° to GO0 C.,
which destroys the alexin. In acquired bactericidal action of the blood,
other substances are important. ( See Bacteriolysis. )
In phagocytosis, the microbes are taken up by the cellular elements
and undergo digestion inside them. In human beings, it is the meso-
dermal element and especially the white blood corpuscles and the endo-
thelium of blood and lymph vessels, which act as phagocytes. The
polymorphonuclear leukocytes have been designated 'micropliages, while
the large mononuclear cells, the large lymphocytes, the giant cells, and the
pulp cells of the spleen and bone marrow are called macrophages. Most
microbes are taken up by microphages, but the tubercle bacillus, the
actinomycosis fungus, and animal parasites are more often engulfed by
macrophages.
The phagocytes are peculiarly susceptible to chemical stimuli (chemo-
taxis). Certain chemical substances of bacterial origin attract leukocytes
GENEKAL FACTS KEGAKDING INFECTION 107
to them in large numbers. They are positively chemotaxic. Other sub-
stances appear to drive leukocytes away from them. They are said to be
negatively chemotaxic. A third group of substances neither attract nor
repel the phagocytes. They are the so-called indifferent substances. A
given substance may be positively chemotaxic in one concentration, and
negatively chemotaxic in another. It seems probable that the leukocytosis
and the leukopenia met with in the infectious diseases are in part to be
explained upon a chemotaxic basis ; in addition, stimulation or depression
of the leukopoietic tissues must also be considered. (See Leukocytosis and
Leukopenia).
Both non-virulent and virulent bacteria may be engulfed by phago-
cytes. Usually the bacteria undergo intracellular digestion and destruction,
but virulent microbes may remain alive and retain their virulence for a
long time within phagocytes.
It was formerly thought that substances exist in the serum that stimu-
late the phagocytes to activity. They were called stimulins. Later studies,
especially those of Wright and Douglas, show that the substances in the
serum, instead of stimulating the phagocytes, act upon the bacteria so as to
fit them for engulfment by the phagocytes. These substances are the
oo-called opsonins and they appear to play an important part in natural
resistance.
It seems probable that certain other substances (lysins, antitoxins) play
some part in natural resistance. They seem to be of far greater importance,
however, in acquired immunities (vide infra).
Natural immunity is rarely absolute, though we know certain examples; thus
no animal, except man, has thus far been found susceptible to scarlet fever; and
human beings are absolutely resistant to cattle plague. Natural resistance is, there-
fore, usually a relative matter, the resistance varying at different times and under
different conditions of nutrition, work, climate, intoxication, mental anxiety, and
the like. An important part of clinical medicine consists in finding out how nat-
ural resistance to disease can be increased by means of dietetic, hygienic, and other
measures.
ii. Antitoxic Resistance
A natural resistance to intoxication also exists in addition to resistance
to infection. This is well shown by comparing the amount of toxin neces-
sary per kilogram of body weight to cause death in different animals.
The amounts of tetanus toxin required for the horse, guinea-pig, rabbit,
and chicken vary as the figures 1 :2 :2,000 :200,000. Measured in the same
way, the mouse is 20,000 times less susceptible to the diphtheria toxin than
the guinea-pig. It was believed by Ehrlich that natural resistance to toxic
substances depends upon failure of the cells to anchor the poison chem-
ically. Studies with Schick's reaction indicate that a large proportion of
children and adults have enough antitoxin to diphtheria in their blood to
protect them from infection. (See Diphtheria.)
108 DIAGNOSIS OF INFECTIOUS DISEASES
References
Addis (T.}. The bactericidal and hemolytic powers of "paraffin," plasma and of serum.
J. Infect. Dis., Chicago, 1912, x, 200-209.
Buchner (H.). Ueber die bakterientodtende Wirkung des zellenfreienBlutserums. Centralbl.
f. Bakteriol u. Parasitenk., Jena, 1889, v, 817; also ibid, vi, 1; also
Munchen. med. Wchnschr., 1889, xxxvi, 415-417.
Die chemische Reizbarkeit der Leukocyten und deren Beziehung zur Ent-
ziindung undEiterung. Berl. klin. Wchnschr., 1890, xxvii, 1084-1089.
Gengou (O.). Contribution a I 'etude de I'origine de Valexine des serums normaux. Ann.
de Vlnst. Pasteur, Paris, 1901, xv, 68-84 & 232-248.
Hahn (M.)» Natiirliche Immunitdt (Resistenz). In: Handb. d. pathogen. Mikroorg.
(Kolle & Wassermann.) 2. Aufl. Jena, 1912, i, 942-1028.
Hektoen (L.) & Ruediger (G. F.). Studies in phagocytosis. J. Infect. Dis., Chicago,
1905, ii, 128-141.
Metschnikoff (E.). Ueber die Beziehung der Phagocyten zu Milzbrandbacillen. Arch. f.
. pathol. Anat. (etc.). Berlin, 1884, xcvii, 502-526.
Etudes sur I'Immunile. Sur la destruction extracellulaire des bacteries dans
Vorganisme. Ann. de Vlnst. Pasteur, Paris, 1895, ix, 433-461.
Miiller (P. T.). Immunitdt gegen Bakterien. In: Handb. d. Biochem. (Oppenheimer) .
Jena, 1910, ii, l.Hlfte, 629-688.
Neisser (M.). Ueber die Vielheit der im normalen Serum vorkommenden Antikorper.
Deutsche med. Wchnschr., Leipzig u. Berlin, 1900, xxvi, 790-792.
Nut tall (G. H. F.). Experiments uber die bacterienfeindlichen Einflusse des thierischen
Korpers. Ztschr. f. Hyg., Leipzig, 1888, iv, 353-394.
Prudden (T. M.}. On the germicidal action of blood serum and other body fluids. Med.
Rec., New York, 1890, xxxvii, 85-88.
Wassermann (A.). Experimentelle Beitrdge zur Kenntnis der naturlichen und kunstlichen
Immunitat. Ztschr. f. Hyg. u. Infectionskrankh., Leipzig, 1901, xxxvii,
173-204.
Wechsberg (F.). Zur Lehre von der naturlichen Immunitdt und liber baktericide Heilsera.
Ztschr. f. Hyg. u. Infectionskrankh., Leipzig, 1902, xxxix, 170-200.
Zinsser (H.). On bactericidal substances extracted from normal leucocytes. J. Med. Re-
search, Boston, 1910, xxii, 397-433.
(c) Acquired Immunity
If a person has once had scarlet fever, smallpox, yellow fever, or
measles, he is protected during the rest of his life from another attack. If
he has had Asiatic cholera, he is protected for some time, hut may, later in
life, have a second attack. If he has had influenza, lobar pneumonia, or
diphtheria, he may gain a protection for a very brief period, hut in a short
time is again susceptible, and, in some instances, more susceptible than if
he had not been previously attacked. The degree and duration of acquired
immunity are therefore variable for the different infections, and, in differ-
ent people, for the same infection. A mild infection seems to yield as high
a grade of immunity as a severe infection. Children who have a mild
attack of scarlet fever, measles, or whooping-cough are therefore to be
regarded as fortunate. Such observations of natural acquired immunity
soon led to the attempt to immunize artificially with attenuated cultures of
bacteria.
GENEKAL FACTS KEGAEDING INFECTION 109
References
Allen (R. W.). Vaccine therapy; its theory and practise. J+ih ed. Philadelphia, 1913.
Egbert (J.) & O'Neill (O.). Sera and vaccines; prophylactic and curative. New York
M. J., 1911, xciv, 970-973.
Irons (E. E.). The principles of specific therapy. In: Therap. Int. Dis. (Forchheimer).
New York, 1914, v, 1-38.
Kolle (W.}. Die Grundlagen derLehre von der erworbenen (aktiven, allgemeinen und lokalen
sowie passiven) Immunitdt. In: Handb. d. pathogen. Mikroorg. (Kolle
& Wassermann.) 2. Aufl. Jena, 1912, i, 905-940.
Pearce (R. M.). The scientific basis for vaccine therapy. J. Am. M. Ass., Chicago, 1913,
Ixi, 2115-2119.
Schorer (E. H.~). Vaccine and serum, therapy, including also a study of infections, theories
of immunity, specific diagnosis and chemotherapy. 2d rev. ed. St. Louis,
1913.
Smith (T.). An attempt to interpret present-day uses of vaccines. J. Am. M. Ass., Chicago,
1913, Ix, 1591-1599.
Wolff-Eisner (A.). Handbuch der Serumlherapie und experimentellen Therapie. Hand-
buchfur Klinik und Praxis. Munchen, 1910, J. F. Lehmann. 408 p. 8°.
i. Antibodies to the Antigens
Acquired immunity is partly due to an intensification of the natural
powers of resistance, but it is principally due to the production of new
protective substances by "the organism and to changed conditions of the
body (allergy), which lead it, on threatened reinfection, to produce the pro-
tective substances in large amounts. These protective substances that
the organism manufactures to overcome infection are known as antibodies.
On the other hand, the substances of parasitic origin that excite the for-
mation of these antibodies are known as antigens.
The antibodies formed include (1) substances that neutralize toxins
(antitoxins), (2) substances that injure or destroy the bacteria (bac-
ieriolysins, etc.), substances that act upon the bacteria, preparing
them for phagococytosis (immune opsonins or bacteriotropins) .
These substances are specific. The diphtheria antitoxin neutralizes
the diphtheria toxin and no other ; the agglutinins for the typhoid bacillus,
agglutinate this and closely allied organisms and no others; the bacterio-
lysins produced in cholera infection, dissolve up the cholera vibrio and
no other.
Though the earlier studies investigated only the antibodies formed
against bacteria and toxins, later work has shown that cells of various
sorts, especially red blood corpuscles, protein substances, ferments, etc.,
can act as antigens, and that they also give rise to specific antibodies (cyto-
lysins, liemolysins, precipitins, antiferments^ etc.).
References
Besredka (A.). De Vanti-endotoxine typhique et des anti-endotoxines, en general. Ann. de
I'lnst. Pasteur, Paris, 1906, xx, 149-154.
110 DIAGNOSIS OF INFECTIOUS DISEASES
Ficker (3f.)» Methoden der aktiven Immunisierung einschliesslich Herslellung von Anti-
genen. In: Handb. d. pathogen. Mikroorg. (Kolle & Wassermann.)
2. Aufl. Jena, 1913, ii, 1, 1-192.
Methoden der Antikorperdarstellung. In: Handb. d. pathogen. Mikroorg.
(Kolle & Wassermann.) 2. Aufl. Jena, 1913, ii, 1, 193-241.
Ford (W. W.). Antibodies to glucosides with special reference to Rhus toxicodendron.
J. Infect. Dis., Chicago, 1907, iv, 541-551.
Landsteiner (/£.)• Immunitdt gegen Korperzellen und Neubildungen. In: Handb. d.
Biochem. (Oppenheimer). Jena, 1910, ii, 1. Hlfte, 542-551.
Michaelis (L.)- Physikalische Chemie der Toxin- AntitoxinUldung. In: Handb. d. Bio-
chem. (Oppenheimer). Jena, 1910, ii, 1. Hlfte, 377-394.
Oppenheimer (C.). Ueber Antitoxine und ihre Beziehungen zu den Toxinen. In: Handb.
d. Biochem. (Oppenheimer). Jena, 1910, ii, 1. Hlfte, 356-376.
Pick (E. P.). Biochemie der Antigene, mit besonderer Berucksichtigung der chemischen
Grundlagen der Antigenspezifizitdt. In: Handb. d. pathogen. Mikroorg.
(Kolle & Wassermann.) 2. Aufl. Jena, 1912, i, 685^868.
Sachs (H.). Antigene und Antikorper. In: Handb. d. Biochem. (Oppenheimer). Jena,
1910, ii, 1. Hlfte, 275-355.
ii. Theories of Antibody Formation
Many theories have been advanced, but the side-chain theory of Ehrlich is the
one that has dominated the thought of investigators, stimulating important
research. This theory has never been completely substantiated, and though, at
present, many of the foremost immunologists accept its tenets gnly in small part,
and in many instances reject it in its entirety, it affords so ready a working hypothe-
sis that it will be given here.
Ehrlich conceived of huge molecules in the protoplasm, each molecule having
a more or less stable central nucleus to which are attached atomic groupings known
as lateral chains, or side-cli(ihi», which, he believes, give the large molecule the
power to enter into union with food substances and with other foreign substances
reaching the cells. Accordingly, these side-chains have also been designated re-
ceptors. A foreign substance reaching a cell combines with its protoplasm only
when it, in turn, possesses a suitable atomic grouping (haptophore group) for
uniting with a receptor of the cell, much as a key fits into a lock, or as the
fingers into a glove. Mere union of the foreign substance with the protoplasm
of the cell does not imply that the former also exerts any influence upon the pro-
toplasm other than mere occupation of the receptor. To influence the protoplasm,
another special atomic grouping is required, a so-called functional group; in the
case of a toxin the functional group is termed a toxophore group.
If a large number of receptors of a given kind in the cells become occupied
by the haptophore groups of a given antigen, the cells begin to form receptors of
the same sort in large amounts (Weigert's "law of regenerative over-compensa-
tion"), and the cells throw them off into the circulation as free antibodies, and
these free antibodies can unite with the haptophore group of the foreign substance
just as well as though they were attached to body-cells. Thus, for example, if
the receptors of a cell have become sufficiently combined with diphtheria toxins
in reaction duly formed receptors will be thrown off into the blood as diphtheria
antitoxins. In other words, the same substance that, attached to the cell, is a
prerequisite of its intoxication becomes a medium for cure when it is free in the
circulating blood.
Examples of such free cellular receptors other than antitoxins are the anti-
ferments, the agglutinins, the precipitins, and various amboceptors to be men-
tioned later.
GEKEKAL FACTS KEGAKDING INFECTION
111
On injecting antigens into an animal there may be a temporary depression
of the mechanism of antibody formation (negative phase 1) ; this is soon followed
by an active production of antibodies (positive phase) ; later on, this over-activity
returns to normal. As a rule, animals do not form antibodies against the sub-
stances of their own bodies, or of the bodies of animals of the same species.
Three kinds of receptors are distinguishable in the cell, designated by Ehrlich
as receptors of the first order, of the second order, and of the third order.
Receptors of the first order possess only one
haptophore group (e.g., antitoxins, antiferments).
They have the power of anchoring only one for-
eign substance with the protoplasmic molecule.
The receptors of the second order possess a hap-
tophore group and a so-called ergophore, or zy-
mophore, group (e. g., agglutinins and precipi-
tins). With the haptophore group, the foreign
substance is anchored to the protoplasm; through
the ergophore group, the protoplasm is influenced.
The receptors of the third order possess two
haptophore groups, one for anchoring a foreign
substance (food molecules, bacteria), the other for
anchoring complements from the blood serum
through which the foreign substance is acted upon.
This second haptophore group is called the comple-
mentophil group. A free receptor of this sort
having two haptophore groups is known as an
amboceptor.
iii. Antitoxins
(C)
Pig. 40.— (A) Receptor of the
First Order; (B) Receptor of
the Second Order; (C) Receptor
of the Third Order.
Powerful antitoxins can 'be produced in ex-
perimental animals against diphtheria toxin,
tetanus toxin, snake venom, and the poisons
of some of the higher plants. The sera conr
taming the first two of these antitoxins
can he carefully concentrated and injected into human heings for thera-
peutic purposes. The immunity thus produced is temporary and is known
as a passive immunity, in contrast with the active immunity produced by
the cells of the organism itself.
Antitoxins in an immune mother can pass through the placental circu-
lation to the child. Antitoxins neutralize their corresponding toxins, but
have no action upon the organisms that form the toxins. The chemical
structure of antitoxins is unknown, hut it is believed by some that they act
by chemical union with the toxins to form a harmless substance.
A toxin has a haptophore group that unites with the cell and a toxo-
phore group that exercises a deleterious effect upon the cell to which the
toxin hecomes attached. The antitoxins are free receptors of the first
order and combine with the haptophore group of the toxin preventing
union of the toxin with the sensitive cells.
The existence of such a "negative phase" is denied by some investigators.
112 DIAGNOSIS OF INFECTIOUS DISEASES
The toxophore group in the toxin is more sensitive than the hapto-
phore group, and when injured by long keeping, or hy heat, the toxin is
transformed into an innocuous modification, the toxoid.
References
Behring (E. v.). Untersuchungen uber das Zustandekommen der Diphtherie-Immunitdt bei
Thieren. Deutsche med. Wchnschr., Leipzig u. Berlin. 1890, xvi, 1145-
1148.
Die Blulserumtherapie bei Diphtheric u. Tetanus. Ztschr.f. Hyg., Leipzig,
1892, xii, 1-9.
Behring (E. p.) & Kitasato (S.). Uebcr das Zustandekommen der Diphtherie-Immunitdt
und der Tetanus-Immunitat bei Tieren. Deutsche med. Wchnschr.,
Leipzig, 1890, xvi, 1113.
Behring (E. v.) & Knorr (A.}. Ueber den Immunisirungswerth und Heilwerth des Tetanus-
heilserums bei weissen Mausen. Ztschr. f. Hyg. u. Infectionskrankh.,
Leipzig, 1893, xiii, 407-426.
Bordet (/.)• Antitoxines et toxines. Ann. de VInst. Pasteur, Paris, 1903, xvii, 161-186.
Calmette (A.). Venoms: venomous animals and antivenomous serum-therapeutics. Transl.
by Ernest E. Austen. New York, 1908, W. Wood & Co. 403 p. 8°.
Contribution a I' etude du venin des serpents. Immunization des animaux
etr-traitement de Venvenimation. Ann. de VInst. Pasteur, 1894, viiit 275-
291.
Dreyer (G.) u. Madsen (T.). Ueber Immunisirung mit den Toxonen des Diphtheriegiftes.
Ztschr.f. Hyg., Leipzig, 1901, xxxvii, 25(>-267.
Ehrlich (P.}. Die Werthbemessung des Diphtherieheilserums und deren theoretische Grund-
lagen. Klin. Jahrb., Jena, 1897, vi, 299-S26.
Heller (0.) & Krumbein (F.). Die Immunisierung grosserer Tiere und die Serumgewin-
nung. In: Handb. d. pathogen. Mikroorg. (Kolle & Wassermann.)
2. Aufl. Jena, 1913, in, 1157-1168. •
Marie (A.) et Tiffeneau (M.). Etude de quelques modes de neutralization des toxines bac-
terienn-es. Ann. de VInst. Pasteur, Paris, 1908, xxii, 289-299; 644-657.
Morgenroth (/.)• Ueber die Wiedergewinnung von Toxin aus seiner Antitoxinverbindung.
Berl. klin. Wchnschr., 1905, xlii, 1550-1554.
Oppenheimer (C.). Toxines and antitoxines. Transl. from the German by C. Ainsworth-
Mitchell. London, 1906. 12°.
Rosenau (M. J.). The immunity unit for standardizing diphtheria toxin (based on Ehrlich? 's
normal serum). Official standard prepared under the Act approved July
1,1902, Washington, 1905. Gov't Print. Office. 92 p. 8°. Forms Bull.
No. 21 of: Treas. Dept. Hyg. Lab., U.S. Pub. Health & Mar. Hosp.Serv.
v. Wassermann (A.) & Wassermann (M.). Antitoxische Sera. In: Handb. d. pathogen.
Mikroorg. (Kolle & Wassermann.) 2. Aufl. Jena, 1913, U, 1, 242-295.
Zinsser (H.). Toxin and antitoxin. In: Infection and Resistance (H. Zinsser}. New
York, 1914. 104-133.
iv. Bacteriolysins and Hemolysins
Serum containing b act erioly sins make the corresponding bacteria
granular and dissolve them. Bacteriolysins have been especially studied
in cholera, in typhoid, and in plague. In bacteriolysis, two distinct inter-
acting substances are concerned. One is thermostable and specific — the
amboceptor or immune body; the other is thermolabile and non-specific —
the complement.
GENERAL FACTS REGARDING INFECTION
113
Amboceptors are non-
dialysable, and may be
kept for years. Comple-
ment is present in normal
blood and degenerates rap-
idly in vitro. There are
several varieties of comple-
ment, and their hapto-
hore groups differ in their
affinities. The comple-
ments possess, besides the
Etaptophore group, func-
tional or aymophore groups.
The latter can be rendered
inactive without injury t(J
the haptophore group (for-
mation of complementoid).
Hemolysins are similar
in structure to bacterioly-
sins, and for hemolysis to
occur three substances, (1)
complement, (2) specific
hemolytic amboceptor, and
(3) red corpuscles must be
present. When red cor-
puscles are mixed with a
fresh serum containing
specific hemolysins, the
blood is laked, that is, the
hemoglobin is dissolved
out of the red corpuscles
and diffused through the
medium.
Normal serum has
some hemolytic effect up-
on the red blood corpus-
cles of a different species
{natural Jiemolysis), but
these hemolytic properties
of the serum of an animal
can be greatly increased if
the animal be subjected to
repeated injections of
washed corpuscles of a for-
114
DIAGNOSIS OF INFECTIOUS DISEASES
eign species (artificial hemolysis). If, for example, a rabbit be subjected
to a series of injections with sheep's red corpuscles, the serum of the rabbit
will quickly hemolyse washed sheep corpuscles in a test tube. These arti-
ficially produced hemolysins are highly specific in their action.
Such a hemolytic serum heated for 30 minutes at 56° C. ceases to be
hemolytic owing to destruction of complement, but when to such a serum,
thus rendered inactive, a little normal serum (not hemolytic in itself) is
added, its hemolytic power is restored, the reactivation being due to the
addition of new complement to the thermostable amboceptor.
In terms of Ehrlich's theory, the hemolytic amboceptor possesses two
haptophore groups, one with a strong avidity for red corpuscles (cytophil
group), and a second for union (with less avidity) with complement (cora-
plementophil group). The cytophil group unites with red corpuscles, even
at low temperatures. For union of the complementophil group with com-
plement, a higher temperature is necessary. The amboceptor alone cannot
hemolyze nor can complement alone; it is the complement that hemo-
lyzes, by acting through the amboceptor ; in other words, the function of
the amboceptor is to act as a medium, connecting the complement with the
red corpuscle. The complement itself here, as in the bacteriolysin, pos-
sesses not only the haptophore group for the union with the amboceptor, but
also a zymotoxic, or ergophore, group
that causes the laking. On heating
to 60° C., the zymotroxic group of the
complement is destroyed, but the hap-
tophore group is uninjured, and can
unite with the complementophil group
of the amboceptor, the complement in
this case having been changed to com-
plementoid. There must be a certain
amount of salt in the fluid in order
that the complement may act. If the
serum be freed from salt by dialysis,
the complement is split into two parts,
one part remmaining in solution., the
other being precipitated. Complement
Corpuscle, (e) Cytophil Group of the itself must therefore have a very com-
Amboceptor, (f) Complementophil -,. . -.
plicated structure.
The researches of Preston Kyes in-
dicate that in hemolytic snake venoms,
lecithin can act as complement.
Recent studies indicate that extracts of certain organs exert a hemo-
lytic effect (organ hemolysis) , not unlike cobra venom hemolysis. This
organ hemolysis appears to depend upon the lipoids in the extract. The
theory has been aolvanced that some of the severe anemias depend upon
Fig. 42.— Schematic Representation of
the Process of Hemolysis, (a) Blood
Corpuscles, (b) Amboceptor, (c) Com-
plement, (d) Receptor of the Blood
Group of the Amboceptor, (g) Hapto-
phore Group of the Complement, (h)
Toxophore (Ergophore) Group of the
Complement. (After DieudonnS.)
GENEKAL FACTS KEGAKDING INFECTION 115
the hemolytic action of such organ lipoids, especially since ethereal
extracts of the dibothriocephalus tape-worm act hemolytically.
According to Bordet, whose views are upheld in this country especially
by F. P. Gay, the process of hemolysis is somewhat different from that
assumed by Ehrlich. Instead of the term amboceptor, Bordet uses the
term substance sensibilatrice, and instead of complement, the term alexin.
According to Bordet, the red corpuscles are injured (sensibilized) by the
substance sensibilatrice, after which the alexin causes laking.
The amboceptor has received various other names (e. g., preparator of
Gruber; fixaieur of Metchniko/f).
The hemolysins which act upon the red corpuscles of a different species
are known as heterolysins. The blood of certain human beings contains
hemolysins that act upon the red corpuscles of other human beings ; that
is, upon the cells of an animal of the same species. Such isolysins (or iso-
hemolysins) may be of considerable importance when blood transfusion is
contemplated for therapeutic purposes. W. L. Moss has worked out
methods for securing human blood which will not act hemolytically on
transfusion (see Diagnosis of Diseases of the Blood).
Hemolysins can themselves act as antigens, and, on injection, give rise
to antihemolysins, which inhibit the hemolytic effect of a serum (produc-
tion of anticomplement, or of anti-amboceptor, or of both).
Complement Deviation. — In studying bacteriolysis, or hemolysis, the
quantitative relations of amboceptor and of complement must be consid-
ered. If, in test tube experiments, the amount of bacteriolytic amboceptor
be greatly increased, while the complement remains unchanged in amount,
there will be no bacteriolysis (Neisser-WecJisberg phenomenon). Here,
probably, the combining power of the bacteria with amboceptors is more
than satisfied, and free amboceptors remain in the surrounding fluid. If
the complement be limited in amount, it will be distributed among the
amboceptors attached to the bacteria 'and the free amboceptors ; thus a part
of the complement will .be deflected (deviated) from the bacteria, and,
with certain quantitative relations, the complement going to the attached
amboceptors will be insufficient to cause bacteriolysis. It is possible that
the attached amboceptors are less avid for complement than the free ambo-
ceptors.
Fixed Complement. — As described above, hemolysis depends upon (1)
red blood corpuscles, (2) specific amboceptors (inactive immune serum),
and (3) complement (fresh normal serum). Similarly, three constitu-
ents (bacteria, specific amboceptor, complement) are necessary for bacteri-
olysis. The complement can be the same in the two processes ; the ambo-
ceptors are different. If one takes, for example, the serum of an animal
immunized against the cholera vibrio, inactivates it by heat, adds cholera
vibrios and complement and allows the mixture to stand for one hour at
body temperature, the bacteriolytic amboceptors and the complement will
116 DIAGNOSIS OF INFECTIOUS DISEASES
be anchored to the bacteria. If to this mixture we next add a hemolytic
system consisting of red corpuscles anchored to hemolytic amboceptors
without complement, no hemolysis will occur ; the blood is not laked
because the complement has been all used up; it has been "bound" or
"fixed."
In another experiment, cholera vibrios are mixed with the inactive
serum of an animal immunized against typhoid ; complement is added, and
the mixture kept for an hour in the thermostat at 37° C. Here specific
bacteriolytic amboceptors for cholera vibrios are absent and the comple-
Fig. 43.— Schematic Representation of Complement Fixation and Hemolysis', (a and b)
Immune Serum, (c) Receptor of the Blood Corpusrli — Hemolytic System, (d) Ambo-
ceptor — Hemolytic System, (e) Complement — Hemolytic System, (f) Antigen Bacillus,
Blood Corpuscle. (After Dieudonn£.)
ment will not be fixed. Now, if a hemolytic system be added (red cor-
puscles, plus specific hemolytic amboceptors), hemolysis will promptly
occur, for the complement is free, and, uniting with the hemolytic ambo-
ceptors, will act through them upon the red corpuscles and will lake the
blood.
Here we have a principle of great help in diagnosis, for, by testing for
complement fixation, we can decide whether or not a serum contains spe-
cific amboceptors for a known bacterium. If the serum examined contain
the specific amboceptor for the known antigen (Bacterium), there will be
no hemolysis when the red corpuscles and hemolytic serum are added. If
it do not contain these amboceptors, hemolysis will occur. The process of
complement fixation is often called the Bordet-Gengou phenomenon. It is>
clinically, especially important in the diagnosis of syphilis (Wassermann
test, q. v.) and of helminthiasis, especially tenia and echinococcus.
References
Belfanti (S.) & Carbone (T.). Produzione di sostanze tossiche net siero di animali inocu-
lati con sangue eierogeneo. Gior. d. r. Accad. di med. di Torino, 1898, 4 *••
Bo time (A.). Opsonine und Vdkzinationstherapie. Ergebn. d. inn. Med. u. Kinderh..
Berlin, 1913, xii, 1-142.
GENEKAL FACTS KEGAEDING INFECTION 117
Bohme (A.}. Bakteriolytische Sera. In: Handb. d. Techn. u. Methodik d. Immunitdts-
forsch. (Kraus u. Levaditi.} Jena, 1909, ii, 366-462.
Bordet (J.) & Gay (F. P.}. Sur les relations des sensibilisalrices avec Vakxine. Ann. d.
I'Inst. Pasteur, Par., 1906, xx, 467-498.
Sur I' agglutination et la dissolution des globules rouges par le serum d'ani-
maux injectes de sang defibrine. Ann. de I'Inst. Pasteur, Paris, 1898, xii,
688-695.
Les proprietes des antisensibilisatrices et les theories chimiques de I'immunite.
Ann. de I'Inst. Pasteur, Paris, 1904, xviii, 593-632.
Brand (E.). Ueber das Verhalten der Komplemente bei der Dialyse. Berl. klin. Wchnschr.,
1907, xxiv, 1075-1079.
v. Dungern (E.} & Coca (A. F.). Ueber Hamolyse durch Schlangengift. Munchen. med.
Wchnschr., 1907, xlvii, 2317-2321.
Ehrlich (P.) & Morgenroth (/.)• Zur Theorie der Lysinwirkung. Berl. klin. Wchnschr.,
1899, xxxvi, 6-9.
Ueber Haemolysine. Berl. klin. Wchnschr., 1899, xxxvi, 481-486.
Ueber Haemolysine. Berl. klin. Wchnschr., 1900, xxxvii, 453-458.
Ehrlich (P.) & Sachs (H.). Ueber den Mechanismus der Amboceptorenwirkung. Berl.
klin. Wchnschr., 1902, xxxix, 492-496.
Ueber den Mechanismus der Antiamboceptorwirkung. Berl. klin. Wchnschr.
1905, xlii, 557; 609.
Ehrlich (P.) & Marshall (H. T.}. Ueber die compleme.ntophilen Gruppen der Ambocep-
toren. Berl. klin. Wchnschr., 1902, xxxix, 585-587.
f errata (A.). Die Univirksamkeit der komplexen Hdmolysine in salzfreien Losungen
und ihre Ursache. Berl. klin. Wchnschr., 1907, xiii, 366-368.
Flexner (5.) & Noguchi (H.}. Snake venom in relation to haemolysis, bacteriolysis and
toxicity. Univ. Penna. Med. Bull., Philadelphia, 1902, xiv, 438-448;
also, J. Exper. Med., Lancaster, 1902, vi, 277-301.
Ford (W. W.}. On the presence of hemolytic substances in edible fungi. J. Infect. Dis.,
Chicago, 1907, iv, 434~439.
Friedberger (E.). Die bakteriziden Sera. In: Handb. d. pathogen. Mikroorg. (Kolle &
Wassermann.) 2. Aufl. Jena, 1913, ii, 1, 296-400.
Gay (F. P.)- The Hxation of alexines by specific serum precipitates. Centralbl. f. Bakteriol.,
1905, Orig. xxxix, 603-610.
Genffou (O.)« Sur les, sensibilisatrices des scrums actifs contre les substances albuminoides,
Ann. de VInst. Pasteur, Paris, 1902, xvi, 735-755.
Hektoen (L.) & Ruediger (G. F.). The antilytic action of salt solutions and other sub-
stances. J. Infect. Dis., Chicago, 1904, i, 379-403.
v. Kanffl-Lenz (E.}. Ueber sogenannte kiinstliche Komplemente. Biochem.Ztschr., Berlin,
1909, xx, 1-9.
Kyes (P.). Venom hemolysis. J. Infect. Dis., Chicago, 1910, Hi, 181-284-
Kues (P.) & Sachs (H.~). Zur Kenntniss der Cobragift activirenden Substanzen. Berl. klin.
Wchnschr., 1902, ii, 20-23; also, iv, 57-60.
Landsteiner (K.}. Zur Kenntnis der specifisch auf Blutkorperchen wirkenden Sera. Cen-
tralbl. f. Bakteriol. (etc.], Jena, 1899, xxv, 546-549.
Hdmagglutinalion und Hamolyse. In: Handb. d. Biochem. (Gppen-
-heimer.) Jena, 1910, ii, 1. Hlfte, 395-541.
Liefmann (H.) & Cohn (M.)« Die Wirkung des Komplementes auf die ambozeptorbela-
denen Blutzellen. Ztschr. f. Immunitatsforsch. u. exper. Therap., Jena,
1910, Orig., vii, 669; viii, 58.
Long cope (W. T.}. Study of the bacteriolytic serum-complements in diseases; a contribution
to our knowledge of terminal and other infections. Univ. of Penna. Med.
Bull, 1903, xv, 331-344; also: J. Hyg., Cambridge, 1903, Hi, 28-51.
Manwaring (W. H.). On the so-called physical chemistry of hemolytic serum. J.
Infect. Dis., Chicago, 1907, iv, '
118 DIAGNOSIS OF INFECTIOUS DISEASES
Marshall (H. T.}. Studies in hcemolysis, with special reference to the properties of the blood and
body-fluids of human beings. J. Exper. M., New York, 1901-5, vi, 347-375.
Morgenroth (/.) & Sachs (H.). Ueber die quantitativen Beziehungen von Amboceptor,
Complement und Anticomplement. Berl. klin. Wchnschr., 1902, xxxix,
Muir (JR.) & Browning (C. //.). On the filtration of serum complement. J. Pathol. &
Bacteriol., Cambridge, 1908-09, xiii, 232-238.
Noguchi (H.). The thermostabile anticomplementary constituents of the blood. J. Exper.
Med., New York, 1906, viii, 726-749.
Ueber die chemische Inaktivierung und Regeneration der Konplemente.
Biochem. Ztschr., Berlin, 1907, vi, 172-184.
Nolf (/*•)• De Vorigine du complement hemolytique et de la nature de Vhemolyse par les
serums. Acad. roy. de Beige. Bull, de la cl. d. sc. Brux., 1908, 748-772.
Quinan (C.). Ueber speciflsche Erythrolyse. Beitr. z. chem. Physiol. u. Path., Brnschwg.,
1904, v, 95-109.
Husk (G. Y.). The effect of benzol inloxica'.ion and consequent leucopenia on the formation
of artificial hemolysins and precipitins. Univ. of Cal. Publications in
Pathology, Berkeley, 1914, ii, 139-145.
Walker (E. W. A.). Immunization against immune serum. J. Pathol. & Bacteriol., Edin-
burgh & London, 1903, viii, 34-51.
Zinsser (H.). Development of our knowledge concerning complement or alexin. In: In-
fection and Resistance (H. Zinsser). New York, 1914. 168-197.
Zinsser (H.) & Johnson (W. C.). On heat-sensitive anticomplementary bodies in human
blood serum. J. Exper. Med., New York, 1911, xiii, 31-42.
v. Opsonins
As has been stated, certain substances in the serum, which render bac-
teria susceptible to phagocytosis, are called opsonins (Wright and Doug-
las), or bacteriotropins (Neufeld-). Those occurring in normal blood
{normal opsonins) are probably entirely different from those occurring
in the blood of immunized animals (immune opsonins; bacteriotropins).
The immune opsonins are, according to Neufeld, thermolabile (consisting
'of complement and another body, • the latter thermostable) and do not
require complement for their activity. ' These substances have been
studied in America especially by Hektoen, Ruediger, Cole, and Ross.
The methods of studying opsonins, \ve owe especially to Wright and
Douglas. Clinically, Wright bases his method of treatment of infections
with vaccines made from the infecting bacteria, upon a determination of
the opsonic index (q. v.), which he uses as a guide for the injections.
References
Adami (J. G.). Inflammation. An introduction to the study of pathology, being the reprint
(revised and enlarged} of an article in Prof. Allbutt's System of Medicine.
London, 1909, MacMillan Co., Ltd. 272 p. 8°.
Bullock (W.} & Western (G. T.). The specificity of the opsonic substances in the blood.
Proc. Roy. Soc., London, 1905^06, S. B., Ixxvii, 531-536.
Cowie (D. M.} & Chapin (W. S.}. On the reactivation of heated normal human opsonic
serum with fresh diluted serum: A contribution to the study of the structure
of opsonins. J. M. Research, Boston, 1907-08, xvii, 57-75.
Experiments in favor of the amboceptor-complement structure of the opsonin
of normal human serum for the staphylococcus albus. J. M. Research,
Boston, 1907-08, xvii, 95-117.
GENERAL FACTS REGARDING INFECTION 119
Cowie (D. M.) & Chapin (W. S.). The separation of opsonic amboceptor and complement
in the cold. J. M. Research, Boston, 1907-08, xvii, 213-217.
Denys (J.) et Leclef (/.)• $wr ^ mecanisme de I'immunite chez le lapin vaccine contre le
streptocoque pyogene. Cellule, Lierre & Louvain, 1895-05, xi, 175-221.
Denys (/.) et Van der Velde (H.). Sur la production d'une antileucocidine chez les lapins
vaccines contre le staphylocoque pyogene. Cellule, Lierre et Louvain, 1895-
96, xi, 357-372.
von Gruber (M.}. Ueber Opsonine. Centralbl. f. Bakteriol. (etc.), Beil. zu 1. Abt.,Jena,
1909, xliv, 2-14.
Hektoen (//.)• On the specificity of opsonins in normal serum. J. Infect. Dis., Chicago,
1908, v, 249-262.
On the mechanism of opsonic action. J. Infect. Dis., Chicago, 1909, vi,
66-67.
Opsonins distinct from other antibodies. J. Infect. Dis., Chicago, 1909,
vi, 78-89.
Variations in the phagocytic and other powers of leucocytes. J. Am. M.
Ass., Chicago, 1911, Mi, 1579-1582.
Hiss (P.) & Zinsser (H.}. Experimental and clinical studies on the curative action of leuco-
cyte extracts in infections. J. M. Research, Boston, 1908, n. s., xiv, 323—
469.
Marchand (Z/.). Elude sur la phagocytose des streplocoques attenues et virulents. Arch, de
med. exper. et d'anat. path., Paris, 1898, x, 253-294. 2 pi.
Michaelis (G.). Grundlagen und Technik der experimentellen spezifischen Bakteriotherapie
(Opsonine). In: Handb. d. pathogen. Mikroorg. (Kolle & Wassermann.)
2. Aufl. Jena, 1913, Hi, 143-166.
Neufeld (F.). Bakteriotropine und Opsonine. In: Handb. d. pathogen. Mikroorg. (Kolle
& Wassermann.) 2. Aufl. Jena, 1913, ii, 1, 401-482.
Neufeld (F.) & Ungermann (E.). Technik und Methodik der Tropinuntersuchung .
Handb. d. Techn. u. Methodik d. Immunitatsforsch. Jena, 1911,Ergnzngsb.
i, 117-143.
Opie (E. L.}. Opsonins of inflammatory exudates. J. Exper. M., Lancaster, Pa., 1907, ix,
515-519.
Riesman (D.). The cellular factor in infectious diseases. J. Am. M. Ass., Chicago, 1915,
lxi:>, 649-652.
Rosenow (E. C.). Human pneumococcal opsonin and the antiopsonic substance in virulent
pneumococci. J. Infect. Dis., Chicago, 1907, iv, 285-296.
Simon (C. E.). The percentage index versus the badllary index in the estimation of the
opsonins. J. Am. M. Ass., Chicago, 1907, xlviii, 139-140.
Tunnicliff (/£.)• On the variations in the phagocytic and coccidal power of the blood in pneu-
monia and scarlet fever. J. Infect. Dis., Chicago, 1911, viii, 302-315.
Wright (Sir A. E.}. Studies on immunization and their application to the diagnosis and
treatment of bacterial infections. New York, 1910, W. Wood & Co. 490 p.
1 ch. 8°.
Zinsser (H.). Phagocytosis. In: Infection and Resistance (H. Zinsser}. New York,
1914. 272-357.
Zinsser (H.) & Cary (E. (7.). On the nature of the opsonic substances of normal sera.
J. Exper. M., Lancaster, Pa., 1914, xix, 345-361.
vi. Precipitins
These are antibodies that precipitate, specifically, protein sub-
stances from solution. The protein injected as an antigen is known as a
precipitinogen. Through the immunizing process, precipitins are formed,
which, when added again to a solution of the original protein (precipitino-
120 DIAGNOSIS OF INFECTIOUS DISEASES
gen or precipitable substance) cause a precipitate to form. Ordinary pro-
tein precipitins are to be distinguished from bacterioprotein precipitins.
The latter were discovered by R. Kraus in 1897, the former by Bordet
and Tschistowitsch.
Ordinary Protein Precipitins. — The serum of an animal immunized
against alien serum will cause precipitates in the alien serum when mixed
with it. The principle is of great value in forensic medicine for differen-
tiating the proteins of human, from those of animal, blood (Uhlenhuth).
Nuttall has applied the principle most extensively in studying the biolog-
ical relationships of animals.
Precipitins contain two groups, a more stable haptophore group, which
unites with precipitinogen, and a more labile functional group, which
causes the precipitation (Kraus and von Pirquet).
The biological test by means of precipitins is much more delicate than
any known chemical test. Solutions of protein 1-100,000 are recognizable
by the use of this method.
Bacterioprotein Precipitins. — Filtrates of old bacterial cultures yield
precipitates with corresponding immune sera. The reaction is specific.
References
Chickering (H. T.). The concentration of the protective bodies in antipneumococcus serum;
specific precipitate extracts. J.Exper. M., Lancaster, Pa., 1915, xxii, 248—
268.
Dold (H.). Die Prdziptine und die Methoden der Prazipitation. Handb. d. Biochem.
Arbeitsm. (Abderhalden) , Berlin, 1913, vii, 588-586.
Hektoen (L.). On rapid production of specific precipitins. Tr. Chicago Path. Soc.,
1913, ix, 55-56.
Klein (H.}. The opsonins in typhoid immunity. J. H. Hosp. Bull., Baltimore, 1907,
xviii, 245-252.
Kraus (R.). Prazipitine (Bakterienprdzipitine) . In: Handb. d. pathogen. Mikroorg.
(Kolle & Wassermann.) 2. Aufl. Jena, 1913, ii, 1, 732-792.
Ueber spezifische Reactionen in kcimfreien Filtraten aus Cholera, Typhus
und Pestbouillonculturen, erzeugt durch homologes Serum. Wien. klin.
Wchnschr., 1897, x, 786-738.
Kraus (jR.) & v. Pirquet (Cl.). Weitere Untersuchungen uber spezifische Niederschlage.
' Centralbl. f. BakterioL, Jena, 1902, xxxii, 60-74.
Michaelis (£.)• Die Prazipitine. In: Handb. d. Biochem. (Oppenheimer) . Jena, 1910,
ii, 1. Hlfte, 552-591.
Norris (C.). The bacterial precipiMns. J. Infect. Dis., Chicago, 1904, i, 463-515.
Uhlenhuth (P.} & Weidanz (O.). Praktische Anleitung zur Ausfiihrung des biologischen
Eiweissdifferenzierungsverfahrens, mit besonderer Berucksichtigung der
forensischen Blut- und Fleischuntersuchung sowie der Gcwinnung prazipi-
tierenden Sera. Jena, 1909, G. Fischer. 252 p. 8°.
Zinsser (H.}. Further studies on the identity of precipitins and protein sens-itizers (albumino-
lysins}. J. Exper. M., New York, 1913, xviii, 219-227.
The phenomena of precipitation. In: Infection and Resistance (H. Zinsser).
New York, 1914.
Zinsser (H.) u. Ostenberg (Z.). Observations on precipitin formation by boiled proteins.
Proc. N. Y. PathoL Soc., 1914, xiv, 78-81.
GENERAL EACTS REGARDING INFECTION 121
vii. Agglutinins
These antibodies, discovered by Gruber and Durham, cause a clump-
ing, or agglutination, of bacteria (bacterio-agglutinins) or of red blood
corpuscles (hemagglutinins) .
Normal serum contains agglutinins, which act upon the most different
kinds of bacteria, if the serum be not markedly diluted (1:10 to 1:20).
These agglutinins are not specific. The serum of a patient or of an animal
immune to a given disease (like typhoid or cholera) from having had the
disease naturally or from artificial immunization, agglutinates the corre-
sponding bacterium in strong dilution (1:100 to 1:5,000, etc.). Such
agglutinins are specific, and are therefore useful for diagnostic purposes
(cf. Widal reaction). Bacteria, if motile, lose their motility when agglu-
tinated, but are not necessarily killed ; they will continue to grow, though
often in the form of long interlaced threads (thread reaction).
Agglutinins are thermostable at 55° to 60° C., but are destroyed at
70° C.
Agglutinins contain two groups, (1) a haptophore group, which unites with
the bacteria, and (2) a functional, or agglutinophore, group, which causes the
agglutination. The latter is the more sensitive, and, when injured without injury
to the haptophore group, the agglutinins are converted into agglutinoids, which
can unite with bacteria without agglutinating them.
An immune serum may agglutinate other bacteria than the homolo-
gous bacterium, if they be closely related to it. Such group agglutination
is met with especially in the typhoid-paratyphoid-colon group. In mixed
infections, a serum may contain "immune" or "major" agglutinins for
both infecting microbes (mixed agglutination).
The saturation experiment of Castellani is used to distinguish between
group agglutination and mixed agglutination. If the serum of a patient
agglutinate typhoid bacteria in great dilution, and paratyphoid bacteria in
almost as great dilution, a portion of serum is mixed with small amounts
of a typhoid culture, allowed to stand for a time, and then centrifugalized.
Should the serum subsequently continue to agglutinate paratyphoid bacilli,
a mixed infection is assumed (mixed agglutination) ; otherwise a group
agglutination is diagnosed.
Injection of red corpuscles of one species into an animal of another
species causes hem agglutinins to appear in the serum ; the immune serum
will clump the red corpuscles bf the animal-species the corpuscles of which
have been used as antigen. Besides these hetero-agglutinins, hemagglutinins
against blood corpuscles of an animal of the same species can be prepared
(iso-agglutinins). As yet they have little, if any, diagnostic importance.
References
Austin (ft. S.} & Frothingham (C., Jr.). A study of human and animal typhoid ag-
Qlutinins. Arch. Int. Med.. Chicago. 1910, vi, 677-689.
122 DIAGNOSIS OF INFECTIOUS DISEASES
Bass (C. C.) & Watkins (J. A.}. A quick macroscopic typhoid agglutination test. Arch.
Int. Med., Chicago, 1910, vi, 717-728.
Bordet (/.)• Le mecanisme de V agglutination. Ann. de VInst. Pasteur, Paris, 1899, xiii,
225-250.
Castellani (A.}. Agglutination bei gemischter Infektion. Ztschr. f. Hyg. u. Infektionskrankh.
Leipzig, 1902, xl, 1-20.
Christian (H. A.}. The cause of a positive agglutination reaction in icterus. Bost. M. &
S. J., 1907, clvi, 536-539.
Cole (R. /.)• Ueber die Agglutination verschiedener Typhusstamme. Ztschr. f. Hyg. u.
Infectionskrankh. Leipzig, 1904, xlvi, 367-370.
Eisenberg (P.) M. Volk (R.}. Untersuchungen uber die Agglutination. Ztschr. f. Hyg.,
1902, xl, 154-195.
Friedberger (E.) . Ueber die Bedeutung unorganischer Salze und einiger organischen krystal-
loider Substanzen fur die Agglutination der Bakterien. Centralbl. f. Bak-
teriol, Jena, 1901, xxx, 336-346.
Gruber (M.} & Durham. Eine neue Methode zur raschen Erkennung des Cholera-
vibrios und des Typhus bacillus. Munch, med. Wchnschr., 1896, xliii,
285-286.
Joos (A.}. Untersuchungen uber die verschiedenen Agglutinine des Typhusserums. Ccn-
tralbl. f. Bakteriol. (etc.), I. Abt., Jena, 1903, xxxiii, Orig., 762-783.
Landsteiner (K.) & von Eisler (M.). Ueber Agglutinin- und Lysinwirkung. Centralbl,
f. Bakteriol. (etc.), I. Abt., Jena, 1905, xxxix, Orig., 309-319.
Miiller (P. T.). Bakterien- Agglutinine und -Prazipiline. In: Handb. d.Biochem. (Oppen-
heimer). Jena, 1910, U, 1. Hlfte, 592-628.
Smith (T.) & Reagh (A. L.). The agglutination affinities of related bacteria parasitic in
different hosts. J. Med. Research, Boston, 1903, ix, 270-300.
Paltauf (U.)« Die Agglutination. In: Handb. d. pathogen. Mikroorg. (Kolle & Wasser-
mann.) Jena, 1904, iv, pt. i, 645-783.
Die Agglutination. In: Handb. d. pathogen Mikroorg. (Kolle & Wasser-
mann.) 2. Aufi. Jena, 1913, ii, 1, 483-654.
Park (W. H.) & Collins (K. R.}. Specific and non-specific or group agglutinins. J.
Med. Research, Boston, 1904, xii, 491-507.
Widal (F.). Reaction agglutinante pendant lafiebre typhoide. Semaine med., Paris, 1897,
xvii, 184.
Zinsser (//.)• The phenomenon of agglutination. In: Infection and Resistance (H. Zins-
ser). New York, 1914. 218-247.
viii. Antiferments
Similar to other antibodies are antiferments. They have been prepared against
the lab-ferment, against trypsin, and against pepsin. (See Examination of the
Blood.)
References
Michaelis (L.). Antifermente. In: Handb. d. Biochem, (Oppenheimer) . Jena, 1910, ii,
1. Hlfte, 707-715.
Morgenroth (/.)• Ueber den Antikorper des Labenzyms. Centralbl. f. Bakteriol., 1899 ,
xxvi, 349-359.
(d) Anaphylaxis; Hyper susceptibility; Allergy
i. History and Definition
Studies on immunity have been directed chiefly to the explanation of the pro-
tection afforded by preceding infection. Since 1902, attention has been directed
toward a contrasting group of phenomena described under different names —
anaphylaxis (Richet), hypersusceptibility (Wolff -Eisner), or allergy (von Pir-
GEKEBAL FACTS REGARDING INFECTION 123
quet). The fundamental observations on which later knowledge of anaphylaxis
is based were made by Hericourt and Richet (1898), when they noted that repeated
injections of eel-serum into dogs causes increased susceptibility to that substance.
Later, Richet (1902) found that if a dog be injected with a poison derived from
the sea-urchin, and several days later be given a second injection, the second dose
need be only £ or ^ as large as the first dose to produce severe or lethal symptoms.
If the animal lives, he recovers more quickly than after the first injection.
Richet therefore assumed that the poison consists partly of an immunizing or
prophylactic principle and partly of a sensitizing or anaphylactic principle. This
was the first sharp separation of the conception of anaphylaxis from that of
immunity. Soon after the appearance of Richet's publications, Arthus confirmed
his observations. Arthus noted that rabbits injected with horse serum become
exquisitely sensitive to a second injection given after an interval of 7 days.
A little later, von Pirquet observed that, on giving a second injection of horse
serum to a child, the symptoms of serum disease did not appear on the 10th day,
as after the first injection, but within 24 hours, from which he drew the conclusion
that, in infections, the disease-exciting agent gives rise to pathological symptoms
only after it is altered by antibodies, and that the incubation period is the
time elapsing before the formation of antibodies. Later, in collaboration with
Schick, the difference between accelerated and immediate capacity for reaction
was recognized by von Pirquet and the diagnostic significance of the latter pointed
out. These authors came to the conclusion that the antibodies produced convert
the foreign body injected (innocuous in itself) into a toxic modification.
In 1902, Theobald Smith had noticed that guinea-pigs used for testing diph-
theria toxin, and for that purpose injected with toxin-antitoxin mixtures, often
died if, after a short interval, they were given a small amount of horse serum by
subcutaneous injection. Otto confirmed and elaborated these findings.
Rosenau and Anderson, in an attempt to explain sudden deaths after treat-
ment by diphtheria antitoxin, made an exact study of the effect of horse serum,
and of other substances, upon guinea-pigs.
In 1904, the subject was taken up by Wolff-Eisner, who introduced the term
hypersusceptibility, and suggested that hay fever and urticaria are to be explained
on this principle.
In 1906, von Pirquet suggested the expression allergy, or clinical alteration
of reaction capacity, as a name for the phenomena formerly included under the
terms anaphylaxis and hypersusceptibility. In America, important contributions
to the subject have been made by Auer and Lewis/ Gay and Southard, Adler,
Pearce, Helmholz, P. W. Clough, Lucas, E. L. Trudeau, V. C. Vaughan, H. G.
Wells, H. Zinsser and C. R. Austrian, besides those already mentioned.
In studies of vaccination and re-vaccination, it has been shown that the change
in the reaction capacity of the body (allergy) is easily elicited by successive vac-
cinations of the skin with cow-pox. The reaction capacity is changed as regards
its time-relations, both qualitatively and quantitatively. On a first vaccination, the
inflammation reaches its mayimum about the llth day. On repeated vaccinations, it
may appear op the Oth to the 4th day after the vaccination (accelerated reaction).
In the allergy following injection of foreign serum, similar temporal changes
in reaction capacity are met with. The normal "serum disease" appears about the
9th day. If more serum of the same sort be injected after an interval of several
months or years, the symptoms of serum disease appear in from 4 to 7 days (accel-
erated reaction). If the second injection be made intravenously at a certain inter-
val after the first, symptoms appear very quickly (immediate reaction).
Besides these temporal changes in reaction capacity, quantitative and qualita-
tive changes are demonstrable.
124
DIAGNOSIS OF INFECTIOUS DISEASES
Davs
'Horse-serum
First injection
Second injection
!Suppos«d 'Immediate anapbylactic
\JSSS* Ycattior>
Fig. 44. — Eftects of Horse-serum in Man. (After C. E. von Pirquet, Arch. Int. Med.>
Any soluble foreign protein (of animal, of vegetable, or of chemical' source)
may act as a sensitizing substance if it reach the blood or lymph in its native or
unaltered state, uncleft. Exceedingly minute quantities suffice to induce sensitiza-
tion. H. G. Wells showed that 0.000.000.05 g. of crystallized egg albumen can
make a guinea-pig sensitive. Ordinarily, 0.1 to 1.0 c.c. of a foreign serum will
so sensitize a guinea-pig that a second injection given intravenously will cause
anaphylactic death.
Sensitization may occur in ways other than by injection. It may be inherited.
It may sometimes be established by feeding a foreign protein. It may occur after
Horse*
serum
/!second\
llnjection
reaction
read ion
Sefum disease
Fig. 45.
Double Reaction after Reinjection of Horse-serum in Man.
Arch. Int. Med.)
(After C. E. von Pirquet,
GEKEKAL FACTS KEGAKDING INFECTION
125
instillation of serum into the conjunctiva, or after inhalation of serum. Guinea-
pigs can be sensitized by inunction of horse-serum-lanolin salve (Clough), or by
vaginal irrigation, or rectal enema. We begin, through such studies, to understand
the origin of the so-called 'idiosyncrasies of man. It is to be kept in mind that
these sensitizations are very specific; thus the organ-proteins of an animal are
different from the serum-proteins of the same animal.
The blood of an animal which has been sensitized to a protein sub-
stance (active anaphylaxis) may, when injected into another animal, lead
to a transference of the allergy to the second animal (passive allergy;
passive anaphylaxis). Anaphylaxis can also be passively transferred from
mother to young. *
Under certain circumstances an allergic condition can be suppressed
(anergy; ant ianaphy laxis ) .
Reference
Doerr (/?.)• Allergie und Anaphylaxie. In: Handb. d. pathogen. Mikroorg. (Kolle &
Wassermann). 2. Aufl. Jena, 1913, ii, 2, 947-1154.
ii. Characters of Allergy, and Symptoms of Anaphylactic Reaction
The three main characteristics of the allergic change are (1) short-
ened incubation period, (2) accelerated course of the phenomena of reac-
tion, and (3) accentuation of the symptoms of reaction. In the typical
acute anaphylactic shock, such as follows injection of serum into a sensi-
tized guinea-pig, there is
restlessness, cough, sud-
den severe dyspnea, soon
followed by clonic
spasms, and by death
within a few minutes.
In milder shock, the
dyspnea is transitory,
the animal recovers
quickly, and, in a few
hours, may seem normal
again. When such an
animal recovers after
re-injection, it is im-
mune for a short time
to subsequent injections
of the same serum (an-
ergy; anti-anaphylaxis).
It has also been
shown that death from
anaphylactic shock is ac-
Fig. 46. — The Large Inflated Lungs were Obtained from a
Typical Fatal Case of Horse-Serum Anaphylaxis in a
Guinea-pig. The Small Collapsed Lungs Belonged to
an Anaphylactic Guinea-pig of the Same Lot which was
Saved by the Injection of Atropin. This Animal Seemed
Normal when Killed. The Picture Shows Strikingly
the Characteristic Lung Picture of Anaphylaxis and
the Remedial Effects of Atropin. The Right Vagus had
been Resected in Each Guinea-pig Thirteen Days Before
the Toxic Injection. (After J, Auer.)
126 DIAGNOSIS OF INFECTIOUS DISEASES
companied by fall in blood pressure (dog), emphysema of the lungs from
bronchospasm (Auer and Lewis), fall of temperature (guinea-pig), and
"chemical rigor" of the myocardium (rabbit). Common to allergy in all
these varieties are (1) leukopenia, (2) loss of the coagulability of the
blood, and (3) disappearance of complement from the blood.
Phenomena of Serum Disease. — The symptoms that follow a single
injection of horse serum, the so-called serum disease (von Pirquet and
Schick), appear, after an incubation period of 8 to 12 days, in the form of
(1) urticaria, usually starting at the site of injection and extending to
other parts of the body, (2) edema, (3) arthralgias, (4) swelling of the
lymph glands, and (5) fever, with albumin and casts in the urine. The
larger the dose of serum, the more marked the symptoms in predisposed
persons.
On re-injection of a serum derived from the same animal species, the
symptoms of serum disease appear more quickly (4 to 7 days). If the
second injection be made in 3 to 8 weeks after the first, over 90 per cent
of those injected will show signs of serum disease. On re-injection after
6 to 9 months, about 50 per cent of the cases show symptoms. Sometimes
a single cubic centimeter, on re-injection, will suffice to cause symptoms.
Care should always be exercised in giving diphtheria antitoxin, inquiry
being made regarding a previous injection. Antitoxins made from ani-
mals other than the horse should be made available, and used for second
injections given after intervals longer than a week.
Clinical Conditions Due to Anaphylaxis. — High fever and urticaria ap-
pear to depend upon anaphylactic reaction to foreign proteins. The study of
bronchial asthma, and of hay fever, bids fair to be revolutionized by the
study of sensitizing "asthmogenic" substances. The tuberculin reactions
of various sorts are believed to be anaphylactic phenomena. Indeed, it
would appear that the symptomatology of all the infectious diseases must
sooner or later be re-written in terms of allergic reaction, and a start in
this direction has already been made.
References
Anderson (J. F.). Anaphylaxis and its relation to clinical medicine. Johns Hopkins
Hosp. Bull, Baltimore, 1910, xxi, 218-223.
Auer (J.). The functional analysis of anaphylaxis. In: Forchheimer's Therapeusis of inter-
nal diseases. New York & London, 1914, v, 39-120.
Auer (J.) & Lewis (P. A.). Acute anaphylactic death in guinea-pigs; its cause and possible
prevention. J. Am. M. Ass., Chicago, 1909, liii, 458-459.
Auer (J.) & Robinson (G. C.). An electro-cardiographic study of the anaphylactic rabbit.
. J. Exper. M., Lancaster, Pa., 1913, xviii, 450-460, 5 pi.
Auer (J.) & Van Slyke (D. D.}. A contribution to the relation between protein cleavage-
products and anaphylaxis. J. Exper. M., Lancaster, Pa., 1913, xvii,
210-217.
Austrian (C. R.). The production of passive hypersensitiveness to tuberculin. A pre-
liminary report. J. Exper. M., Lancaster, Pa., 1912, xv, 149-162.
GENEBAL FACTS BEGABDING INFECTION" 127
Biedl (A.) & Kraus (/£.)• Experimentelle Studien iiber Anaphylaxie. 4- Zur Charak-
teristic des anaphylaktischen Shocks. Ztschr. f. Immunitdtsforsch. u. exper.
Therap., Jena, 1910, vii, 205-222.
Coca (A. F«). The site of reaction in anaphylactic shock. Ztschr. f. Immunitdtsforsch. u.
exper. Therap., Jena, 1914, Orig., xx, 622-643.
Die Ursache des pldtzlichen Todes bei intravenoser Injektion artfremderBlut-
korper. Virchow's Arch. f. path. Anat. (etc.}, Berlin, 1909, cxcvi, 92-107,
Ipl.
Cowie (D. M.). Studies on the incubation period. I. Serum disease. Am. J. Dis. Child.,
Chicago, 1914, vii, 258-291.
Dold (#.)• Das Bakterien-Anaphylotoxin und seine Bedeutung fur die Infektion. Jena,
1913, G. Fischer. 80 p. roy. 8°.
Friedberger (/?.)• Die Anaphylaxie. Deutsche Klinik, Berlin, 1911, xiii, Ergnzngsbd.,
U, 619-726.
Die Anaphylaxie mil besonderer Beriicksichtigung ihrer Bedeutung fur
Infektion und Immunitdt. Deutsche med. Wchnschr., Leipzig u. Berlin,
1911, xxxvii, 481-487.
Friedberger (E.) & Mita (5.). Ueber Anaphylaxie. Ztschr. f. Immunildtsforsch. u. exper.
Therap., Jena, 1911, x, 216-281.
Gautier (P.). Accidents seriques graves a la suite d'une injection de serum antitetanique
onze ans apres une injection de serum antidiphterique. Rev. med. de la
Suisse Rom., Geneve, 1914, xxxiv, 114-116.
Gay (F. P.) & Southard (E. E.). On serum anaphylaxis in the guinea-pig. J. Med.
Research, Boston, 1907, xvi, 143-180, 6 pi; 1908, xviii, 407-431; 1908,
xix, 1-34.
Goodall (E. W.}. Serum rashes. In: Syst. Med. (Allbutt & Rolkston), 8°, London, 1911,
ix, 113-117.
Hericourt (J.) et Richet (Ch.). Nouvelles experiences sur le traitement de la tuberkulose
experimental. Compt. Rend. Soc. Biol, Paris, 1898, 225-230.
Jobling (J. W.}, Petersen (W.) & Eggstein (A. A.). Mechanism of anaphylactic shock.
J. Exper. M., Lancaster, Pa., 1915, xxii.
Kastle (I. H.), Healy (D. G.) & Buckner (G. D.). The relation of calcium to anaphy-
laxis. J. Infect. Dis., Chicago, 1913, xii, 127-132.
Lewis (P. A.). The relation of hypersusceptibility to immunity. Arch. Int. Med., Chicago,
1909, iv, d 28-537.
Mclntosh (/.)• Critical review: anaphylaxis and its bearing on medicine. Quart. J. Med.,
Oxford, 1914, vii, 272-290.
Manwaring (W. H.). Der physiolooiscJie Mechanismus des anaphylaktischen Shocks.
Ztschr. f. Immunitdtsjorsch. u. exper. Therap., Jena, 1911, viii, 1-23.
Michaelis (L.). Anaphylaxie. In: Handb. d. Biochem. (Oppenheimer) . Jena, 1910, ii,
1. Hlfte, 689-706.
Moro (E.). Experimentelle und klinische Ueberempfindlichkeit (Anaphylaxie) . In: Ergebn.
d. allgem. Pathol, etc. (Lubarsch & Ostertag). Wiesb., 1910, xiv, Abt. i,
429-593.
Moss (W. L.) & Brown (G. L.). Variations in the leukocyte count in normal rabbits, in
rabbits following the injection of normal horse serum, and during a cutane-
ous anaphylactic reaction. Johns Hopkins Hosp. Bull., Baltimore, 1911 ,
xxii, 258-268.
Otto (#.)• Das Theobald Smithsche Phdnomen der Serum- Ueber empfindlichkeit. Gdnkschr.
f. d. verstorb. Generalstabsarzt d. Armee, v. Leuthold, Berlin, 1906, i,
153-172.
Pearce (R. M.) & Eisenbrey (A. B.). The physiology of anaphylactic "shock" in the dog.
Tr. Cong. Am. Phys. & Surg., New Haven, 1910, viii, 402-413.
Pfeiffer (H.}, Die Arbeitsmethoden bei Versuchen uber Anaphyfaxie. Handb. d. Biochem,
Arbeitsm. (Abderhalden), Berlin, 1911, v, 525-562.
128 DIAGNOSIS OF INFECTIOUS DISEASES
Pfeiffer (H.). Ueber das verschiedeneVerhalten der Korpertemperatur nach Injektion und
nach Reinjektion von artfremden Serum. Wien. klin. Wchnschr., 1909,
V. Pirquet (C.). Allergie. Ergebn. d. inn. Med. u. Kinderh., Berlin, 1908, i, 420-464;
1910, v. 459-539.
Allergie. Berlin, 1910, J. Springer. 96 p. 4°.
Allergy. Arch. Int. Med., Chicago, 1911, mi, 259-288; also 383-435.
Klinische Studien liber Vakzination und vakzinale Allergie. Leipzig u.
Wien, 1907, F. Deuticke. 198 p., 1 pi. 8°.
von Pirquet (C.) & Schick (#.)• Zur Theorie der Inkubationszeit. Wien. klin. Wchnschr.,
1903, xvi, 758; 1244.
Die Serumkrankhcit. Leipzig u. Wien, 1905, F. Deuticke. 146 p. 8°.
Jtichet (C.)» De Vanaphylaxie alimenlaire. Ann. de Vlnst. Pasteur, Paris, 1911,
580-592.
Robinson (G. C.) & Auer (/.)• Disturbances of the heart-beat in the dog caused by serum
anaphylaxis. J. Exper. M., Lancaster, Pa., 1913, xviii, 556-571, 4 pl>
Rosenau (M. J.) & Anderson (J. F.). A study of the cause of sudden death following the
injection of horse serum. Washington, 1906, Govt. Print. Office. 95 p.,
8°. Forms Bull. No. 29 of Treas. Dept. Mar. Hosp. Serv., Hyg. Laborat.
A review of anaphylaxis with especial reference to immunity. J. Infect.
Dis., Chicago, 1908, v, 85-105.
Seligmann (E.). Anaphylaxie. In: Handb. d. Biochem. (Oppenheimer). Jena, 1913,
Ergdnzungsbd., 248-326.
Sewall (Henry) & Powell (Cuthbert). Studies in the relations of the hypersusceptibility
and insusceptibility induced in guinea-pigs by tfie instillation of horse serum
into the nose. Arch. Int. Med., Chicago, 1915, xvi, 605-632.
Smith (H. L.). Buckwheat poisoning. With report of a case in man. Arch. Int. Med.,
Chicago, 1909, Hi, 350-859.
Vaughan (V. C.). The relation of anaphylaxis to immunity and disease. Am. J. M. Sc.,
Philadelphia & New York, 1913, cxlv, 161-177.
Vaughan (V. C., Jr.). Sensitization and its relation to practical medicine. Internal. Clin.,
Philadelphia, 1911, 21 s., iv, 131-148.
Vaughan (V. C.), Gumming (J. G.) & Wright (J. H.). Protein fever. Ztschr. f. Im-
munitdlsforsch. u. exper. Therap., Jena, 1911, Orig., ix, 458-489.
Vaughan (V. C.), Vaughan (V. C., Jr.] & Wright (J. H.). The ferment produced in
protein-sensitization. Ztschr. f. Immunitatsforsch. u. exper. Therap.,
Jena, 1911, Orig., xi, 673-682.
Weaver (G. H.}. Serum disease. Arch. Int. Med., Chicago, 1909, in, 485-513.
Weil (R.). Studies in anaphylaxis. J. Med. Research, Boston, 1914, xxx, 299-364.
Wells (H. G.). Studies on the chemistry of anaphylaxis. III. Experiments with isolated
proteins, especially those of the hen's egg. J. Infect. Dis., Chicago, 1911,
ix, 147-171.
Studies on the chemistry of anaphylaxis II. J. Infect. Dis., Chicago, 1909,
vi, 506-522.
Wells (H. G.) & Osborne (T. !?.)• Is the specificity of the anaphylaxis reaction dependent
on the chemical constitution of the proteins or on their biological relations?
J. Infect. Dis., Chicago, 1913, xii, 341-358.
Zinsser (H.). Anaphylaxis. In: Infection and Resistance (H. Zinsser}. New York,
1914. 358-445.
Zinsser (H.) & Dwyer (J. G.). The aggressin-like action of anaphylotoxin. Proc. Soc.
Exper. Biol. & Med., New York, 1914, xi, 74-76.
iii. Antianaphylaxis
Methods of desensitizing sensitized persons, that is, the production of
so-called anti-anaphylaxis, or anergy, should be more carefully studied. In
GENERAL FACTS REGARDING INFECTION
129
animals, desensitization can be produced by the intravenous injection of a
minute quantity of the antigen, or of a series of graded doses thereof
(Besredka). In animals, a whole series of substances may on injection
prevent the anaphylactic reaction; among these may be mentioned NaCl,
BaCl2, peptone, ether, atropin, urethan, adrenalin, and chloral hydrate.
In man, severe serum anaphylaxis is not very common, especially
since we have learned to take certain precautions (use of old serum; use
of purified serum ; avoidance of repetition of horse serum injections ; cau-
tion in patients who suffer from asthma or who have asthmatic antece-
dents). In patients who have had antitoxin before, I have sometimes given
a small amount of serum by the rectum on the day preceding re-injection of
diphtheria antitoxin. If we fear anaphylaxis, it is well to use the desen-
sitizing methods of Besredka, to be on the safe side. In urgent cases, e. g.,
Days . . . .
2)Jnjectioo
Horsa-
setum''
IPIL , , ,
I
|FF^rm-.j
Antibody
i
hrcsbold -J \[
>f death O*«l
)— Threshold Of
i observation
Fig. 47.— Anci-Ry — Anti-anaphylaxis. (After C. E. von Tirquct, Arch. Int. Med.)
of cerebrospinal meningitis, Besredka advises 1 c.c. of a 10 per cent solu-
tion of serum intravenously; after 4 minutes, 3 c.c. more; and 10 minutes
later 10 c.c. ; after 2 more minutes 25 c.c. of the dilution. Eour minutes
after this last dose, the patient is desensitized and may receive 10-30 c.c.
of undiluted serum, either intravenously or intraspinally.
The danger seems to be greatest in patients who suffer from vasomotor
instability, or from vagotony. The fatal cases in human beings have most
often been asthmatics, or persons with asthmatic antecedents.
130 DIAGNOSIS OF INFECTIOUS DISEASES
References
Besredka (A.). De V anti-anaphylaxie par la voie digestive. Compt. Rend. Soc.BioL, Paris,
1911, Ixx, 203-205.
Besredka (A.} & Steinhardt (/?.)• De I'anaphylaxie et de I' anti-anaphylaxie vis-a-vis du
serum de cheval. Ann. de I'Inst. Pasteur, Paris, 1907, xxi, 117-127.
Du mecanisme de I' anti-anaphylaxie. Ann. de I'Inst. Pasteur, Paris,
1907, xxi, 384-891.
Koessler (K. K.). Experiments on antianaphylaxis. Trans. Pathol. Soc., Chicago, 1913,
ix, 39-43.
Weil (,R.) & Coca (A. F.}. The nature of anti-anaphylaxis. Ztschr. f. Immunitatsforsch.
u. Exper. Therap., Jena, Orig., 1913, xvii, 141-155.
Weil (/£•)• Experiments in antisensitization: a contribution to cellular dynamics in im-
munity. Ztschr. f. Immunitatsforsch. u. exper. Therap., Jena, 1914,
Orig., xxiii, 1-31.
iv. Theories of Allergy
It seems certain that the active agent in anaphylaxis circulates in the blood
(passive transference!), though it doubtless is derived from the body cells. Some
think that this is a single substance (anaphylactin] . Others believe that the
"anaphylactins" vary in the different allergic states. Von Pirquet calls the sub-
stance ergin, and believes it to be an antibody, produced by the antigen, and
capable of converting the latter into a poisonous substance.
On account of the resemblance of anaphylactic shock to the anaphylactoid
phenomena (Auer), which appear in poisoning by a first injection of peptone,
or of certain other substances, the theory has been advanced that some protein
cleavage ("parenteral digestion theory" of anaphylaxis) must occur during the
anaphylactic reaction, and this view receives much support from experiment
(Vaughan; Schittenhelm and Weichardt; Biedl and Kraus). The view generally
held at present is that a first parenteral introduction of protein into the body
causes sensitization by the production of antibodies (proteolytic ferment?) which,
on subsequent injections, unite with the antigen to lead, in some way, to intoxica-
tion by a protein cleavage-product that excites the symptoms of anaphylaxis
(Vaughan). Vaughan has shown that any protein can be split into a toxic frac-
tion (alcohol-soluble) and a non-toxic fraction, and that, on first injection into
a guinea-pig, the toxic fraction will cause symptoms and anatomical signs like
those of anaphylactic shock. Strange to say, the toxic fraction does not sensitize,
but the non-toxic fraction can sensitize against the whole protein molecule, though
not against itself.
In general anaphylaxis, the poison appears to act upon the central nervous
system, especially upon the vasomotor center; this action can be inhibited by
narcosis with ether, ethyl chlorid, and urethane (Besredka).
By far the best reviews in English of the present state of our knowl-
edge regarding anaphylaxis are to be found in Auer's article "The Func-
tional Analysis of Anaphylaxis," in Forchheimer's "Therapeusis of Inter-
nal Diseases," 1914, V, 39-120, in Zinsser's article in his "Infection and
Resistance" and in von Pirquet's articles on "Allergy."
THE BODY TEMPEEATUEE 131
B. The Body Temperature
Measurements of the body temperature form an important part of
every clinical study.
1. Heat Regulation
In warm-blooded animals (homoiothermic) , a tolerably constant temperature
is maintained within the body, despite the temperature of its surroundings; in the
cold-blooded animals (poikilothermic) , the temperature of the body changes with
that of its surroundings. In man, the temperature normally remains fairly con-
stant, varying not more than 1° to 1.5° F. in the 24 hours.
Animal heat arises from the combustion going on in the. body (oxidation of
proteins, fats and carbohydrates by the inhaled oxygen). A human being of aver-
age weight and at rest uses up in twenty-four hours about 2400 calories; of these
about 80 per cent are given off in radiation, conduction and evaporation of water
from the skin, about 12 per cent by evaporation from the lungs, while about
8 per cent are used up in warming the food intake and the inspired air. Oxida-
tive processes in all the organs give rise to heat, but the largest amounts of heat
are produced in the muscles, and in the glandular tissues generally, especially in
-39°
\
-38°
TW'ature ^ \ =^-- JT^n^f
Normal Work Rest, fasting Normal Chill Fastigium Crisis \ Normal
Sweating
Heat production
— -Heat loss Subnormal
Fig. 48. — Diagram Showing Mechanism of Heat Regulation Under Different Conditions. (After
H. H. Meyer and R. Gottlieb, "Pharmacology, Clinical and Experimental," published
by J. B. Lippincott Co., Phila.)
the liver. The self-regulatory mechanisms are partly physical, partly chemical,
in nature. In man, physical regulation predominates. Among the physical meth-
ods of regulation are included:
(1) Artificial regulation, by means of clothing and housing.
(2) Natural regulation*, (a) Through circulatory changes (anemia or hyperemia
of the skin), (b) Evaporation of water from the skin and lungs. The chemical
regulation occurs through increase or decrease of the oxidative processes going on
in the body. These have to do with heat production in contrast with the physical
regulation, which has to do with heat dissipation. Many factors influence heat
I production; among the more important are (1) bodily exercise, (2) food intake,
(3) influences acting upon catabolism, especially certain internal secretions (e.g.,
thyroid) and ferments, especially the oxidases.
The automatic self-regulation is often disturbed in disease so that the
organism is no longer able to maintain the normal temperature. Owing
132 DIAGNOSIS OF INFECTIOUS DISEASES
to a disproportion between heat formation and heat dissipation the tem-
perature may become higher than normal (fever, or pyrexia), or lower
than normal (subnormal temperature).
Fever is usually due to increased heat production rather than to
lessened heat loss, especially in the infectious diseases. During a chill,
there is rapid increase in temperature owing to the muscular contractions
during the rigor. Heat loss is somewhat diminished as a rule while the
temperature is rising, though when the temperature reaches higher levels
the loss of heat is usually increased. During the sweat following a chill,
heat dissipation may be greatly increased (from cutaneous hyperemia and
evaporation of water). Every gram of water evaporated from the skin
withdraws from the body about 0.6 calories or about 1/7 of the heat that
arises from the combustion of 1 gram of protein, or of carbohydrate, in the
body. A loss of 4 liters of sweat could withdraw 2400 calories, or an
amount equal to the daily loss of an individual at rest.
In heat regulation, a number of centrifugal nerves, going to the muscles, blood
vessels, sweat glands and respiratory organs are concerned. These nerves appear
to stand under the dominion of a nerve center for heat regulation. The location of
this center has not been definitely determined. Puncture of the corpus striatum
causes increase of temperature through increased heat production, owing chiefly to
increased carbohydrate combustion (0. Scholtze). Fasting animals, and glycogen-
free animals, react very little to such a puncture.
It seems probable that the mechanism of heat regulation is acted upon by sub-
stances like peptones, bacterial proteins, toxins, and certain salts. Large amounts
of these substances cause a rapid fall in temperature, smaller ones a rise in tem-
perature. Substances that increase temperature are said to be pyrogenic.
Increased loss of heat may be due to reflex influences that act by increasing the
respiration or through the vasodilators; and, again, reflex influences may cause
fever through vasoconstriction, though the fevers usually designated as reflex (gall-
stone fever; urethral fever) are probably not reflex, but due to the setting free of
pyrogenic substances in local infectious processes.
2. Measurement of the Body Temperature (Thermometry)
For this purpose a clinical thermometer, exactly tested, is used. In this
country, and in England, the Fahrenheit scale is employed, while on the
Continent, the Centigrade scale is in use. Quick-registering, maximal
thermometers are now universally employed.
The temperature may be taken by mouth (under the tongue), in the
axilla, or by rectum. In this last, the temperature is 0.5° to 1° C.
higher. For exact measurement, rectal temperatures are the more satis-
factory, and they should always be used for taking the temperature in
children, in very old people, or in adults with disturbed mentality.
In ordinary clinical work the temperature is taken at least twice a day,
but, when the temperature is varying much, it may be desirable to measure
THE BODY TEMPEEATUEE 133
it more frequently (every 2, 4, or 6 hours). The results are recorded on
a temperature chart, in the form of a continuous curve. Such continuous
curves, with accompanying pulse curves and respiration curves, as charted
by a trained nurse, are very helpful for quick orientation in clinical
studies.
For converting the scale of one thermometer into that of another, the
following formulae are used :
F = Fahrenheit.
C = Centigrade.
E = Eeaumur.
To convert Fahrenheit to Centigrade 5 (F— 32) = ^
y
To " Centigrade to Fahrenheit J C+32 =F
o
To " Fahrenheit to Eeaumur 4 (F~32)=R
9
QT>
To " Eeaumur to Fahrenheit ™_i_32 = F
4
Thus
96° F. = 35.5° C. 99° F. = 37.2° C. 103° F. = 39.5° C.
97° F. = 36.1° C. 100° F. = 37.8° C. 104° F. = 40° C.
98° F. = 36.6° C. 101° F. = 38.3° C. 105° F. - 40.5° C.
98.6° F. = 37° C. 102° F. = 38.9° C. 106° F. = 41.1° C.
For the conversion of degrees Fahrenheit to degrees Centigrade, I have
found the following diagonal line on millimeter paper very convenient.
The ordinates represent °C., the abscissae °F. I am indebted to our physi-
cist, Professor Joseph S. Ames, for calling my attention to this simple
plan. (See next page.)
Reference
Bolton (H. C.). Evolution of the thermometer, 1592-1743. 12°. Easton, Pa., 1900.
3. Normal Temperature of the Human Body
The normal rectal temperature of the human body varies between 98.-
5°-98.9° F., the axillary temperature between 97.6°-9S.3° F. Plethoric
individuals show a little higher temperature ; delicate, anemic individuals
a little lower.
During the 24 hours the normal temperature varies slightly, in the
form of a curve which is higher in the evening than in the morning, after
eating than when fasting, and after exercise than when resting; the tem-
perature rises also after a hot bath. The minimal temperature of the 24
134
DIAGNOSIS OF INFECTIOUS DISEASES
°F-95 96 97 98 99 100 101 102 103 104 105 106 107 108
Fig. 49. — Easy Method of Translating Degrees Centigrade Into Degrees Fahrenheit and vice
versa. Note that the Vertical Lines Correspond to Degrees Fahrenheit, and the Horizontal
Lines to Degrees Centigrade where the mm. Chart is Cut by the Black Oblique Line.
(Courtesy of Prof. J. S. Ames.)
hours is observed between 2 A. M. and 6 A. M., the maximal temperature
between 5 p. M. and 8 p. M. When patients lie in bed the whole 24 hours,
the daily variations are much less than when they are up and about.
The temperature of sucklings and of young children is normally a little
higher than that of adults.
4. Fever
Fever is the name given to pathological elevations of the body tempera-
ture.
(a) Febrile Temperatures
The following fever scale shows, at a glance, the terms ordinarily in use
to designate the different deviations from normal temperature :
Name. Fahrenheit.
Subnormal temperature
(collapse) Below 96.8°
Subfebrile temperature 99.5°-100.4°
Slight fever " 100.4°-101.2°
Moderate fever " 101.2°-103.2°
Rather high fever " 103.2°-105°
Very high fever Above 105°
Hyperpyrexia " 107°
Centigrade.
Below 36.0°
" 37.5°-38°
" 38? -38.4°
" 38.4°-39.5°
" 39.5°-40.5°
Above 40. 5°
" 41.6°
THE BODY TEMPERATURE 135
In rare cases, temperatures have been recorded as high as 113° F., or
even as high as 122° F. (English Commission).
The lowest temperatures observed in human beings have been in cases
of brain tumor, especially of tumors of the fourth ventricle, 73.4° P.
(Lemcke), S6°-89.6° F. (Reinhold).
The daily variations in the temperature curve are more outspoken in
febrile patients than in healthy individuals. The temperature often falls
markedly in the early morning hours (morning remission), to rise consid-
erably in the later part of the day (evening exacerbation). Occasionally,
an opposite behavior is met with, the temperature being higher in the
morning than in the evening (inverted type).
With the sudden onset of high temperature in infectious disease, the
patients often suffer from chilly sensations, or have an outspoken rigor or
chill. This is especially often met with in malaria, in sepsis, in endocar-
ditis, and in the beginning of lobar pneumonia. The patients complain
bitterly of cold, their teeth chatter, and the whole body may shake. The
skin is pale and cool (vasoconstriction). After the chill, there may be
marked cutaneous hyperemia with sweating, especially if the temperature
fall rapidly.
(6) Different Types of Fever
An analysis of various fever curves permits of a subdivision into several
types, according to the variations shown. The more important of these
are the following:
i. Continued Fever (Febris continual
Here the curve is fairly level, the daily variations being slight, not
greater than 1° C. Such a continued fever is seen especially in the second
stage of typhoid fever, in most of the acute exanthemata, in croupous
pneumonia, in tuberculosis, etc.
ii. Remittent Fever (Febris remittens)
Here there are marked daily variations, greater than 1° C., a fall in
temperature occurring usually in the morning hours, though even then the
temperature does not reach normal. Such a remittent fever is seen in the
third stage of typhoid fever (amphibolous period), in acute articular rheu-
matism, in various septic diseases, in pulmonary tuberculosis (hectic fever
with night sweats) .
iii. Intermittent Fever (Febris intermittens)
Here the minimal temperature in the 24 hours may be normal or sub-
normal, while the maximal temperature may be very high. Brief periods
136 DIAGNOSIS OF INFECTIOUS DISEASES
of fever (febrile paroxysms} alternate with brief afebrile intervals (apy-
rexia). Such an intermittent fever is met with especially in malaria of dif-
ferent types (quotidian, tertian, quartan), in sepsis, in miliary tuberculosis,
'etc,
iv. Recurrent Fever (Febris recurrens)
Here several days of fever are followed by several days of apyrexia.
Such a recurring fever is characteristic of the relapsing fever due to the
Spirochaeta obermeieri. It is sometimes met with in Malta fever, and in
some cases of Hodgkin's disease (recurring fever of Pel).
(c) Stages of the Febrile Course
A single fever curve is divisible into three parts :
1. Stage of rising temperature (stadium increment!), with or with-
out chill.
2. The height of the fever (fastigium or acme).
3. Stage of falling temperature (stadium decrementi or deferves-
cence). The temperature may fall suddenly (crisis), often accompanied
by sweating, as in lobar pneumonia ; or slowly (lysis), the temperature be-
coming markedly remittent or intermittent and taking several days to be-
come normal, as at the end of typhoid fever.
When the temperature falls quickly, but is followed by a slight single
elevation, we speak of a protracted crisis. When the temperature rises
unusually high, just before the crisis, we speak of a " critical perturbation/'
In typhoid fever, between the fastigium and the stadium decrementi, there
is often a period of markedly remittent temperature known as the period
of steep curves, or so-called amphibolous stage.
References
Burdon-Sanderson (Sir /.), Pembrey (M. S.) & White (W. H.). Fever. In: Syst.
Med. (Allbutt & Rollestori). London, 1910, i, 818-861.
Kocher (R. A.). Ueber die Grosse des Eiweisszerfalls bei Fieber und bei Arbeitsleistung.
Deulsch. Arch. f. klin. Med., Leipzig, 1914, cxv, 82-123.
Liidke (H.). Ueber Ursachen und Wirkungen der Fiebertemperalur. Ergebn. d. inn.
Med. u. Kinderh., Berlin, 1909, iv, 493-522.
McCallum (W. G.). Fever. In: Harvey Lectures, New York, 1908-1909, 27-68. Also:
Arch. Int. Med., Chicago, 1908-1909, ii, 569-602.
Moffitt (H. C.). A contribution to the study of long-continued fevers. Am. J. M. Sc.,
Philadelphia & New York, 1907, cxxxiv, 644-657.
Ott (Isaac}. Fever, its thermotaxis and metabolism. New York, 1914, P. B. Hoeber.
166 p. 12°.
Welch (W. H.}. The Cartwright lecture on the general pathology of fever. Med. News,
Philadelphia, 1888, Hi, 365, 393, 539, 565. Also: Med. Rec., New York,
1888, xxxiii, 373; 401; 457.
Wunderlich (C. R. A.). Das Verhalten der Eigenwdrme in Krankheiten. Leipzig, 1870,
0. Wigand.
APPLICATIONS OF BACTEKIOLOGICAL METHODS 137
G. Clinical Applications of Bacteriological
Methods
For purposes of clinical diagnosis in the infectious diseases, an ac-
quaintance with bacteriological methods is essential. Every medical stu-
dent is nowadays trained in the study and isolation of the pathogenic forms
of hacteria. The methods of bacteriology are fully described in the special
text-books on the subject. Here only a few of the methods particularly
applicable in clinical work are given. For other methods the student may
consult the treatises of V. A. Moore, Hiss and Zinsser, E. O. Jordan, Kolle
and Wassermann, Kraus and Levaditi, Brugsch and Schittenhelm, Park
and Williams, E. R. Stitt, and others.
References
Besson (A.). Technique microbiologique et serotherapie (microbes palhogenes de I'homme
et des animaux). Guide du medecin et du vetennaire pour les travaux du
laboratoire. 3d ed. Paris, 1904, J. B. Bailliere & fils. 847 p. 8°.
Also: 5th ed., 1911.
Friedberger (E.) & Reiter (H.). Die allgemeinen Methoden derBakteriologie. In: Handb.
' d. pathogen. Mikroorg. (Kolle & Wassermann). 2. Aufl. Jena, 1912, i,
293-554.
Hiss (P. H.) & Zinsser (//.). A text-book of bacteriology. New York & London, 1910,
D. Appleton & Co. 745 p. 8°.
Jordan (E. O.). A text-book of general bacteriology. 4th ed. Philadelphia & London,
1914, W. B. Saunders Co. 643 p. 8°.
Koch (/£.)• Untcrsuchungen uber Bacterien. Verfahren zur Untersuchung, zum Conser-
viren und Photographiren der Bacterien . Beitr. z. Biol. d. Pflanz., Breslau,
1877, ii, 899-434.
Kolle (W.) & Wassermann (A.). Handbuch der pathogenen Mikroorganismen. 2d ed.
Jena, 1912-1913, G. Fischer. 8v. 4°.
Krause (P.). Klinische Bakteriologie. In: Lehrb. d. klin. Diagnoslik (P. Krause). 2d
ed. Jena, 1913, 778-837.
Mallory (F. B.) & Wright (J. H.) Pathological Technique. 5th ed. Philadelphia &
London, 1911.
Muir (R.) & Ritchie (/.). Manual of bacteriology. 6th ed. London, 1913, H. Frowde,
etc. 760 p. 6 pi. 8°.
Park (W. H.} & Williams (A. W.). Pathogenic microorganisms. 5th ed. New York &
Philadelphia, 1914, Lea & Febiger. 709 p. 8°.
Stitt (E. JR.) Practical bacteriology, blood work and animal parasitology, etc. 3d ed.
Philadelphia, 1913, P. Blakision's Son & Co. 423 p. 4 pi. 8°.
Weigert (C.). Ueber eine Mykose bei einem neuqeborenen Kinde. Jahresb. d. schles.
Gesellsch. f. vaterl. Kult., Breslau, 1876, liii, 229.
1. Collection of Material for Bacteriological
Examination
Great care must be taken in collecting material to avoid contamination with
extraneous bacteria.
Secretions. — Secretions from the oral, nasal and pharyngeal cavities and from
the urethra, vagina or cervix are best collected by means of a sterile platinum loop.
138 DIAGNOSIS OF INFECTIOUS DISEASES
If possible, smears and cultures should be made immediately, as the materials often
dry in transport, in which case certain microorganisms (e. g., gonococci, meningo-
cocci) die out. When the physician cannot make the examinations himself, he may
secure the material by means of a sterile swab, and inclose it in a sterile test tube,
such as is now provided by the Health Department of every town.
Sputum. — This, as ordinarily collected, is worthless for bacteriological exami-
nation. According to Luetscher, sputum is best collected by placing a sterile Petri
dish beside the patient and explaining to him that what is wanted is not saliva nor
ordinary pharyngeal hawkings, but the sputum which can be felt to come from the
bronchi. It is best to secure that coughed up in the morning from the depth of
the bronchi. It is desirable that this should be worked up as quickly as possible.
If sputum, so collected, be washed thoroughly by the bacteriologist in several Petri
dishes of sterile salt solution, the pathogenic agents can usually be obtained, in
almost pure culture, from the interior of the washed mass.
Feces should be collected directly, in a large sterile glass vessel. For amebse,
the mucus obtained in the eye of a rectal tube may be examined.
Urine. — This should be drawn by sterile catheter after thorough cleansing of
the meatus and glans. The centrifugate may be examined microscopically, by cul-
tural methods, or by animal inoculation.
Exudates, Transudates, Pus and Cerebrospinal Fluid.— These are best col-
lected with the aid of a sterile aspirating syringe.
Blood. — If only small amounts are required (search for malarial parasites,
Widal test, opsonic index, etc.), the blood can be obtained from the lobule of the
ear, or the tip of the finger, after carefully cleansing with alcohol and ether and
drying. (See Examination of Blood.) If larger amounts are needed (blood cul-
ture; Wassermann test; other complement fixation tests), 20-100 c.c. of blood can
easily be withdrawn from a vein at the bend of the elbow by means of a suitable
syringe (Luers; Record). A ligature is placed around the upper arm and made
tight enough to obstruct the venous flow without obliterating the radial pulse.
Aseptic precautions !
C. E. Simon's Method. — When it is not feasible to secure blood as above, a
sufficient quantity of blood for the Wassermann test (0.5-1.5 c.c.) can be secured by
freely puncturing the lobule of the ear at its margin and then "milking" the ear
into a little glass tube, measuring about 5 cm. in length with a diameter of 5-6 mm.,
the individual drops being scooped up with the edge of the tube.
K. D. Blackfan's Apparatus for Collecting Infants' Blood for the Wassermann
Reaction. — The methods usually employed for obtaining blood from infants are in
the majority of instances extremely unsatisfactory. The veins are too small to
enter and it is a tedious, difficult and painful procedure to collect the necessary
amount of blood by puncturing the fingers or toes.
The apparatus herein described is a simple, inexpensive device by which the
necessary amount of blood can be obtained easily, with a minimum of discomfort
to the patient and in a comparatively short space of time. The time spent in col-
lecting the blood averages about 2 minutes.
The apparatus, as shown in Fig. 50, consists of a glass cylinder (A) If inches
in diameter; the large end is ground smooth and the other end (B) is drawn out
for the attachment of a small hand suction pump (C) ; an outlet (D), which is fused
at an angle to the under surface of the cylinder, 1/2 inch from the large end, and a
collecting tube (E). The collecting tube (E) fits over the outlet (D), the connec-
tion being made air-tight by means of a small piece of rubber tubing. The tube in
which the blood is collected may be the size which is used in the laboratory test,
obviating the necessity of transferring the blood to another tube.
Technic with Blackfan's Apparatus. — The technic is as follows: Connect the
APPLICATIONS OF BACTEEIOLOGICAL METHODS 139
apparatus for use. The patient may be placed in either the upright or recumbent
posture. The most convenient site is on the back just below the angle of the scap-
ula, though any other surface of the body may be used. Having cleansed the area
with alcohol and ether, one or two small punctures are made through the skin with a
sharp-pointed scalpel or Hagedorn needle and the apparatus is quickly applied.
With but little suction-force the blood will flow from the wound through the outlet
and into the collecting tube. After a sufficient amount has been collected, the tube
is taken off, a cotton plug is inserted and the tube containing the blood is set aside
until the examination is made. The wound is covered with a collodion dressing
and the resulting swelling rapidly subsides with no discomfort to the patient.
Fig. 50.— Suction Apparatus for Collecting Blood for the Wassermann Reaction, (A) Suction
Glass Connecting at (B) with Suction Pump (C) ; the Blood Flows Through (D) Con-
nected by Rubber Stopper with an Ordinary Test Tube (E). (After K. D. Blackfan.)
Blood may be collected by this method from the older children and adults, as
well as infants, in a much shorter time and with less difficulty than by entering
a vein.
The glass apparatus can be made in the laboratory or by a glass blower and the
suction pump can be obtained through any surgical supply house.
With sufficient care, blood so obtained may be used also for blood-cultures from
infants' blood, though there will often be contaminations by skin cocci.
Of course, blood obtained in this way should never be used for a blood count,
hemoglobin estimations or for physical and chemical determinations, as the result
would be of no value. For serological tests, however, this method is very valuable.
2. Kinds of Bacteria Often Found
In Nasal Secretion. — Staphylococci ; diphtheria bacilli; lepra bacilli;
meningococci ; encapsulated bacilli in ozena and in rhinoscleroma.
In Conjunctival Secretion. — Gonococci; influenza bacilli; diphtheria
bacilli ; xerosis bacilli ; pneumococci (serpiginous ulcer).
140 DIAGNOSIS OF INFECTIOUS DISEASES
In Pus. — Pyogenic cocci ; colon bacilli ; bacillus pyocyaneus ; tubercle
bacilli.
In Pharyngeal Exudate. — Diphtheria bacilli; streptococci; fusiform
bacilli; a spirillum (Plant-Vincent's angina); meningococci ; pneumo-
cocci; influenza bacilli.
In Sputum. — Tubercle bacilli ; pneumococci ; influenza bacilli ; strepto-
cocci ; staphylococci ; actinomyces ; glanders bacilli ; anthrax bacilli ; plague
bacilli.
In Feces. — B. typhosus; B. paratyphosus; B. dysenteric; B. coli;
cholera vibrios ; dysenteric amebse ; tubercle bacilli, etc.
In Urethral and Other Genital Secretions, and in the Urine. — Gono-
cocci ; tubercle bacilli ; typhoid bacilli ; streptococci ; staphylococci ; colon
bacilli; smegma bacilli.
In Pleural Tappings. — Pneumococci ; streptococci ; tubercle bacilli.
In Peritoneal Tappings. — Colon bacilli ; typhoid bacilli ; streptococci ;
gonococci ; tubercle bacilli.
In Cerebrospinal Fluid. — Meningococci; tubercle bacilli; pneumo-
cocci ; influenza bacilli ; trypanosomes.
In Blood. — Typhoid bacilli ; paratyphoid bacilli ; streptococcus vir-
idans ; streptococcus hemolyticus ; other streptococci ; staphylococcus ; pneu-
mococcus ; anthrax bacilli ; plague bacilli ; bacilli typhi-exanthematici, etc.
3. Microscopic Examinations for Bacteria
(a) Examination of Dried, Fixed, and Stained Smears
This is the most useful method for quick clinical orientation.
The Smear. — A minute amount of the material is evenly spread on a clean
cover glass or slide, in a very thin layer, by means of a platinum loop or the end
of a clean match.
Air-Drying. — The preparation is allowed to dry completely in the air ; the proc-
ess may be hastened by holding the smear, with the film side up, a few inches from
a very low gas flame, avoiding, however, any temperature that could coagulate pro-
tein, since the fixation should not be made until the air-drying is complete.
Fixing. — For fixing, the smear is passed three times directly through the flame,
with the film side up. This coagulates the protein, making it insoluble. Care must
be taken to avoid over-heating. A still better fixation, desirable when one wishes
to study the finer details of malarial parasites in blood preparations, or to under-
take differential staining or polar staining in diphtheria bacilli or plague bacilli,
can be obtained by immersing the smear for 15 to 20 minutes in absolute alcohol,
in a mixture of alcohol and ether, or, best of all, for 3 to 5 minutes in absolute
methyl alcohol, instead of passing through the flame.
Staining. — This is done by one of the methods described below, and the smear
is then washed in water, under the tap, inclining the smear slightly, beneath a
delicate stream, so as to protect the film as much as possible. If preferred, a
chemical wash bottle may be used. If there be any doubt as to the film side of the
preparation, it can usually be detected by scratching the surface with a pin.
APPLICATIONS OF BACTEKIOLOGICAL METHODS 141
The smear is next dried between folds of filter paper, several layers thick, the
paper being pressed directly upon the smear and stroked gently until dry. The
drying can be completed by holding the smear, film side up, high above a small
flame.
The smear is now ready for microscopic examination with the oil immersion
lens. If the smear has been made upon a slide, a drop of cedar oil is placed di-
rectly upon it, and the immersion lens run into it (open diaphragm) ; or a drop of
neutral Canada balsam and a cover glass may be applied, pressed down gently so
as to form a thin layer, after which a drop of cedar oil is placed on the surface of
the cover slip before examination with the immersion. If the smear has been made
upon a cover slip, this is mounted in a thin film of neutral Canada balsam, on a
clean slide, and examined in the same way.
(6) Examination of Unstained Fresh Preparations
The infectious agent can often be seen in unstained fresh preparations
of the material collected.
Thus, if malaria be suspected, a drop of blood taken from the ear, on an
absolutely clean cover glass, may be placed upon an absolutely clean slide,
when the drop will flatten out into a layer one corpuscle thick. (See Exam-
ination of Blood.) A drop of cedar oil is applied, and the examination
made immediately with an oil immersion lens (medium or small dia-
phram). The pigment of the parasite may first catch the eye when the gen-
eration is near maturity. Young parasites are difficult to recognize at first,
though with a closed diaphragm they may be recognized, especially the
forms that show ameboid movements. Such an examination should
always be supplemented by the study of a fixed smear, stained by Wilson's
or Giemsa's method.
In pus from subcutaneous abscesses, if blastomyces (oidiomycosis) be
suspected, the doubly contoured parasites are easily recognizable in the
fresh slide.
If amebic dysentery be suspected, a particle of mucus from the stool
can be examined fresh beneath the cover slip, on a warm slide and warm
stage. The typical subdivision into ectosarc and endosarc, the active ame-
boid movement, and the phagocyted red corpuscles are characteristic.
(c) Examination in Hanging Drop
This is rarely used for the direct examination of material collected from the
patient, but is very helpful for the study of particles of living cultures derived from
such material.
The slide about the edge of the cavity in a hollow slide is surrounded with
vaseline. With a sterile oese, a small drop of the culture is placed in the middle of
a clean cover slip, lying on a piece of white paper, or a small drop of salt solution
or sterile bouillon can be placed upon the cover slip and inoculated with a minute
particle of solid material containing the bacteria, with a sterile platinum needle.
The glass slide, with the cavity downward, is now laid upon the cover slip so that
the drop comes directly in the middle of the cavity; it is then pressed gently into
142 DIAGNOSIS OF INFECTIOUS DISEASES
the vaseline. The slide is next carefully turned over so that the cover glass is
above, and the drop hangs from its under surface into the cavity.
The slide is now placed under the microscope. With the low power and closed
diaphragm, the edge of the drop is first sought and brought exactly into the middle
of the field. A drop of cedar oil is next applied to the cover slip, the diaphragm
opened about 1/3, and the oil immersion fixed upon the edge of the drop. This
found, the slide may be cautiously moved as the bacteria in the hanging drop are
sought for and studied. The method is especially useful in studying motility.
4. Methods of Staining Bacteria and Parasites
The ordinary stains of the bacteriological laboratory are employed. The
basic dyes, like methylene blue, gentian violet, and fuchsin, stain bacteria
and cell nuclei intensively. Sometimes a contrast stain with an acid dye,
like eosin, is also used.
The dyes are kept in 2 per cent aqueous solution, or, better, in 5 per
cent alcoholic solution, to be diluted just before use with 4 to 10 parts of
water.
(a) General Stains
i. Alkaline Methylene Blue (Loeffler)
The stain consists of 30 ccm. of a saturated alcoholic solution of methylene
blue with 100 c.c. 0.01 per cent KOH.
ii. Carbol-Fuchsin (Ziehl-Neelsen)
The stain consists of 1.0 gram fuchsin, 5.0 acid carbol liq., 10.0 alcohol, 100.0
aqua distillata. The solution keeps well. If diluted 10 times it stains all ordinary
bacteria in a few seconds. To stain tubercle bacilli it is applied in an especial
way (vide infra).
Hi. Anilin Water Gentian Violet (Ehrlich)
Five c.c. anilin oil are thoroughly shaken with 100 c.c. distilled water, and
filtered through a moist filter. In the filtrate, 4 grams of gentian violet are dissolved.
The solution is to be filtered again, just before use. The stain does not keep well,
spoiling in two or three weeks. Instead of adding the crystals of gentian violet,
11 c.c. of a saturated alcoholic solution of gentian violet may be used.
iv. Wilson's and Giemsa's Stain (Methylene Azure and Eosin)
(See Staining of Blood Smears.)
These stains are especially useful for demonstrating malarial parasites, spiro-
chfletes, and trypanosomes.
(6) Special Stains
i. Gram's Stain
The method consists in staining the bacteria with gentian violet, and treating
the smear with Lugol's solution, through which a union of iodin with the stain
APPLICATIONS OF BACTERIOLOGICAL METHODS 143
occurs, after which the smear is washed in alcohol. Certain bacteria retain the
stain and are called Gram-positive; others decolorize and are said to be Gram-
negative.
Technic, — 1. Stain with warm anilin gentian violet for two minutes.
2. Place in Lugol's solution (iodin 1, KI 2, distilled water 300) for from \
to 2 minutes. The specimen turns black.
3. Wash in absolute alcohol until the color just ceases to be visible to the naked
eye.
4. Counterstain with 2 per cent aqueous solution of Bismarck brown.
5. Wash in water, dry, and mount.
The Gram-positive bacilli will be stained violet; the Gram-negative
bacilli will be stained brown.
Gram-positive Bacteria. — (1) Nearly all cocci (staphylo, strepto,
pneumo) except gonococci and meningococci ; (2) diphtheria bacilli; (3)
anthrax bacilli ; (4) tetanus bacilli ; (5) tubercle bacilli ; (6) lepr a bacilli,
etc.
Gram-negative Bacteria. — (1) Gonococcus; (2) meningococcus ; (3)
micrococcus catarrhalis; (4) typhoid bacillus, and paratyphoid bacillus;
(5) influenza bacillus ; (6) B. coli; (7) B. pyocyaneus; (8) B. mallei; (9)
B. pestis; (10) cholera vibrio; (11) B. dysenterise ; (12) Friedlander's
bacillus; (13) whooping-cough bacillus (Bordet) ; (14) bacillus of soft
chancre, etc.
ii. Stains for Tubercle Bacilli, and Other Acid-Fast Bacilli
These bacilli stain with difficulty, probably on account of the waxlike
.substance they contain. Once stained, unlike other bacteria, they hold the
stain tenaciously, even in the presence of acid ; they are "acid-fast." If a
second dye be used as a counterstain, it will color the bacteria which are
"non-acid-fast."
1. Method of Ziehl- Neelsen. — 1. Stain for 1 to 2 minutes in concentrated carbol-
fuchsin, heating until steam comes off.
2. Wash quickly in water.
3. Decolorize in 5 per cent H2S04 for 2 to 5 seconds, or in 3 per cent HC1-
alcohol, or in 30 per cent aqueous HN03 solution, for 1 to 3 seconds.
4. Wash in 70 per cent alcohol until almost colorless.
5. Rinse in water.
6. Counterstain with weak methylene blue solution, 5 to 10 seconds.
7. Wash again in water, dry, and mount.
All acid-fast bacilli, including tubercle bacilli, stain bright red; other bacteria,
cell nuclei, and mucus, stain pale blue. Besides tubercle bacilli (human, bovine,
avian, etc.), a number of other bacilli are acid-fast (pseudo tubercle bacilli, smegma
bacilli, lepra bacilli).
II. Method of Fraenkel-Gabbett. — Here the decolorizing and counterstaining
are done simultaneously. After staining in hot carbol-fuchsin, the specimen is
rinsed in water and placed in the following solution: Methylene blue 2.0, acid
sulphuric concentrated 25.0, alcohol 50.0, distilled water 100.0. It is left here about
144 DIAGNOSIS OF INFECTIOUS DISEASES
5 minutes, until the preparation looks slightly blue. It is then rinsed thoroughly
in water, dried, and mounted.
Either of the above methods is useful for staining tubercle bacilli in sputum,
urine, feces, or cerebrospinal fluid.
III. Antiformin Methods. — These are used for demonstrating tubercle bacilli,
present in small quantities, in blood, sputum, or tissue. The antiformin, which is
a mixture of hypochlorit of soda and NaOH, quickly destroys all organic sub-
stances (including bacteria), except acid-fast bacteria, which still retain their form,
vitality, and colorability. Urinary sediments containing tubercle bacilli, treated
with antiformin and injected into guinea-pigs, cause infection, showing that the
tubercle bacilli are not killed.
Several antiformin methods have been used. Uhlenhuth's seems as good as any.
The material is dissolved up in an equal volume of 15-20 per cent antiformin solu-
tion by allowing the mixture to stand for 10-12 hours in the thermostat at body
temperature. The tubercle bacilli can be obtained in concentrated aggregate by
centrifugali zing. The centrifugate is used for staining, or for animal experiments.
A quick method has been introduced by Lorenz. From 2 to 10 c.c. of sputum
are shaken in a test tube for about 5 minutes with two or three times as much 15
per cent solution of antiformin. The shaking is continued until the mixture is
homogeneous, then boiled and strongly centrifugalized for about 15 minutes. The
sediment is spread on a glass slide, diluted with a few oeses of water, dried, fixed
in a flame, and stained.
Methods have been introduced for differentiating tubercle bacilli from other
acid-fast bacilli (Korallin method, and House's method). For these, the special
text-books must be consulted. They are not absolutely reliable, and, where there is
doubt, cultures should be made, or animal inoculations undertaken.
iii. Stains for Treponema pallidum
The material can be obtained from a mucous patch in the mouth, from a
hard chancre, or from other luetic lesions. In the case of hard chancre, the
surface is first touched several times with a hit of cotton wet in ether, then
cautiously scraped with a knife short of hemorrhage, after which a scraping
is cautiously made from the middle to the periphery of the chancre until a
little bloody serum just appears. It is well to examine a droplet of this
fresh, by "dark-field illumination"; often the spirochsetes can be seen in
lively rotary motion. A drop is taken up with the edge of a thoroughly
clean glass slide, or cover slip, and spread upon a similarly clean slide by
stroking. If the smear be correctly made, single intact red corpuscles will
be scattered in it. The smear is dried in the air and fixed in the flame in
the ordinary way.
Methylene Azure Eosin. — The preparation is stained with Wilson's or
Giemsa's stain (20 drops to 20 c.c. of water). Some of the diluted stain is placed
on the slide, which is clean, warmed over the flame until steam arises, but short of
boiling. The first stain is poured off and fresh stain added and heated, and this
process repeated several times. The quicker the staining is carried on, the better.
Wash in water, and dry. Red blood corpuscles and spirochastes are stained a
bright red color and look granular.
India Ink Method. — A drop of serum obtained from the chancre as above de-
scribed is mixed evenly with a drop of fluid India ink of the best quality on a glass
APPLICATIONS OF BACTEKIOLOGICAL METHODS 145
slide, after which an even thin smear is made with the end of another slide, or
with the edge of a cover slip, allowed to stand £ minute, and dried. Examine at
once with oil immersion lens.
The spirochsetes are seen as glistening, silverlike cork-screws, lying on a homo-
geneous brown background. This method
can be warmly recommended for clinical
diagnosis.
References
Cohn (J. S.). On the means of finding the
Spirochceta pallida, with
special reference to the India
ink method. Interstate M.
J., St. Louis, 1911, xviii,
26-31.
Geraghty (J. T.). The practical value of the
demonstration of Spirochasta
pallida in the early diagnosis
of syphilis. Johns Hopkins
Hosp. Bull., Baltimore,
1908, xix, 364-367.
Ueber den Nachweis der Spi-
rochceta pallida im Ausstrich
mittelst der Silbermethode.
Berl klin. Wchnschr., 1907,
xliv, 400.
Stern (M.).
Fig. 51. — India Ink Preparation from a
Luetic Papule — Papulopustular Syphi-
lide in an Infant. (After E. Moro in E.
Leer's "Lehrb. d. Kinderheilkunde,"
published by G. Fischer, Jena.)
White (B) & Avery (O. T.). The treponema pallidum. Observations on its occurrence and
demonstration in syphilitic lesions. Arch. Int. Med., 1909, Hi, J^ll-^21.
iv. Stains for Capsules
Several methods are in use. Two of the better known stains will be given here.
Welch's Method. — After fixation, place a drop of glacial acetic acid on the
smear. After a few seconds pour off the acid and cover smear with anilin,
water gentian violet, renewing the stain several times. When staining is complete
(3-5 minutes) wash preparation in 2 per cent salt solution and examine in this
solution.
Johne's Method. — 1. Stain with 2 per cent aqueous solution of gentian violet,
warming for 2 minutes.
2. Wash in water, decolorize in 1 to 2 per cent acetic acid for 6-10 seconds.
3. Wash in water and examine in the same. (In Canada balsam the capsules
disappear.)
v. Stains for Spores
Moeller's method is often used. Fix a cover slip in the ordinary way, and
immerse for from 5 seconds to 10 minutes in 5 per cent solution of chromic acid,
the time varying for the different varieties of bacteria, and to be tested in each case.
W<ish in water, stain in steaming carbol-f uchsin 1 minute, decolorize for 5 seconds in
5 per cent H2S04, wash in water, counterstain with aqueous methylene blue solution,
wash, dry, mount. The spores will be stained red, the bodies of the bacteria blue.
Another method consists in placing some of the material in \ c.c. salt solution,
and adding to this \ c.c. filtered carbol-f uchsin solution. Place the test tube in
boiling water for 10 minutes. Place a droplet on a glass slide and warm. When
dry, fix in the flame and decolorize in equal parts of absolute alcohol and water
146 DIAGNOSIS OF INFECTIOUS DISEASES
(if necessary, acidulating with HC1) ; wash in water; counterstain with Loeffler's
methylene blue.
vi. Stains for Flagella
I. Bunge's Method. — With the point of a platinum needle, place a minute par-
ticle of a young agar-slant-culture .(not bouillon culture) in a small droplet of
water on a cover slip. Mix well, make a smear, dry quickly. Immerse the cover
slip in Bunge's mordant (25 c.c. of a 25 per cent ferric chlorid solution, plus 75
c.c. saturated solution of tannic acid) for 1 minute, heating until steam comes off.
Wash in water and dry. Float on carbol-gentian-violet, and warm gently. Wash
in water; dry; mount in balsam.
II. Zettnow's Method. — SOLUTION A. — 10 g. Tannin dissolved in 150 c.c. dis-
tilled water.
SOLUTION B. — Tartar emetic 2 g. dissolved in 40 c.c. hot distilled water. '
Warm A. to 40° C. (not above 45° C.) ; to it add gradually 27-28 c.c. of Sol. B.,
or until the precipitate which arises does not materially diminish after a few
minutes' shaking. This mordant is ready for use at once and can be kept for months
by adding a large thymol crystal.
TECHNIC. — Place some of the mordant in a test tube after shaking the flask well.
Boil until clear. Lay the cover slip in a box-glass with the film side down, and pour
the warm mordant over it. Leave the cover slip in until the cooling mordant begins*
to become turbid ; then remove the cover slip and wash with water ; then fasten it in
a Cornet forceps and set on edge to drain and dry. Now lay the cover slip horizon-
tally and cover it with a solution of methylamine silver made by shaking 2-3
grams silver sulphate violently with 200 grams water until saturated. Of this solu-
tion, one part is diluted with 1 part distilled water, and then mixed with 33 per cent
methylamine solution until the precipitate first arising again dissolves. Warm the
cover slip, covered with silver solution, in a low flame until vapor begins to come
off; wash with water, and dry. The silver sulphate is made by precipitating silver
nitrate solution with magnesium sulphate or sodium sulphate.
The flagella are stained black ; in many bacteria they are attached all
around the body of the bacterium (peritrichous) ; in others, there is only a
single flagellum at one end (monotrichous) .
5. Bacterial Cultures for Clinical Diagnosis
Both fluid and solid media are used. Among the fluid media, bouillon,
plain or enriched, and peptone solution are most employed. For the isola-
tion of typhoid bacilli, Conradi's bile medium (ox bile 900 c.c. ; glycerin
100 c.c. ; peptone 20 grains) is often used. Plain milk and litmus milk are
also valuable for differential diagnosis.
Among the solid media, coagulated blood serum, especially Loeffler's
serum, to which 1 per cent glucose bouillon has been added, is much
used, for the isolation of diphtheria bacilli. Potato, gelatin, and especially
agar, either plain, or agar to which glycerin, blood, glucose/ or other sub-
stances have been added are in daily use.
Reliable media can now be purchased. If one makes one's media, it
APPLICATIONS OF BACTEKIOLOGICAL METHODS 147
may be convenient to use instead of agar, the so-called ragit (Merck),
which simply needs to be dissolved up to be ready for use.
Certain special media have been found useful in making cultures from
stools when it is desired to isolate typhoid, paratyphoid and colon bacilli.
Several of the more important follow.
Lactose-litmus-imtrose agar (Drigalski and Conradi), by means of which we
find out whether a bacterium can decompose the milk sugar with formation of acid
which reddens litmus. The medium should be prepared as directed in Hiss and Zins-
ser's Text-book. In addition to litmus and lactose it contains crystal violet to inhibit
the growth of bacteria other than B. typhosus or B. coli. On this medium, typhoid
bacilli, paratyphoid bacilli (A and B), and dysentery bacilli, grow as blue- colonies,
while the colon bacillus grows as red colonies.
Fuchsin-sulphite agar (Endo). To a liter of 3 per cent neutral agar are
added 10 c.c. of 10 per cent soda solution, 10 g. lactose, 5 c.c. saturated fuchsin
solution (filtered) ; then add 25 c.c. freshly prepared solution of sodium sulphite (10
per cent) . This medium is clear when the reaction is alkaline and sodium sulphite is
present. It should be kept in the dark, and air-tight. For use, it is poured into
Petri dishes.
Bacteria that convert the milk sugar into lactic acid grow as red colonies, while
other bacteria form colorless colonies. Endo's fuchsin agar can be prepared quickly
by the use of the so-called Endo-capsule (Merck).
Malachite-Green Agar. — This consists of 3 per cent neutral agar plus 5 c.c. nor-
mal NaOH (per liter) plus 1 per cent nutrose plus 1 c.c. of a 1 per cent solution of
malachite green (C. P. Hochst) in water and alcohol. According to H. Schindler, it
is best to make tests with varying amounts of malachite green in the medium until
one gets the composition in which most typhoid colonies and fewest colon colonies
will grow. The medium has the advantage of inhibiting the growth of B. coli and
various other bacteria.
Hints for Culture. — For the diagnosis of diphtheria, slants of Loeffler's
medium are very satisfactory. For blood and sputum cultures, blood-agar
Petri plates are desirable. For cultures from the stools, the special media
of Drigalski and Conradi, Endo, etc., are useful.
For the exact determination of the bacterial species obtained, all the
ordinary methods of the bacteriological laboratory must be employed in the
clinical laboratory (blood cultures, surface cultures on various media,
animal experiments, etc.).
If the presence of anaerobic bacteria be suspected, oxygen-free growth
should be attempted (pyrogallic acid method; hydrogen or illuminating-gas
method ; mechanical method ; plastillin method of Lentz and Heim). (See
Special Texts.)
In studying the biological properties of bacteria, the capacity for fer-
mentation of sugars and proteins, for the formation of alkali or acid, H2S
or indol, the oxygen-need, the reducing capacity, the toxin production, and
the production of pigment, may need investigation.
The value of blood-cultures is often so great from a diagnostic point of view
that it is a pity that they are not more often made outside of the hospitals. Satis-
148 DIAGNOSIS OF INFECTIOUS DISEASES
factory blood-cultures can be made by any physician who has had elementary
training in bacteriology, though he may require the assistance of a trained labora-
tory worker in the interpretation of the results.
The patient's arm is thoroughly washed with green-soap followed by 70 per
cent alcohol. An Esmarch bandage, or a length of rubber tubing, is applied about
the upper arm tightly enough to cut off the venous flow but not to obliterate the
radial pulse. The veins of the forearm are thereby distended and show prom-
inently. In fat people, in women, and in cachectic patients, this maneuver may
not suffice to render the veins visible. They must then be palpated by passing the
fingertips gently across the forearm. The veins are readily felt as corids in the
subcutaneous tissues. If the patient clench and unclench the fist the veins often
become more prominent. In very difficult cases immersion of the arm in hot
water (with the bandage on) will often be of use. As a rule, no difficulty is expe-
rienced in finding a suitable vein. The easiest to enter with a needle are not the
most superficial veins, but those whose attachment to the deep fasciae renders
them less mobile — a point on such a vein is hence selected. If palpation has been
necessary, the skin is again cleansed with alcohol. Keep the patient's fingers and
flies off this prepared area. Nothing should touch the needle nor the skin where
the needle is to enter.
A 10-20 c.c. Luer, or Record syringe with a sharp needle (No. 18-20) and a
hemostat should meantime have been boiled for three minutes in a shallow pan.
(Caution: remove the piston for boiling). The water is carefully drained off.
The barrel is picked out, the piston fitted into it, and then with a sterile hemostat
the needle is picked up and fitted on and the obturator gently pulled out from
the lumen of the needle.
The point of the needle is then passed through the skin overlying the vein,
with a quick thrust, and then more slowly it is pushed through the wall of the
vein itself. In this way one avoids passing completely through the vein. When
the point of the needle enters the lumen of the vein, blood mounts into the syringe.
The piston is slowly drawn out until the requisite amount of blood is obtained.
If the flow becomes very slow it is best to stop, as too great delay at this stage
will result in clotting inside the syringe. Ten c.c. are sufficient. The constrictor
is loosened before the needle is withdrawn. The cotton stopper of a tube of
media is then flamed over an alcohol lamp, withdrawn and held between two fingers,
the mouth of the tube flamed, and the proper quantity of blood delivered into the
media, after which the tube is plugged. Each tub) or flask of media is thus
rapidly inoculated in succession. If desired, some of the blood may be placed
in an empty tube for the Wassermann or Widal test. The syringe should be
washed with cold water before clotting in the barrel occurs.
Since outside hospitals it is often awkward to melt down agar, and to pour
plates, reliance is usually placed upon the liquid media of which the various
bouillon and bile medias are the standbys. It is probably better to deliver the
blood from the syringe into a small sterile flask, containing a few c.c. of sterile
1 per cent sodium citrate to prevent coagulation. The flask is then taken to the
laboratory where transfers to suitable media are made.
Recently, there have been placed upon the market vacuum tubes (Keidl) con-
taining sterile citrated-glucose-bouillon. A needle and rubber connection are fur-
nished, which are boiled and then fitted over the point of the vacuum tube. The
needle is introduced into the vein and the fine point of the tube broken by bend-
ing the rubber connection. The vacuum draws blood into the citrated media. The
tube can then be taken to the laboratory. Empty tubes may be used for collecting
blood for the Wassermann test,
APPLICATIONS OF BACTEEIOLOGICAL METHODS 149
References
Canon. Die Bakteriologie des Blutes bei InfektionskrankJieiten. Jena, 1905, G. Fischer.
256 p. 8°.
Fried (G. A.} & Sophian (A.). Investigations concerning the value of the microscopic ex-
amination of the blood for bacteria. Am. J. M. Sc., Philadelphia & New
York, 1911, cxlii, 88-92.
Jochmann (G.}. Ueber die Bakteriamie und die Bedeutung der bakteriologischen Blut-
untersuchung fur die Klinik. Ztschr. f. klin. Med., Berlin, 1904, liv,
408-447.
Judd (C. C. W.} & Simon (C. E.}. The vacuum tube of Keidel as applied to blood-cul-
ture work. J. Am. M. Ass., Chicago, 1915, Ixiv, 822. '
Libman (E.). On some experiences with blood-cultures in the study of bacterial infections.
Johns Hopkins Hosp. Bull., Baltimore, 1906, xvii, 215-228.
On certain features of the growth of bacteria on media containing sugars and
serum, with remarks upon the acid production. J . Med. Research, Boston,
1901, n. s., i, 84-96.
Noguchi (Hideyo). On the application of certain cultivation methods to the study of infec-
tious diseases. Berl. klin. Wchnschr., Berlin, 1914, li, 509-11.
6. Animal Inoculations, and Virulence Tests
Subcutaneous, intravenous, intraperitoneal and subdural injections of
the bacteria under examination may be necessary, especially in testing
virulence. Certain bacteria are virulent for certain animals, not for others,
a point often useful in diagnosis.
In a number of instances, bacteria can be most easily isolated in pure
culture by passing the material through a susceptible animal. This is
especially true of the bacillus of tetanus, the tubercle bacillus, the anthrax
bacillus, and the pneumococcus.
If sputum contain the pneumococcus, a small portion of it placed under
the skin at the root of the tail of a mouse will lead quickly to the death of
the animal, and the pneumococcus can be obtained in pure culture from the
heart's blood. If a few cubic centimeters of the blood of a human being
suffering from lobar pneumonia be injected into the ear vein of a rabbit,
the rabbit will often die within 24 hours, and enormous numbers of pneu-
mococci in pure culture can be found in the heart's blood.
If the centrifugate of the urine, in a case of renal tuberculosis, be
injected into the peritoneum of a guinea-pig the animal may be killed at
the end of 2 or 3 weeks and tuberculous lesions found, from which tubercle
bacilli may be grown in pure eulture.
Eats are very susceptible to plague ; rabbits to staphylococci, streptococci
and pneumococci ; dogs to malignant edema ; guinea-pigs to tuberculosis and
glanders; mice and rats to anthrax.
For details of animal inoculations special text-books on bacteriology
should be consulted.
150 DIAGNOSIS OF INFECTIOUS DISEASES
D. Clinical Applications of Immunological
Methods
The newer knowledge of immunity and anaphylaxis (allergy) has
already been utilized in clinical diagnosis, especially in certain serodiag-
nostic reactions.
Among the antibodies utilized for clinical diagnostic tests are (1) agglu-
tinins, (2) lysins, (3) precipitins, (4) opsonins, and (5) ergins. The
principles underlying these tests have been described above. Here the
technic of some of the tests themselves will be given.
References
Citron (/.). Immunity; methods of diagnosis and therapy, and their practical application.
TransL from the German by A. L. Garbat. Philadelphia, 1912, P. Bla-
kistoris Son & Co. 209 p. 8°.
Dick (G. F.). Immunological reactions in diagnosis. In: Forchheimer's Therapcusis of
internal diseases. New York & London, 1914, v, 121-168.
Dieudonne (A.}. Immunitdt, Schutzimpfung und Serumtherapie. 8th ed. Leipzig, 1913.
248 p.
Kolmer (John Albert}. A practical textbook of infection, immunity and specific therapy,
with special reference to immunologic technic. With an introduction by
A. J. Smith. Ill by E. F. Faber. Philadelphia & London, 1915, W. B.
Saunders Co. 908 p.
Much (H.). Die Immunitatswissenschaft. Sine kurzgefasste Uebersicht uber die biolo-
gische Therapie und Diagnostik. 2. Aufl. Wurzburg, 1914, C. Kabitzsch.
286 p. 8°.
Sachs (H.} & Ritz (H.). Experimentette spezifische Diagnostik mittels Agglutination, Bak-
terizidie (Lyse) und Komplementbildung. In: Handb. d. pathogen. Mi-
kroorg. (Kolle & Wassermann). 2. Aufl. Jena, 1913, Hi, 1-122.
Simon (Charles E.). An introduction to the study of immunity, including chapters on
serum-therapy, chemotherapy, and serum-diagnosis. 2d ed. Philadelphia
& New York, 1913, Lea & Febigcr. 352 p. 8°.
Weichardt (W.). Jahresbericht ueber die Ergebnisse der Immunitdtsforschung und deren
Grenzivissenschaften, der Chemotherapie, Zoonosologie, Hygiene, etc. Stutt-
gart. Vols. i-4x, 1905-1914.
1. Tests for Agglutinins
Agglutination reactions may be employed either for the identification of
a given organism (with an immune serum) or for the recognition of the
nature of an immune serum (with a known bacterium). Thus, in the for-
mer instance, an emulsion of an unknown bacterium is treated with diluted
immune serum (antityphoid, anticolon, antidysentery, etc.) ; in the latter
instance the unknown serum is tested against a series of known bacteria.
The most important clinical agglutination reaction is the so-called Widal
reaction in typhoid fever, though the same principle has also been utilized
for diagnostic purposes in paratyphoid, in meningococcus infections, and in
Malta fever.
APPLICATIONS OF IMMUNOLOGICAL METHODS 151
(a) The Widal Reaction
This may be carried out by the microscopic or by the macroscopic
method. For the former, only a few drops of blood are necessary ; for the
latter 1-5 c.c. are desirable.
In addition, known typhoid
bacilli of agglutinable strain
must be available, preferably
an 18 to 24-hour old bouillon
culture, or a thin suspension
of bacilli made by rubbing up
a small loop of the growth,
from an 18-hour agar culture,
in 5. c.c. of sterile 0.8 per
cent ISTaCl solution.
Microscopic Test. — The ex-
amination is made in the
hanging drop (see above).
The serum is diluted, first
with 24 parts of salt solution
by means of a mixing pipet,
and from this other dilutions
—1:50, 1:100, and 1:200—
are prepared. A drop of each
dilution— 1 :25 to 1 :200— is
placed upon a cover slip by
means of a platinum loop, and
a small drop of the fresh
bouillon culture, or agar
growth in suspension added.
The vaselined hollow slide is
then applied, and the speci-
mens examined at once, with
a high-power dry lens. If
large clumps of bacteria are
visible, the preparation is dis-
carded, and the suspension of
bacilli centrifugalized for a
minute or two. This throws
any clumps to the bottom, and
the supernatant fluid may be used for making new preparations. When
satisfactory specimens, free from clumped organisms, have been obtained,
they are set aside for from -J to 1 hour and then re-examined. If the
reaction be positive, the bacilli will have, lost their motility, and will be
Fig. 52.— Widal Reaction— Half Schematic; (a).
Typhoid Bacilli Free ; (b) Typhoid Bacilli
Agglutinated. (After H. Schottmiiller in
Mohr and Staehelin's "Handb. d. inner. Med.,'?
published by J. Springer, Berlin.)
152 DIAGNOSIS OF INFECTIOUS DISEASES
gathered in clumps of variable size. Ordinarily, complete clumping in
1 hour with a serum dilution of 1 :50 is regarded as a positive reaction of
diagnostic value. The highest dilution which causes clumping and lessens
motility is called the agglutination titer of the serum.
Macroscopic Test. — In each of a series of small test tubes 0.5 X 5 cm.,
place 1 c.c. of varying dilutions of serum (1:10; 1:50; 1:100; 1:200,
etc.), and, in a control tube, 1 c.c. of normal salt solution. To each tube add
1 c.c. of the bacterial suspension. Place the tubes in the thermostat, at the
body temperature, for 3-7-12 hours. If the reaction be positive, the bac-
teria will settle to the bottom as a white flocculent sediment, leaving the
fluid above them clear and contrasting sharply with the control tube in
which there is a granular deposit and a uniformly turbid supernatant fluid.
The macroscopic method is the one of choice where exact results are
desired.
METHOD or BASS AND WATKINS. — Bass and Watkins have devised a
rapid macroscopic test using formalinized bacilli instead of living or-
ganisms. Briefly stated, the method is as follows: One or two drops of
blood, diluted with 4 volumes of water, is mixed on a glass slide with an
equal amount of the test suspension (10,000 millions bacilli per 1 c.c. of
1.7 per cent NaCl and 1 per cent formalin). The slide is slowly tilted to
and fro. If the reaction be positive, a grayish sediment settles in a minute
or less ; when the reaction is negative, the mixture remains clear.
TICKER'S TYPHOID DIAGNOSTICUM. — This is a purchasable suspension of dead
agglutinable typhoid bacilli (Merck) used for macroscopic tests as above. The
dealers supply both a typhoid, and a paratyphoid strain.
One can, if he wishes, use cultures killed in the laboratory instead. A bouillon
culture (Erlenmeyer flask) of an agglutinable strain 24 hours old is killed by the
addition of formalin, in such amounts that the total mixture contains 1 per cent
f ormaldehyd. Allow to stand "for 3 days in the thermostat ; centrif ugalize ; wash the
bacilli twice with sterile salt solution, centrifugalizing each time, dilute with salt
solution to the original volume, and preserve in sterile glass bulbs in the ice-box.
Such material will keep for months.
Judgment of the Agglutination Reaction. — Agglutination in dilutions
under 1 : 50 are of no diagnostic value, since normal serum may possess
some agglutinating power. Agglutination in dilutions of 1:50 and in
liigher dilutions possess diagnostic value. In exceptional instances, agglu-
tination of typhoid bacilli in 1—50 dilution has been noted in cases of
tuberculosis and of jaundice. In typhoid fever, the reaction is rarely posi-
tive until the beginning of the second week in bed, and it is frequently
negative until the third week, and, occasionally, until late in convalescence.
In rare instances of undoubted typhoid, as proven by positive blood culture,
the Widal reaction may remain negative throughout. The reaction may
remain positive for several weeks or months after the infection ; indeed, it
is sometimes present years after typhoid fever. When the reaction per-
APPLICATIONS OF IMMTOTOLOGICAL METHODS 153
sists for such a long period, persistent local infections (bones, gall-blad-
der) may be suspected. Probably all typhoid carriers yield a positive
Widal reaction.
It will be interesting to learn how long the Widal reaction remains posi-
tive after prophylactic inoculation against typhoid.
~No parallelism exists between the severity of the case and the amount
of agglutinins formed.
It is interesting that some strains of typhoid bacilli yielding a negative
result in dilutions of 1:50 and 1:100 yield a definitely positive result in
higher dilutions (1 : 500 ; 1 : 1000).
In cases of group reaction, one may determine the agglutination titer
for each organism of the group, or one may adopt Castellani's method of
mixing a portion of immune serum with each of the members of the group,
centrifugalizing, and testing the supernatant fluid for its agglutination
titer for the other members. (For References, see pp. 121-122.)
2. Tests for Lysins (Bacteriolysins; Hemolysins)
The substances concerned have already been described. Two main clin-
ical applications are used: (a) Pfeiffer's experiment, and (b) complement
fixation tests.
(a) Pfeiffer's Experiment
If an immune serum from the rabbit (against cholera or typhoid) be inactivated
by heat and injected, with its corresponding (homologous) bacteria, into the peri-
toneal cavity of a guinea-pig, and a little of the peritoneal exudate obtained by
means of fine glass capillaries be examined at intervals (immediately, after 5 min-
utes, 15 minutes, 30 minutes, etc.) in hanging drop preparations, it will be
observed that the bacteria quickly lose their motility, swell up, become granular, and
in three-quarters of an hour or an hour are completely dissolved (bacteriolysis}.
The complement of the guinea-pig's peritoneal fluid has reactivated the amboceptors
of the immune serum and caused bacteriolysis.
The reaction is strongly specific, and is of great importance, especially in the
diagnosis of cholera, when it is desirable to establish without doubt the diagnosis in
the first cases of the disease at the beginning of an epidemic by isolating the cholera
vibrio in cultures and establishing the identity of the cultivated vibrio.
Diagnosis of an Unknown Bacterium by Bacteriolysis with a Known Immune
Serum. — In actually performing the experiment for clinical purposes, it is desir-
able to use immune serum of known strength, dried in vacuo. This can now be pur-
chased, put up in small brown glass tubes containing 0.2 grams. In cholera, the
strength of the immune serum must be so great that 0.0002 c.c. suffices completely to
bacteriolyze 2 mg. (1 oese) of an eighteen-hour agar culture of cholera bacilli,
placed with it in the peritoneal cavity of the guinea-pig, within 60 minutes ; in other
words, it must possess a bacteriolytic titer of at least 1:5000.
TECHNIC. — Four guinea-pigs, each weighing approximately 200 g., are required.
Guinea-pig A receives 5 times the titer dose, i. e., 1 mg. of an immune serum with
a titer of 1 :5000.
154 DIAGNOSIS OF INFECTIOUS DISEASES
Guinea-pig B receives 10 times the titer dose, i. e., 2 mg. of an immune serum
with a titer of 1:5000.
Guinea-pig C, a control animal, receives 50 times the titer dose, i. e., 10 mg. of
normal rabbit's serum.
The serum injected into the peritoneal cavity of each of these three animals is
first mixed with 1 oese of an agar culture of the suspected bacterium (18 hours at
37° C.) rubbed up in 1 c.c. bouillon (not in salt solution or peptone water).
Guinea-pig D receives 1 oese of the bacterial culture in 1 c.c. bouillon, without
other admixture, in order to find out whether the culture is virulent for the guinea-
pig or not.
If, in the first two animals, A and B, bacteriolysis occur within 20 minutes, or at
the latest within one hour, while in animals C and D, bacteriolysis has not occurred,
the reaction is positive, and the microorganism is proven to be the suspected infec-
tious agent.
Diagnosis of an Unknown Immune Serum by Bacteriolysis of a Known Bac-
terium.— One can, on the other hand, use the same principle for determining
whether a serum derived from a patient suspected to have typhoid or cholera, or
from a convalescent from these diseases,- contains immune bodies (bacteriolysins
against the typhoid bacillus, or against the cholera vibrio). The suspected serum
(usually in dilutions of 1:20, 1:100, 1:500) is injected, together with the bacteria,
into the peritoneal cavity of the guinea-pig; examinations are made, at intervals,
up to 1 hour, to see whether the organisms undergo granular disintegration and
lysis.
Bacteriolysis in Vitro. — The method described above requires a living animal;
the test is done in vivo. It can also be carried out in vitro (Stern and Korte). In-
activated typhoid serum (in different dilutions) is mixed in test tubes with serum
containing complement (fresh rabbit serum) and with known typhoid bacilli; the
mixture is allowed to stand for 45 to 60 minutes, after which agar plates are made to
determine in what dilutions the serum has killed, or markedly diminished, the growth
as contrasted with the control tests in which inactivated normal serum was used
instead of immune serum. In typhoid fever, positive results are usually obtainable
with dilutions of 1 : 1000, and even in less concentration.
Reference
Pfeiffer (#.)• Untersuchungen uber das Choleragift. Ztschr. f. Hyg. u. Infectionskrankh.,
Leipzig, 1892, xi, 893-412.
Die Differenlialdiagnose der Vibrionen der Cholera Asiatica mil Hiilfe der
Immunisirung. Ztschr. f. Hyg., Leipzig, 1895, xix, 75-100.
Weitere Mittheilung uber die specifischen Antikorper der Cholera. Ztschr.
f. Hyg., Leipzig, 1895, xx, 198-219.
NOTE. — For other references, see pp. 116-118.
(b) Complement Fixation Tests
As has been fully described above, by complement fixation is meant the
fact that when antigen and specific antibody are mixed together, the com-
plement present becomes anchored, so that no complement is available for
an introduced hem oly tic system (hemolytic amboceptor + red corpuscles),
and no hemolysis results.
Complement is fixed in the presence of amboceptor and bacterial anti-
gen (Bordet-Gengou phenomenon) ; it is also fixed in the presence of pre-
APPLICATIONS OF IMMUNOLOGICAL METHODS 155
cipitin and protein-antigen (Gengou-Moreschi phenomenon). Both these
forms of complement fixation have been used in clinical diagnosis.
If one immunize a large rabbit by injecting it on several (3-4) occa-
sions, 4-6 days apart, with the washed corpuscles from 1.0-10.0 c.c. of
sheep's blood (asepsis!), the rabbit's serum in 10-12 days, after the last
injection will possess in favorable cases a strong specific hemolytic power
for sheep's corpuscles, the hemolysis depending upon the cooperation of two
substances, (1) specific hemolytic amboceptor, and (2) non-specific normal
complement.
If such an immune serum be rendered inactive by heat, it will still con-
tain hemolytic amboceptor but no complement.
Now, if a given antigen be mixed with the (homologous) amboceptor to
which it can, on injection, give rise, the two unite to form a compound
which has an extraordinary affinity for free complement; the compound
formed by their union binds the complement firmly, while either antigen or
amboceptor alone possesses only slight affinity for such complement. If
one suspect that a patient's serum contain a certain specific amboceptor,
and, to a portion of this serum, some corresponding antigen (extract of
syphilitic liver, typhoid bacilli, etc.) be added, together with a little fresh
complement, and the whole be kept at 37° C. for a short time, the comple-
ment will be liound (fixed, or anchored), if the suspected amboceptor be
present. Now, since in this fixation all free complement has been used up,
if the hemolytic system be introduced (sheep's red corpuscles + hemolytic
amboceptor in the form of inactivated immune serum), no hemolysis will
occur because of the lack of free complement (positive reaction for comple-
ment fixation) ; but should we be wrong in our surmise regarding the pres-
ence, in the patient's serum, of an amboceptor corresponding to the antigen
used, the complement will not be bound, and so free complement will be
available to activate the hemolytic amboceptor, and the red corpuscles of the
hemolytic system will be laked; in other words, hemolysis will occur
(negative reaction for complement fixation).
The method has been used for the diagnosis of typhoid fever, of tubercu-
losis, of chronic gonorrhea, and of certain other infectious diseases, but it
has scored its greatest triumph in the serum diagnosis of syphilis, for
which purpose it was applied first by Wassermann, Neisser and Bruck
(1906), the test being generally known as the Wassermann reaction. They
used an extract of the liver of a luetic fetus as antigen. About the same
time, Detre used as antigen an extract of condylomata.
References
Bordet (/.)• La fixation de Valexine et sa signification pour Vimmunite. Ztschr. f. 7m-
munitatsf., Ref., Jena, 1909, i, Theil ii, 1-88.
Clowes (G. H. A.}. Deviation of complement by means of the serum of sarcoma rats. J.
Am. M. Ass., Chicago, 1909, Hi, 408.
156 DIAGNOSIS OF INFECTIOUS DISEASES
Dean (H. 72.) . The relation between the fixation of complement and the formation of a pre-
cipitate. Ztschr. f. Immunitdtsforsch. u. exper. Therap., Jena, 1912-13,
Orig., xiii, 84-122.
Jacoby (M.) & Schutze (A.). Ueber die Inaktivierung dcr Komplemente durch Schutteln.
Ztschr. f. Immunitdtsforsch., Jena, 1909-10, Orig., iv, 730-739.
Marks (H. K.}. The thermostability of the midpiece of complement. Ztschr. f. Immunitdls-
forsch. u. exper. Therap., Jena, 1911, Orig., xi, 18-30.
Meakins (J. C.). The method of "fixation of complement " in the diagnosis of meningo-
coccus and gonococcus infections. Johns Hopkins Hosp. Bull., Baltimore,
1907, xviii, 255-258.
Moreschi (C.). Zur Lehre von den Antikomplementen. Berl. klin.Wchnschr., 1905, xlii,
1181-1185.
Also: 1906, xliii, 100-104.
Neufeld (F.) & Handel. Ueber Komplementbindung und Komplementablenkung bei 0°
und bei 37°. Arb. a. d. k. Gsndhtsamte, Berlin, 1908, xxviii, 198-212.
Skwirnsky (P.). Ueber den Mechanismus der Komplementbindungen. Ztschr. f. Immuni-
tdtsforsch. u. exper. Therap., Jena, 1910, v, 538-571.
Zinsser (H.}. Practical applications of the complement-fixation method. In: Infection and
Resistance (H. Zinsser). New York, 1914, 198-217.
i. Wassermann Reaction ( Wa.-R.)
• It was first shown that the serum of syphilitic patients, mixed with salt
solution extracts of syphilitic organs (liver of congenital syphilis) as anti-
gen, would absorb complement. From this it was assumed that the salt
solution extract of luetic organs contains syphilitic antigen, and also that
the blood serum of syphilitic patients contains specific (syphilitic) anti-
bodies (amboceptor).
It turns out from later studies that alcoholic extracts and acetone extracts of
luetic liver work as well as saline extracts, and, moreover, extracts from perfectly
normal tissues (human heart, guinea-pig's heart) work as well as those from syphil-
itic organs, especially if a little cholesterin be added.
The antigen appears to be a lipoid body, possibly related to lecithin, and the
antibody in the serum of syphilitic patients can scarcely be an amboceptor in the
sense of Ehrlich, but seems rather to be some substance with a marked affinity for
lipoid bodies. It has been called the lipoidophilic antibody (C. E. Simon).
As a hemolytic system, sheep's corpuscles, together with the antiserum
made by injection of sheep's corpuscles into rabbits and inactivated by heat
so as to contain only amboceptor, was used, and, for complement, fresh
guinea-pig's serum was employed.
Before carrying out the test, certain control experiments must be made
to determine the activity of the extract, of the hemolysin, and of the com-
plement, and to make sure that the serum to be tested does not, of itself,
inhibit hemolysis (autotropic serum).
Technic. — The five substances necessary for the test are (1) the antigen,
(2) the serum suspected to contain the amboceptor corresponding to the
antigen, (3) complement, (4) hemolytic amboceptor s, (5) corresponding
red corpuscles.
APPLICATIONS OF IMMTOTOLOGICAL METHODS 157
1. The ANTIGEN, as originally obtained, is a watery extract made as
follows : A weighed amount of the liver of a macerated syphilitic fetus is
cut into small pieces, ground up, shaken for 24 hours in 4 times its weight
of salt solution (0.85 per cent) containing 0.5 per cent carbolic acid, the
coarser particles removed by a gauze filter, and the mixture briefly centrifu-
galized (half a minute). The centrifugate thus obtained is not a solution,
but a homogeneous, fairly stable suspension. It is kept in a dark flask, in
the ice-box, and should always be well shaken before using. The amount of
extract necessary to combine complement is determined in a preliminary
experiment, and it is also ascertained whether the extract alone will hemo-
lyze red blood cells without the presence of either complement or hemo-
lysin. Practically, only those antigens are used of which 0.4 c.c. will not of
itself fix the complement.
Many workers use, instead of the above watery extract, an acetone
extract, made by extracting 1 gram dried substance of luetic liver, normal
heart or guinea-pig's heart, rubbed up in a mortar with pure acetone.
The suspension is placed^for 8-10 hours in the thermostat at 37° C., and
then for the same length of time in a shaking machine, after which
it is allowed to stand half a day at the room temperature, and then filtered.
The flask should be closed air-tight with a rubber stopper.
Extracts (aqueous or acetone) must be tested out to see (1) whether
they are suitable for the Wassermann reaction, and (2) if found suitable,
what amounts it is best to use to secure reliable results.
Noguchi has prepared an antigen by using the acetone-insoluble fraction
of alcoholic extracts, since he has found that the antigen thus prepared is
free from the decomposition products of protein, such as albumoses and pep-
tones, which are capable of "proteotropic ferment fixation." The heart,
liver or kidney of man or animal is hashed and extracted with 10 volumes
of absolute alcohol for several days at 37° C. This extract is filtered, the
filtrate evaporated in vacuo to dryness, extracted with ether, the ethereal
extract concentrated, and mixed with 10 volumes of pure acetone. The
insoluble precipitate is collected, dissolved in a minimal amount of absolute
methyl alcohol, and kept in ampules as a stock solution. For use, enough
stock solution is dissolved in salt solution to make a solution containing
0.3 per cent of the original lipoids. This can be kept on ice until it is used.
Noguchi has also prepared an antigen from pure cultures of Trepo-
nema pallidum.
Very recently antigens made of alcoholic extract of beef-heart to which
0.05 per cent cholesterin is added, have come into use. Such cholesterinized
alcohol-extract antigens promise well. They may come into general use.
In such testing of antigens, we make use of a positive standard serum
(luetic) and of a negative standard serum (non-luetic), controlled just
before testing by a reliable standard antigen extract. We also control all
the reagents (sera and extracts) individually with the hemolytic system.
158 DIAGNOSIS OF INFECTIOUS DISEASES
to see if any one of them, with double the amount used in any test, will by
itself inhibit hemolysis. Rough tests are first made for orientation with 5
doses of the extract (0.2; 0.1; 0.05; 0.025; 0.0125). If we find, for
example, that the extract tested works well in the amounts 0.05 and 0.025,
we then make tests of the efficiency of the extract in comparison with that
of a well-tested standard extract, and raise and lower the dose of the new
antigen until results are reached that are, as near as possible, like those
obtainable with the standard antigen. The amount of new extract that does
this is used as the ordinary dose. The extracts remain fairly constant in
activity, so that the dose, once determined, can be relied upon as correct
for a considerable period. Antigen when added to a hemolytic system in
sufficient concentration will inhibit hemolysis. Since this effect is produced
by the action of the concentrated antigen upon the complement it is spoken
of as the anticomplementary property of the antigen. In titrating the anti-
gen we observe, in the series with normal serum, whether any anticomple-
mentary action is observable and what is the least concentration of antigen
which will produce such an effect. In the positive-serum series we observe
what is the smallest amount of antigen that will cause complete inhibition
of hemolysis; this amount is usually spoken of as one unit of antigen.
Double this amount (e. g., two units) should not be a sufficient amount to
cause any anticomplementary action: and if it does the antigen should be
discarded as unreliable.
2. The SERUM of patients suspected to contain syphilitic antibody is
heated in small test tubes for half an hour at 56° C. As controls, sera
from healthy patients are used.
Anticomplement may develop in sera that have stood for some time ; it
is destroyed by heat. Blood drawn after meals may be rich in anticomple-
mentary substances. For this reason it is best to draw the blood for a
Wassermann reaction before a meal.
Cerebrospinal fluids may be tested in the same way as serum. They
need not be inactivated before use ; indeed, as far as the complement itself
is concerned, serum need not be inactivated, if acetone extracts be used
(Noguchi), but in order to get rid of certain other substances it is best to
heat the sera.
3. As COMPLEMENT, fresh guinea-pig's serum is used, diluted 1 : 10
with salt solution. The guinea-pig is bled from the carotid artery. The
clot is broken up with a glass rod during its formation, and the whole
quickly centrifugalized. Fresh serum can thus be obtained in a few
minutes.
Instead of sacrificing a guinea-pig each time complement is desired, if
only a little be required, it can be obtained by anesthetizing the animal and
drawing off 3-5 c.c. directly from the heart by means of an aspirating
needle.
Serum over 24 hours old should never be used.
APPLICATIONS OF IMMUHOLOGICAL METHODS 159
4. For HEMOLYTIC AMBOCEPTOR the inactivated serum of a rabbit that
has been immunized against sheep's corpuscles by 3 injections 5 days apart
into the ear vein, or intraperitoneally, first with 2.0 c.c. concentrated red
corpuscles, second with 1.5 c.c. of equal parts of corpuscles and salt solu-
tion, and third with 1.0 c.c. of a mixture of equal parts of corpuscles and salt
solution, is used. Dick advises 3 c.c. of blood at the first injection, 6 c.c. at
the second, 10 c.c. at the third, 15 c.c. at the fourth, and 20 c.c. at the fifth;
the injections are then given 5 days apart.
This hemolytic serum must be titrated before use. We prepare a series
of solutions varying in strength from 1 : 300 to 1 : 3000 and test 0.25 c.c. of
each dilution with 0.25 c.c. of complement (1 :10), and 0.25 c.c. of sheep's
corpuscles (5 per cent). The amount of fluid in each tube is brought up to
1.25 c.c. with salt solution. The titer of the amboceptor should be at least
such that 0.5 c.c. of a 1:2000 dilution (in salt solution) will completely
hemolyze 0.5 c.c. of a 5 per cent suspension of washed sheep's corpuscles in
the presence of 0.5 c.c. of a 1:10 dilution of guinea-pig's serum (comple-
ment) within 30 minutes at 37° C. This hemolytic serum after inactiva-
tion may be kept on ice in small sterile tubes.
5. The SHEEP'S CORPUSCLES are obtained from defibrinated sheep's
blood (taken either from the ear, or, through a needle or cannula, from the
V. jugularis, into a sterile flask containing glass pearls), centrifugalized,
and then washed and centrifugalized three times with salt solution. The
last centrifugate is drawn up with a graduated pipet and mixed with 19
volumes of 0.8 per cent salt solution so as to make a 5 per cent suspension of
corpuscles. Since the blood of the sheep varies somewhat, and the fragility
of the corpuscles is sometimes increased, the preliminary hemolytic experi-
ment (q. v.) is needed as a control of the sheep's corpuscles, as well as to
inform us about the laking power of the amboceptor used.
Preliminary Hemolytic Experiment
This experiment (see below) is for the purpose of establishing the
strength of the hemolytic system to be chosen; that is, the amount of ambo-
ceptor necessary for the actual experiment. The amount may vary, because
the content of a guinea-pig's serum in active complement varies consider-
ably. The poorer a guinea-pig's serum is in complement, the greater the
amount of amboceptor that must be added to make sure that a part of the
corpuscles will not remain unaltered.
The task of this preliminary experiment is then to establish the simple
laking dose of the amboceptor, by which is meant the smallest amount of
amboceptor that, along with 0.5 c.c. of complement in 1 :10 dilution, is
able completely to lake 0.5 c.c. of 5 per cent suspension of sheep's corpuscles
after standing 1 hour at the body temperature. At the end of an hour, one
notes which of the tubes, a, b, or c, is completely laked. Since d and e
160 DIAGNOSIS OF INFECTIOUS DISEASES
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APPLICATIONS OF IMMUIsrOLOGICAL METHODS 161
contain no amboceptor they should show no laking ; d is to prove that the
complement does not of itself lake red corpuscles, and e to prove that the
corpuscles are suitable and the salt solution isotonic.
In the protocol, the successive steps of the technic of the experiment are
numbered in blackface type.
The Principal (Diagnostic) Experiment
After the preliminary hemolytic experiment has been carried out as
above, we can proceeed to the making of an actual test, or the so-called
Principal or Diagnostic Experiment. The following is the Wassermann
System now in use in the bacteriological division of the laboratory of the
Medical Clinic at the Johns Hopkins Hospital (Dr. Arthur Bloomfield in
charge at time of writing).
REAGENTS :
1. Salt solution (.85 per cent) .
2. Sheep's red blood corpuscles (5 per cent suspension).
3. Patient's serum (diluted 1 : 5 with salt solution and inactivated) .
4. Antigen (previously titrated and used in less than one-half the anticom
plementary dose). Two varieties of antigen are used for each test.
5. Complement (fresh guinea-pig serum, diluted 1:10 with salt solution).
6. Antisheep rabbit's immune serum (containing hemolytic amboceptor
against sheep's blood).
TECHNIC (see Protocol) :
Three tubes (I, II and III) are introduced as general controls.
Tube I contains only salt solution and corpuscles.
Tubes II and III both contain the hemolytic system with one of the
two antigens used in double the amounts used in the test.
There are three tubes (1, 2, and 3) for each patient.
Tube 1 contains only the hemolytic system, with double the amount
of patient's serum used in the test. This is the anticomple-
mentary control for patient's serum.
Tubes 2 and 3 are the actual "test" tubes ; each, however, contains a
different antigen.
The total volume of fluid in each tube is 1.25 c.c.
The complement, and hemolytic serum have been titrated in the
Preliminary Hemolytic Experiment.
162 DIAGNOSIS OF INFECTIOUS DISEASES
PROTOCOL OF THE PRINCIPAL OR DIAGNOSTIC EXPERIMENT
Tube No.
Salt Sol.
Antigen
Patients'
Serum
Comp
men
le-
t
Hemo-
lytic
Serum
Corpus
3les
Total VoL
of Tube
Salt sol. and cor-
puscle control. . . .
Control for antigen
A
Ill
II
1
.5A
...
.25
h— I
g
.25
.25
.25
—
2
1.25
1.25
Control for antigen
B
I
.5B
.25
1
.25
.25
C
cr
9
1.25
n
Patient A
1
5
.25
#•
.25
.25
•
1.25
(Known positive.)
2
3
.25 A
.25B
.25
.25
.25
.25
£
cc
-i
0
.25
.25
.25
.25
£
00
^1
0
1.25
1.25
Patient B
4
.5
.25
c"'
.25
.25
o*
1.25
(Known negative.)
5
6
.25 A
.25B
.25
.25
.25
.25
M>-
tr
c
.25
.25
.25
.25
1— 1
g*
1.25
1.25
Patient C
7
5
25
i
.25
.25
p
1.25
(To be tested.)
8
9
.25 A
.25B
.25
.25
.25
.25
.25
.25
.25
.25
1.25
1.25
* Water bath.
Results: Tube III should show no hemolysis.
Tubes II and I should be completely hemolyzed; i. e., the antigen is not anti-
complementary in double the amount used in the test.
Tubes 1, 4, 7, etc., should be completely hemolyzed; i. e., the patient's serum
is not anticomplementary in double the amount used in the test.
Tubes 2, 3, 5, 6, 8, 9, etc., will, or will not, be hemolyzed, depending upon
whether, or not, the complement has been fixed.
Hemolysis = no fixation = negative test.
Absence of hemolysis = fixation = positive test.
Since human serum may sometimes contain antisheep amboceptors, a
negative reaction may be obtained, even though much complement is fixed.
To guard against this, such natural antisheep amboceptor may be removed
by Simon's method :
C. E. Simon's Method of Removing Antisheep Amboceptor. — To remove any
natural antisheep amboceptors from the blood, Simon dilutes the inactivated serum
with 5 volumes of a standard sheep's-corpuscle emulsion, inactivates for 30 minutes
in the water bath, and then removes the amboceptor-laden corpuscles by centrif ugali-
zation. Any complementoid that may be simultaneously present is then gotten rid
of at the same time (in the presence of natural antisheep amboceptors). After
centrifugalization, the supernatant fluid is pipeted off and combined with the vari-
ous reagents in the usual manner.
Noguchi's Method of Avoiding Negative Reactions Due to the Presence in the
Human Serum of Antisheep Amboceptor. — For this purpose, Noguchi advises the
use of a human hemolytic system instead of the sheep hemolytic system of the orig-
inal Wassermann reaction. The full details of the method are to be found in
Noguchi's book, and also in Ralph Webster's Diagnostic Methods. Webster uses
this method as a routine, and asserts that, in his experience, "it is somewhat more
reliable than the original Wassermann test in obscure cases." (See following table.)
APPLICATIONS OF IMMUNOLOGICAL METHODS 163
Condition
Number of
Cases
Wassermann
Positive
Noguchi Positive
Primary syphilis
208
88 per cent
94 per cent
Secondary syphilis
669
92 per cent
98 per cent
Tertiary syphilis
Latent syphilis . .
455
305
74 per cent
54 per cent
83 per cent
68 per cent
Congenital syphilis
Cerebrospinal syphilis. . . .
79
55
98 per cent
73 per cent
98 per cent
80 per cent
Grading the Positive Reactions. — By making the double sets of experi-
ments (Citron; Noguchi), one set (A) containing the amount of patient's
serum and antigen given above, and the second set (B) containing half as
much serum and half as much antigen, a rough quantitative report can be
made, since the degree of inhibition of hemolysis varies according to the
amount of syphilitic antibody present.
In Tube A, Noguchi uses 0.1 c.c. of aqueous extract antigen plus 0.1
c.c. of acetone-insoluble antigen ; in Tube B only the acetone-insoluble anti-
gen (0.1 c.c.).
If the serum be rich in syphilitic antibody, complete inhibition will oc-
cur in B as well as in A; such a reaction is marked "quadruple plus"
(H — | — h +)• When the inhibition is incomplete in B but complete in
A, the reaction is designated "triple plus" (H — | — h). When hemolysis
is complete in B, and inhibition complete in A, the reaction is said to
be "double plus" (+ +). If there be only partial inhibition in A, and
complete hemolysis in B, it is said to be "single plus ( + ). (See Plate II.)
Tube A
Tube B
Half Quantities of Suspected
Serum and of Antigen
Grade of Reaction
Complete inhibition.
Complete inhibition.
Complete inhibition.
Partial inhibition . .
Complete inhibition
Partial inhibition
Complete hemolysis
Complete hemolysis
Clinical Value of the Wassermann Reaction. — This reaction is of
the greatest importance for the diagnosis of syphilis, and for the control
of therapy in syphilis. During the past few years, in the clinic in which I
work, between 50 and 100 W^assermann tests have been made- per week
(P. W. Clough; C. E. Austrian; W. A. Baetjer; K. W. Major; T. P.
Sprunt; S. R. Miller; A. L. Bloomfield), and we have come to place great
reliance upon results obtained when the technic outlined above is strictly
followed.
164 DIAGNOSIS OF INFECTIOUS DISEASES
A well-marked positive reaction is pathognomonic of syphilis (pro-
vided the patient is not suffering from scarlet fever, sleeping sickness, lep-
rosy, or framhesia). Slight reactions are not to be regarded as positive;
other tests should be done later. According to J. H. Richards (1913), the
Wassermann reaction is often positive in diabetic acidosis in the absence of
any luetic infection.
Single negative reactions do not rule out lues. The reaction may be
negative in the blood and positive in the cerebrospinal fluid.
A serum that yields a negative reaction may become positive after a
few doses of mercury, or after a single small salvarsan injection (provoca-
tive stimulation).
After prolonged treatment with mercury, iodids, or salvarsan, a serum
formerly positive may become negative, and later on, after treatment has
been stopped for some time, it may become positive again. At least 3 weeks
should elapse after antiluetic treatment before making the test.
It is a safe rule to insist upon negative reactions, at intervals of 3
months, for at least 1 year after treatment has ceased before the patient
can be pronounced free from infection. According to Craig and Nichols,
the use of alcohol can exert a profound effect upon the results of a Wasser-
mann test; it is asserted that through alcohol, a positive test can be con-
verted into a negative one within 24 hours. Hough finds in dementia para-
lytica that alcohol has some influence, though not so great as in Craig's
experience.
In primary lues, all cases examined are positive at the end of the fourth
week after the appearance of the chancre (Swift) ; in 1 case, a positive
Wassermann reaction was found 8 days after exposure and 14 days before
the initial lesion appeared (Lesser). Probably 65 to 95 per cent of all
primary cases will yield a positive Wassermann reaction. In secondary
lues, the Wassermann reaction is positive in 75 to 95 per cent of the cases ;
in hereditary hies, in 90 to 100 per cent. In cerebrospinal lues about 90
per cent of the patients have a positive reaction in the blood serum
(Naegeli).
Nearly all general paretics yield a positive reaction in both the blood
(80 to 100 per cent) and the cerebrospinal fluid (73 to 100 per cent), while
50 to 75 per cent of tabetics yield a positive reaction in either the blood or
the cerebrospinal fluid.
In the following table, taken from Noguchi's excellent monograph, the
results of many observers in the different forms of lues are summarized.
References
Bailey (C. H.}. The value of absorption methods in the Wassermann test. Arch. Int. Med.,
Chicago, 1912, ix, 551-556.
Black fan (K. D.). Apparatus for collecting infants' blood for the Wassermann reaction.
Am. J. Dis. Child., Chicago, 1912, iv, 83-84.
PLATE II
fv
Very strongly positive
Wassermann Reaction
Positive
Wasserrnann Reaction
(+*)
Weakly po
Wassermann Reaction
Negative
Wasserrnann Reaction
APPLICATIONS OF IMMUNOLOGICAL METHODS 165
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166 DIAGNOSIS OF INFECTIOUS DISEASES
Blackfan (K. D.}, Nicholson (S. T., Jr.) & White (T. W.}. A study of the Wasser-
mann reaction in 100 infants. Am. J. Dis. Child., Chicago, 1913, vi,
162-165.
Boas (Harold). Die Wassermann1 sche Reaktion mit besonderer Beriicksichtigung ihrer
klinischen Verwertbarkeit. Mit einem Vorwort von A. Wassermann. 2.
Aufl. Berlin, 1914, S. Karger. 250 p.
Bottler (R.}. Ueber die Brauchbarkeit von Rinderherzextract mit Cholesterinzusatz bei
der Wassermanrischen Reaktion. Arch. f. Dermat. u. Syph., Leipzig u.
Wien, 1913, cvi, 259-264.
Cecil (R. L.} & Lamb (A. R.}. Observations on the complement-fixation test for syphilis
with cadaver serum. Arch. Int. Med., Chicago, 1913, xi, 249-257.
Citron (/•)• Die praktischen Ergebnisse der Serodiagnostik der Syphilis. Ergebn. d. inn.
Med. u. Kinderh., Berlin, 1909, iv, 319-402.
dough (P. W.}. Clinical experience with the Wassermann reaction in the Johns Hopkins
Hospital. Johns Hopkins Hosp. Bull, Baltimore, 1910, xxi, 70-75.
Coca (A. F.} & L'Esperance (Elsie £.)• A modification of the technique of the Wasser-
mann reaction. Arch. Int. Med., Chicago, 1913, xi, 84-91.
Dexter (R.} & Cummer (C. L.). The occurrence of native sheep amboceptor in human
serum and its importance in the performance of the Wassermann reaction.
Arch. Int. Med., Chicago, 1912, ix, 605-608.
Dick (G. F.}. On the origin and action of hemolytic complement. J. Infect. Dis., Chicago,
1913, xii, 111-126.
Fildes (P.) & Mclntosh (/.)• The Wassermann reaction and its application to neurology.
Brain, London, 1913-14, xxxvi, 193-254.
Gay (F. P.). A comparison between the Bordet-Gengou fixation reaction and the Wassermann
reaction, based on the relative dosage of the reacting substances. Univ.
Calif. Publ. Path., Berkeley, 1911-12, U, 23-28.
Henes (E., Jr.). Cholesterinemia and the Wassermann reaction. J. Am. M. Ass., Chi-
cago, 1915, Ixiv, 1969-1972.
Holt (L. E.}. The Wassermann reaction in hereditary syphilis, in congenital deformities,
and in various other conditions in infancy. Am. J. Dis. Child., Chicago,
1913, vi, 166-170.
Judd (C. C. W.). A comparison of cholesterinized and non-cholesterinized artificial anti-
gens in the Wassermann reaction. J. Am. M. Ass., Chicago, 1914, Ixiii,
313-316.
Kolle (W.} & Stiner (O.). Die Verwendung von Azetonextracten zur Serum-Diagnostik der
Syphilis. Deutsche med. Wchnschr., Leipzig u. Berlin, 1911, xxxviii,
1739-1741.
Major (R. H.}. The Wassermann reaction in the Johns Hopkins Hospital. Johns Hop-
kins Hosp. Bull, Baltimore, 1913, xxiv, 175-178.
McCrae (T.}, Eisenbrey (A. B.) & Swift (H. F.}. The use of pure lipoids and alcoholic
extracts with active and inactive serum in the complement-fixation tests for
syphilis. Arch. Int. Med., Chicago, 1910, vi, 469-477.
Noguchi (H.). The relation of protein, lipoids and salts to the Wassermann reaction. J.
Exper. M., Lancaster, Pa., 1909, xi, 84-99.
A new and simple method for the serum diagnosis of syphilis. J. Exper.
M., Lancaster, Pa., 1909, xi, 392-401.
Serum diagnosis of syphilis and luetin reaction, together with the butyric
test for syphilis. 3d ed. Philadelphia & London, 1912, J. B. Lippincott
Co. 320 p. 8°.
Pearce (R. M.). The Wassermann reaction in the pathology, diagnosis and treatment of
syphilis. Arch. Int. Med., Chicago, 1910, vi, 478-516.
Forges (O.) & Meier (G.). Ueber die Rolle derLipoide bei der Wassermann' schen Syphilis-
reaktion. Berl. klin. Wchnschr., 1908, xlv, 731-736.
APPLICATIONS OF IMMTOTOLOGICAL METHODS 167
Sachs (H.}. Ueber den Einfiuss des Cholesterins auf die Verwendbarkeit der Organextrakte
zur Wassermann' schen Syphilisreaktion. Berl. klin. Wchnschr., 1911,
xlviii, 2066-2067.
Sternberg (C.). Versuche uber die Wassermann' sche Reaktion. Wien. klin. Wchnschr.,
1914, xxvii, 545-549.
Stone (W. /.)• Comparative Wassermann, cobra, and globulin tests in syphilis, with a re-
port of one hundred and five reactions. Med. Rec., New York, 1914,
Ixxxvi, 545-547.
Swift (H. F.). The use of active and inactive serum in the complement-deviation test for
syphilis. Arch. Int. Med., Chicago, 1909, iv, 494-501.
A comparative study of serum diagnosis in syphilis. Arch. Int. Med.,
Chicago, 1909, iv, 376-405.
Uhle (A. A.) & MacKinney (W. H.}. Comparative results of the Wassermann test. A
clinical study. J. Am. M. Ass., Chicago, 1915, Ixv, 863-866.
Walker (I. C.) & Swift (H. F.}. A study of the addition of cholesterin to the alcoholic ex-
tracts of tissues used for antigens in the Wassermann reaction. J. Exper.
M., New York, 1913, xviii, 75-95.
West on (P. Cr.)» The preservation of reagents used in the Wassermann reaction. J. Med.
Research, Boston, 1915, xxxii, 391-398.
ii. Complement-Fixation Test for Differentiation of Human from Animal Blood
(Gengou-Moreschi Phenomenon)
Here, use is made of complement-fixation for forensic purposes (Neisser and
Sachs). It has the same value as the precipitin test (q. v.) but is more difficult to
carry out, and, though more sensitive, is less specific. For the technic, the original
articles may be consulted.
iii. Complement-Fixation in the Diagnosis of Echinococcus
The serum of patients suffering from echinococcus invasion can be recognized by
the use of the complement-fixation test in which the unaltered hydatid fluid of
infected sheep is used as antigen. Or an antigen may be made by extracting the
walls of echinococcus cysts with water or with alcohol. The reaction was positive in
10 out of 12 cases examined by Thomsen and Magnussen. According to Meyer and
Hahn, it is a group reaction, the test being positive with different forms of tenia.
References
Rey (Charles). La reaction deWeinberg. Lyon, 1914, A. Rey. 116 p. No. 132. 8°.
Thomsen (O.) & Magnussen (£.)• Ueber spezifische Antikorper bei Echinokokken-
kranken. Berl. klin. Wchnschr., 1912, xlix, 1183.
Weinberg (M.). Sero-diagnostic de I'echinococcose. Ann. de I'Inst. Pasteur, Paris, 1909,
xxiii, 472-502.
iv. Complement-Fixation in the Diagnosis of Gonococcal Infections
This method, applied first by Mueller and Oppenheim (1906) has been
used in this country especially by Schwartz and McNeil, O'Neil, Kyes, and
168
DIAGNOSIS OF INFECTIOUS DISEASES
Keidel and seems to be valuable in the diagnosis of chronic gonococcal infec-
tions (gonococcus arthritis, etc.).
Cultures of the gonococcus on salt-free veal agar, neutral to phenolphtha-
lein, are used as antigen ; it is best to have cultures from at least a dozen
strains, and to mix them. For details of preparation of the antigen, see
the article of Schwartz and McNeil. The gonococcus antigen sold by Parke,
Davis & Co. is said to work well.
Technics. — The Tiemolytic amboceptor is titrated in the ordinary way. In a
series of hemolyzing tubes is placed 0.5 c.c. of complement (1:10). Each of the
tubes then receives varying amounts of antisheep rabbit serum, and the total quan-
tity in each tube is then brought up to 1.5 c.'c. with physiological salt solution. With
a pipet, 0.5 c.c. of washed sheep's corpuscles (5 per cent suspension) is next added
to each tube, so that the total volume in each tube is now 2 c.c. The rack of tubes is
then placed in the thermostat at 37° C. for 1 hour, at the end of which time one notes
the smallest amount of hemolytic amboceptor that has caused complete hemolysis.
This amount is designated 1 unit of hemolytic amboceptor; in subsequent tests, 2
units are used.
In titrating the antigen, a rack containing a double row of tubes is used. Into
each tube of the back row is placed 0.1 c.c. of normal human serum from a per-
son certainly free from gonococcal infection, while into each tube in the front
row is placed the same amount of human serum from a patient suffering certainly
from gonorrhea and known to have a serum strongly positive. If such a serum be
not available, the same amount of antigonococcic serum, prepared for therapeutic
purposes, may be used in its place. Increasing quantities of gonococcus antigen are
now introduced into each consecutive pair of front and back tubes, and the quantity
of fluid in each tube brought up to exactly 1 c.c., after which 0.5 c.c. of complement
(1 part of guinea-pig's serum -\- 9 parts physiological salt solution) is added. The
rack of tubes is then placed in the thermostat at 37° C. for 1 hour, after which 0.5
c.c. of sheep's corpuscles (5 per cent suspension) and 2 units of hemolytic ambocep-
tor are added to each tube. The rack of tubes is then replaced in the thermostat for
another hour, after which the tubes are examined; the smallest amount of antigen
that has caused complete inhibition of hemolysis with the gonorrheal serum but
which has net interfered with hemolysis with the normal serum is called the unit of
antigen. Two units of antigen are used in subsequent tests. Therefore one should
observe whether two units of antigen show any tendency to inhibit hemolysis in
the series with normal serum. If so, the antigen should be discarded, and a fresh
antigen prepared.
The Actual Test. — After both hemolytic amboceptor and antigen have been
titrated, the 12 test tubes are arranged in a rack as in the following diagram :
Fig. 53.— Arrangement of Test Tubes for the Gonococcal Complement-Fixation Test,
(After G. F. Dick.)
APPLICATIONS OF IMMUJSTOLOGICAL METHODS 169
The contents of the tubes are as follows :
TABLE SHOWING ARRANGEMENT OF TUBES FOR COMPLEMENT-FIXATION TEST nsr
GONOCOCCAL INFECTIONS
Tube Number
Patient's
Serum c.c.
Normal Serum
c.c.
Positive
Serum c.c.
Antigen Units
1
0.05
0
0
2
2
0.1
0
0
2
3
O.C5
0
0
0
4
0 1
0
0
o
5
0
0 05
0
2
6
0
0 1
0
2
7
0
0 05
0
0
8
0
0.1
0
0
9
10
11
0
0
0
0
0
0
0.05
0.1
0.05
2
2
0
12
0
0
0.1
0
Enough physiological salt solution is added to make the contents of each tube
measure 1.5 c.c. The whole rack is then placed in the thermostat at 37° C. for 1
hour.
To each tube the secondary hemolytic system is now added, that is, in each tube
is placed 2 units of hemolytic amboceptor and 0.5 c.c. of sheep's corpuscles (5 per
cent suspension), and the rack of tubes replaced in the thermostat for another hour.
The tubes are then examined. If the reaction be positive, Tubes 1 and 2 and
Tubes 9 and 10 should show no hemolysis; in all the other tubes, the corpuscles
should be completely hemolyzed. If preferred, Noguchi's human system can be used
instead of the sheep system, just as with the Wassermann test.
Results of the Gonococcus Complement ^Fixation Test. — The reaction
is rarely positive before the fourth week of the disease, and then only in
acute cases with complicating prostatitis or arthritis. Once present, the
reaction usually persists for a couple of months ; should it be present still
longer, it indicates the persistence of the infection.
The test is usually negative in uncomplicated acute anterior urethritis,,
hut here smears yield the positive diagnosis.
In chronic posterior urethritis, prostatitis, vesiculitis and gonorrheal
stricture, 5/6 of the cases yield a positive reaction (O'Neil).
In females, the majority of cases of infection of the lower genital tract
yield a positive reaction.
In pelvic infections, the reaction is also usually positive, especially if
the cervix uteri he involved.
In gonorrheal arthritis, the reaction is usually positive.
In vulvovaginitis in children, the reaction is positive (McNeil).
The test differs from the Wassermann reaction in that it is biologically
specific, depending upon a specific antigen-antibody interaction. Accord-
ingly, non-gonorrheal cases never yield a positive reaction (Schwartz and
McNeil),
170 DIAGNOSIS OF INFECTIOUS DISEASES
The test requires, as Irons emphasizes, a considerable degree of skill
for its performance, and adequate controls are essential. It is important to
remember that a negative result does not exclude gonococcal infection.
In cases of gonococcal arthritis, the reaction may vary from positive to
negative within a few days, but if in a case of arthritis the reaction is per-
sistently negative when repeated at intervals of 4 to 7 days, it is strong
evidence against a gonococcal origin.
In our clinic, and in Young's urological clinic, this test, by Keidel, has
been of considerable help in differential diagnosis.
References
McNeil (A.). Complement- fixation in gonococcal infections. Am. J. Obst., New York, 1913,
Ixviii, 603-609.
Muller (R.) & Oppenheim (M.). Ueber den Nachweis von Antikorpern im Serum eines
an Arthritis gonorrhoica Erkrankten mittels Komplementablenkung. Wien.
klin. Wchnschr., 1906, xix, 894.
Schwartz (H. T.) & McNeil (A.). The complement-fixation test in the diagnosis of gono-
coccic infections. Am. J. M. Sc.} Philadelphia & New York, 1911f cxli,
693-709.
3. Tests for Precipitins
Clinically, the precipitin tests are useful as biological blood tests in
medico-legal cases (Uhlenhuth).
Reference
Uhlenhuth (P.) & Steffenhagen (K.). Die biologische Eiweiss-Differenzierung mittels
Prdzipitation mil besondererBeriicksichtigung der Technik. In: Handb. d.
pathogen. Mikroorg. (Kolle & Wassermann). 2. Aufl. Jena. 1913. Hi,
257-336.
(a) Precipitin Test for Human Blood
The suspected material is dissolved in salt solution and diluted so that 1 c.c., on
boiling with a drop of 25 per cent HN03, shows only a slight opalescence.
Six small tubes are placed in a rack. In tubes I and II are placed 1 c.c. of the
solution of the suspected material, in Tubes III and IV, 1 c.c. of diluted cat's or
dog's blood, in Tube V, 1 c.c. of salt solution, and in Tube VI, 1 c.c. of a 1 : 1000
solution of human blood. Next, 0.1 c.c. of serum from a rabbit immunized against
human blood is added to each of the tubes except Tube II, which receives 0.1 c.c. of
normal rabbit's serum. The serum added is allowed to flow down the side of each
tube. The tubes are left at the room temperature, without shaking, for 20 minutes,
and then examined. If the suspected material is human blood, a precipitate will
be seen in Tubes I and VI, while Tubes II, III, IV and V will remain clear.
The test is very sensitive; dried blood-stains 50 years old, or older, are
recognizable.
APPLICATIONS OF IMMUNOLOGICAL METHODS 171
References
Nuttall (G. H. F.). Blood-immunity and blood^relationship; a demonstration of certain blood-
relationships amongst animals by means of the predpitin test for blood.
Including original researches by G. S. Graham-Smith and T. S. P. Strange-
ways. Cambridge Univ. Press, 1904, xii. 444 P- 8°.
Uhlenhuth (Paul [Theodor]) & Weidanz (O.). Praktische Anleitung zur Ausfuhrung
des biologischen Eiweissdifferenzierungsverfahrens, mit besonderer Beriick-
sichtigung der forensischen Blut- und Fleischuntersuchung, sowie der
Gewinnung prdzipitierender Sera. Jena, 1909, G. Fischer. 246 p. 8°.
(b) Predpitin Test for Meningococcal Infection
Vincent and Bellot have devised a diagnostic test for epidemic cerebrospinal
meningitis dependent upon a precipitin reaction. They add 1 drop of antimeningo-
coccus serum to 3-6 c.c. of cerebrospinal fluid (cleared by centrifugation), and allow
to stand for 8-12 hours at 50° -53° C. A precipitate, it is asserted, indicates a men-
ingococcic infection, even in the absence of meningoeocci from smears and cultures.
4. Tests for Immune Opsonins (Bacteriotropins)
Technic. — Leukocytes, serum and bacteria in definite proportions are mixed in
a test tube Phagocytosis occurs, the leukocytes engulfing the bacteria. Stained
preparations are made and 100 leukocytes counted, as well as the number of bacteria
visible within them. The average number per leukocyte is called the pliagocytic
count, while the number obtained by dividing this by the phagocytic count as
obtained in a normal person is called the opsonic index; thus, if the average number
of organisms per cell is 5 when the patient's serum is used and is 10 when nor-
mal serum is used, the opsonic index of the patient for the particular bacterium used
will be 0.5. According to Wright and Bulloch, the opsonic index in normal persons
varies between 0.8 and 1.2.
The technic is difficult and time-consuming and only laboratory men working
constantly with it can obtain reliable results. The diagnostic value is much disputed.
In our clinic, we gave the methods a fair trial (Cole and others) and have
abandoned them as far as practical clinical work is concerned. When variations in
index beyond the limits of error occur, other changes, easier to recognize, will per-
mit of a diagnosis. The details of the technic can be found in Wright's articles, and
also in C. E. Simon's Infection and Immunity.
5. Tests for Ergins
When the human body is in an allergic, or anaphylactic, state, inocula-
tion with the corresponding antigen (or allergin) calls forth a specific reac-
tion, probably due to union of the allergin with certain specific antibodies
(ergins).
Certain clinical allergic tests are much in use; notably (1) the tuber-
culin tests, (2) the luetin test, (3) Austrian's ophthalmo-reaction in
typhoid, and (4) Pfeiffer's anaphylactic protein test.
172 DIAGNOSIS OF INFECTIOUS DISEASES
(a) Tuberculin Tests
i. Subcutaneous Tuberculin Reaction (Koch)
When old tuberculin (Koch) is injected, subcutaneously, into healthy
people, considerable quantities can be borne without any symptoms, while
luberculous patients react to very small doses (0.1-1 mg.) with outspoken
symptoms.
Three forms of reaction are distinguished: (1) a general reaction, (2) a
focal reaction, and (3) a puncture or local reaction.
General Reaction. — Fever, malaise, headache, pains in the limbs, palpi-
tation, nausea and vomiting. The most important symptom is the rise of
temperature.
Fig. 54. — Chart Illustrating a Characteristic Tuberculin Reaction. (Prom L. Hamnaan and
S. Wolman.)
Focal Reaction. — Evidences of irritation in the diseased tissue ; thus, in
pulmonary tuberculosis, increased rales, cough, and sputum ; or, in tuber-
culosis of the skin, eye or larynx, a visible flare-up of the inflammatory
process.
Puncture Reaction, or Local Reaction. — Eedness and swelling and pain
at the site of the aseptic injection. The regional lymph glands are often
swollen and tender.
In making this test, the patient should be afebrile, and the temperature should
be recorded every 2 hours during the 48 hours preceding. On the third day, the dose
APPLICATIONS OF IMMUNOLOGICAL METHODS 173
is administered subcutaneously, pref-
erably in the back (between the scap-
ulae). It is best to give 1/5 mg. as
the initial dose, 1 mg. as the second,
and 5 mg. as the end dose in adults
(Hamman and Wolman), at intervals
of 3 days when more than one dose
is required. A rise of temperature
to 100° F., or higher, is regarded as
a positive reaction. As a diluent of
the tuberculin, 0.8 per cent salt solu-
tion, containing 0.25 per cent car-
bolic acid, is used.
If there be no reaction after three
injections given as above, it can be
assumed that the patient is free from
active tuberculosis. The test is con-
tra-indicated after hemoptysis or
hematuria. Careful physical exam-
inations of the patient should be
made just before each injection is
given and the results closely com-
pared with the findings after the
test.
ii. Cutaneous Tuberculin Reaction
(von Pirquet)
This is especially useful for
the diagnosis of tuberculosis in
young children.
Technic. — Cleanse the skin of the
flexor surface of the forearm with
alcohol or ether; apply a small drop
of old tuberculin at each of two
points about 10 cm. apart. With
von Pirquet's "borer," or with a
needle, or the point of a scalpel, make
a superficial abrasion, first in the
skin midway between the two drops,
and then in the center of each drop
of tuberculin. It is best to avoid free
bleeding; it is enough to scarify so
that a few small points of blood ap-
pear. Leave exposed to the air for
5 to 10 minutes ; this insures the max-
imum amount of absorption. Then
gently wipe with absorbent cotton,
avoiding the control point. No dress-
ing is required.
After 24 hours the inoculated
points are carefully compared with
LO
cv)
174 DIAGNOSIS OF INFECTIOUS DISEASES
the control between them. If the borer has been used, the control shows a trau-
matic reaction; if the inflammatory areola be 5 millimeters or more wider than the
control, the reaction is definitely positive. (See Plate III, Fig. 4.)
In scrofulous children, the skin about the area of reaction may show a
number of small elevated nodules, and similar nodules may appear at the
same time upon the limbs and trunk. The reaction is specific. Tubercu-
lous patients react unless the tuberculosis be (1) very acute (general mili-
ary tuberculosis, tuberculous meningitis, galloping phthisis), (2) the end-
stage of a chronic process, or (3) associated with other acute infections.
For diagnostic purposes, the reaction is very valuable in schools, and in
children under two years of age ; in older children and in adults, it is posi-
tive in more than 70 per cent of all examined, and is, therefore, of no diag-
nostic value in them.
Other Tuberculin Reactions Applied to the Skin
These include (a) the percutaneous tuberculin test (Moro), in which 50 per
cent tuberculin-lanolin is rubbed into the skin for 1 minute, and (b) the intracuta-
neous tuberculin test (Mendel-Mantoux), in which a dilute solution of old tuber-
culin is injected into the skin through a fine needle, as in the Schleich method of
local anesthesia. The information furnished by this test is intermediate in value
between that given by the conjunctival and the cutaneous tests.
The so-called differential cutaneous reaction of Detre, intended to decide
between human and bovine tuberculosis, is of doubtful value.
Attempts at quantitative tuberculin tests for determining the degree of sensitive-
ness have been made by White and Graham, by White and Van Norman, and by
Boardman.
iii. Conjunctival Tuberculin Test or Ophthalmo-Reaction
(Cahnette; Wolff-Eisner)
In this test, a salt-solution dilution of tuberculin is instilled into the
conjunctival sac. The appearance of a conjunctivitis in 12 to 24 hours is
the criterion of a positive reaction.
Technic, — Freshly prepared sterile dilutions (1:100; 5:100) of old tuberculin
(Hb'chst) in normal salt solution are used. The eyes are inspected to exclude dis-
ease and to make sure that the conjunctivae of the two sides correspond in appear-
ance. The lower lid is drawn forward while the patient looks lateralward, and 1
drop of the weaker solution is placed at the medial canthus with an eye-dropper (or,
better, with Baldwin's capillary pipet) , avoiding lacrimation. Examine at the end
of 24 hours.
Three groups of positive reactions are distinguished :
1. Mild reaction: Redness at the medial canthus (caruncle), and on
the inner surface of the lower lid.
2. Medium reaction: The same, plus involvement of -the conjunctiva
bulbi.
APPLICATIONS OF IMMTOTOLOGICAL METHODS 175
3. Violent reaction: Purulent conjunctivitis, rarely with vesicles.
If the reaction be negative, a drop of the 5 per cent solution may be
placed in the other eye. If it yield a positive reaction, not much stress is
laid upon it, but if it yield a negative reaction, this speaks strongly against
active tuberculosis.
Precautions. — The conjunctival test should never be repeated in the
same eye for fear of overwhelmingly severe reaction, due to local sensitiza-
tion. The test should not be made if the eye be in any way diseased, or if
the adjacent skin be affected. It is also best avoided in manifestly scrofu-
lous children and in aged persons. If these precautions be observed, one
may, in my experience, use the ophthalmic test without fear of untoward
symptoms.
Value of the Ophthalmo-Reaction. — I lay great stress upon a positive
reaction with 1 per cent solution as indication of the presence of "clinical"
tuberculosis. A negative result with 1 per cent solution is of but little
value, but a negative result with 5 per cent solution is of real value in
helping to exclude clinical tuberculosis.
References
Austrian (C. /?.). Hyper sensitiveness to tuberculo-protein and to tuberculin. Johns
Hopkins Hosp. Bull, Baltimore, 1913, xxiv, 141-147.
Baldwin (E. R.). Hypersusceptibility to tuberculin in tuberculosis: its physiological and
clinical importance. Yale M. J., New Haven, 1908-9, xv, 257-280.
Conclusions from 1,087 conjunctival tuberculin tests by a uniform method.
Rep. VI., Internal. Cong. Tuberculosis, 1908, i, 487-494; also: J. Am. M.
Ass., Chicago, 1909, Hi, 603-605.
Antituberculin or tuberculin-precipitin serums. J. Med. Research, Bos-
ton, 1904, xii, 235-242.
Calmette (A.). The ophthalmo-reaction to tuberculin, a new means of diagnosing tuberculosis
in man. Internal. Clin., Philadelphia, 1907, 17. s., iv, 120-124.
Cattermole (G. H.). Tuberculin tests in children of Colorado. J. Am. M. Ass., Chicago,
1915, Ixv, 782-785.
Evans (G. H.} & Whitney (J. L.}. A preliminary report on the diagnostic value of the
intracutaneous tuberculin test. Arch. Int. Med., Chicago, 1910, vi, 307-318.
Gelien (Johanna) & Hamman (L.). The subsequent history of one thousand patients
who received tuberculin tests. Johns Hopkins Hosp. Bull., Baltimore,
1913, xxiv, 180-186.
Hamill (S. Af.), Carpenter (H. C.) & Cope (T. A.). A comparison of the von Pirquet,
Calmette and Moro tuberculin tests and their diagnostic value. Arch. Int.
Med., Chicago, 1908, ii, 405-447.
Hamman (L.) & Wolman (S.}. Tuberculin in diagnosis and treatment. New York &
London, 1912, D. Appleton & Co. 395 p. 8°.
Krause (A. K.}. Experimental studies on tuberculo-protein hypersensitiveness and their
possible applications. Baltimore, 1911. 8°.
Krumbhaar (E. B.) & Musser (J. H., Jr.). Diagnostic value of percutaneous tuberculin
test (Moro). Am. J. M. Sc., Philadelphia & New York, 1914, n. s.,
cxlvii, 540-549.
Riviere (C.) & Morland (E. C.). Tuberculin treatment. London, 1912. 8°.
von Pirquet (C.). The cutaneous tuberculin test. Arch. Pediat., New York, 1910, xxvii,
161-166. [Discussion] 233.
176 DIAGNOSIS OF INFECTIOUS DISEASES
White (W. C.) & Graham (D. A. L.~). A quantitative modification of the von Pirquet
tuberculin reaction and its value in diagnosis and prognosis. J. Med.
Research, Boston, 1909, xx, 347-357.
Wolff-Eisner (A.). The ophthalmic and cutaneous diagnosis of tuberculosis. Together
with a discussion of the clinical methods for the early diagnosis of pul-
monary tuberculosis. Transl. from the German by B. I. Robert. New
York, 1908, W. Wood & Co. 215 p. 8°.
Theoretical and practical considerations concerning the significance of
the conjunctival reaction (Ophthalmo-tuberculin test). J. Am. M. Ass.,
Chicago, 1909, Hi, 622-625.
(b) Epiphanin Reaction (Weichardt)
The presence of either antigen, or of antibodies, in minute traces can be demon-
strated by the epiphanin reaction (Weichardt), which depends upon the accelera-
tion of diffusion when antigen and antibodies are brought together in certain
dilutions.
The test can be made with Weichardt's difEusiometer (Zentralbl. f. d. gesamte
Phys. u. Path. d. Stoffwechsels, 1911, Nr. 9). It has been made more delicate by
introducing a second system (Ba(OH)2 and H2S04) and noticing whether there is a
dislocation of the end-reaction with phenolphthalein as indicator, as contrasted with
controls, through the antigen-antibody union. We probably have to deal here with
absorption changes of a changing colloid (Schade).
The simpler modification of the test suggested by v. Angerer and Stotter (1912)
is the one now generally used.
References
Angerer (K.) & Stotter (//.)• Ueber Versuche Antigen-Antikorperwirkungen sichtbar zu
machen. Munchen. med. Wchnschr., 1912, lix, 2035-2037.
Friedmann (U.}. Experimentelle Diagnostik mittels physikalischer bzw. physikalisch-
chemischer Methoden. In: Handb. d. pathogen. Mikroorg. (Kolle &
Wassermann). 2. Aufl. Jena, 1913, Hi, 123-142.
Weichardt (W.}. Ueber weitere Versuche, Antigen-Antikorperwirkungen sichtbar zu
machen. Berl. klin. Wchnschr., 1911, xliii, 1935-1937.
(c) Meiostagmin Reaction (Ascoli)
This reaction depends on the principle that, on adding antigen to diluted serum,
changes occurring in a colloid system can be recognized by changes in the surface-
tension of the fluid. In case the antigen unites with antibodies in the serum, the
surface-tension is diminished. This can be measured by dropping the serum from a
small tube (Traube's stalagmometer) . The drops become smaller and their number
greater.
Reference
Ascoli (M.). Die spezifische Meiostagminreaktion; eine physiologisch-chemische Immuni-
tdtsreaktion. Munchen. med. Wchnschr., 1910, Ivii, 62.
(d) Potassium-Iodid-Starch Method for Measuring the Excitation
of Catalyser Action by Proteotoxic Substances
(Weichardt and Kelber)
Cleavage products of proteins and other toxic substances can influence catalysers
such as hemoglobin and colloidal metals (e. g., colloidal osmium) in a characteristic
APPLICATIONS OF IMMUNOLOGICAL METHODS 177
way. This influence on the catalyser can be measured quantitatively by the method
of Weichardt and Kelber. (See original article, Munch, med. Wchnschr., 1912,
Nr. 35:)
These tests may be valuable for investigative work, but as yet are not clinically
applicable.
(e) Luetin Test (Noguchi)
This is a cutaneous reaction for syphilis similar to the intracutaneous
test for tuberculosis. The luetin is injected with a fine needle just beneath
the epidermis, the needle being advanced for a short distance. The devising
of the test became possible after ISToguchi grew Treponema pallidum in pure
culture.
Technic. — Luetin consists of killed cultures of Treponema pallidum in thin
emulsion. As a control fluid, a preparation made from the sterile culture medium is
employed. The arms are sterilized with alcoholic sublimate solution. The left arm
is injected intradermally with 0.07-0.10 c.c. of luetin at two points 5 cm. apart. The
right arm is similarly injected with the control fluid. In non-syphilitic indi-
viduals, the reactions (traumatic) are identical in the two arms, appearing as a small
rosy areola, with or without slight swelling, from 24 to 48 hours after injection,
and disappearing within 48 hours without induration. In syphilitic patients, the
reactions may differ markedly on the two sides. At the site of the luetin injection
a large reddish, indurated papule may appear in 24 to 48 hours, about 7 to 10 mm.
in diameter; it increases in size and becomes surrounded by a red zone (papular
reaction) . It may require 4 to 5 days for evolution and then gradually undergo
involution, turning bluish red, then fading, to disappear entirely in about 2 weeks.
Or, it may, about the fourth day, become vesicular, and a day or two later purulent
(pustular reaction) . In this case, the pustule usually ruptures, and a crust forms;
after the crust falls off, an indurated nodule remains for weeks or months. This
pustular type of reaction is common in late hereditary syphilis, in tertiary lues, and
in secondary lues after treatment with salvarsan.
In rare instances, the reaction seems to be negative at first, but after 10 days, or
later, the inoculated points become markedly inflamed, sometimes with pustule for-
mation (torpid form of reaction) .
Value of the Reaction. — The Noguchi luetin test seems to he especially
serviceable in the recognition of (1) congenital lues, (2) latent syphilis,
and (3) the late stages of lues in adults. The method has been carefully
controlled in the clinic in which I work by Wolfsohn (1912), who found
that, in tabes and in dementia paralytica, the reaction may be delayed for
from 9 to 30 days. A reaction sometimes occurs at the control site, espe-
cially in tertiary lues. The luetin test is a good supplement to the Wasser-
mann reaction since it often yields positive reactions in the luetic conditions
in which the Wassermann reaction is occasionally negative.
Long continued treatment, still short of cure, tends to render the luetin
reaction more evident ; while it makes the Wassermann reaction negative.
References
Benedek (L.). Ueber Hautreaktionen mit Noguchi' s Luetin bei Paralytikem. Munchen.
med. Wchnschr., 1913, Ix, 2038-2037.
178 DIAGNOSIS OF INFECTIOUS DISEASES
Brown (A.}. The luetin reaction in infancy. Am. J. Dis. Child., Chicago, 1913, vi, 171-178.
Foster (G. /?.)• The Noguchi luetin reaction in syphilis. Am. J. M. Sc., Philadelphia,
1913, cxlvi, 645-659.
Kaliski (D. /.)• The luetin skin reaction in syphilis. New York M. J., 1913, xcviii, 24-28.
McNeil (H. L.)» Experiences with Noguchi's luetin test for syphilis. J. Am. M. Ass.t
Chicago, 1914, Ixii, 529-531.
Mutter (R.) & Stein (R. O.). Cutireaktion bei Lues. Mittheilung 8. Bericht iiber 530
Impfungen mit Drusenluetin. Uebersicht der Arbeiten mit Kultur- und
Organluetin. Wien. med. Wchnschr., 1913, Ixiii, 2614-2621.
Noguchi (JET.). La luetine-reaction (cuti-reaction de la syphilis). Presse med., Paris,
1913, xxi, 757-759.
Rytina (A. G.). The luetin skin test in the diagnosis of syphilis. Med. Rec., New York,
1913, Ixxxiii, 384-388.
Simpson (C. A.). Luetin skin reaction in diagnosing syphilis. South. M. J., Nashville,
1913, vi, 234-236.
Ziegel (H. F. L.)« The practical value of Noguchi's luetin reaction. Arch. Int. M'ed.,
Chicago, 1912, ix, 520-524.
(/) Typhoprotein Conjunctival Test, or Typhoid- Ophthalmo-
Reaction (Chantemesse; Austrian)
The method is of value, especially if the antigen be prepared by Aus-
trian's method (10 mg. of dry bacillary protein added to 1 c.c. distilled
water).
Technic. — One drop of a solution of the dry bacillary protein (0.0005 gram) is
instilled into the conjunctival sac after slightly everting the lower lid, and the
eye examined, at short intervals, during the first 24 hours. Two kinds of reac-
tion are met with: (a) the typical diagnostic reaction and (b) the atypical non-
diagnostic reaction.
TYPICAL OR DIAGNOSTIC REACTION. — This appears in 1 to 5 hours
after instillation, and is usually maximal within 6 to 10 hours (injection of
vessels of conjunctiva of lower lid, reddened or purplish caruncle, slight
edema of lid, drop of pus). Usually the conjunctiva of the lower lid shows
a bright purple color and looks velvety. There is slow subsidence after 10 to
20 hours. It may require 10 days for complete subsidence. There is no
pain or photophobia. The congestion persists for at least 24 hours.
ATYPICAL, NON-DIAGNOSTIC REACTION. — Normal persons, and patients
other than typhoids, may show an atypical or non-specific reaction (greater
injection of conjunctiva bulbi, more pus) ; less reaction in palpebral con-
junctiva and caruncle, fading rapidly in 4 to 14 hours.
Value of Reaction. — When typical, it agrees closely with the results of
blood cultures, helping to establish the diagnosis earlier in the disease than
the Widal reaction.
References
Austrian (C. R.). The ophthalmo-reaction in typhoid fever. Johns Hopkins Hosp. Bull.,
Baltimore, 1912, xxiii, 1-9.
APPLICATIONS OF IMMUNOLOGICAL METHODS 179
Chantemesse (A.). L'ophthalmo-diagnostic de la fievre typholde. Bull. acad. de med..
Paris, 1907, 3. s., Iviii, 138.
See also: Deutsche med. Wchnschr., Leipzig u. Berlin, 1907, xxxiii, 1246;
1572.
Floyd (C.) & Barker (W. W.). General susceptibility in typhoid and colon infection as
shown by the ophthalmic test. J. M. Research, Boston, 1909, xx, 95-104.
Gay (F. P.) & Force (J. 2V.). A skin reaction indicative of immunity against typhoid.
Arch. Int. Med., Chicago, 1914, xiii, 471-479.
Hamburger (W. W.). The ocular typhoid reaction; preliminary report of a modification of
the ocular test of Chantemesse. J. Am. M. Ass., Chicago, 1908, 1, 1344.
(fir) Anaphylactic Test for Protein (Pfeiffer)
For forensic purposes, the anaphylactic phenomenon in the guinea-pig,
as shown either by death in convulsions from anaphylactic shock, or by a
sudden fall of temperature or fever, with fall of blood-pressure and later
eosinophilia may be utilized for testing a suspected protein. A guinea-pig
is injected with 0.1 c.c. of blood serum, or with a small amount of protein
of known origin. After 14 to 21 days, 1.0 to 2.0 c.c. of a solution of pro-
tein, suspected to be the same as that by which the animal has been sensi-
tized, is injected. If the suspicion be correct, the guinea-pig will show a
marked fall in temperature and will probably die in acute anaphylactic
shock. This method can be employed instead of the precipitin method,
especially if the material has undergone marked change. Briick has used
the method of passive anapliylaxis to demonstrate idiosyncrasy to antipyrin.
'
SECTION II
SPECIAL DIAGNOSIS OF THE INFECTIOUS DISEASES
A bird's-eye view of the principal infectious diseases and the etiological
agents concerned in them can be obtained by a study of the following tables.
ETIOLOGICAL AGENTS IN THE PKINCIPAL INFECTIOUS
DISEASES
I. VEGETABLE MICROORGANISMS
(a) Cocci as Infectious Agents
i. Streptococcus: Erysipelas; anginas; phlegmons; septicemias; peri-
tonitis ; endocarditis acuta ; endocarditis lenta ; bronchopneumonia ;
acute rheumatic fever.
ii. Staphylococcus : Furunculosis ; septicemias, and especially pyemia;
endocarditis ; osteomyelitis.
iii. Pneumococcus : Croupous pneumonia; otitis; meningitis; perito-
nitis; endocarditis; arthritis; pericarditis; empyema.
iv. Gonococcus: Urethritis; prostatitis; epididymitis ; orchitis; pye-
litis; vulvovaginitis ; pelvic peritonitis; salpingitis; endometritis ;
endocarditis; polyarthritis; ophthalmia neonatorum.
v. Meningo coccus: Epidemic cerebrospinal meningitis ; polyarthritis.
vi. Micrococcus mellitensis: Malta fever.
(&) Bacilli as Infectious Agents
i. Pneumobacillus (Friedlander) : Pneumonia; serositis; meningitis,
ii. Scleroma Bacillus: Rhinoscleroma.
iii. Bacillus anthracis: Anthrax*
iv. Bacillus edemce malignce: Malignant edema.
v. Bacillus aerogenes capsulatus (Welch and Nuttall) : Gas gangrene.
vi. Bacillus tetani: Tetanus.
vii. Bacillus influenza;: Influenza (nasopharyngitis ; paranasal sinu-
sitis; bronchitis; bronchopneumonia; meningitis; encephalitis;
endocarditis, etc.).
viii. Bacillus of Bordet and Gengou: Whooping-cough.
ix. Bacillus pestis: Bubonic plague (bubo; sepsis; pneumonia).
xt Bacillus typhosus: Typhoid fever.
180
ETIOLOGICAL AGENTS IN INFECTIOUS DISEASES 181
xi. Bacillus paratyphosus A and B and Manchuriensis : Paratyphoid
fever.
xii. Bacillus coli communis: Peritonitis; cholangitis; pyelitis; cystitis,
xiii. Bacillus dysenterice (Shiga; Flexner) : Bacillary dysentery,
xiv. Bacillus of Ducrey: Soft chancre (ulcus molle).
xv. Bacillus diphtherias (Loeffler) : Diphtheria (throat; nose; larynx),
xvi. Bacillus pyocyaneus: Green pus; various inflammations,
xvii. Bacillus mallei: Glanders (skin; lymphatics; lungs, etc.).
xviii. Bacillus tuberculosis (Koch) : Tuberculosis (general miliary;' pul-
monary; meningeal; serosal; articular; cutaneous; urogenital,
etc.).
xix. Bacillus leprce: Leprosy.
xx. Bacillus cholerce asiaticce (Koch) : Asiatic cholera,
xxi. Bacillus lacti morbi: Milk sickness.
xxii. Bacillus proteus vulgaris: Acute infectious jaundice (epidemic
catarrhal jaundice; Weil's disease),
xxiii. Bacillus typhi-exanthematici: Typhus fever.
(c) Coarser Forms of Fungi as Infectious Agents
i. Hyphomycetes:
(a) Aspergillus: Aspergillosis (lungs; skin; ear; nose; cornea).
(b) Mucor: Mucor-mycosis (lung; ear; intestine).
(c) Achorion: Favus (skin; sepsis).
(d) Tricophyton •: Eingworm.
(e) Microsporon furfur' Pityriasis versicolor.
(f) Microsporon minutissimum : Erythrasma.
ii. Blastomycetes:
(a) Blastomyces and Oidium: Dermatitis; metastatic granuloma.
(b) Thrush fungi: Thrush (parasitic stomatitis),
iii. Sporotrichum or Sporothrix: The Sporotrichoses.
iv. Streptothrix (The Streptotrichoses) :
(a) Streptothrix actinomyces: Actinomycosis (head; neck;
lungs; intestines; bones).
(b) Mycetoma fungi: Madura foot.
(c) Other Streptothrix forms: The pseudo-actinomycoses.
(d) Discomyces: The Gougerot-Carougeau nocardiosis.
II. ANIMAL MICROORGANISMS (PROTOZOA)
(a) Rhizopoda as Infectious Agents
i. Entameba histolytica:
(a) Amebic dysentery.
(b) Tropical liver abscess.
(c) Pyorrhea alveolaris.
182 DIAGNOSIS OF INFECTIOUS DISEASES
(5) MastigopJiora as Infectious Agents
i. Trypanosomidce :
(a) Trypanosoma gambiense: Sleeping sickness; trypanosome
fever.
(b) Typanosoma rliodesiense: Kaodzera.
(c) Schizotrypanum cruzi: Chagas' disease,
ii. Piroplasmidce :
(a) Leishmania (donovani) : Kala-Azar.
(b) Leishmania (infantum) : Infantile Kala-Azar.
(c) Leishmania (tro pica) : Oriental sore (Delhi boil).
iii. Plasmodidce:
(a) Plasmodium vivax: Tertian malaria.
(b) Plasmodium malarice (Laveran) ; Quartan malaria.
(c) Plasmodium immaculatum (sive prcecox) (Grassi and Fe-
letti) : Estivo-autumnal malaria.
iv. Spirochceta obermeieri, duiioni, novyi, carteri: Relapsing fever,
v. Treponema pallidum (Spirochceta pallida) : Sypbilis and para-
syphilis.
vi. Treponema pertenu : Yaws or f rambesia.
vii. Treponema pallidum: Granuloma venereum.
viii. Gangosa.
ix. Verruga peruana.
x. Bartonia bacilliformis: Oroya fever.
(c) Sporozoa as Infectious Agents
III. FlLTRABLE VlRUSES (Ul,TRAMICROSCOPIc)
(a) Pasteur's Virus: Rabies (hydrophobia; lyssa).
(b) Reed, Carroll and Agramonte's Virus: Yellow fever.
(c) Ashburn and Craig's Virus: Dengue fever.
(d) Flexner and Noguchi's Virus: Poliomyelitis (Heine -Medin
disease).
(e) Loeffler and Frosch's Virus: Stomatitis epidemica (foot and mouth
disease) ; Doerr and Russ's Virus: Pappataci fever; Peyton
Rons' s Virus: Sarcoma.
IV. UNKisrowiT INFECTIOUS AGENTS
(a) The Acute Exanthemata
i. Scarlet fever,
ii. Measles,
iii. Rubeola.
iv. Rubeola scarlatinosa (Fourth Disease).
DISEASES DUE TO COCCI 183
v. Chickenpox (Varicella).
vi. Smallpox ^ariola).
vii. Vaccinia (Cowpox and vacination).
viii. Sweating Sickness (Febris miliaris).
ix. Rocky Mountain Spotted Fever.
(&) Non-exanihematous Diseases
i. Mumps (Parotitis epidemica).
I. DISEASES DUE TO VEGETABLE MICROORGANISMS
A. Diseases Due to Cocci
1. Diseases Due to Streptococci
The pathogenic streptococci, more often than any other bacteria, are the
cause of septicemia. Over 60 per cent of general infections in which bac-
teria can be grown from the blood are due to streptococci. (Plate III,
Figs. 2 and 3.)
These cocci grow in shorter or longer chains. They do not decolorize
by Gram. They grow well on ordinary media, not liquefying gelatin.
Several varieties of streptococci are differentiate by cultivation on
blood-agar plates, in which they show differences (1) in hemolysin forma-
tion and (2) in pigment production (Schottmiiller).
1. Streptococcus pyogenes or Streptococcus vulgaris hemolyticus.
—Each colony in the blood-agar plate is surrounded by a circular clear area,
due to the absorption of hemoglobin (hemolysis).
2. Streptococcus viridans. — This grows more slowly on blood-agar
plates, often not appearing for several days. The colonies develop as fine
greenish points, in the depth usually smaller in size than the head of a pin.
Those on the surface may be somewhat larger, and are blackish green or
gray. There is no clear area of hemolysis about the colony. Milk is coagu-
lated in from 1 to 3 days.
3. Streptococcus putridus. — Strictly anaerobic ; does not cause hemol-
ysis on blood-agar plates. Cultures have a foul odor (H2S). Colony
white. Does not coagulate milk. Non-pathogenic for animals.
4. Streptococcus mucosus. — Cocci in capsulelike hull. Aerobic, and
facultative anaerobe. Milk coagulated in 24 to 48 hours. Colonies on
blood-agar dark green; larger than head of a pin in 24 hours. Highly
pathogenic for animals (white mice, rabbits).
Of the above four varieties, the first, or Streptococcus Tiemolyticus, is
the most common cause of sepsis ; Streptococcus viridans is the cause of
184
DIAGNOSIS OF INFECTIOUS DISEASES
subacute infectious endocarditis (endocarditis lenta), while Streptococcus
putridus is often the septic agent in infections following abortion.
Hosp. Bull, Balti-
Preliminary notes.
References
Cole (R. /.)• Experimental streptococcus arthritis. Johns Hopkins
more, 1905, xvi, 114-115.
Floyd (C.) & Wolbach (S. B.). On the differentiation of streptococci.
J. M. Research, Boston, 1914, xxix, 493-530.
Fuller (C. A.) & Armstrong (V. A.). The differentiation of fecal streptococci by their fer-
mentative reactions in carbohydrate media. J. Infect. Dis., Chicago, 1913,
xiii, 442-462.
con Lingelsheim (W.). Streptokokken. In: Handb. d. pathogen. Mikroorg. (Kolle &
Wassermann). 2. Aufl. Jena, 1912, iv, 458-512.
McLeod (J. W.) & M'Nee (J. W.). On the ancemia produced by the injection of the hemo-
lysin obtained from streptococci, and on the question of natural and ac-
quired immunity to streptolysin. J. Pathol. & Bacteriol., Cambridge, 1913,
xvii, 524-537.
Meakins (J. C.). Phagocytic immunity in streptococcus infections. J. Exper. Med.,
Lancaster, Pa., 1909, xi, 815-824.
Neufeld (F.). Treten im menschlichen Blute nach uberstandener Streptococcenkrankheit
Antikorper auff Deutsche med. Wchnschr., Leipzig u. Berlin, 1897, xxiii,
162-164-
Neufeld (F.) & Rimpau (W.). Ueber die Antikorper dcs Streptokokken- und Pneumo-
kokken-Immur) serums. Deutsche med. Wchnschr. , Leipzig u. Berlin, 1904,
xxx, 1458-1460.
Schottmiiller (#.) & Barfurth (W.}. Die Bactericidie des Menschenblutes Streptokokken
gegenuber als Gradmesser ihrer Virulenz. Beitr. z. Klin. d. Infektions-
krankh. u. z. Immunitdtsforsch., Wiirzburg, 1914, Hi, 291-318.
. 56. — Purpura in Septicemia. (Me4- Service, J. H. H.)
PLATE III
Fig. 1. — Conradi-Drigalski Plate. B.
typhosus — Blue Colonies. B. coli —
Red Colonies. (After L. Mohr u. R.
Staehelin, "Handb. d: inner. Med.,"
published by J. Springer, Berlin.)
(2) -^^^
Fig. 2. — Differentiation of Streptococci
on Blood-agar Plate. (1) Streptococ.
Tulgar. hac.molyticus, (2) Strepto-
coccus mitior. (After G. Jochmann,
in L. Mohr u. R. Staehelin, "Handb.
d. inner. Med.," published by .T.
Springer, Berlin.)
Fig. 3. — Pus with Streptococci. (After G. Jochmann, in L. Mohr u. R. Staehelin, "Handb.
inner. Med.," published by J. Springer, Berlin.)
Fig. 4. — Quantitative Gradation of the Cutaneous Reaction After von Pirquet. (After P.
Krause, "Lehrb. d. klin. Diagnostik d. inner. Krankh.," published by G. Fischer, Jena.)
DISEASES DUE TO COCCI
185
Swift (H. F.) & Thro (W. C.). A study of
streptococci with the comple-
ment-fixation and congluti-
nation reactions. Arch. Int.
Med., Chicago, 1911, vii,
Henry H. aet."54>
Weaver (G. H.}. Anlistreptococcus serum.
In: Therap. Int. Dis. (Forch-
heimer). New York & Lon-
don, 1914, v, 652-656.
(a) Streptococcal Septicemia
The cocci causing septicemia may
enter the blood (1) through the
urogenital tract, especially in puer-
peral sepsis, (2) through the
throat (after tonsillitis, diphtheria,
scarlatina), (3) through the middle
ear (otogenous sepsis), (4) through
the skin (wounds, erysipelas), (5)
occasionally, through the lungs and
pleura, or (6) through the digestive
tract (ulcers after typhoid or dysen-
tery.
Metastatic infections of the or-
gans are rare in streptococcal sepsis,
though common in staphyloccocal sep-
sis. "Purulent metastases may, how-
ever, occur in the joints or lungs.
Endocarditis is a common complica-
tion. The fever is usually markedly
remittent; it may be continuous or
intermittent. Not infrequently a
hemorrhagic diathesis develops, and
a petechial or purpuric rash is seen
on the skin.
References
Fig. 57. — Streptococcus Sepsis ; Endocardi-
tis ulcerosa. (Personal Observation.)
In: Syst. Med. (Allbutt & Rollestori). 8°.
Am. J. M. Sc., Phila-
Cheyne (W. W.}. Septicaemia and pyaemia.
London, 1910, i, 865-891.
Churchman (J. W.}. Cutaneous manifestations of septiccemia.
delphia & New York, 1913, cxlvi, 833-836.
Jochmann (G.). Septische Erkrankungen. In: Handb. d. inn. Med. (Mohr & Staeheliri),
Berlin, 1911, i, 578-716.
Koch (.R.)« Untersuchungen uber die Aetiologie der Wundinfectionskrankheiten. Leipzig,
1878, F. C. W. Vogel. 80 p. 8°.
Lister (J.). On the relation of minute organisms to unhealthy processes arising in wounds
and to inflammation in general. Tr. Internal. M. Cong., London, 1881, i,
311-323.
186
DIAGNOSIS OF INFECTIOUS DISEASES
Welch (W. H.). Conditions underlying the infection of wounds. Tr. Cong. Am. Phys. &
Surg., New Haven, 1892, ii, 1-28.
Widal (F.), Courmont (J.) [et al.]. Streptococcie, Staphylococcie, Pneumococde, Coli-
bacillose. Paris, 1912, J. B. Bailliere & fits. 145 p. 8°. [Nouv.
traite de med. de therap., x.]
(b) Endocarditis lenta (Subacute Infectious Endocarditis)
Symptoms. — Onset insidious ; slight fever at first, later high and inter-
mittent with or without chills ; gastro-intestinal disturbances common ;
sweating; progressive weakness and emaciation; signs of valvular disease
usually present but often lacking; palpable spleen ; pains in bones, joints, or
muscles; tenderness over lower sternum; progressive anemia; painful
erythematous nodules; sallow facies; pigmentation; petechiae. The
patients have nearly all had rheumatic endocarditis in earlier life.
Diagnosis. — This is usually easy if the blood culture is properly made
(Streptococcus viridans). In the differential diagnosis, rheumatic endo-
carditis, typhoid fever, malarial fever, tuberculosis, and Bantis disease,
should be considered. (See next page.)
FOR THE DIFFERENTIATION OF THE ENDOCARDITIS-COCCI, "THE FOLLOWING TABLE
is USEFUL (AUSTRIAN)
PNEUMOCOCCUS
STREPTOCOCCUS
Cocci OF ENDOCARDITIS LENTA
A
B
Capsule
1. Diagnostic
or
2. Not present
1. Non-diagnostic
or
2. Not present
Not present
Not present
Gram
Positive
Positive
Positive
Positive
Blood-plates
Green, no clear
zone
1. Gray, clear
zone, or
2. Green, no
clear zone, or
3. Moist white
growth
1. Green, no clear zone
or
2. Moist or dry white growth, no
clear zone
Tnulin fermentation
. +
(occasionally — )
— (rarely +)
+
—
Precipitation
Serum, Glucose-
Agar
- (rarely +)
+
+
+
Solution by Bile. . .
+
-
-
-
Appearance in 1st
culture
24-48 hrs.
24-48 hrs.
24-96 hrs.
Usually late. Smaller and grow
more poorly than pneumo- or
streptococci
Libman considers these endocarditis-cocci as attenuated streptococci.
Rosenow regards them as attenuated pneumococci. Schottmuller regards them as
Streptococcus mitior or viridans.
DISEASES DUE TO COCCI
187
Prognosis. — The disease is nearly always fatal, but the fever may con-
tinue for months or even 1 to 2 years before death.
NOTE. — For further description and references, see Part VI.
(c) Erysipelas
Definition. — Erysipelas is an acute inflammation of the skin, spreading
through the lymphatics, nearly always due to Streptococcus hemolyticus.
Symptoms — The streptococcus enters through some small lesion on
skin or mucous membrane,
very often on the face, fol-
lowing a scratch, insect bite,
or an excoriation about the
nose or lip. The erysipela-
tous dermatitis may occur on
any part of the body from
infection of a wound, or of
an ulcer. It is not uncom-
mon, in the new born, at the
umbilicus. ••
The incubation period
varies in length from a few
hours to 3 to 7 days. The
onset is usually sudden, with
chill, fever, and vomiting.
A sharply limited area of
redness appears on the skin
of the face, trunk, or ex-
tremities. This area is
swollen, hot, and tender.
The surface is tense and
often glazed; vesicle forma-
tion is common. In facial
erysipelas the features are
characteristically altered by
the swelling; the nose broad-
ens, the lips become thick,
the ears huge and stiff, as if
made of red wax. The eyes
are swollen shut; but it is
very rare to see any conjunc-
tivitis. Though the spread is
rapid, it is often checked Fig. 58.— Erysipelas,
where the skin is tight (chin,
margin of hair, upper neck). The swelling and redness of the area first
affected may disappear and desquamation begin while the disease is still
188 DIAGNOSIS OF INFECTIOUS DISEASES
spreading at the margin. The course is often rapid, the disease terminating
in from 4 to 8 days. More rarely, the process advances further and further
and may wander over a large part of the body (erysipelas migrans). The
adjacent lymph glands are swollen and tender. The fever, high at onset,
is usually continuous or slightly remittent for an average of 4 to 6 days ;
it may end by crisis or by lysis. Ten per cent of the cases are afebrile.
Leukocytosis is the rule. Headache, anorexia and weakness are usual.
The patients are restless, and may be dull, or delirious (drinkers). Re-
lapses are common. Erysipelas may affect the throat or tonsils; occa-
sionally it involves the larynx, and causes edema of the glottis. The mor-
tality varies from 4 to 7 per cent.
Complications. — Bronchitis, bronchopneumonia, septicemia, metastatic
arthritis or meningitis, furunculosis.
Diagnosis. — Usually easy. Occasionally the disease is confused with
phlegmon, anthrax, or erythema. It is not to be mistaken for the erysipe-
loid of Rosenbach (in which a butterfly-shaped area of redness appears
over the nose and cheeks in butchers, cooks, etc.).
References
Anders (J. M.). The complicating conditions, associated diseases, and mortality rate in ery-
sipelas. Internal. M. Mag., Philadelphia, 1893, ii, 799-804.
Also: Tr. Pan-Am. M. Cong., 1893, Washington, 1895, pt. 1, 264-268.
Armstrong (G. E.). Erysipelas of the face, followed by double cerebral abscess. Canada
M. & S. J., Montreal, 1884-85, xiii, 170-172.
Also: Canada M. Rec., Montreal, 1884-85, xiii, 2.
Atkinson (I. E.). A clinical study of erysipelas in infants. Med. Rec., New York, 1887,
xxxii, 618-622.
Douglas (K. M.}. Erysipelas in the surgical hospital, 1891-96. Edinb. Hosp. Rep., 1898,
v, 363-371.
Fehleisen (X.). Die Aetiologie des Erysipels. Berlin, 1883, T. Fischer. 38 p. 8°.
Fox (T. C.). Dermatoses of streptococcic origin. In: Syst. Med. (Allbutt & Rolleston). 8°.
London, 1911, ix, 161-185.
Henry (Andre}. De la peritonite erysipelateuse, en parliculier au cours de I'erysipele de la,
face[Lyon]. Saint-fitienne, 1914, "La Loire." 71 p. No. 116. 8°.
Jochmann (G.). Erysipel. In: Handb. d. inn. Med. (Mohr & Staehelin). Berlin, 1911,,
i, 717-736.
Ochsner (A. J.). The treatment of erysipelas with strong alcohol. Am. J. Surg. & Gynea
Kansas City, 1893-94, iv, 167-169.
Packard (F. A.}. Erysipelas. Am. Text-Bk. Dis. Child. (Starr). 2d ed. Philadelphia.,
1898, 221-230.
Rosenbach (F. J.). Ueber das Erysipeloid. Arch. f. klin. Chir., Berlin, 1887, xxxvi,,
346-351.
Experimentelle morphologische und klinische Studie uber die krankheits--
erregende Mikroorganismen des Schweinerotlaufs, des Erysipelas und'.
der Mdusesepsis. Ztschr. f. Hyg. u. Infektionskrankh., Leipzig, 1909,,
Ixiii, 343-369.
Thomas (W. T.). Ichthyol in erysipelas. Liverpool M.-Chir., 1893, xiii, 483-485.
Winslow (12.) • A case of gangrenous erysipelas, with remarks on the etiology and treatment
of erysipelas. Maryland M. J., Baltimore, 1890-91, xxiv, 447-449.
DISEASES DUE TO COCCI 189
(d) Streptococcal Puerperal Sepsis
Puerperal fever is the most important form of streptococcal sepsis. It
is most often due to the aerobic Streptococcus hemolyticus; while, in septic
abortion, the infection is most often caused by the anaerobic Streptococcus
putridus. The general infection may follow any one of several forms of
local streptococcus infection: (1) endometritis ; (2) thrombophlebitis, in
which there is a chill at the end of the first, or the beginning of the second
week after delivery, followed by high fever and sweating, and later chills
every two or three days; (3) pelvic peritonitis or parametritis (lymph-
ogenous form of puerperal sepsis).
Diagnosis. — This is usually easy when the signs of infection follow a
birth, or an abortion. Extragenital diseases like typhoid, tuberculosis,
malaria, and scarlet fever must be ruled out. Gynecological examinations,
blood cultures, and cultures from the lochia are helpful.
References
Bacon (C. S.}. Puerperal infection in private practice. J. Am. M. Ass., Chicago, 1902,
xxxviii, 1243.
Hirst (B. C.). Lectures on puerperal sepsis. Med. Times & Hosp. Gaz., London, 1896,
xxiv, 703, 735, 767, 783.
Holmes (O. W.}. The contagiousness of puerperal fever. N. Eng. Q. J. M. & S., Bost.,
1842-3, i, 303-330.
Lambert (S. W.) & Painter (H. McM.}. Fever in the puerperal woman. Soc. Lying-in
Hosp. N. York Med. Rep. (1893), 1894, 24-99, 3 ch.
Schottmuller (H.). Ueber bakteriologisclis Untersuchungen und ihre Methoden bei Febris
puerperalis. Munchen. med. Wchnschr., 1911, Iviii, 787-789.
Semmelweis (I. P.). Die Aetiologie, der Begriff und die Prophylaxis des Kindbettfiebers.
Pest, Wien & Leipzig, 1861, C. A. Hartleben. 543 p. 8°.
Slemons (J. M.). Placental bacteremia. J. Am. M. Ass., Chicago, 1915, Ixv, 1265-1268.
Symposium on puerperal fever. Practitioner, London, 1905, Ixxiv, 289-435.
(e) Streptococcal Sinus Thrombosis (Otogenous Sepsis)
Symptoms. — The onset is usually sudden, with nausea, vomiting, head-
ache, vertigo, chills, and fever. Tenderness over the mastoid with swell-
ing is frequently observed. If the thrombus extends into the jugular vein,
it may be palpable in front of the M. sternocleidomastoideus. A blood
culture from an arm vein often shows the presence of Streptococcus Jiemo-
lyticus. Libman recommends simultaneous cultures from blood of an arm
vein and from blood obtained by sinus puncture.
References
Libman (E.) & Celler (H. L.). The importance of blood cultures in the study of infections
of otitic origin. Am. J. M. Sc., Philadelphia & New York, 1909, cxxxviii,
409-427.
Schottmuller (H.). Zur Redeutung der bakteriologischen Blutuntersuchung bei otogener
Sepsis. Beitr. z. Klin. d. Infektionskrankh. u. z. Immunitdtsforsch.,
Wiirzburg, 1914, Hi, 265-276.
190
DIAGNOSIS OF INFECTIOUS DISEASES
(/) Streptococcal Angina
Ordinary sore throats, especially acute tonsillitis, are very often due
to Streptococcus hemolyticus. Not infrequently, they form the starting
point of a general sepsis, of an endocarditis, of a metastatic arthritis, or of
an embolic nephritis.
The absorption of streptococcus toxins (without bacterisemia) not
infrequently leads to diffuse renal intoxication (large white kidney).
I
A
-
( x' v!
"*„•**
B
3jf
Fig. 59. — (A) Swollen Glands of the Neck in Septic Sore Throat; (B) Streptococci from Septic
Sore Throat (Drawn by Max Broedel.) (After k. P, Hamburger, J. H. H. Bull.)
DISEASES DUE TO COCCI 191
Recently, peculiar epidemics of streptococcal angina, with bubolike
enlargement of the cervical lymph glands, have been met with in America,
especially in Baltimore, in Boston, and in Chicago. In a number of these
cases, a general streptococcal septicemia, or a streptococcal peritonitis, has
been met with as a complication.
References
Beall (K. H.). Glandular fever. Texas State J. M., Fort Worth, 1911-12, vii, 222.
Burns (J. E.~). Glandular fever. Report of an epidemic in the children's ward of the Union
Protestant Infirmary. Arch. Int. Med., Chicago, 1909, iv} 118-125.
Capps (J. A.}. Epidemic streptococcus sore throat; its symptoms, origin and transmission.
J. Am. M. Ass., Chicago, 1913, Ixi, 723-724.
Capps (J. A.) & Davis (D. /.). An epidemic of streptococcus sore throat in Jacksonville,
Illinois, which was traced to the milk of cows affected with streptococcus
mastitis. Tr. Ass. Am. Physicians, Philadelphia, 1914, xxix, 279-293.
Hamburger (L. P.}. The Baltimore epidemic of streptococcus or septic sore throat, and its
relation to a milk supply. Johns Hopkins Hosp. Bull., Baltimore, 1913,
xxiv, 1-11.
Jackson (L.). Experimental streptococcal arthritis in rabbits. A second study dealing with
streptococci from the milk epidemic of sore throat in Chicago, 1911-12.
J. Infect. Dis., Chicago, 1913, xii, 364-385.
Korsakoff (N. 5.). Beitrdge zur Lehre des Driisenfiebers. Arch. f. Kinderheilk., Stuttgartf
1905, xli, 321-357; 1905, xlii, 193-247.
Mann (T. A.). Study of an outbreak of septic sore throat occurring in Concord (N. H.\
January, 1912. J. Infect. Dis., Chicago, 1913, xii, 481-497.
Martin (H. H.). Report of a case of general sepsis following peritonsillar abscess. South.
M. J., Nashville, 1913, vi, 661-564.
(gr) Acute Rheumatic Fever
(Acute Articular Rheumatism; Polyarthritis rheumatica acuta)
Definition. — Acute rheumatic fever is an acute, non-contagious, infec-
tious disease, usually beginning with angina, and characterized by fever,
sweating, and an excruciatingly painful, serous inflammation of a number
of joints, which become involved one after the other, with strong tendency
to complicating thrombo-endocarditis, the whole disease process, especially
the pains, reacting promptly to salicylate therapy. It is sometimes fol-
lowed (in children) by chorea.
Etiology. — The virus was, until recently, entirely unknown. Hundreds
of careful blood cultures, in the clinic in which I work, were, up to the end
of 1913, uniformly sterile, and cultures made from the joints were sterile.
English observers (Poynton and Payne) had found a diplococcus in the
blood, and many other microorganisms have been described in the disease.
Eecently, Eosenow (Chicago) has isolated streptococci from joints, tonsils,
and regionary lymph glands, which, by animal passage and by other means,
he believes he can convert into typical hemolytic streptococci on the one
hand, and into pneumococci on the other. On animal inoculation, these
192 DIAGNOSIS OF INFECTIOUS DISEASES
cocci give rise to polyarthritis, myocarditis, and myositis. This work ia
exceedingly interesting and further studies in the same direction should
be closely watched.
My own observations had, up to the time of Rosenow's work, kept me skepti-
cal regarding a bacterial etiology. I was strongly of the opinion that acute
articular rheumatism was due to some virus wholly different from any ordinary
form of bacterium, a virus that seemed to attack primarily the tonsils, with
subsequent virusemia metastatic virus-infection of the joints and sometimes of
the endocardium.
Rosenow is, however, such a careful worker, that any statement he makes
must be given serious consideration. At my request, one of our staff, Dr.
Arthur Bloomfield, went to Chicago, where Dr. Rosenow kindly instructed him
in his technic of making cultures from the blood and from the lymph glands in
acute and in chronic polyarthritis. On returning to the clinic in Baltimore, Dr.
Bloomfield has been able, by these methods, to isolate from the blood and from
the lymph glands, in arthritis cases, streptococci, apparently identical with those
described by Rosenow. There can be no doubt that by Rosenow's method, bacteria
can be grown from many patients when cultures made in the ordinary way
remain sterile.
Rosenow had found in his studies on the transmutation of pneumococci and
streptococci that oxygen pressure plays an important role in bringing about
changes in these organisms; it occurred to him that the bacteria in rheumatic cases
might be exceedingly sensitive to oxygen and that the negative cultures in acute
rheumatism might be due to failure to supply and maintain the proper oxygen
tension in the culture media. He devised a technic, by which in the same tube
of medium, not only aerobic and anaerobic conditions are provided, but also all
degrees (a gradient) of oxygen pressure between these two extremes. The blood,
freed from hemoglobin and from complement, or the exudate from a joint, is
mixed with ascites-dextrose agar (first melted and then cooled to a point just
short of consolidation), in a tall test tube, so that on solidification, a tall column
of solid inoculated medium results; at the surface, aerobic conditions exist;
at the bottom, the conditions are anaerobic; in between, the inoculated material
is exposed to a gradient of oxygen tensions. By this method Rosenow got
pure cultures of streptococci from the joint fluid in acute rheumatism in 16 out
of 19 non-fatal cases, fnd from the blood in 5 out of 8 cases.
These strains of streptococci all differ in one respect or another from Strepto-
coccus viridans, on the one hand, and from Streptococcus hemolyticus, on the other.
They vary in virulence ; they produce much acid in media containing dextrose ; they
tend to change in their properties on cultivation; they grow better than ordinary
streptococci at low temperatures; they are more virulent for frogs than are either
pneumococci or ordinary streptococci. Injected into rabbits and dogs, they are
said by Rosenow to exhibit not only an affinity simultaneously for the several serous
membranes (endocardium, pericardium, and joint membranes), but also a tendency
to localize in the experimental animals at sites corresponding roughly to the sites
of the lesions in the human cases whence they were isolated. Thus with strains
from human cases without myositis, the experimental animals did not develop
myositis, while strains derived from myositic lesions in man gave rise to non-
suppurative myositis and myocarditis in the animals, in addition to arthritis and
endocarditis. After cultivation and animal passage, however, this localization-
specificity is said soon to be lost. Rosenow (1912) believes that he can convert,
by appropriate means, these rheumatic strains of streptococci into other members
DISEASES DUE TO COCCI 193
of the streptococcus group and vice versa. His experiments on mutation make
him believe that these and other streptococci, grown in symbiosis with other bacteria
and under varying degrees of oxygen pressure, may acquire new properties; he
thinks that streptococci may thus undergo change in the human body, in the
tonsils, for example. It is his opinion, also, that the more chronic forms of
arthritis, such as one called chronic progressive polyarthritis, are due to streptococci
with distinctive cultural and pathogenic features, which are in keeping with the
types of the disease in which they occur in man.
Rosenow's Technic. — Dr. Arthur Bloomfield has kindly furnished me with the
following details. For the isolation from blood and tissues of. organisms that
do not grow readily under conditions of complete aerobiosis or anaerobiosis, Rose-
now uses the following method:
1. BLOOD CULTURES. — Fifteen to 30 c.c. of blood, drawn by venepuncture, are
introduced into citrate solution to prevent clotting, and the mixture laked by
adding about 10 volumes of sterile distilled water. This solution is now centri-
fuged at high speed for about 2 hours, the clear supernatant fluid decanted, and
the sediment inoculated. Tubes of 1 per cent glucose agar (.5 per cent acid)
are boiled for several minutes to drive off as much oxygen as possible, and then
cooled to about 50° C. About J volume of ascitic fluid, which has been heated at
60° C. for about 24 hours, is added, and small amounts of the blood sediment are
now introduced with a sterile pipet. The tube is not shaken, but after thoroughly
flaming the plug and the top of the tube, it is inverted once to distribute the
inoculated material through it. The column in the tube is about 10 cm. high.
The colonies appear, after incubation, as opaque grey bodies and are easily
distinguishable from the tissue particles which may be present in the tubes. To
subculture the colonies, the tubes are broken and the organisms fished out and
transferred to blood agar or to serum slants, or stabs may be made into solid
tubes of ascites-dextrose agar.
2. CULTURES FROM TISSUES. — The lymph gland, or other piece of tissue, is
dipped into boiling water for an instant to kill any bacteria on the surface, and
is then immediately inserted into a sterile box containing a mortar, so arranged
that, by means of an opening in the side to which a glove is attached, the tissue
can be ground up under perfectly sterile conditions. A satisfactory apparatus
can be improvised from a five-pound ether can. The fragments of tissue and
the juice are next inoculated into the glucose-ascites-agar tubes in exactly the same
way as for the blood sediment described above.
The principle of this method lies in the fact that varying grades of oxygen
tension are offered to the organisms in addition to aerobic and anaerobic conditions.
The view of Sahli that acute articular rheumatism is a sepsis due to an'
attenuated staphylococcus or streptococcus had been less in favor since the con-
ception of acute infectious pseudorheumatisms has had more acceptance. Rose-
now's results lend new interest to Sahli's view.
The disease is most common in youth and during adolescence; it is. not
very common after middle life, though its residues (valvular disease of the
heart ; adherent pericardium) are often seen.
Symptoms. — The onset is usually sudden, often after tonsillitis (70-80
per cent of the cases) ; or a short period of arthralgia, myalgia, and malaise,
with fever that rises rapidly may precede the outspoken joint involvement.
Inflammation of several joints develops, usually within 24—48 hours, the
disease jumping from joint to joint characteristically, causing swelling,
redness and excruciating pain, especially when the joints are moved. The
194 DIAGNOSIS OF INFECTIOUS DISEASES
swelling is mainly periarticular, but effusion into the joint is not uncom-
mon. The order of frequency of involvement is as follows: knee, ankle,
shoulder, wrist, elbow, hip, hand, and foot. The sternoclavicular, temporo-
maxillary, and vertebral joints are not, as a rule, involved. The inflamma-
tion subsides in one joint while increasing in others, and, after the arthritis
has subsided, no residual deformities remain. There is a great tendency to
recurrences.
The fever is irregular, being usually markedly remittent; deferves-
cence is by lysis. Tachycardia may be pronounced. An apical systolic
bruit is frequently heard, even in the absence of endocarditis.
Characteristic, in typical cases, are the profuse sour sweats, as a result
of which sudaminal vesicles (miliaria crystallina and, less often, miliaria
rubra) develop. Simple erythema, erythema multiforme and nodosum,
urticaria, or purpura may be associated. Subcutaneous fibroid nodules are
sometimes seen, especially in children; they are most numerous along
fasciae, and on the tendons about the fingers, hands, wrists, scapulas, elbows,
knees, and spine.
Anorexia, thirst, and perspiration are prominent symptoms. There is
commonly a febrile nephropathy with very acid urine. A marked second-
ary anemia quickly develops, and the blood shows a leukocytosis (10,000-
18,000), with P. M. ~N. increase from the beginning. In chorea, the eosin-
ophils may be increased to 10 per cent (Macalister).
The course is very variable ; the duration is probably not influenced by
salicylates; most cases continue for several weeks, but there are shorter
attacks lasting 1-2 weeks.
The mortality is low (2-4 per cent), but the outlook for the distant
future is often gloomy on account of the frequency of an associated endo-
carditis, myocarditis, or pancarditis.
Complications. — Endocarditis is extremely common ; it affects especial-
ly the mitral valve, but sometimes both the mitral and the aortic valves, and
usually leads to permanent valvular lesions (stenoses; insufficiencies);
pericarditis and myocarditis are common ; more rarely pleuritis is seen ;
occasionally, hemorrhagic nephritis, or peritonitis, develops. In one group
of cases, erythema multiforme is common. A purpuric form is sometimes
met with (peliosis rheumatica). In children, chorea minor is a frequent
complication or sequel ; it seems to be due to a cerebral localization of the
causative streptococci, perhaps of a modified strain (Dick and Rothstein,
1913). A very dangerous complication is the rheumatic hyperpyrexia, or
cerebral rheumatism (not to be confused with salicylate delirium!), in
which the temperature may rapidly rise to 106° or to 108° F., with
delirium, convulsions, coma, and death. Recurring rheumatic iritis is not
uncommon. Old rheumatic hearts are especially predisposed to secondary
septic infection (endocarditis lenta, etc.). Enlargement and tenderness of
the thyroid are not uncommon (Vincent) ; some authors regard acute rheu-
DISEASES DUE TO COCCI 195
matic fever as the commonest provocative cause of Graves' s disease (Mou-
riquand and Bouchut).
Diagnosis. — In children, and in young adults, the typical picture, with
tonsillitis, fever, and polyarthritis flying from joint to joint, reacting
promptly to salicylates, and prone to endocardia! complications, is not diffi-
cult to recognize. It is sometimes hard to rule out an acute infectious
pseudorheumatism (Bouchard), or so-called rheumatoid disease (Ger-
hardt), including the polyarthritides due to gonococci, pneumococci, etc.
The arthropathy following serum injections (diphtheria antitoxin) may
be confused with acute rheumatic fever.
Sometimes, the early stage of a primary chronic progressive polyar-
thritis may be so acute as to simulate acute rheumatic fever, but, in this
disease, the jaw joint, the sternoclavicular joint, and the cervical spine are
not infrequently affected — joints that are only rarely involved in acute
rheumatic fever. The quick appearance of muscular atrophies, and the
absence of tendency to endocarditis and to other serous membrane involve-
ments help to differentiate.
The postscarlatinal polyarthritis is not a true polyarthritis rheumatica.
Acute osteomyelitis can be distinguished (1) by the positive blood
culture for staphylococci, and (2) by rontgenograms of the bones.
Acute gout rarely offers difficulty in diagnosis (nocturnal onset ; sites of
predilection; family history; disturbed purin metabolism; response to
colchicum).
Whether a chronic articular rheumatism due to the same virus as that
which causes true rheumatic fever ever occurs, is much disputed (T.
McCrae). The question can scarcely be settled until the virus of acute
rheumatic fever is definitely established, and its presence or absence in the
chronic processes determined. Some think that Jaccoud's rheumatismus
fibrosus is a true chronic rheumatism. The tendency now is to reserve the
term rheumatism for diseases caused by the virus that is responsible for
acute rheumatic fever, and not to apply it to other forms of arthropathy.
References
Beattie (J. Af.). Relapses in acute articular rheumatism. Liverpool M.-Chirurg. J., 1913,
xxxiii, 487-500.
Beattie (J. M.) & Yates (A. G.). The bacteriology of rheumatism — further evidence in
favour of the causal relationship of streptococci. J. Pathol. & BacterioL,
Cambridge, 1912-13, xvii, 538-551.
Church (Sir W. S.) & Bulloch (IF.). Rheumatic fever. In: Syst. Med. (Allbutt &
Rollestori). 8°. London, 1909, ii, pt. i, 594-645.
Cole (R. /.). Experimental streptococcus arthritis in relation to the etiology of acute articular
rheumatism. J. Infect. Dis., Chicago, 1904, i, 714-737.
Etiology of acute articular rheumatism. New York M. J. [etc.], 1906,
Ixxxiii, 534-538.
Faber (H. K.). Experimental arthritis in rabbit. Contribution to pathogeny of arthritis in
rheumatic fever. J. Exper, M-, Lancaster ', Pa., 1915, xxii,
196 DIAGNOSIS OF INFECTIOUS DISEASES
Haskell (R. H.). Mental disturbances associated with acute articular rheumatism. Am. J.
Insan., Baltimore, 1914, Ixxi, 361-381.
Jochmann ((*.)• Der akute Gelenkrheumatismus (Polyarthritis rheumatica, Rheumatismus
articulorum acutus). In: Handb. d. inn. Med. (Mohr & Staehelin) , Ber-
lin, 1911, i, 736-758.
Kemp (C. G.). On the prognosis of acute articular rheumatism, with special reference to the
cardiac manifestations. Quart. J. Med., Oxford, 1914, vii, 251-271.
Klotz (O.). Arterial lesions associated with rheumatic fever. J. Path. & Bacteriol., Cam-
bridge, 1913, xviii, 259-269.
Osier (W.). On the visceral complications of erythema exudativum multiform*. Philadel-
phia, 1895. 18 p. 8°. Repr. from Am. J. M. Sc., Philadelphia, 1895,
n. s., ex, 629-646.
Poynton (F. /.). Remarks on the infective nature of rheumatic fever, illustrated by the
study of a fatal case. Brit. M. J., London, 1904, i, 1117-1120.
Rheumatic fever. Mod. Med. (Osier). 8°. Philadelphia & New
York, 2d ed., 1914, i, 974-1008.
The prevention of acute rheumatism. Amer. Med., Burlington, Vt. &
New York, 1915, n. s., x, 351-857.
Poynton (F. J.) & Paine (A.}. Researches on rheumatism. London, 1913, J. & A.
Churchill. 461 p. 8°.
Pribram (A.). Der akute Gelenkrheumatismus. Spez. Path. u. Ther., herausgegeben von
Nothnagel. v, 2. Halfte. Wien, 1901, A. Holder.
Der acute Gelenkrheumatismus (Rheumatismus articularis acutus}. Wien,
1899, A. Holder. 574 P- 8°.
Forms pt. i, v. 5, of: Spec. Path. u. Therap. (Nothnagel).
Rosenow (E. C.). The etiology and specific treatment of rheumatism. In: Forchheimer,
Therap. of Int. Dis., New York, 1914, v, 509-516.
Ruhr ah (/.)• Infectious diseases, including acute rheumatism, croupous pneumonia, and
influenza. Progr. Med., Philadelphia & New York, 1914, i, 145-270.
Smith (Lewis). Some clinical observations on the cardiac manifestations of acute rheu-
matism. Practitioner, London, 1912, Ixxxviii, 46-54-
Thalhimer (W.) & Rothschild (M. A.). On the significance of the submiliary myocardial
nodules of Aschoff in rheumatic fever. J. Exper. M., Lancaster, Pa.,
1914, xix, 417-428.
Vincent (M.). Sur la signe thyro'idien dans le rheumatisme aigii. Semaine med., Paris,
1908, xxviii, 527.
(h) Chronic Streptococcal Arthritis
Recent bacteriological studies have shown that a certain proportion
of the cases of chronic arthritis are due to infection with Streptococcus.
It is not often possible to demonstrate the streptococcus in these cases
in the joints themselves except at autopsy, but now and then cultures
from the regional lymph glands reveal the presence of numbers of these
bacteria. In such cases the primary focus of streptococcus infection
should be sought for.
Reference
Davis (D. J.). Chronic streptococcus arthritis. J. Am. M. Ass., Chicago, 1913, Ixi, 724-727,
DISEASES DUE TO COCCI 197
2. Diseases Due to Staphylococci
The Pathogenic Staphylococci. — These include the Staphylo coccus aur
reus, the Staphylo coccus albus, and the Staphylococcus citreus. Of these,
the aureus is the most pathogenic. The albus is always present in the
human skin, and is often spoken of as the "skin-coccus" ; it sometimes gives
rise to local and to general infections. The individual cocci are round,
smaller than streptococci, and are usually arranged in grapelike bunches.
They grow well on ordinary media, liquefying gelatin. They stain with
ordinary anilin dyes, and are Gram-positive. On blood-agar plates, two
kinds of colonies are seen at the end of 24 hours: — (1) in the depth, black
points without hemolytic areas about them, and (2) on the surface, white
and golden-yellow colonies surrounded by clear areas, due to absorption of
hemoglobin. These surface colonies show hemolysis owing to the presence
of more oxygen there than in the depth.
Staphylococci give rise to a poison which hemolyses the red corpuscles
(staphylolysin) , and to another which destroys the white corpuscles (leuko-
cidin). The principal poisoning in staphylococcus infections, however,
seems to be due to endotoxins arising from the bodies of the Staphylococci
themselves.
Portals of Entry. — Those most often concerned are (1) wounds, tears,
punctures, pricks, or scratches of the skin, followed by local inflammation
(furunculosis, carbuncles, panaritium, acne) and sometimes by general
sepsis; (2) the mucous membrane of the urogenital tract (bladder, pelvic
organs, and kidney), and (3) the mucous membrane of the throat (tonsils,
pharynx).
Multiple purulent metastases are very common in staphylococcus sepsis
(lung abscess, endocarditis, abscesses in heart, spleen, kidneys, joints, and
bone-marrow). When the cocci go over into the blood, the blood culture is
sometimes positive, but is often negative, as the cocci are quickly removed
from the blood by the organs (in contrast with streptococcus sepsis).
(a) Staphylococcal Septicemia
Symptoms. — There is high fever, usually continuous, or slightly remit-
tent, rarely accompanied by chills; often relative bradycardia; palpable
spleen; hyperleukocytosis ; delirium; signs of metastases (lung abscess,
septic endocarditis, polyarthritis, meningitis).
Diagnosis. — Blood culture ; urine culture ; finding of primary focus of
infection ; cultures from metastatic abscesses.
References
Jochmann (G.). Staphylokokkensepsis. In: Handb. d. inn. Med. (Mohr & Staeheliri).
Berlin, 1911, i, 658-680.
198 DIAGNOSIS OF INFECTIOUS DISEASES
Neisser (M.). Staphylokokkenimmunitat. In: Handb. d. path. Mikroorg. (KolU & Was-
sermann), Jena, 1904, 1150-1160.
Die Staphylokokken. In: Handb. d. pathogen. Mikroorg. (Kolle & Wasser-
mann). 2. Aufl. Jena, 1912, iv, 856-420.
Neisser (M.) & Wechsberg (F.). Ueber das Staphylotoxin. Ztschr. f. Hyg., Leipzig,
1901, xxxvi, 299-347.
(b) Acute and Chronic Osteomyelitis
Etiology. — Osteomyelitis is nearly always due to infection with
Staphylococcus aureus; occasionally it may be due to streptococci, or to
pneumococci.
Symptoms. — The onset is usually acute, with fever, chills, and pains in
one or more of the bones (femur, tibia), followed by swelling of the part,
and later, by necrosis and sequestrum-formation. There is often pus for-
mation, with abscess.
Diagnosis. — Blood cultures are nearly always positive at some stage of
the disease. Rontgenograms are helpful in the diagnosis of this con-
dition.
Differential Diagnosis. — A number of conditions should be ruled out
especially in children (fracture; Barlow's disease with its painful sub-
periosteal hemorrhages). In the more chronic forms of osteomyelitis in
which the swelling arises gradually, the patient being, perhaps, afebrile,
the differential diagnosis is usually more difficult than in the acute cases.
In addition to chronic osteomyelitis due to staphylococci or streptococci, we
must think of cold abscess, of sparotrichosis, of neoplasm, and of gumma.
(See Part XL)
References
Berg (A. A.). A case of acute osteomyelitis of the femur, with general systemic staphylococcus
aureus infection, terminating in recovery. Ann. Surg., Philadelphia, 1900,
xxxi, 332-339.
Elsberg (C. A.). On the treatment of chronic osteomyelitis and of chronic bone cavities by the
iodoform wax filling. Ml. Sinai Hosp. Rep., 1903-04, New York, 1905,
iv, 322-328.
Gar re (C.). Ueber besondere Formen und Folgezustdnde der akuten infektiosen Osteomyelitis.
Beitr. z. klin. Chir., Tubingen, 1893, x, 241-298, 2 pi.
Jordan (M.). Ueber atypische Formen der akuten Osteomyelitis. Beitr. z. klin. Chir.,
Tubingen, 1895-96, xv, 467-464.
Lexer (E.). Die Aetiologie und die Microorganismen der akuten Osteomyelitis. Samml.
kUn. Vortr., n.F., Leipzig, 1897, No. 173 (Chir., No. 49), 659-698.
Makins (G. H.) & Abbott (F. C.). Forty-one fatal cases of acute infective osteomyelitis,
terminating with pyaemic symptoms, contrasted with two hundred cases of
ordinary pyaemia. St. Thomas's Hosp. Rep., 1889-90, London, 1901,
n. s., xix, 193-217.
Nichols (E. H.). Acute, subacute and chronic infectious osteomyelitis; its pathology and
treatment. J. Am. M. Ass., Chicago, 1904, xlii, 439-466.
Oechsner (J. F.). Acute suppurative osteomyelitis; the importance of its early recognition
and treatment. N. Orl. M. & S. J., 1904, Mi, 378-390.
Taylor (R. T.). The clinical aspect, symptoms and differential diagnosis of osteomyelitis.
N. York M. J., 1902, Ixxv, 841-847.
DISEASES DUE TO COCCI 199
(c) Furunculosis
In this condition, local areas of inflammation occur in the subcutaneous
tissue. In the center of each area, containing masses of staphylococci, is
a core of necrotic tissue; outside this there is edema, with leukocytic
infiltration. As the hoil ripens, the tissues undergo softening, and the
leukocytes increase in number with pus formation. The boil will often
break, if left to itself, or if it be poulticed. The infection usually begins in
a hair follicle. Sites of predilection are the back of the neck, the nates, the
external genitalia, the axillae and the external auditory canal. Diabetes
strongly predisposes to such infections and widespread furunculosis is also
common during convalescence from typhoid fever. A furuncle on the
upper lip is especially dangerous owing to the frequent involvement of the
facial veins with pyemia as a sequel. The so-called carbuncle of the neck
may consist of a single boil, or of a group of conglomerate furuncles (com-
mon in the senile, and in diabetes). Before the bacteriological era, such
staphylomycotic carbuncles were sometimes confused with anthrax.
References
Fox (T. C.). Dermatoses of staphylococdc origin. In: Syst. Med. (Allbutt & Rolle$tori).
8°. London, 1911, ix, 185-201.
Waugh (J. F.). Vaccine therapy in dermatology with special reference to acne and furuncu-
losis. In: Therap. Int. Dis. (Forchheimer) . New York & London, 1914,
v, 625-636.
3. Diseases Due to Pneumococci
The Pathogenic Pneumococci. — TheDiplococcus pneumonia? ( Weichsel-
baum), Pneumococcus (Fraenkel) or Micrococcus lanceolatus (Welch) is
met with usually in pairs, each individual coccus being lancet-shaped;
sometimes chains of 4 to 6 occur. It stains easily with ordinary basic
anilin dyes and is Gram-positive. In preparations made from the tissues
or fluids of infected animals and man, it is seen to be surrounded by a
capsule, each capsule inclosing 2 cocci ; in cultures it often grows without
capsule.
Growth will occur, though feebly, on ordinary media at 37° C. The
pneumococcus grows much better on media containing human serum. It
dies out easily, unless frequently transplanted, though it may live for some
time in dry sputum or in dry blood.
In most cases, it is easily recognizable by its morphology, but it is best
isolated by the injection of suspected material into a mouse, or a rabbit;
in these animals it quickly gives rise to pneuniococcus septicemia, and
may, after 24 hours, be obtained in pure culture from the blood. Normal
sputum usually contains the pneumococcus (hence the sputum septicemia
[Sternberg; Pasteur] on injection of sputum into rabbits, or mice); in
200 DIAGNOSIS OF INFECTIOUS DISEASES
man, it is a harmless occupant of the mouth cavity in 50-70 per cent of
normal individuals.
Differentiation of Pneumococci from Streptococci. — Blood-agar plates
are helpful.- The pneumococeus differs from Streptococcus hemolyticus in
that the colonies grow green and are not surrounded by hemolytic zones.
It differs from Streptococcus viridans in (1) its lancet shape, (2) its cap-
sule formation in animals, (3) the more intense green color of its colonies
on blood-agar, (4) its stronger growth in the depth of blood-agar, (5) its
inability to precipitate serum-glucose-agar, and (6) its power of ferment-
ing inulin. E. C. Rosenow believes that he can, by transfer methods, con-
vert certain streptococci into pneumococci and vice versa.
Mice and rabbits are most susceptible to pneumococeus infection,
minute amounts of virulent pneumococci killing them within three days,
often within 24 hours, from septicemia.
Strains of Pneumococci. — Cole and Dochez, and Dochez and Gillespie,
Rockefeller Hosp., ~N. Y., confirming and extending the earlier work of
Eyre and Washbourne, and of Neufeld and Haendel, have shown that
pneumococci, isolated from pneumonia, are divisible into four groups. This
fact may prove to be important in the development of a specific therapy, as
powerful antisera have been produced against two of the groups.
The cocci belonging to each of the first two groups are said to be specific,
as far as the immunity to which they give rise is concerned. The immune
serum (horse) arising from injections of a pneumococeus belonging to
Group I, has a specific protective action against all pneumococci belonging
to Group I, but does not protect against pneumococci belonging to Groups
II, III, or IV. Similarly, a pneumococeus belonging to Group II will
yield, on injection, a serum protective against all cocci belonging to Group
II, but against no other cocci. Group III contains all the pneumococci of
the type of Pneumococeus mucosus. On injection it has not been found
possible to produce a protective serum against any member of this group.
Group IV includes all pneumococci against which the serums prepared by
injection of pneumococci belonging to Groups I and II are ineffective and
which by cultural or pathogenic qualities can be shown not to belong in
Group III. An immune serum prepared by injection of a pneumococeus
belonging to Group IV is protective against the strain used, but will not
protect against other strains belonging to Group IV, nor will it protect
against the races belonging to Groups I, II, and III. The pneumococci
belonging in Groups I and II can also be easily recognized by agglutination
tests made with the respective immune sera. Pneumococci belonging to
Group III are easily recognized by their cultural and pathogenic charac-
ters. Membership in Group IV is determined by exclusion.
P. W. Clough has demonstrated an increase of phagocytic power for
the homologous (virulent) pneumococeus in the blood serum of patients
after the crisis in pneumonia.
DISEASES DUE TO COCCI 201
References
Axenfeld (Th.). Pneumokokkenconjunctivitis. In: Handb. d. pathogen. Mikroorg. ( Knlle
& Wassermanri). 2. Aujl. Jena, 1913, vi, 572-586.
Bull (C. G.)« Mechanism of curative action of antipneumococcus serum. J. Exper. M.t
Lancaster, Pa., 1915, xxii, 457-465.
The mechanism of the action of antipneumococcic serum. Proc.Soc. Exper.
Biol. & Med., New York, 1914-15, xii, 143-151.
Cory (C.) & Lyon (/. /*.)• Pseudomembranous inflammation of the mucous membranes
caused by the pneumococcus. Tr. Ass. Am. Physicians, Philadelphia,
1901, xvi, 879-392.
Clough (P. TF.). Development of antibodies in the serum of patients recovering from acute
lobar pneumonia. Johns Hopkins Hosp. Bull., Baltimore, 1913, xxiv,
295-306.
Cole (R. /.)• Blood cultures in pneumonia. Johns Hopkins Hosp. Bull., Baltimore,
1902, xiii, 136-139.
Toxic substances produced by pneumococcus. J. Exper. M., Lancaster,
Pa.. 1912, xvi, 644-664.
Pneumococcus infection and immunity. J . Am. M. Ass., Chicago, 1912,
lix, 693-697.
The production of methemoglobin by pneumococci. J. Exper. Med., Lan-
caster, Pa., 1914, xx, 363-378.
Pneumococcus infection and lobar pneumonia. Arch. Int. Med., Chicago,
1914, xiv, 56-93.
Pneumococcus hemotoxin. J. Exper. Med., Lancaster, Pa., 1914, xx, 346-
362.
Pneumococcus infection and immunity. New York M. J., New York,
1915, ci, 1-7, 59-62.
Dochez (A. R.) & Cole (R. /.)• Pneumococcus infection. In: Therap. Int. Dis. (Forch-
heimer). New York & London, 1914, v, 472-508.
Dochez (A. R.) & Gillespie (L. /.)• A biologic classification of pneumococci by means
of immunity reactions. J. Am. M. Ass., Chicago, 1913, Ixi, 727-732.
Gay (F. P.) & Chickering (H. T.}. Concentration of the protective bodies in antipneumo-
coccus scrum by means of specific precipitation. Proc. Soc. Exper. Biol.,
New York, 1915, xii, 115.
Hanes (F. M.). Pneumococcus meningitis. Johns Hopkins Hosp. Rep., Baltimore, 1910,
xv, 247-276.
An immunological study of pneumococcus mucosus. J. Exper. M., Lan-
caster, Pa., 1914, xix, 38-51.
Howard (C. P.). Pneumococcic arthritis: report of three cases. Johns Hopkins Hosp.
Bull, Baltimore, 1903, xiv, 803-806.
Jobling (J. W.} & Strouse (5.). Studies on ferment action. V. Immunization with pro-
teolytic cleavage products of pneumococci. J. Exper. M., Lancaster, Pa.,
1912, xvi, 860-867.
Jochmann (G.)« Pneumokokkensepsis. In: Handb. d. inn. Med. (Mohr & Staehelin).
Berlin, 1911, i, 681-695.
Kinyoun (J. J.) & Rosenau (M. J.}. Infections caused by the pneumococcus. (Pre-
liminary note.) Rep. Superv. Surg.-Gen. Mar. Hosp., Washington,
1897, 762-766.
Neufeld (F.). Ueber eine spccifische bakteriolytische Wirkung derGalle. Ztschr.f. Hyg. u.
Infectionskrankh., Leipzig, 1900, xxxiv, 4^4~4^4-
Neufeld (F.) & Handel (L.). Pneumokokken. In: Handb. d. pathogen. Mikroorg. (Kolle
& Wasscrmann). 2. Aufl. Jena, 1912, iv, 513-588.
Rosenow (E. C.). Human pneumococcal opsonin and the antiopsonic substance in virulent
pneumococci. J. Infect. Dis., Chicago, 1907, iv, 285-296.
Transmutations within the streptococcus-pneumococcus group. J. Infect.
Dis., Chicago, 1914, xiv, 1-32, 1 pi.
202 DIAGNOSIS OF INFECTIOUS DISEASES
St rouse (£.)• Experimental studies on pneumococcus infections. J. Exper. Med., Lan-
caster, Pa., 1909, xi, 743-761.
Strouse (5.) & Clough (P. W.). Blood cultures in pneumonia. Johns Hopkins Hosp.
Bull., Baltimore, 1910, xxi, 247-251.
Welch (W. H.}. The Micrococcus lanceolatus, with especial reference to the etiology of acute
lobar pneumonia. Johns Hopkins Hosp. Bull., Baltimore, 1892, Hi,
125-139.
(a) Croupous Pneumonia (Lobar Pneumonia)
This disease is nearly always due to some member of one or another of
the four groups of pneumococci above described. In a few cases the causal
agent is Friedlander's bacillus. (For symptoms, diagnosis, etc., see Diag-
nosis of Diseases of the Lungs. )
(6) Pneumococcal Septicemia
Definition. — In human pneumococcus infections, primarily local, the
cocci may go over into the blood and multiply there. If only a few reach
the blood, and there be no marked multiplication, we speak of a "pneumo-
coccus bacteriemia." But the blood may contain a large and increasing
number of the cocci; we then speak of "pneumococcus sepsis." Such a
pneumococcus sepsis may follow pneumonia, otitis media, an angina, or a
cholecystitis. The severer toxic symptoms in fatal cases of pneumonia
probably depend, in most instances, on pneumococcus sepsis.
Symptoms. — In pneumococcus sepsis, the fever is, as a rule, high and
continuous, though in some cases it is markedly intermittent. Suppura-
tive metastases are not uncommon, and are usually fatal. Ulcerative
pneumococcus endocarditis and pneumococcus meningitis are serious com-
plications. Occasionally, a metastatic pneumococcus arthritis is met with ;
it is usually suppurative.
4. Diseases Due to Gonococci
The Gonococcus (Neisser). — This is a biscuit-shaped or coffee-bean-
shaped coccus, occurring in pairs (diplococci), the adjacent edges of the
cocci in each pair being flattened. In gonococcal inflammations, the proto-
plasm of the leukocytes is often crowded with pairs of gonococci (intracellu-
lar cocci).
The gonococcus stains with ordinary anilin dyes, but it is Gram-nega-
tive, an important point in diagnosis. In fixing the smear, overheating
should be avoided; during the Gram-staining, the stain should not be
allowed to evaporate ; the decolorization in alcohol should be thorough.
The gonococcus does not grow well on ordinary media. It grows best
on more highly albuminous media, and especially well on ascites-agar, or
hydrocele-fluid agar, though it grows fairly well on blood-agar without
DISEASES DUE TO COCCI 203
hemolysis. The nutrient medium should be neutral or very feebly acid.
The optimal temperature for growth is 35°-3T° C. ; a rise above this endan-
gers the life of the organism, and, as E. E. Irons suggests, it is well to set
the regulator of the thermostat at 35° C., so that, if a slight unavoidable
rise of temperature occurs, it will not be great enough to kill the culture.
The organisms are easily demonstrable in the pus of gonorrheal urethri-
tis or conjunctivitis, and in the exudate of gonococcal endocarditis and
gonococcal arthritis. In smears stained with alkaline methylene blue,
they are visible chiefly as intracellular cocci. If such cocci are found also
to be Gram-negative they are probably gonococci. Care must be taken not
to confuse the gonococcus with (1) the meningococcus, (2) non-hemolyzing
streptococci, (3) micrococcus catarrhalis, (4) coccoid forms of B. coli,
and ( 5 ) the pseudo-gonococcus.
References
Barker (L. F.). Bilateral exostoses on the inferior surface of the calcaneus, gonorrhoeal in
origin (Pododynia gonorrhoica) . Johns Hopkins Hosp. Bull., Baltimore,
1905, xvi, 384-385.
Bruck (C.). Immunitdt bei Gonorrhoe. In: Handb. d. pathogen. Mikroorg. (Kolle &
Wassermann). 2. Aufl. Jena, 1912, iv, 721-736.
Cole (Rufus). Gonococcus infections. Mod. Med. (Osier). 8°. Philadelphia & New
York, 2d ed., 1914, i, 743-765.
Harris (N. A/.) & Haskell (L. W.). Concerning a case of suppurative myositis caused by
micrococcus gonorrhoeas (Neisser). Johns Hopkins Hosp. Bull., Balti-
more, 1904, xv, 395-397.
Irons (E. E.). Gonococcemia, with a report of six cases in which the gonococcus was isolated
from the blood during life. Arch. Int. Med., Chicago, 1909, iv, 601-627.
Gonococcal infections. Therap. Int. Dis. (Forchheimer}. New York &
London, 1914, v, 579-624.
Koch (J.). Gonorrhoe. In: Handb. d. pathogen. Mikroorg. (Kolle & Wassermann) .
2. Aufl. Jena, 1912, iv, 655-720.
Neisser (A.). Ueber eine der Gonorrhoe eigenthumliche Micrococcusform. Berlin, 1879,
L. Schumacher. 8°. Also repr. from Centralbl. f. d. med. Wissensch.,
Berlin, 1879, xvii, 497-500.
Pearce (Louise}. A comparison of adult and infant types of gonococci. J. Exper. Med.,
Lancaster, Pa., 1915, xxi, 289-803.
M'Donagh (J. E. R.) & Klein (B. G.). The treatment of gonorrhoeal infections by vac-
cines and the regulation thereof by the complement-fixation test. J. Path.
& Bacteriol, Cambridge, 1912-1913, xvii, 559-580.
Smith (G. G.). The complement-fixation test in the management of gonococcus vulvo-
vaginitis. Am. J. Dis. Child., Chicago, 1913, v, 313-316.
(d) Gonococcal Inflammations of the Urogenital Organs
The gonococcus is a common cause of urethritis (see Gonorrhea), pros-
tatitis, cystitis, epididymitis, pyelitis, vulvovaginitis, endometritis, pelvio
peritonitis, and salpingitis. In the male, gonococcal epididymitis, and in
the female, gonococcal salpingitis, are among the commonest causes of
sterility. (See Part X.)
204 DIAGNOSIS OF INFECTIOUS DISEASES
(6) Gonococcal Conjunctivitis (Ophthalmia neonatorum)
This is one of the commonest causes of blindness. About a quarter of
the blind children in the schools for the blind in the United States owe their
blindness to gonococcal infections. It is rarer now than formerly, for many
obstetricians have adopted Crede's method (1881) of instilling one or two
drops of a solution of silver nitrate into the conjunctional sac of the new-
born, irrespective of whether gonorrhea is supposed to be present in the
mother or not. A single instillation of a 1 per cent solution in each eye
has been found to be sufficient ; the stronger solution may excite a "silver
catarrh."
Reference
Crede-Hdrder (C. A.). Die Augeneiterung der Neugeborenen (Aetiologie, Pathologic,
Therapie und Prophylaxe). Berlin, 1913, S. Karger. 144 p.
(c) Gonococcal Endocarditis (Endocarditis gonorrheicd)
This is often one of the most prominent symptoms of a general gonococ-
cus sepsis. It is usually associated with gonococcal polyarthritis. The
endocarditis may be combined with pericarditis and myocarditis due to
the same coccus. A gonococcal pleuritis is occasionally observed.
Gonococci were isolated from the blood of living patients suffering
from gonococcal endocarditis by Thayer and Lazear and by Thayer and
Blumer (1895). They were demonstrated in blood cultures in cases of
gonococcal arthritis by Hewes (1894) and by Ahmaner.
References
Harris (N. M.) & Dabney (W. M.). Report upon a case of gonorrhoeal endocarditis in a
patient dying in the puerperium, with reference to two recent suspected
cases. Johns Hopkins Hosp. Bull, Baltimore, 1901, xii, 68-77.
Jochmann (G.). Gonokokkensepsis. In: Handb. d. inn. Med. (Mohr & Staehelin).
Berlin, 1911, i, 696-700.
Thayer (W. S.) & Blunter (G.). Endocardite ulcereuse blennorrhagique. Septicemie
Aborigine blennorrhagique. Arch. d. med. exper. et d'anat. path., Paris,
1895, vii, 701-718.
Thayer (W. S.} & Lazear (J. W.}. A second case of gonorrhoeal septicaemia and ulcer a-
tive endocarditis, with observations upon the cardiac complications of gonor-
rhoea. J. Exper. M., New York, 1899, iv, 81-116.
(d) Gonococcal Polyarthritis (Gonorrheal Rheumatism)
Here we deal with a metastatic infection, usually of several joints, fol-
lowing gonococcal inflammation of the urogenital system, or, rarely, of the
conjunctiva. At the outset a number of joints, are involved (polyarthritis) ;
later, the inflammation becomes most marked, as a rule, in a single joint
(monarthritis), most often one knee-joint, or one ankle-joint. Occasion-
DISEASES DUE TO COCCI 205
ally, a joint suppurates. The symptoms are but little relieved by salic-
ylates or by potassium iodid. Exacerbations and recurrences are very
common and often run parallel to exacerbations of tbe primary urethritis
or prostatitis. The complement-fixation test is positive.
References
Cole (R. /.) & Meakins (J. C.). The treatment of gonorrheal arthritis by vaccines. Johns
Hopkins Hosp. Butt., Baltimore, 1907, xviii, 223-232.
Hagner (F. /2.). Successful cultivation of gonococcus in two cases of gonorrhoeal arthritis
and one of tenosynovitis, with remarks on a new medium. Johns Hop-
kins Hosp. Bull, Baltimore, 1897, viii, 121-124.
Wolbarst (A. L.). Gonorrhoeal arthritis. Am. Med., Burlington, Vt., & New York, 1915,
n. s., x, 410-420.
(e) Gonococcal Iritis
This occurs not infrequently as a metastatic complication in gonococcal
polyarthritis, or after it. Recurrences of the iritis are common ; it is not
certain whether they represent a renewal of the infection or an allergic local
reaction due to the sudden setting free of gonococcus protein elsewhere in
the body.
5. Diseases Due to Meningococci
Meningococcus, or Diplococcus intracellularis meningitidis ( Weichsel-
baum). — This organism closely resembles the gonococcus in its biscuit-
shaped morphology. In a meningeal exudate, obtained by lumbar puncture,
the cocci are chiefly intracellular, though some extracellular cocci may also
be seen. The meningococcus stains easily with methylene blue and with
other basic anilin dyes. It is Gram-negative. In cultures, the size of the
individual cocci is variable ; along with small forms, one sees some giant
cocci, three or four times as large as the others. The individual cocci also
take the stain with variable intensity.
This coccus grows best at 37° C., and on media containing human or
animal serum. Blood-agar, ascites-agar, and hydrocele-agar are excellent
media for the cultivation of it. The growth is particularly good on ascites-
agar to which some glucose has been added. In using blood-agar as a
medium, the proportion of 2 c.c. liquid agar to 3 c.c. human blood is most
suitable.
The meningococcus quickly dies out in cultures, unless transplanted
every 5 days. It is also very sensitive to light and to drying. It is almost
non-pathogenic for animals, except young guinea-pigs and mice. Injected
into the subarachnoid space of monkeys, it causes meningitis. Dead cocci,
injected into rabbits and horses in increasing doses, yield a serum rich in
206
DIAGNOSIS OF INFECTIOUS DISEASES
specific agglutinin; this is most helpful in the recognition of suspicious
colonies, grown on ascites-agar.
In testing for meningococcus carriers by cultures from the pharynx, a
number of organisms must be ruled out (Micrococcus catarrhalis, Diplococ-
cus crassus, Diplococcus flavus, and Micrococcus cinereus). For methods,
see special texts.
(a) Epidemic Cerebrospinal Meningitis
(Cerebrospinal Fever, Meningitis meningococcica)
Definition. — An acute contagious disease, usually occurring in epi-
demics; due to infection of the leptomeninges with the meningococcus,
•which is demonstrable in fluid obtained by lumbar puncture.
FteubenE. aet.4-
JZl
107
Fig. 60.— Temperature Chart of Epidemic Cerebrospinal Meningitis. (Personal Observation.)
DISEASES DUE TO COCCI
207
Epidemiology. — The disease is spread, apparently, less by direct contact
with the patient than by the intermediation of so-called healthy menin-
gococcus carriers, that is, healthy individuals who harbor meningococci in
the nasopharynx. In mining districts, especially, the father of a sick child
carries the meningococcus to the mines, and contaminates other fathers,
who, as meningococcus carriers, on go-
ing to their homes, infect their own
children.
Incubation Period. — This is usu-
ally short, rarely exceeding 2 or 3
days.
Symptoms. — The onset is sudden,
with violent headache, vomiting, STIFF-
NESS IN THE NECK, chills, and fever
(in contrast with the slow onset in
tuberculous meningitis). The blood
shows a polymorphonuclear leukocytosis
(10,000-20,000).
When the disease is fully developed,
the pain in the head, photophobia,
irritability, restlessness, vomiting, ri-
gidity of the neck, general cutaneous
hyperesthesia, rigidity of the legs, and
KERNIG'S SIGN (inability to assume or to be placed in a sitting position
without flexion at the hip and knee) are very characteristic. Muscular
rigidity often leads to orthotonus, or to opisthotonus. Tremors of mus-
cles, tonic and clonic spasms, ankle- and patellar-clonus, are common.
Fig. 61. — Epidemic Cerebrospinal Men-
ingitis—Retraction of the Neck. (After
J. Ibrahim, in E. Feer's "Lehrb. d.
Kinderheilkunde," published by G.
Fischer, Jena.)
Fig. 62.— Epidemic Cerebrospinal Meningitis. (Med. Service, J. H. H.)
208
DIAGNOSIS OF INFECTIOUS DISEASES
Fig. 63.— Brudzinski's "Identical Reflex" or "Frog Sign"
in Meningitis. Method of Eliciting it by Flexing
the Head on the Trunk. (From W. P. Northrup's
Article, J. Am. M. Ass.)
BRUDZINSKI'S SIGNS, (1) flexion of head on chest, causing flexion at the
hips and knees (frog sign), and (2) flexion of one thigh on abdomen,
causing similar flexion on
the opposite side (contra-
lateral reflex), are present.
Symptoms referable to in-
volvement of the individ-
ual cerebral nerves (eye
muscle paralyses, optic
neuritis, deafness) are of-
ten seen, but less frequent-
ly than in tuberculous
meningitis. Occasionally,
focal symptoms (hemi-
plegia, convulsions) occur.
Delirium is common, often
followed by stupor and
coma. The fever is re-
mittent or intermittent.
The reflexes may be either
increased or diminished ;
the patellar reflexes are
often absent ; Babinski's
Fig. 64.— Brudzinski's "Contralateral Reflex" in Men- "phenomenon of the toes"
ingitis. Method of Eliciting It. Passive Flexion of may be positive, in adults,
One Leg Causes Reflex Flexion of the Other Leg. . , Sp0ond wppk of
(From W. P. Northrup's Article, J. Am. M. Ass.)
the disease. A measles-
like EXANTHEM, or roseola, is sometimes seen and petechige are common
(spotted fever). Herpes of the face, lips and ears — usually extensive — is
present in the majority of cases, except in children under 3 years of age,
in whom it does not occur.
Complications. — A large number of different complications may occur ;
the commonest are polyarthritis, endocarditis, and bronchopneumonia.
Course of the Disease. — This varies all the way from the extremely
acute type (foudroyant) known as MENINGITIS SIDERANS (in which death
occurs in a few hours), to the protracted cases with prolonged meningeal
suppuration and intermittent course. In the majority of cases, the conva-
lescence sets in within a week, or death occurs before that time. In the pro-
tracted cases, HYDROCEPHALTTS iNTERNUS often develops ; the patients be-
come afebrile, emaciate rapidly, suffer from flexion-contractures of the
lower extremities, and periodic vomiting.
In some cases, especially in children, the symptoms are peculiar, in
that rigidity of the neck and Kernig's sign are absent. In such ATYPICAL
FORMS, bulging of the fontanelles, and hyperalgesia on passive move-
DISEASES DUE TO COCCI 209
ments of the legs, would lead one to make a lumbar puncture, especially in
an epidemic.
Diagnosis. — In outspoken cases, especially in epidemics, the disease can
scarcely he overlooked. In sporadic cases, and in atypical forms, the dis-
ease may go unrecognized unless lumbar puncture is done. The cerebro-
spinal ftuid contains many polymorphonuclear leukocytes with intracellular
(and extracellular), Gram-negative, meningococci.
Differential Diagnosis. — 1. From meningismus (in typhoid, pneu-
monia, scarlet fever, etc.). In this, there may be rigidity of the neck, a
positive Kernig's sign, hyperesthesia, and increased pressure of cerebro-
spinal fluid, but the fluid contains neither pus cells nor bacteria. In
typhoid, the leukopenia and the positive blood culture are helpful in dif-
ferentiation.
2. From secondary meningitides, following otitis media, paranasal
sinusitis, etc. (streptococci, staphylococci, pneumococci, influenza bacilli).
The bacteriological examination of the fluid (Gram-positive cocci; bacilli)
distinguishes these from meningococcus infections.
3. From tuberculous meningitis. In this the onset is slow, herpes is
usually absent, the spinal fluid may be clear, or only slightly turbid, and
the sediment consists chiefly of mononuclear lymphocytes, not of polymor-
phonuclear leukocytes. Tubercle bacilli can often be demonstrated in the
fluid obtained by lumbar puncture.
Sequelae. — These, like the mortality, have been greatly reduced since
the introduction of the treatment with Flexner's antimeningitis serum.
Formerly, hydrocephalus, deafness, blindness, paralyses and imbecility
were common sequels.
The mortality has been reduced by the serum treatment from 75 per
cent to about 25 per cent. When epidemics prevail, immunization by .dead
cultures (Sophian and Black) might be considered as a measure of per-
sonal prophylaxis.
(6) Meningococcal Arthritis
(Polyarthritis meningococcica)
This is occasionally met with as a complication of cerebrospinal menin-
gitis ; it may also occur in the absence of meningitis.
(c) Meningococcal Sepsis
In the bibliography an increasing number of reports on meningococcal
sepsis are met with, in which the meningococcus has been grown in blood
cultures.
References
Bovaird (D., Jr.). Meningococcus septicemia with sterile cerebrospinal fluid; iridocyclitis;
Flexner's serum; recovery. Arch. Int. Med., Chicago, 1909, iii, 267-269.
210 DIAGNOSIS OF INFECTIOUS DISEASES
Bray (H. A.}. Chronic meningococcus septicaemia associated with pulmonary tuberculosis.
Arch. Int. M., Chicago, 1915, xvi, 487-502.
Brudzinski (/.)• Experimentelle Untersuchungen uber den kontralateralen Reflex und
liber das Nackenphdnomen an den unteren Extremitdten. Wien. klin.
Wchnschr., 1911, xxiv, 1795-1798.
Un signe nouveau sur les membres inferieurs dans les meningites chez
les enfants. Arch, de med. d. en/., Paris, 1909, xii, 745-752.
Bruynoghe (JZ.)» Le diagnostic de la meningite cerebro-spinale par le procede de deviation
du complement. Centralbl. f. Bakteriol. [etc.], 1. Abt., Jena, 1911, Ix,
Orig., 581-588.
Cecil (R. L.) & Soper (W. B.). Meningococcus endocarditis, with septicemia. Its bear-
ing on the mode of infection in epidemic cerebrospinal meningitis. Arch.
Int. Med., Chicago, 1911, viii, 1-16.
Councilman (W. T.), Mallory (F. B.} & Wright (J. H.}. Epidemic cerebrospinal
meningitis. Am. J. M. Sc., Philadelphia & New York, 1898, cxvt
251-270.
Gushing (H.} & Sladen (F.). Obstructive hydrocephalus following cerebrospinal menin-
gitis with intraventricular injection of antimeningitis serum (Flexner). J.
Exper. Med., Lancaster, Pa., 1908, x, 548-556.
Davis (D. /.)• Studies in meningococcus infections. J. Infect. Dis., Chicago, 1907, iv,
558-581.
Elser (W. J.) & Huntoon (F. M.). Studies on meningitis. J. Med. Research, Boston,
1909, xx, 371-541.
Flexner (5L). Experimental cerebrospinal meningitis and its serum treatment. J. Am. M.
Ass., Chicago, 1906, xlvii, 560-566.
Experimentelle Cerebrospinalmeningitis und ihre Serumbehandlung. Cen-
tralbl. f. Bakteriol. [etc.], 1. Abt., Jena, 1907, xliii, Orig., 99-112.
Experimental cerebrospinal meningitis in monkeys. J. Exper. Med., Lan-
caster, Pa., 1907, ix, 142-167.
The present status of the serum therapy of epidemic cerebrospinal menin-
gitis. J. Am. M. Ass., Chicago, 1909, liii, 1443-1445.
The results of the serum treatment in thirteen hundred cases of epidemic
meningitis. J. Exper. Med., Lancaster, Pa., 1913, xvii, 553-576.
Accidents following the subdural injection of the antimeningitis serum. J.
Am. M. Ass., Chicago, 1913, Ix, 1937-1940.
Flexner (S.) & Barker (L. F.). A contribution to our knowledge of epidemic cerebrospinal
meningitis. Am. J. M. Sc., Philadelphia, 1894, cvii, 155-172, 259-276.
The recent outbreak of epidemic cerebrospinal meningitis at Lonaconing
and other places in the valley of George's Creek, Maryland. Johns Hopkins
Hosp. Bull., Baltimore, 1893, iv, 68-71.
Flexner (5.) & Jobling (J. W.}. Serum treatment of epidemic cerebrospinal meningitis.
J. Exper. Med., Lancaster, Pa., 1908, x, 141-203.
Gdppert (F.). Ueber Genickstarre. Ergebn. d. inn. Med. u. Kinderh., Berlin, 1909, iv,
165-254.
Heiman (H.} & Feldstein (5.). Meningococcus meningitis. Philadelphia & London
[1913], J. B. Lippincott Co. 327 p. 8°.
Herrick (J. B.}. Concerning Kemig's sign in meningitis. Am. J. M. Sc., Philadelphia
& New York, 1899, cxriii, 85-44.
Jochmann (G.). Meningitis cerebrospinalis epidemica. In: Handb. d. inn. Med. (Mohr
& Staehelin). Berlin, 1911, i, 759-799.
Kernig (W.). Ueber ein wenig bemerktes Meningitis-Symptom. Berlin klin. Wchnschr.,
1884, xxi, 829-832.
Koplik (H.}. Epidemic cerebrospinal meningitis. Mod. Med. (Osier). 8°. Philadelphia
& New York, 2d ed., 1914, i, 594-619.
Kutscher (K. H.). Uebertragbare Genickstarre. In: Handb. d. pathogen. Mikroorg.
(Kolle & Wassermann). 2. Aufl. Jena, 1912, iv, 589-654.
DISEASES DUE TO COCCI 211
Lyons (R.). Cerebrospinal meningitis; a further discussion of certain signs and symptoms.
South. M. J., Nashville, 1914, vii, 534-537.
Cerebrospinal meningitis, with special reference to serum therapy. Pan-
Am. S. & M. J., New Orleans, 1914, xix, 55-59.
Major (R. H.) & Nobel (Edmund). The glycyl-tryptophan reaction in meningitis. Arch.
Int. Med., Chicago, 1914, xiv, 383-387.
Navarro (D.). On the bacteriology of Cerebrospinal fever. Brit. J. Child. Dis., London, 1915,
xii, 193-198.
Netter (A.) & Debre (R.). La meningite cerebro-spinale. Paris, 1911, Masson & Cie,
292 p. 8°.
Northrup (W. P.}. New reflex signs in meningitis diagnosis. J. Am. M. Ass., Chicago •,
1911, Ivi, 114-115.
Ormerod (J. A.). Cerebrospinal fever. In: Syst. Med. (Allbutt & Rolleston). 8°. Lon-
don, 1910, i, 923-942.
Osier (TF.). The arthritis of Cerebrospinal fever. Boston M. & S. J., 1898, cxxxix, 641-643.
Peters (E. A.). Note on nasal conditions of Cerebrospinal meningitis. J. LaryngoL, London,
1915, xxx, 267-269.
Robinson (G. C.}. The blood-pressure in epidemic Cerebrospinal meningitis. Arch. Int.
Med., Chicago, 1910, v, 482-490.
Sachs-Miike. Untersuchungen uber das Vorkommen von MeningokoJcken und Pseudo-
meningokokken im Nasenrachenraum Gesunder. Klin. Jahrb., Berlin,
1911, xxiv, 425-450.
Sladen (F. J.}. Epidemic Cerebrospinal meningitis and serum therapy at the Johns Hop-
kins Hospital. Johns Hopkins Hosp. Rep., Baltimore, 1910, xv, 397-540.
Sophian (A.) & Black (/.)• Prophylactic vaccination against epidemic meningitis. J.
Am. M. Ass., Chicago, 1912, lix, 527-531.
Epidemic Cerebrospinal meningitis. In: Therap. Int. Dis. (Forchheimer) .
New York & London, 1914, v, 517-578.
Sternberg (C.). Meningococcus. Ergebn. d. allg. u. path. Anat. [etc.], Wiesb., 1910, xiv,
1. Abt., 136-168.
Vincent (H.} & Bellot. Les porteurs de meningocoques et la prophylaxie de la meningite
cerebro-spinale par la disinfection de lew naso-pharynx. Bull, et mem.
Soc. med. d. hop. de Paris, 1909, 3e s., xxriii, 184-188.
Nouvelles recherches suf le precipito-diagnostic de la meningite cerebro-
spinale. Bull, et mem. Soc. med. d. hop. de Paris, 1909, 3e s., xxvi,
952-961.
Weichselbaum (A.}. Ueber die literarischen Schicksale des " Diplococcus intracellularis
meningitidis " und seine dtiologische Bedeulung. Centralbl. f. Bakteriol.
[etc.], 1. Abt., Jena, 1903, xxxiii, Orig., 510-531.
Wollstein (Martha). Parameningococcus and its antiserum. J. Exper. Med., Lancaster,
Pa., 1914, xx, 201-217.
6. Diseases Due to the Micrococcus melitensis
The Micrococcus melitensis, isolated by Bruce (1887), is a very small
coccus. It is Gram-negative, and grows best on 20 per cent ascites-agar.
It does not liquefy gelatin. It is pathogenic for monkeys, and gives rise in
these, and in rabbits, to specific agglutinins. It is one of those micro-
organisms that are most often the cause of accidental infections in bac-
teriological laboratories; thus, MacFayden lost his life from infection in
the laboratory with Micrococcus melitensis. The coccus can be killed in
milk by heating at 60° C. for 20 minutes (M. J. Kosenau).
212 DIAGNOSIS OF INFECTIOUS DISEASES
(a) Undulant Fever
(Malta Fever, Mediterranean Fever)
Definition. — This is a septicemia, with chronic course, due to Micro-
coccus melitensis, and characterized by periods of fever, interrupted by
apyretic intervals; hence the name "undulant fever."
Occurrence. — It is met with on the shores of the Mediterranean Sea,
and in various tropical countries (Asia, Africa, America). An endemic
center of the disease exists in a goat-raising section along the Rio Grande
in Texas (Gentry and Ferenbaugh).
Portals of Entry. — It gains entrance chiefly by way of the alimentary
tract, from drinking raw goats' milk containing the cocci ; occasionally, by
insect bites, or by contact (urine; dust).
Incubation Period. — This is 6 days, as proven by laboratory infection.
Symptoms. — These are indefinite at the onset (headache; anorexia;
tired feeling in the limbs). The temperature rises gradually, though oc-
casionally, the onset is sudden, with chills. Sweating, nausea, and insom-
nia are common. The abdomen is tender ; constipation is marked ; some-
times there is irregular diarrhea. In mild cases, the temperature may
gradually fall at the end of 10 days. In severer cases, it lasts longer. After
a few days of apparent convalescence, the temperature, in the majority of
cases, rises again and remains elevated for 2 or 3 weeks. The patient
grows anemic, and the spleen becomes enlarged and tender. The blood
shows a leukopenia. Tenderness and swelling of the joints, and metastatic
orchitis are common complications. The hair often falls out. Periods of
fever and of apyrexia may alternate for months.
Diagnosis. — This is easy, if blood culture be made (Micrococcus meli-
tensis). In the recognition of the coccus, the agglutination test (Konrich),
and the complement-fixation test (Sicre) are helpful.
Differential Diagnosis. — (1) From typhoid fever and paratyphoid; (2)
from malaria; (3) from acute and subacute rheumatic fever, and from
infectious arthritis.
Prognosis. — In general, the outlook is favorable, the mortality being
only about 2 per cent.
Prophylaxis. — Cows and goats become infected and their milk, when
taken unboiled, causes the disease in human beings (English Mediter-
ranean Fever Commission). The disease usually disappears from a com-
munity, if only boiled milk is taken, though infection may occasionally
arise in other ways than through milk. The urine of patients should be
disinfected.
References
Bruce (David). Malta fever. Mod. Med. (Osier}. 8°. Philadelphia & New York.
1907, Hi, 17-28.
Eyre (J. W. //.)• Mittelmeerfieber. In: Handb. d. pathogen. Mikroorg. (Kolle & Wasser-
mann). 2. Aufl. Jena, 1912, iv, 421-452.
DISEASES DUE TO BACILLI 213
Irons (E. E.)« Malta fever. In: Therap. Int. Dis. (Forchheimer) . New York & London,
1914, v, 661-664-
Notter (J. L.). Malta fever. In: Syst. Med. (Allbutt & Rolleston). 8°. London, 1910,
w, pt. 2, 422-435.
Wellman (C.), Eustis (A.) & Schochet (S. S.). Malta fever in Louisiana. Report of
a positive case in a series of forty-six agglutination tests with Microbacillus
melitensis. Am. J. Trop. Dis. [etc.], New Orleans, 1913, i, 893-396.
B. Diseases Due to Bacilli
1. Diseases Due to the Pneumobacillus (Friedlander)
Pneumobacillus (Friedlander). — This is a short, plump, encapsulated
rod, which forms a naillike growth on gelatin at room temperature and is
pathogenic for rabbits.
It occasionally causes a croupous pneumonia; it has also been found as
a cause of serositis, and of meningitis.
Reference
Abel (R.~) & Hallwachs (W.). Die Kapselbacillen (Bac. pneumoniae Friedlander und ver-
wandte Bacillen). In: Handb. d. pathogen. Mikroorg. (Kolle & Wasser-
mann). 2. Aufl. Jena, 1913, vi, 515-544.
2. Diseases Due to the Scleroma Bacillus
Bacillus of Rhinoscleroma (von Frisch). — This bacillus closely re-
sembles Friedlander's pneumobacillus, but is less virulent for animals.
It is the cause of rhinoscleroma.
(a) ^Rhinoscleroma
This is a chronic, fatal disease of the air passages, infiltrating (in the
form of bluish-red hard nodules) the skin and the mucous membrane of the
nose, mouth, palate, pharynx, larynx, or external auditory canal. The
infiltrations may feel as hard as ivory. In the nose, they lead to narrow-
ing of the nasal cavities, and obstruct the breathing. The disease belongs
among the "infectious granulomata" (along with tubercle, gumma, etc.).
The nodules of rhinoscleroma show, however, no tendency to later
softening.
The histology of the infiltrated area is characteristic (masses of plasma
cells, together with groups of large clear cells (dropsical degeneration) con-
taining the scleroma bacilli).
214 DIAGNOSIS OF INFECTIOUS DISEASES
References
Babes (F.). Das Rhinosklerom (Sklerom). In: Handb. d. pathogen. Mikroorg. (Kolle &
Wassermann). 2. Aufl. Jena, 1913, v, 1237-1256.
Whitfield (A.). Rhinosderoma. In: Syst. Med. (Allbutt & Rollestori). 8°. London,
1911, ix, 532-534*
3. Diseases Due to the Anthrax Bacillus
Anthrax Bacillus. — The Bacillus anthracis is a large, straight, non-
motile rod occurring singly or in chains, in cultures often assuming a
thread form. It stains easily with basic anilin dyes, and is Gram-
positive. Outside the body, spore forms that are very resistant develop.
The bacilli do not sporulate except in the presence of oxygen.
The bacilli are pathogenic for many animals (especially, cattle and
sheep).
(a) Human Anthrax
Men are usually infected from hides, from wool, or from rags. The
spores may infect the skin (anthrax carbuncle, malignant pustule, anthrax
edema) or they (or the bacilli in raw meat) may be swallowed and give rise
to intestinal anthrax, with symptoms of severe hemorrhagic enteritis. In a
third form, the spores may be inhaled and give rise to pulmonary anthrax
(woolsorter's disease; rag-picker's disease) characterized by hemorrhagic
pneumonia, hemorrhagic pleurisy, and mediastinitis.
In all three forms of anthrax, the bacilli may spread through the lym-
phatics, and reach the blood, giving rise to anthrax septicemia.
Laboratory workers, and veterinarians, should exercise the greatest care
in autopsy ing anthrax cadavers (rubber gloves).
References
Blumer (G.) & Young (H. H.). A case of anthrax septicaemia in a human being asso-
ciated with acute anthrax endocarditis and peritonitis. Johns Hopkins
Hosp. Bull, Baltimore, 1895, vi, 127-132.
Gibier (P.). De r aptitude communiques aux animaux d sang froid d contracter le charbon
par Velevation de leur temperature. Compt. rend. Acad. d. Sc., Paris, 1882,
xciv, 1605.
Irons (E. E.). Antianthrax serum. In: Therap. Int. Dis. (Forchheimer). New York &
London, 1914, v, 658.
Koch (R.}. Untersuchungen uber Bacterien. Die Aetiologie der Milzbrandkrankhe.it,
begriindet auf die Entwicklungsgeschichte des Bacillus anthracis. Beitr. z.
Biol d. Pflanz.,Breslau, 1877, ii, 277-308.
von Kordnyi (F.). Milzbrand, Rotz, Actinomykosis, Maul- und Klauenseuche. Spec.
Path. u. Therap., Nothnagel, Wien, 1897, v, 5. Theil, 1. Abth., 1-149.
Pasteur (L.). Sur Vetiologie du charbon. Compt. rend. Acad. d. Sc., Paris, 1880, xci, 86-94.
Nouvelles observations sur Vetiologie et la prophylaxie du charbon. Compt.
rend. Acad. d. Sc., Paris, 1880, xci, 697.
Also: Bull. Acad. de Med., Paris, 1880, 2e s., ix, 1138-1143.
Sur la longue duree de la vie des germes charbonneux et sur leur conservation
dans les terres cultivees. Compt. rend. Acad. d. Sc., Paris, 1881, xcii, 209-
211.
DISEASES DUE TO BACILLI 215
Pasteur (L.). DP la possibilite de rendre les moutons refractaires au charbon par la methode
des inoculations preventives; avec la collaboration de MM. Chamberland et
Roux. Compt. rend. Acad. d. Sc., Paris, 1881, xcii, 662; 666.
Compte rendu sommaire des experiences faites a Pouilly-le-Fort, pres Melun,
sur la vaccination charbonneuse ; avec la collaboration de MM. Chamber-
land et Roux. Compt. rend. Acad. d. Sc., Paris, 1881, xcii, 1378-1383.
Sobernheim (<?.)• Milzbrand. In: Handb. d. pathogen. Mikroorg. (Kolle & Wasser-
mann). 2. Aufl. Jena, 1913, Hi, 583-716.
4. Disease Due to the Bacillus of Malignant Edema
Bacillus of Malignant Edema. — This resembles the anthrax bacillus in
its shape (rods, threads). It also is Gram-positive. It differs from the
anthrax bacillus in being strictly anaerobic.
In human beings it can, though rarely, give rise to a form of gas gan-
grene, resembling that due to the gas bacillus of Welch.
Reference
von Werdt (F.). Malignes Oedem. In: Handb. d. pathogen. Mikroorg. (Kolle & Wasser-
mann). 2. Aufl. Jena, 1912, iv, 837-864.
5. Disease Due to the Gas Bacillus (Welch and Nuttall)
Bacillus aerogenes capsulatus (Welch and Nuttall). — This is com-
monly known as the gas bacillus, and is somewhat similar in form to the
anthrax bacillus. It is Gram-positive, often shows capsule formation, is
strictly anaerobic, and is pathogenic for guinea-pigs and for sparrows. E.
Fraenkcl's Bacillus phlegmonis emphysematosae is probably identical with
Welch's bacillus.
(a) Gas Gangrene (Hospital Gangrene)
This disease, formerly so common as a complicating infection of wounds
in the surgical wards of hospitals, is now very rare. It is, however, occa-
sionally seen, and I saw it, when in Manila in 1899, follow a bullet wound
in an unfortunate American soldier. Reports indicate that the infection
has been met with among the wounded in the great war now going on in
Europe.
The tissues swell, become discolored, and crackle under the finger. On
incision, a turbid, sanguinolent, dirty-looking exudate is visible, in smears
of which the thick gas bacilli are visible. The gas bacillus can also cause
distention of the uterus in puerperal infection (tympania uteri) ; it may
also give rise to gas cysts in the lymph vessels of the vagina (colpohyper-
plasia cystica).
The gas bacillus is, however, much more frequently met with at
autopsy in the so-called frothy organs, or foamy organs (liver, spleen, kid-
neys) in which spherical cavities due to post mortem multiplication of the
bacilli with gas formation are seen. The brain and liver, on section, may
show holes like those of Swiss cheese.
216
DIAGNOSIS OF INFECTIOUS DISEASES
References
Barrett (G. M.). Gas bacillus infection.
265.
Calif. State J. M., San Francisco, 1915, xiii, 260-
Baugher (A. H.}. The bacillus aerogenes capsulatus in blood cultures with recoveries. J.
Am. M. Ass., Chicago, 1914, Ixii, 1153-1155.
Klotz (O.) & Holman (W. L.). Infection by the gas bacillus in coal miners. J. Infect.
Dis., Chicago, 1912, ix, 251-264.
sports of cases of infection due to the bacillus aerogenes capsulatus
Boston M. & S. J., Boston, 1900, cxlii, 532-538.
Johns Hop-
Thorndike (P.). Clinical \
of Welch.
Welch (W. H.}. Morbid conditions caused by Bacillus aerogenes capsulatus.
kins Hosp. Bull, Baltimore, 1900, xi, 185.
Welch (W. HJ & Nuttall (G. H. F.). A gas-producing bacillus (Bacillus aerogenes cap-
sulatus, nov. spec.) capable of rapid development in the blood vessels after
death. Johns Hopkins Hosp. Bull., Baltimore, 1892, Hi, 81-91.
von Werdt (F.). Der Gasbrand und seine Erregcr. In: Handb. d. pathogen. Mikroorg.
(Kolle & Wassermann). 2. Aufl. Jena, 1912, iv, 878-908.
6. Diseases Due to the Tetanus Bacillus
Tetanus Bacillus. — Bacillus tetani (Mcolaier, 1884) is character-
ized by the presence of a terminal spore, which makes it resemble in
form a nail or a pin. It is
slightly motile, Gram-positive,
strictly anaerobic, and patho-
genic for animals. It was first
grown in pure anaerobic cul-
ture by Kitasato (1887), who
proved that it multiplies in
loco, giving rise to a powerful
toxin (tetanus toxin), which ex-
tends along the nerves to the
nerve, centers and causes a fatal
intoxication of the brain un-
less early neutralized by tetanus
antitoxin. The normal habitat
of B. tetani is the intestinal
tract of herbivorous animals,
hence its occurrence in manure,
in garden earth, in street dust,
etc. The house fly may help to distribute tetanus spores. The spores
are very resistant.
(a) Human Tetanus
(Lockjaw, Trismus)
Definition. — This is an intoxication of the nervous system with tetanus
toxin, leading to tonic spasm of the muscles; it is due to infection of a
wound with B. tetani.
Fig. 65. — Tetanus Bacilli.— Nail Forms. (After
W. Kolle and H. Hetsch, "Die experimented
Bakteriologic, etc.," published by Urban &
Schwarzenberg, Berlin.)
DISEASES DUE TO BACILLI 217
Portal of Entry. — If a penetrating wound be contaminated with garden
earth, manure, or street dirt, infection is liable to occur. In America,
Fourth of July wounds (blank cartridges) have frequently been followed
by fatal tetanus.
Diphtheria antitoxin may be contaminated with tetanus toxin and
cause death, as in the lamentable experience in St. Louis (1901), when 7
children succumbed to tetanus thus caused (Bolton, Fisch, and Walden).
Vaccine virus and bacterial vaccines may, if not properly controlled, be
contaminated by tetanus spores. A United States law (1902) now
requires that all serums and vaccines sold in interstate traffic be first tested
upon animals to insure freedom from contamination. Gelatin often con-
tains tetanus spores and human tetanus has been produced by injection of
imperfectly sterilized solutions of gelatin, used as a hemostatic. Human
infection is usually preceded by a known trauma (tetanus traumaticus) .
Sometimes the mode of infection is entirely unknown (tetanus idiopatli-
icus). Formerly, in a few cases, it was thought to follow exposure to cold
(tetanus rheumaticus) . The two latter forms may be instances of infec-
tion by inhalation of tetanus spores, though this is not certain.
Incubation Period. — This varies from 3 to 20 days; it is usually
between 4 and 10 days.
Symptoms. — The patients first notice a feeling of stiffness and tension
in the masseters, and in the muscles of the face and neck. The tonic spasm
of the muscles of the face gives rise to a characteristic rigid appearance
resembling a smile (risus sardonicus). Later, the muscles of the trunk
become involved and there may be marked over-extension of the back, the
body being supported by the head and the heels (opisthotonos) ; or there
may be rigidity of the trunk and extremities in a straight line (ortho-
tonos) ; or spasm of the abdominal muscles so that the body is bent for-
ward (emprostJiotonos). External stimulation (noises, etc.) may excite a
paroxysmal increase of spasm, associated with violent pain and dyspnea.
There is no fever at first ; later, the temperature rises, especially just before
death. The mind is usually clear throughout. Constipation is marked,
and defecation is painful. When the face is the portal of entry, facial
paralysis occurs and there is difficulty in swallowing (tetanus facialis,
head tetanus, tetanus hydropJiobicus).
In the Southern States, especially among the poor, infection at the
umbilicus in the new-born is not uncommon (tetanus neonatorum).
The tetanus sometimes seen in puerperal infections (tetanus, puer-
peralis) is usually severe.
Course of the Disease. — In the severer forms, death .occurs within 3 or
4 days after the appearance of the symptoms. If the patients live for a
week, they usually recover. In the milder forms, the incubation period is
longer, and all the symptoms are milder. The mortality, before the
serum treatment, varied from 50 per cent to 90 per cent.. Since the cam-
218 DIAGNOSIS OF INFECTIOUS DISEASES
paign for a "safe and sane" celebration of July 4th, for the radical treat-
ment of penetrating wounds, and for prophylactic inoculation with anti-
toxin, has been carried on, a great many cases of tetanus have undoubtedly
been prevented.
Diagnosis. — This is usually easy from the history and the symptoms.
In doubtful cases, meningitis,, strychnin poisoning, and rabies should be
borne in mind. Once symptoms have appeared, it is usually too late to save
the patient; the all-important thing is to prevent the development of
tetanus!
References
Anderson (J. F.). The danger and prevention of tetanus from Fourth of July wounds. Pub.
Health Rep. U. S. Mar. Hosp. Serv., Washington, 1908, xxiii, 857-861.
Ashhurst (A. P. C.) & John (R. L.). The rational treatment of tetanus, with a report of
twenty-three cases from the Episcopal Hospital, Philadelphia. Am. J. M.
Sc., Philadelphia & New York, 1913, cxlvi, 77-117.
Baccelli (G.). Sulla curd del tetano. Lavori d. Cong, di med. int., 1905, Roma, 1906, xv, 5-14.
Behring (E.) & Ransom (F.). Ueber Tetanusgift und Tetanusantitoxin. Deutsche med.
Wchnschr., Leipzig u. Berlin, 1898, xxiv, 181-185.
Bennecke (//.). Ueber die Leukocytose bei Tetanus. Mitt. a. d. Grenzgeb. d. Med. u.
Chir., Jena, 1912, xxiv, 319-338.
Besredka (A.}. De la fixation de la toxine telanique par le cerveau. Ann. de Vlnst. Pasteur,
Paris, 1903, xvii, 138-147.
Eisendrath (D. N.). The prevention of tetanus. J. Am. M. Ass., Chicago, 1904, xlii,
1276-1278.
Fotheringham (J. T.}. A case of tetanus, with recovery, treated by carbolic acid injections.
Can. Med. Ass. J., Toronto, 1914, iv, 898-902.
Hill (E. IF.). Tetanus. Arch. Int. Med., Chicago, 1911, viii, 747-788.
Huber (G.). Zur Symptomatologie und Serumtherapie des Tetanus traumalicus. Beitr. z.
klin. Chir., Tubing. , 1912, Ixxvii, 139-236.
Kitasato (5.).' Ueber den Tetanusbacillus. Ztschr. f. Hyg., Leipzig, 1889, vii, 225-233.
Experimentelle Untersuchungen uber das Tetanusgift. Ztschr. f. Hyg. u.
Infectionskrankh., Leipzig, 1891, x, 267-305.
Knorr (A.). Das Tetanusgift und seine Beziehungen zum thierischen Organismus. Munch.
med. Wchnschr., 1898, 321; 362.
v. Lingelsheim (H. A. W.}. Immunitdt bei Tetanus. Handb. d. path. Mikroorg. (Kolle
& Wassermann), Jena, 1904, iv, 2. Teil, 983-1000.
Tetanus. In: Handb. d. pathogen. Mikroorg. (Kolle & Wassermann). 2.
Aufl. Jena, 1912, iv, 737-787.
Madsen (T.). Ueber Tetanolysin. Ztschr. f. Hyg. u. Infectionskrankh., Leipzig, 1899,
xxxii, 214-238.
Marie (A.} & Morax (F.). Recherches sur I' 'absorption de la toxine lelanique. Ann. de
Vlnst. Pasteur, Paris, 1902, xvi, 818-832.
Meltzer (S. /.) & Auer (J.}. The effects of intraspinal injection of magnesium salts upon
tetanus. J. Exper. M., New York, 1906, viii, 692-706.
Mendl (/.). Beitr ag zur Kenntnis des Stoffwechsels bei Tetanus traumaticus. Zischr.f.
klin. Med., Berlin, 1908, Ixv, 141-160.
Meyer (H.} & Ransom (F.). Untersuchungen uber den Tetanus. Arch. f. exper. Path,
u. Pharmakol., Leipzig, 1903, xxxix, 369-416.
Nicolaier (A.}. Ueber infektiosen Tetanus. Deutsche med. Wchnschr., Berlin, 1884, x,
842-844*
DISEASES DUE TO BACILLI 219
Noguchi (H.). On the influence of tissues, cholesterin and cholesterin esters upon the pro-
duction of tetano-spasmin and tetano-lysin in fluid cultures, Proc. N.
York Path. Soc., 1907-08, vii, 87-90.
Norris (G. W.). Tetanus: a study of fifty-seven cases from the records of the Pennsylvania
Hospital. Phila. M. J., 1903, ix, 835-838.
Park (W. H.). Tetanus. In: Therap. Int. Dis. (Forchheimer). New York & London,
1914, v, 456-471.
Robertson (H. E.). A new method for the prophylactic application of tetanus antitoxin.
J. Am. M. Ass., Chicago, 1915, Ixv, 793-794.
Rosenbach (F. J.}. Zur Aetiologie des Wundstarrkrampfes beim Menschen. Arch. f.
klin. Chir., Berlin, 1887, xxxiv, 306-317.
Roux & Barrel. Tetanus cerebral et immunite contre le tetanos. Ann. de VInst. Pasteur,
Paris, 1898, xii, 225-239.
Roux (E.) et Vaillard (L.)« Contribution a V etude du tetanos. Ann. de VInst. Pasteur.,
Paris, 1893, vii, 65-140.
Ruediger (E. H.). The duration of passive immunity, with special reference to that against
tetanus. Bull. Manila M. Soc., 1911, Hi, 83, 98.
Wassermann (A.) & Takaki (T.). Ueber tetanusantitoxische Eigenschaften des normalen
Centralnervensy stems. Berl. klin. Wchnschr., 1898, xxxv, 5-6.
7. Diseases Due to the Influenza Bacillus
Influenza Bacillus. — Bacillus influenzce (E. Pfeiffer, 1892-3) is an
extremely minute bacillus, rather irregular in length, with rounded ends,
and very difficult to grow. It stains best with dilute carbol-f uchsin ; it is
Gram-negative, non-motile. It is aerobic, and grows best on blood-agar, on
which it appears as minute, colorless, transparent colonies. Because it
grows only on hemoglobin-containing media, it is classed among the "hemo-
globinophil" bacilli. It is often difficult to distinguish it from similar
bacilli (pseudo-influenza bacilli, bacillus of trachoma, bacillus of whooping-
cough, xerosis bacilli), but the grouping in smears of purulent secretion is
considered characteristic. The organisms rarely form chains, but lie in
irregular thick clusters, without parallelism.
(a) Influenza (La Grippe)
Definition. — An infectious and highly contagious disease, due to
Bacillus influenzce,, occurring generally in epidemics ; after each epidemic it
continues to appear sporadically for several years.
In the great epidemics thousands are attacked within a very brief
period. Thus half the inhabitants of a district may be attacked within a
few weeks. The morbidity is great, the mortality usually small.
Portal of Entry. — Usually, the bacillus enters through the respiratory
tract, probably, chiefly by "droplet-infection."
Symptoms. — The incubation period is usually from 1 to 4 days. The
symptoms vary according to the predominant localization of the bacilli or
their toxins. The onset is usually sudden, often with chills and fever.
Herpes simplex is very often present In most cases, the attack is quickly
220
DIAGNOSIS OF INFECTIOUS DISEASES
over. In others, it may be prolonged. Convalescence is frequently tedious,
and relapses are common. Four principal types of influenza are distin-
guished and, in all, marked
prostration and debility are J~^0\jIT 3.€t,
prominent features. *—
1. Influenza of the respira-
tory tract, with rhinitis, laryn-
gitis, tonsillitis, tracheobron-
c h i t i s, paranasal sinusitis.
These cases are often compli-
cated by influenzal pneumonia
and pleurisy.
2. So-called influenzal fe-
ver with headache, prostration,
myalgias, anorexia, and de-
pression, without catarrhal
symptoms.
3. Gastro-intestinal influ-
enza with high fever, anorexia,
herpes, and severe diarrhea.
4. Influenza of the central
nervous system. Several se-
vere forms of influenzal infec-
tion of the central and periph-
eral nervous system occur, e. g.,
influenzal meningitis, influen-
zal encephalitis, influenzal
polyneuritis, and influenzal
neuralgias (persistent). Dr.
B. A. Cohoe has reported a
case of influenzal meningitis,
from my service.
Pure influenzal infections
do not necessarily change the
leukocyte count. In mixed in-
fection with streptococci and
pneumococci, leukocytosis is
seen. One attack does not confer immunity, but rather predisposes to
other attacks.
Complications. — Endocarditis, meningitis, orchitis, nephritis, polyar-
thritis, conjunctivitis, and especially otitis media, may occur during the
acute process or as sequelae.
Patients with phthisical or bronchiectatic cavities are often influenza-
bacillus carriers, and may be responsible for a revival of epidemics from
Fig. 66. — Influenza. (Personal Observation.)
DISEASES DUE TO BACILLI 221
year to year when climatic conditions increase disposition in a community.
F. P. Lord of Boston found influenza bacilli in the sputum in a large
proportion of expectorating patients in an interepidemic period. Boggs
has called attention to the presence of influenza bacilli in the sputum from
bronchiectatic cavities.
References
Axenfeld (77i.). Conjunctivitis des Koch-Weeksschen Bacillus und der Influenzdbacillen.
In: Handb. d. pathogen. Mikroorg. (Kolle & Wassermann). 2.Aufl
Jena, 1913, vi, 545-571.
Boggs (T. JR.). The influenza bacillus in bronchiectasis. Am. J. M. Sc., Philadelphia &
New York, 1905, cxxx, 902-911.
Cohoe (B. A.). Influenzal meningitis. Am. J. M. Sc., Philadelphia & New York, 1909,
cxxxvi, 74-88.
Davis (D. J.). Influenza and influenzal pneumonia, their etiology and complications, and
the occurrence of influenza bacilli in various infectious diseases. Arch.
Int. Med., Chicago, 1908, ii, 124-138.
Influenzal meningitis. Arch. Int. Med., Chicago, 1909, iv,
Jochmann (G.). Influenza. Ergebn. d. allg. Path. u. path. Anat., Wiesbaden, 1909,
xiii, Abt. i, 107-134-
Lord (F. T.}. Influenza. Mod. Med. (Osier}. 8°. Philadelphia & New York, 2d ed.,
1914, i, 534-549.
The etiology of an epidemic of influenza. Pub. Mass. Gen. Hosp., Boston,
1909, ii, 715-719.
Netter (A.), Hudelo (L.) [et al.]. Grippe, Coqueluche, Oreillons, Diphterie. Paris,
1913, J. B. Bailliere & fils. 172 p. 8°. [Nouv. traite de med. de
therap., ix.]
Rhea (L. /.). Cerebrospinal meningitis due to bacillus influenzas. A report of two cases
from one of which the organism was obtained in pure culture from the cir-
culating blood eighty-five days before death. Arch. Int. Med., Chicago,
1911, viii, 133-140.
Ross (A.) & Moore (A. E.}. A case of influenzal meningitis. Brit. M. J., London, 1913,
1056-1058.
Scheller (R.). Die Gruppe der hdmoglobinophilen Bakterien. In: Handb. d. pathogen.
Mikroorg. (Kolle & Wassermann). 2. Aufl. Jena, 1913, v, 1257-1
Thurs field (H.}. Influenzal septicaemia, with a short review of the present status of bacillus
influenzce. Quar. J. Med., Oxford, 1910, iv, 7-13.
Wollstein (M.). Influenzal meningitis and its experimental production. Am. J. Dis.
Child., Chicago, 1911, i, 4^-58.
8. Diseases Due to the Bacillus of Bordet and Gengou
Bacillus of Bordet and Gengou. — This bacillus closely resembles the in-
fluenza bacillus, but is slightly larger and shows less tendency to pleomor-
phism. It is usually present in the sputum of whooping-cough patients,
and has been cultivated on a glycerin-potato-blood-agar medium (Bordet).
It is a bi-polar-staining bacillus; Bordet and Gengou believe that it is the
etiological agent in whooping-cough since in their hands the serum from
convalescents from whooping-cough yields a positive agglutination reac-
tion, or more often a complement-fixation reaction, with their bacillus.
Frankel, however, could cultivate this bacillus in only 8 out of 38 cases;
222 DIAGNOSIS OF INFECTIOUS DISEASES
moreover, serum from convalescents never agglutinated it, and complement
fixation was positive in only 1 of 5 cases tested. Similar reports are made
by Scheller (1912), Odaira (1911), Wollstein (1909), and Weil (1913).
Many still believe that the disease is due to the bacillus influenzas.
Czerny thinks that whooping-cough is not an etiological unity, but may be
due to different infectious agents. If there is one specific agent, the
whooping-cough due to it may be called "essential whooping-cough," and
the other forms, "symptomatic whooping-cough." Apparently in the
spasmophil diathesis, a cough like that in pertussis may occur in the
absence of any specific infectious agent.
Luetscher, however, finds the I3ordet-Gengou bacillus present in many
cases of whooping-cough in Baltimore. According to Mallory and Horner,
the bacilli are present in great numbers on the surface of the tracheal
epithelium, where they mechanically paralyze the cilia. The question of
the etiology of pertussis is not yet wholly satisf acorily settled.
(a) Whooping-cough
(Pertussis, Tussis convulsiva, Fr. Coqueluche)
Definition. — A disease directly contagious, especially in its early stages,
characterized by paroxysms of coughing, often accompanied by vomiting,
and occurring, usually, in epidemics among children. The cough in the
convulsive stage sets in with a series of 5-30 short expiratory coughs, fol-
lowed by a loud inspiratory noise (whoop). For the etiology, see above.
Susceptibility. — Among animals, dogs, cats, and monkeys are known to
be susceptible. Children between 6 months and 5 years of age are extremely
susceptible, but the disease may occur at any age. One attack usually
yields permanent immunity.
. Nature of the Disease. — According to Reyher, the pertussis syndrome
may arise :
1. From an intense stimulus, exerted upon the respiratory mucous
membrane, most often by an exogenous cause (essential whooping-cough).
The exciting stimulus can be conditioned by (a) the production of special
irritants by an infectious agent; (b) the localization of an infectious agent
at a site of predilection for reflex cough (e. g., regio inter arytenoidea) ; (c)
the factors (a) and (b) together.
2. From a heightened irritability of the nervous system of the sick
child, in which an ordinary catarrh may suffice for the production of the
syndrome; here an endogenous cause plays the main role (symtomatic
whooping-cough). This is observed (a) in children with spasmophil diath-
esis, when they contract an ordinary respiratory cough; (b) in older
neuropathic persons in the same circumstances.
3. From a combination of the effect of an intense stimulus with a
heightened irritability.
DISEASES DUE TO BACILLI 223
Symptoms. — These come on after an incubation period of, ordinarily,
3 to 8 days.
In the catarrhal siage,, they consist of sneezing, running of the nose,
headache, lacrymation, cough and slight fever, lasting 3 to 14 days.
The convulsive, stage is characterized by an irrepressible feeling of
tickling in the larynx and repeated paroxysms of coughing, each followed
by a whoop. At the end of a paroxysm, viscid, glassy sputum is expec-
torated (or expelled by gagging or vomiting movements) ; on microscopic
examination this sputum is characterized by the presence of large amounts
of squamous epithelium, each cell stuffed full of small short bacilli. The
paroxysms may be so severe as to cause asphyxia. There is often vomiting,
epistaxis, conjunctival hemorrhage, and involuntary urination and defeca-
tion. After a paroxysm there is a brief period of exhaustion and sweating.
The child may then resume its play and act as though it were perfectly
well. A child may suffer from 10 to 15 or more attacks per day. The
severer attacks occur in the night and toward morning. Paroxysms are
often precipitated by emotion, crying, pharyngeal irritation, dust, etc.
This convulsive stage lasts from 2 to 6 weeks ; it may sometimes continue
for several months. Convalescence is gradual.
In epidemics, mild and abortive cases may be seen. The white cell
count in the blood is usually increased. On physical examination, signs of
diffuse bronchitis, and, in severe cases, of pulmonary emphysema and of
dilatation of the right heart are found.
Complications. — Capillary bronchitis; bronchopneumonia (very fatal
in young children, especially if rachitic or scrofulous) ; emphysema; pneu-
mothorax; apoplexy.
Sequelae. — Emphysema; pulmonary tuberculosis; tuberculous men-
ingitis.
Diagnosis. — This is easy, as far as the clinical syndrome is concerned,
in typical cases with the whoop. The diagnosis is often difficult, or impos-
sible, in the catarrhal stage, especially when there is no history of exposure.
But if we assume the existence of (1) an "essential (specific) whooping-
cough," and (2) a "symptomatic (non-specific) whooping-cough," there
will often be great difficulty in distinguishing the two. One may make
(1) cultures for the Bordet-Gengou bacillus, and (2) serodiagnostic tests
in the later disease or in the convalescence for agglutination and for com-
plement fixation ; but the antibodies develop too late in the disease to per-
mit of an early serodiagnosis (better and Weil, 1913).
In the catarrhal stage, or in rudimentary forms, we may (1) seek a
history of exposure, (2) look for a lyrnphocytosis, (3) look for pale urine
of high specific gravity rich in uric acid ; but these are not wholly satisfac-
tory data on which to make a diagnosis !
In sucklings and in children up to 2 years of age, we should ascertain
whether or not the signs of a spasmophilia (Chvostek's facial phenomenon,
224 DIAGNOSIS OF INFECTIOUS DISEASES
increased electrical excitability of the nerves) are present. In case they
are present we should be cautious in making the diagnosis of an essential
or specific whooping-cough; it may be only a symptomatic whooping-
cough in a spasmophilic child, due to an ordinary catarrh (Czerny) ; the
latter diagnosis is strongly supported if there be (1) no outspoken catar-
rhal stages preceding the convulsive attacks, and (2) no copious excretion
of mucus containing flat epithelium full of bacilli, at the end of the
paroxysm.
Tuberculosis of the bronchial glands may cause similar paroxysms
(rontgenogram ; percussion; tuberculin test; course).
Hysterical cough may simulate whooping-cough, but there is no vomit-
ing after the paroxysms and no preceding catarrhal stage; usually there
are no paroxysms at night and other signs of hysteria are present.
References
Barach (J. H.). Morphology of the blood in pertussis. Arch. Int. Med., Chicago, 1908f
i, 602-614.
Bordet (J.) & Gengou (O.)» Le microbe de la coqueluche. Ann. de I'lnst. Pasteur,
Paris, 1906, xx, 731-741.
Czerny (A.). Zur Lehre vom Keuchhusten. Jahrb. f. Kinder h., Berlin, 1915, n. s., Ixxxi,
473-481.
Kolmer (J. A.). A study of the blood in pertussis. Arch. Int. Med., Chicago, 1909, iv,
81-96.
Krause (P.). Keuchhusten. In: Handb. d. inn. Med. (Mohr & Staehelin) , Berlin, 1911,
i, 195-206.
Mallory (F. B.) & Homer (A. A.}. Pertussis: The histological lesion in the respiratory
tract. J. Med. Research, Boston, 1912-13, xxvii, 1 15-123.
Mallory (F. B.), Horner (A. A.) & Henderson (F. F.). The relation of the Bordet-
Gengou bacillus to the lesion of pertussis. J. M. Research, Boston, 1913,
xxvii, 391-397.
Mosenthal (H. O.). The leucocyte count of normal institutional children and those suffer-
ing from pertussis. Arch. Pediat., New York, 1908, xxv, 831-837.
Netter (A.) & Weil (M. P.). La deviation du complement par le bacille de Bordet et Gengou
dans la coqueluche. Compt. rend. Soc. deBiol, Paris, 1913, Ixxiv, 236-238.
Olmstead (M.) & Luttinger (P.). Complement fixation in pertussis. Arch. Int. Med.,
Chicago, 1915, xvi, 67-85.
Reyher (P.)» Keuchhusten. In: Spez. Pathol. u. Therap. inn. Krankheiten. (Kraus &
Brugsch), Berlin, 1914, ii, 1, 431-467.
Ruhrah (John). Whooping-cough. Mod. Med. (Osier). 8°. Philadelphia & New
York, 2d ed., 1914, i, 656-663.
Sill (E. M.). Whooping-cough (Pertussis). In: Therap. Int. Dis. (Forchheimer). New
York & London, 1914, v, 300-312.
Smith (E.). Whooping-cough. In: Syst. Med. (Altbutt & Rolleston). 8°. London,
1909, ii, pt. i, 571-585.
Wollstein (M.). A study of the bacteriology of pertussis, with special reference to the agglu-
tination of the patient's blood. J. Exper. M., New York, 1905, vii, 335-
342.
The Bordet-Gengou bacillus of pertussis. J. Exper. M., Lancaster, Pa.,
1909f xi, 41-54.
DISEASES DUE TO BACILLI
9. Diseases Due to the Plague Bacillus
225
Blague Bacillus. — Bacillus pestis usually assumes the form of a short
rod, but it is often polymorphous; its ends are rounded; polar stain-
ing is visible in methylene blue preparations; it is Gram-negative. 'The
bacillus is non-motile. It grows well on gelatin, at low temperatures, and
is non-liquefying. It is pathogenic for mice, rats, and squirrels. The
bacillus belongs to the hemorrhagic-septicemia group. It builds no true
toxin, but injures through its endotoxins.
(a) Plague
Definition. — An infection due to Bacillus pestis, usually causing
swelling of the nearest lymph gland (bubo) ; it may, however, give rise to
septicemia, or to pneumonia.
Portals of Entry. — The bacillus usually enters through a minute wound
(flea-bite) in the skin (axillary and inguinal buboes) ; occasionally,
entrance is by inhalation (plague pneumonia). Epidemics in rats usually
precede the larger human epidemics. Rat fleas (Pulex cheopis) are con-
Fig. 67. — Pulex irritans. (After W. Braun, "Die tbierischen Parasiten des Menschen," pub-
lished by Bale Sons & Danielsson, London.)
cerned in the transfer of the bacilli from rat to rat, and possibly also from
rat to man. The Pulex irritans or common flea differs somewhat from the
rat flea.
When plague is epidemic, the morbidity increases from October to
February and March, and then declines.
In Egypt, the small epidemics are of the bubonic type and due to
infection from rats. In winter, the cases are often of the pneumonic type
and the infection is direct from man to man (Gottschlich).
Incubation Period. — Two to 5 to 10 days.
226 DIAGNOSIS OF INFECTIOUS DISEASES
Symptoms. — After a brief prodromal period (malaise, anorexia, head-
ache, pain in hack) there is usually a sudden onset with chill, violent
headache and vertigo, often with nausea and vomiting, high fever, delir-
ium. In one or two days a bubo, a plague pustule, or a plague pneumonia
becomes demonstrable. As members of a Commission to the OHent
(1899), Flexner and I, with Drs. Flint and Gay, had opportunity of
studying the disease, clinically and at autopsy, with Lowson in Hong Kong.
Later, with Flint, I saw 800 cases in one day at the Plague Hospital
in Poona, near Bombay. On the average, a new patient entered the hos-
pital every 8 minutes, and a plague cadaver was carried out every 10
minutes of the day.
In 1900, Flexner, Novy and I, as a Commission appointed by the
U. S. Government, confirmed the diagnosis of the existence of plague in
San Francisco, after which the admirable Campaign of Extermination
was undertaken by the local authorities in cooperation with the United
States Public Health Service.
THE PLAGUE BUBO. — The lymph gland nearest the portal of entry be-
comes large and tender (primary bubo) ; thence, the bacilli may enter the
blood and cause general infection, with metastatic involvement, and swell-
ing of distant lymph glands (secondary buboes). The juice aspirated
from the swollen lymph glands contains enormous numbers of plague
bacilli.
PLAGUE PUSTULE, OR CARBUNCLE. — This is a bluish red, painful infil-
tration of the skin, varying in size from that of a hemp-seed to that of a
quarter, with vesicle formation ; the turbid fluid contents contain enormous
numbers of plague bacilli. This skin-plague is usually metastatic in origin.
PNEUMONIC PLAGUE. — This is the severest form of plague and is almost
uniformly fatal. The hemorrhagic sputum contains plague bacilli. Heart
failure occurs early, death ensuing in from 2 to 5 days after onset of the
infection. Secondary buboes are not uncommon. (Plate IV, Fig. 2.)
Diagnosis. — This is easy in epidemics. It is often difficult to recog-
nize the first case, though this is, of course, extremely important. The
bubonic form is sometimes confused with • inguinal buboes due to soft
chancre, or to gonorrhea. If plague be suspected, the lymph gland should
be aspirated, and the juice examined bacteriologically. Smears stained
in carbol-methylene-blue reveal the polar-staining bacilli ; the nature of the
bacillus can be confirmed by cultures and by inoculations of guinea-pigs.
Recently a plaguelike disease due to Bacillus tularense has been discovered by
McCoy and Chapin in California, and observed by Wherry and Lamb in Ohio.
The patients present an ulcerative conjunctivitis involving the palpebral conjunc-
tivae and accompanied by enlargement of the preauricular and the cervical lymph-
glands on the side affected, fever, and prostration. The disease appears to be
contracted from rodents (ground-squirrels, wild rabbits), possibly through the
intermediation of insects (fleas, flies).
DISEASES DUE TO BACILLI 227
References
Bacot (A. W.) & Martin (C. J.). Observations on the mechanism of the transmission of
plague by fleas. J. Hyg., Cambridge, 1913-14, xii, 423-439, 2 pi.
Bannerman (W. B.). The plague prophylactic. 2d revised ed. Govt. Central Press,
Bombay, 1905.
Barber (M. A.}. Studies on pneumonic plague and plague immunization. XI. The in-
fection of guinea pigs, monkeys, and rats with doses of plague bacilli,
., M
ranging from one bacillus upwards. Philippine J. Sc., Manila,
mi (B.), 251-254.
Barker (L. F.}. On the clinical aspects of plague. Tr. Ass. Am. Physicians, Philadelphia,
1901, xvi, 459-480. -
Barker (L. F.) & Flint (J. M.). A visit to the plague districts in India. New York
M. J., 1900, Ixxi, 145-154.
Blue (R.}. Anti-plague measures in San Francisco, California, U.S. A. J. Hyg., Cam-
bridge, 1909, ix, 1-8.
Boelter (W. R.}. The rat problem. London, 1907.
Calvert (W. J.). Plague. Mod. Med. (Osier}. 8°. Philadelphia & New York, 2d ed.t
1914, i, 620-638.
Chick (H.} & Martin (C. J.). The fleas common on rats in different parts of the world
and the readiness with which they bite man. J. Hyg., Cambridge, 1911,
xi, 122-136.
Danysz (/.)• Un microbe pathogene pour les rats. Ann. de I'Inst. Pasteur, 1900, xiv, 193-
201.
Dieudonne (A.} & Otto (R.). Pest. In: Handb. d. pathogen. Mikroorg. (Kolle & Wasser-
mann). 2. Aufl. Jena, 1912, iv, 155-355.
Flexner (S.}, Novy (F. G.) & Barker (L. F.). Report of the commission appointed by
the Secretary of the Treasury for the investigation of plague in San Fran-
cisco. Rep. Superv. Surg.-Gen. Mar. Hosp., Washington, 1901, 524-535.
Also: Pub. Health Rep., U. S. Mar. Hosp. Serv., Washington, 1901,
xvi, 801-816.
Flint (J. M.). Notes on the plague in China and India. J. H. H. Bull, 1900, xi, 119-127.
Lewin (Alex. v.). Neuere Forschungen uber die Epidemiologie der Pest. Ergebn. d. inn.
Med. u. Kinderh., Berlin, 1913, x, 818-868.
McCoy (G. W.}. Studies upon plague in ground squirrels. U. S. Public Health Serv.
Bull. 'No. 43. Washington, 1911. 71 p. 8°.
The susceptibility to plague of the weasel, the chipmunk, and the pocket
gopher. J. Infect. Dis., Chicago, 1911, viii, l$-Jfi.
Payne (J. F.}, Bulloch (W.} & Douglas (S. R.}. Plague. In: Syst. Med. (Allbutt &
Rolleston). 8°. London, 1910, U, pt. 2, 358-422.
Rowland (S.). Besredka's method of vaccination. J. Hyg., Cambridge, Univ. Pr., 1912,
xi, Plague Supplement ii, 344~349-
Rucker (W. C.}. Bubonic plague, a menace to American seaports. Public Health Rep.,
Washington, 1915, xxx, 1140-1146.
The relation of rodent plague to human infection. J. Am. M. Ass.,
Chicago, 1915, Ixv, 1767-1769.
Strong (R. P.). Summary of the clinical features of pneumonic plague as observed in the
Manchurian epidemic. Rep. Internal. Plague Conf., Manila, 1912,
428-432.
Summary of bacteriology and pathology of pneumonic plague. Rep.
Intern. Plague Conf., Manila, 1912, 433-457.
Protective inoculation against plague. J. Med. Research, Boston, 1908,
xviii, 325-346.
Strong (R. P.) & Teague (O.). Method of infection in pneumonic plague. J. Am. M.
Ass., Chicago, 1911, Ivii, 1270.
Studies on pneumonic plague and plague immunization. V. Clinical ob-
servations. Philippine J. Sc., Manila, 1912, vii (B.), 181-185.
228 DIAGNOSIS OF INFECTIOUS DISEASES
[Various Authors.] Plague suppressive measures in California. Ann. Rep. Surg.-Gen.
Mar. Hosp., Washington, 1910, 174-187.
[Various Authors.] The rat and its relation to the public health. U. S. Public Health
Serv. Bull. No. 30. Washington, 1910. 254 p. 8°.
Wherry (W. /?.)• A plague-like disease of California ground squirrels affecting man, in Ohio,
with a demonstration of specimens. J . Am. M. Ass., Chicago, 1915, Ixv,
1549-1550.
10. Diseases Due to the Typhoid Bacillus
Typhoid Bacillus. — Bacillus typhosus (Eberth-Gaffky) is a short
rod with rounded ends, actively motile (peritrichous flagella), staining
with ordinary dyes, but Gram-negative. It is easily grown on ordinary
media, not liquefying gelatin. It can be distinguished from 13. coll by
various special cultural tests (Drigalski-Conradi medium, Endo's fuchsin-
sulphite-agar, litmus milk, indol formation, etc., q. v.)9 and from />. coli
;^$V: /i/ >£?;•#'
... .%\% : \ / >•' ' v • . . . " • X W V % • V . */
••• **•*/***• *"•*». *••.*•*• *.*»V"*%
\\ .*v « • ^ * • .** w>v^ V v« *
* * * * " * * *
Fig. 08. — This Map for 1907 Shows a Large Number of Cases Distributed Evenly Throughout
a City. Many of These Cases Were Probably Caused by Infected Water, but it is Hard
to Separate the Cases Caused by Water-borne Infection from Those Caused by Flies.
(After W. R. Stokes and F. W. Hachtel, Arch. Int. Med.)
DISEASES DUE TO BACILLI 229
n
Fig. 69.— The Map for 1900 Shows a Typical Milk Epidemic, as Shown by Large Number of
Black Pins in Upper Portion of Map. The Rest of the City, when Compared with the
Map of 1907, Shows a Much Smaller Number of Cases. (After W. R. Stokes and F. W.
Hachtel, Arch. Int. Med.)
and B. paratypliosus by serological reactions (agglutiniii test, bacteriolysin
test).
The typhoid bacillus belongs to the so-called typhoid-colon group, which
includes also the bacillus of hog-cholera, Gartner's bacillus, the paratyphoid
bacillus, the dysentery bacillus, Bacillus fecalis alcaligenes, and the bacil-
lus of mouse typhoid.
In the table following the discussion *of the paratyphoid diseases, the
characteristics of several of the members of the group are synoptically
arranged.'
(a) Typhoid Fever
(Typhus abdominalis)
History. — Through the careful analysis of clinical symptoms and the
study of pathological anatomy, a group of fevers known as typhoid fever
was gradually separated from other conditions, especially from typhus
exanthematicus, relapsing fever,, plague, and yellow fever. It was only
after the development of etiological studies, and especially after the intro-
230
DIAGNOSIS OF INFECTIOUS DISEASES
duction of bacteriological methods and biological immunity reactions that
this "clinical typhoid fever" could be further analyzed, and divided into
several distinct diseases on the ground of etiology (B. iypliosus, B. paraty-
phosus A, B. paratyphosus B, etc.). We now speak of these, taken together,
as the typhoidal diseases, and, among them, distinguish (1) typhus ab-
dominalis, (2) paratyphus, and (3) typhus manchuricus.
Definition of True Typhoid Fever (Typhus abdominalis). — An infec-
tious disease with continued fever due to the B. typhosus, which is always
present in the blood of patients suffering from the disease ; the fever lasts
usually from 2 to 4 weeks. The disease is clinically characterized by a
palpable spleen, rose spots, leukopenia and a pulse-temperature curve
that shows a relative bradycardia. It is occasionally complicated by in-
testinal hemorrhage, or by perforative peritonitis. The mortality of the
disease varies between 8 per cent and 12.per cent, in most epidemics.
Epidemiology. — Every case of typhoid comes from some preexisting
case, directly or indirectly. The typhoid patient gives off typhoid bacilli,
chiefly through the feces, sometimes also through the urine; other people
are less often infected by direct contact with the sick than by indi-
rect transmission through polluted drinking-water, milk, or food, such
pollution often being due to the so-called typhoid bacillus hosts (i. e.,
persons who have never had typhoid or who have had an attack and
Fig. 70. — The Spring in the Brickyard Furnished an Abundant Supply of Clear Water. Fol-
lowing the Development of a Typhoid Case in the Cottage on the Hill, 108 of the 20O
Workmen in the Brickyard Became 111 with Typhoid Fever. (After E. O. Jordan, J. Am.
M. Ass.)
continue to give off from their bodies bacilli, for a shorter or longer period,
thus menacing the health of people about them).
Human beings who harbor typhoid bacilli are, as we have said, spoken
of as typhoid hosts. Among them, those who are suffering from typhoid,
or who have earlier had typhoid, are called typhoid-bacillus excretors,
while those who have never had typhoid, or at any rate are not known to
have had it, are called typhoid-bacillus carriers. The condition of "host"
may be temporary or chronic. Most chronic typhoid hosts are women,
DISEASES DUE TO BACILLI
231
perhaps because they more often suffer from gall-stones. Only 1 to 4 per
cent of typhoid excretors become chronic typhoid hosts, though many are
temporary hosts for a few months after defervescence.
Large epidemics, and those of sudden outbreak, are due nearly always
either to a contaminated water supply or to a contaminated milk supply.
Small epidemics may be due to contaminated foods (oysters, butter, etc.).
Food may be infected either by a human typhoid host or by flies. The
infection atrium in human beings is nearly always the digestive tract.
Disposition. — Age is important, the majority of the patients infected
being between the 15th and the 35th year, over half the cases occurring
between the 15th and 25th years. Sex is important only in as far as the
exposure to infected material differs. Strong, healthy, young people are
fully as often infected as feebler persons. House infection (family infec-
tion) is common (contact, common drinking-water and food). Sporadic
cases of typhoid are usually due to contact infection, often from carriers.
TYPHOID FEVER BY MONTHS
1904 1905 1906 1907
JFMAMJJASONOMFMAMJJASONDIJFMAMJJASONOlJFMAM JJASOND
469
Fig. 71.— This Chart Shows the Typical Seasonal Rise in the Cases of Typhoid Fever During
the Months of July, August and September When Flies are Most Prevalent. (After
W. R. Stokes and F. W. Hachtel, Arch. Int. Med.)
232
DIAGNOSIS OF INFECTIOUS DISEASES
The morbidity from typhoid fever is highest in the summer and
autumn months. The cases are fewest from January to April.
Incubation Period. — This is somewhat uncertain; it is believed to be,
usually, 3 or 4 days, but occasionally shorter (1 to 2 days), or longer (2
to 3 weeks).
Symptoms. — During the incubation period, certain prodromata may be
felt — anorexia, slight headache, insomnia, malaise, bronchitis.
The patient then begins to have FEVER, which follows a characteristic
course, gradually rising (stadium incrementi), then remaining continuous
(acme), then becoming markedly remittent or intermittent (amphibolous
stage), and finally ending by lysis (defervescence), to be followed by a
few days of subnormal temperature in the early part of convalescence.
George Z. aet.25
Fig. 72. — Temperature Chart of Typhoid Fever. (Personal Observation.)
It is practically convenient to classify the clinical symptoms and the
pathological changes according to the weeks of the disease. This practice,
though convenient, is purely schematic, and every physician is familiar
with marked deviations from the scheme.
The Typical Course of Typhoid Fever.
FIRST WEEK (STADIUM INCREMENTI. HYPERPLASIA OF PEYER'S
PATCHES). — The fever curve shows a steplike ascent, the temperature
DISEASES DUE TO BACILLI
233
each morning and evening being higher than that of the day before, until
by the 3rd or the 5th day, it may be 104° or 105° F. Among the symp-
toms of the first week are : headache ; pain in the back ; chilly sensations ;
sometimes actual rigor ; anorexia ; disinclination for exercise ; coated tongue
with red edges ; often epistaxis ; slight abdominal distention ; usually con-
stipation, rarely diarrhea ; sometimes, palpable spleen ; pulse slow, con-
Vir&'J&aet.'SLQ
Fig. 73.— Typhoid Fever— Initial Staircaselike Rise. (Personal Observation.)
trasted with the elevation of temperature, often dicrotic ; sometimes rhon
chi in the lungs. The psyche may be a little dulled ; there is rarely delir-
ium at this stage (initial delirium). The skin is dry and hot. No herpes.
No coryza. There is almost always a leukopenia (W. B. C. 3,500 to 7,000)
with relative increase in the large mononuclear cells. The blood culture is
positive for B. typhosus in over 90 per cent of the cases if made during the
first week. The Widal test is negative at this stage. The ophthalmic reac-
tion of Austrian is usually positive. The diazo-reaction of Ehrlich is
often positive in the urine after the middle of the first week, though, if
the patients drink much water, it may not appear.
234
DIAGNOSIS OF INFECTIOUS DISEASES
SECOND WEEK ( FIRST HALF OF STADIUM ACMES. NECROSIS AND
SLOUGHING OF PEYER'S PATCHES). — The temperature curve during the
second week shows a continuous fever, with slight morning remissions.
The pulse, in relation to height of fever, may be only slightly accelerated (a
striking feature) ; it is usually dicrotic. All the subjective symptoms are
exaggerated until the 10th day, when the headache usually stops, and the
patient becomes more apathetic and dull, "typhoid state," or he may
becomes restless and delirious, especially at night. In the severer cases, one
may notice jumping of the tendons (subsultus tendinum), or a tendency
to pick at the bed-clothes (carphologia). Involuntary urination and defeca-
tion are not uncommon in soporous patients.
From the 8th day on, rose spots may appear on the abdomen, the
chest, and the back, coming in "crops." This typhoid roseola, when pres-
ent, is very helpful for diagnosis. In neglected mouths, we see sordes on
lips, teeth and tongue. The spleen, as a rule, becomes palpable. Meteor-
ism may develop; there is gurgling in the right iliac fossa on palpation.
Sometimes there are pea-soup stools (3—4) ; cultures from the stools yield
typhoid bacilli (Drigalski-Conradi medium; Endo agar). Some of the
patients are constipated. There is usually a febrile nephropathy (oliguria,
albuminuria, cylindruria). A diffuse bronchitis can usually be made out
on auscultation. The leukopenia continues and the blood culture is still
positive, but there are fewer bacilli per cubic centimeter of blood. The
Fig. 74.— Typhoid Fever— Amphibolus Stage — 2-Hour Chart.
DISEASES DUE TO BACILLI
235
g 3 g CT CT
sssi
Widal reaction sometimes becomes
positive during the second week,
though it often remains negative.
Intestinal hemorrhage is not un-
common at this stage, due to oozing
from the hyperemic, spongy Peyer's
patches.
THIRD WEEK (SECOND HALF
OF STADIUM ACMES. CONTINUED
SLOUGHING OF PETER'S PATCHES,
WITH FORMATION OF INTESTINAL
ULCERS). — The temperature chart
may continue as a fastigium, but it
now often enters upon the period of
"steep curves" due to marked morn-
ing remissions and evening exacer-
bations (amphibolous stage). To-
ward the end of the week, the even-
ing temperature may begin to fall
and the stadium decrements com-
mences.
Intestinal hemorrhage is less
common than in the second week.
From this time on, the danger of
perforation of an ulcer and of per-
forative peritonitis must be kept in
mind. Bed-sores (decubitus) are
prone to develop in the very sick,
especially when the skin is neg-
lected or in dull patients with uri-
nary incontinence; skillful nursing
will usually prevent them. Broncho-
pneumonia or circulatory failure
may complicate the clinical picture.
The mental state is often clearer
than in the second week.
FOURTH WEEK (LYTIC FALL OF
c^§^^§ = = =.= ~s TEMPERATURE, OR STADIUM DECRE-
Fig. 75.— Chart Showing Loss of Weight in MENTI. HEALING OF ULCERS ).
Typhoid Fever Despite a Food Intake Aver- mr v • jj i
aging 2,000 Calories per Day. (After J. The Subjective Symptoms nOW grad-
from w. Coieman's Article, Am. j. ually disappear. The temperature
falls, and the pulse becomes slower ;
there is often an outspoken bradycardia, though in severe cases, a slight
tachycardia may develop, due to myocardial weakness. The spleen may
236
DIAGNOSIS OF INFECTIOUS DISEASES
8
2 S
:>< * w-" on
oai
JS;
CO "^t Csl CD
C > C4 --
OlJttf
oovz
mv
owe
OOZQ
OOC7
00CF
OCFZ
O O O CJ
§ § 8 S
«O ITJ "si CO C\J —
Fig. 76. — Chart Showing that Weight Equilibrium Can
be Maintained by the High Calory Diet in Typhoid
Fever. (After W. Colenmn, Am. J. M. Sc.)
cease to be palpable. The meteorism disappears. The tongue begins to
clean and the appetite to return. The thirst lessens. The patient looks
somewhat emaciated and shows a moderate grade of secondary anemia.
FIFTH WEEK (SUBNORMAL TEMPERATURE. CONVALESCENCE). — The
temperature now becomes subnormal, and remains so for from 6 to 8 days.
s ^ The urine increases in
^tc-joco in cr> — CD o o o
o o o at eg ro co <Ni o o g
turns and usually be-
comes ravenous. The
body weight begins to in-
crease. The spleen is no
longer palpable (except in
cases liable to relapse).
There is a rather marked
bradycardia. Sometimes
desquamation of the skin
occurs, or falling out of
the hair. In patients
who have become greatly
exhausted and emaciated,
a post-typhoid psychosis
may develop (exhaustion
psychosis).
Variations from the
Typical Course of Ty-
phoid Fever. - - MILD
FOKMS. — In some cases,
the fever is never high
and is over in a few days
(typhus levissimus). In
a few cases, the symptoms
may be severe at first,
with high fever, and
then quickly disappear
(typhus aboriivus) .
When the fall of temper-
ature is by crisis, sporad-
ic typhus fever, or Brill's
disease may be suspected; if the blood culture be negative for B. typhosus
and for B. paratypliosus, a guinea-pig should be injected and the tempera-
ture curve watched (Anderson's test for Brill's disease, q. v.) and an an-
aerobic culture made by Plotz's method for B. typhi-exanthematici.
Many patients go to bed as soon as the temperature begins to rise,
but, in some, the general symptoms are so slight, or the infected are so
DISEASES DUE TO BACILLI
237
indiscreet, that the pa-
tients walk about (ty-
phus ambulatorius)
until they are sur-
prised, perhaps, by an
intestinal hemorrhage,
or by the symptoms of
perforative peritonitis.
Recrudescences
and Relapses in Ty-
phoid Fever. — In the
stadium decrement!,
the temperature, in-
stead of continuing to
fall, may rise again
(recrudescence or in-
ter current relapse ) ,
or, in the period of
convalescence, after
the temperature has
been normal, or even
subnormal for from 1
to 50 days, it may
gradually rise again,
the patient passing
through a second usu-
ally shorter and often
less severe attack ( true
relapse or recidive).
A patient may suffer
from two, three, or
even more of these re-
lapses. At the begin-
ning of every relapse,
blood cultures show a
renewal of the bacil-
1 e m i a . Autopsies
made in such cases
show involvement of a
new set of Peyer's
patches, or of solitary
follicles, with each re-
lapse. Such relapses
are often attributed
Fig. 77.— Typhoid Relapses. (Med. Service, J. H. H.)
238
DIAGNOSIS Of INFECTIOUS DISEASES
by the patient or his friends to dietetic errors. The real cause of relapse
is wholly unknown. This much is certain — the bacilli reappear in the
blood and the mesenteric lymph system becomes reinfected.
Complications of Typhoid Fever. — A number of these are of great
importance, especially (1) intestinal hemorrhage, (2) intestinal perfora-
tion, (3) venous thrombosis. Other complications to be kept in mind are,
Fig. 78. — Cellular Infiltration into Heart Muscle in Typhoid Fever. The Large Number of
Eosinophils is Noteworthy. (After L. Hamman, Arch. Int. Med.)
(4) bronchopneumonia, (5) otitis media, (6) my ocardial. insufficiency,
(7) pleuritis, (8) nephritis, (9) cystitis, (10) parotitis, (11) abortion
(in pregnant women), (12) meningismus and, rarely, meningitis, (13)
thrombosis of cerebral arteries, (14) typhoid spine, (15) cholecystitis,
(16) furunculosis, and (IT) peripheral neuritis.
In rare cases, the typhoid bacilli localize in the lung, kidney or men-
inges, and set up violent local inflammations (pneumotyphus, nepliro-
typlius, meningotyphus).
DISEASES DUE TO BACILLI 239
INTESTINAL HEMORRHAGE. — This complication occurs most often be-
tween the 6th and the 20th day, though hemorrhage may occur as early as
the 6th or later than the 36th day. A patient may have a single hemor-
rhage, or he may have two, three, four, or more. In small hemorrhages,
the blood is usually mixed with the feces, which have a black or tar-like ap-
pearance. If the bleeding be profuse, or the intestinal peristalsis lively, red
blood may be passed. The quantity of a single hemorrhage may vary from
a tablespoonful to a liter or more ; a larger hemorrhage may be signalled by
a fall of several degrees of temperature, even to subnormal, while the pulse
becomes small, and it and the breathing are accelerated ; the skin grows sud-
denly pale and cool. The leukocytes are slightly increased. Such symp-
toms justify the diagnosis of hemorrhage even before the blood has been
passed in the feces. The cerebral symptoms are often considerably relieved
by intestinal hemorrhage. The death rate in cases complicated with hem-
orrhage is probably three times greater than the average in cases without
hemorrhage.
INTESTINAL PERFORATION AND PERFORATIVE PERITONITIS. — This
dreadful complication fortunately occurs in only a small percentage of the
cases (2-3 per cent) ; it is accountable, however, for from 6 to 12 per
cent of the deaths in typhoid fever. It occurs most often in the 3rd, the
4th, or the 5th week, and is more often seen in the cases in which the gen-
eral symptoms are severe, though occasionally it is met with in very mild
cases. It may occur as late as the 100th day. Usually, there is only one per-
foration, but there may be two, or even several. The site of perforation is
in the base of an ulcer, most often at the lower end of the ileum, occasionally
in the colon, rarely in the upper part of the small intestine, or in the vermi-
form appendix. The immediate cause of perforation may be extension of
the necrosis to the surface; more often it is the result of rupture of the
thinned wall from gaseous distention or from violent peristalsis ; occasion-
ally, it follows attempts at defecation.
The most important symptom of perforation is a sudden pain in the
abdomen, referred either to the whole abdomen, or to a definite spot in the
right iliac fossa. This is usually followed by colicky pains, hiccough, and
later, by nausea and vomiting. On gentle palpation, local tenderness and
muscle spasm can often be made out. Obliteration of liver dullness and
abolition of abdominal breathing are early and important indications of
this disease.
The patient has an anxious expression at first ; later on, when perfor-
ative peritonitis has developed, he may become euphoric, though restless.
The pulse is usually accelerated and feeble. The face looks pinched, pale
and slightly cyanotic, and the body may be covered with a cold sweat. The
feet and hands and the end of the nose grow cool, the temperature begins
to rise ; the white cell count in the blood rises, and the polymorphonuclears
may become relatively increased.
240
DIAGNOSIS OF INFECTIOUS DISEASES
The blood-pressure often rises sharply at the time of perforation,
though it may remain unchanged. A patient who complains of abdominal
pain, especially of sudden pain, should be carefully watched for the signs
described; should they appear, perforation has almost certainly occurred,
and will be followed by increasing distention, lessened respiratory move-
ment of the abdomen, increase of the tenderness, the rigidity and the
effC
Fig. 79. — Typhoid Perforation.
muscle spasm, along with signs of free fluid in the peritoneal cavity.
The diagnosis of the condition should be made before general perito-
nitis develops, since if perforation has occurred, the earlier the operation is
done, the greater the chance of saving the patient. Every hour counts.
Two, or three, out of every five cases of perforation in typhoid fever can be
saved if operation be skillfully done within a few hours after perforation
has occurred. It is better in doubtful cases to operate quickly than to wait,
even if now and then the abdomen be opened in the absence of perforation.
VENOUS THROMBOSIS. — This, when it occurs, most often involves the
femoral vein. After complaint of pain and tenderness in Scarpa's tri-
angle, the pulse becomes accelerated, the lower extremity begins to swell,
DISEASES DUE TO BACILLI 241
and the white cell count in the blood begins to increase. The swelling of
the leg continues usually for from 4 to 6 weeks, after which it gradually
decreases, though there may be a tendency to edema of the leg ever after.
Other veins occasionally become thrombosed. Lewis Conner has called
attention to the frequency of pulmonary infarction in cases of typhoid
thrombophlebitis.
OTHER COMPLICATIONS. — These have been referred to above. For a
discussion of (1) the causes of chills, (2) the skin complications, and (3)
the bone lesions that may occur, the articles of McCrae and of Cursch-
mann should be consulted. In Lewis Conner's article will be found an ex-
cellent account of the various post-typhoidal elevations of temperature
that may be met with.
Diagnosis of Typhoid Fever. — This is usually easy before the end of
the first week, even early in the first week, if the following points be kept
in mind:
(1) Increasing fever, pulse slow in relation to the elevation of the
temperature; (2) headache; (3) leukopenia ; (4) absence of coryza, and of
herpes; no malarial parasites in the blood; (5) blood culture in Conradi's
bile medium; (6) ophthalmo-reaction, as modified by Austrian.
I would emphasize especially the importance of the blood culture for
the early diagnosis of typhoid fever. Any physician can draw blood, asep-
tically, from the vein at the bend of the elbow, and place some of it in a
tube of sterile bile bouillon. It should then be sent to a bacteriological
laboratory for incubation and study. A positive result can be obtained in
90 per cent of the early cases in from 16 to 24 hours.
I would also emphasize the fact that the Widal reaction is of very lit-
tle value in the early diagnosis of typhoid fever, though it may be very
helpful, later on, in cases of doubtful diagnosis in which the blood culture
has been negative. In the second week, the occurrence of typical rose spots
is most helpful in diagnosis.
Differential Diagnosis. — Certain febrile diseases, without positive
physical findings at the beginning, may closely resemble typhoid fever.
We must differentiate it :
1. From central pneumonia (leukocytosis ; herpes ; rontgenogram ;
tachypnea).
2. From miliary tuberculosis (blood culture negative for B. typhosus;
tubercle bacilli occasionally demonstrable in 'blood if 10 c.c. be received in
3 per cent acetic acid and treated with 2 per cent antiformin solution and
examined microscopically; rontgenogram of lungs; choroidal tubercles;
cyanosis; dyspnea; family history; evidences of earlier tuberculosis).
3. From septicemias due to staphylococcus, streptococcus, etc., includ-
ing osteomyelitis (the blood culture and leukocytosis decide in all these
cases).
4. From meningitis (lumbar puncture; polymorphonuclear leukocy-
242
DIAGNOSIS OF INFECTIOUS DISEASES
tosis ; blood culture negative for typhoid). A meningismus in typhoid fre-
quently simulates meningitis.
5. From typhus exanthematicus or Brill's disease (blood culture;
tachycardia; eruption; Anderson's guinea-pig test, q. v.).
6. From relapsing fever (spirochetes in stained blood-smear; tem-
perature chart).
7. From the different varieties of malaria (parasites in the blood;
blood culture negative).
8. From secondary syphilis (negative blood culture ; positive Wasser-
mann; remains of chancre).
9. From trichinosis (negative blood culture ; outspoken eosinophilia ;
histology of excised muscle; history of eating raw ham or sausage).
10. From influenza (herpes; often coryza; negative blood culture).
11. From ulcerative endocarditis (cocci in blood culture; leukocytosis ;
lieart murmurs; conjunctival petechige).
Prophylaxis of Typhoid Fever. — The secret in prophylaxis is to remem-
ber that the source of all new typhoid infections (in the last analysis) is the
infected human being (B,. Koch). The early diagnosis of typhoid cases,
the disinfection of excreta, the bacteriological control of typhoid hosts,
including the bacillus carriers, the protection of the water, the milk, and
the food supply, the avoidance of infection by direct contact (fingers!),
and the campaign against flies, are important measures.
Typhoid Hosts. — The healthy carrier presents a difficult problem. A
reasonable man may, if he be a chronic host, be led to disinfect his feces
and his urine, but the majority of carriers can scarcely be induced or
forced to take such precautions. It is impracticable to isolate all carriers,
but care should be taken to see to it that they engage in occupations that
have nothing to do with the preparation, or transport, of foods, milk, or
drinking-water. It was hoped that extirpation of the gall-bladder would
cure the chronic
carrier, but the re-
sults of operation
liave been unsatis-
factory. No cure
for the carrier has
yet been devised.
Most chronic hosts
yield a positive
Widal reaction !
Preventive In-
OClllation. The GX-
v^pTirp in ^rmtli
"^
Africa during the
T> ^rr J J.T.
-^oer War; and tne
NONE-
STRICKEN
(b)
Fig. 80.— Results of Typhoid Inoculation. (a) Jacksonville,
Fla., 1898, Seventh Army Corps, TJ. S. Army, 10,759 Men,
None Given Typhoid Vaccine, (b) TJ. S. Army, San An-
tonio, Tex., 12,801 Men, All Given Typhoid Vaccine. (After
E. O. Jordan— copied from Washington State Board of
Health Bulletin, May, 1912, in J. Am. M. Ass.)
DISEASES DUE TO. BACILLI 243
experience of the United States Army during the recent mobilization on
the Mexican border, prove conclusively the value of preventive inocula-
tion against typhoid. Three successive injections of the dead bacilli, in
suitable numbers, protect for 1-2-3 years or longer. The work of Major
F. F. Kussell of the United States Army in connection with prophylactic
vaccination has been notable.
(b) Gastroenteritis Due to Bacillus typhosus
(Gastroenteritis typhosa)
In rare instances, the typhoid bacillus, instead of causing typhoid fever,
gives rise to an acute gastroenteritis of sudden onset, with vomiting and
violent diarrhea, abdominal pain, and fever, lasting two or three days. The
typhoid bacillus can be grown from the feces. A few bacilli may get over
into the blood, and the serum later agglutinates the typhoid bacillus. Here
we have to deal with a wholly different disease from typhoid fever; in
gastroenteritis typhosa, it is the surface of the intestinal mucous mem-
brane which is attacked, as in Asiatic cholera, while in true typhoid fever
it is the mesenteric lymph paths and the lymphatic tissue of Peyer's patches
and the solitary follicles that are predominantly involved.
References
1. Larger General Articles
Curschmann (//.). Typhoid fever and typhus fever. Edited, with additions, by William
Osier. Authorized translation from the German, under the editorial super-
vision of Alfred Stengel. Philadelphia & London, 1901, W. B. Saunders
Co. 646 p. 8°. NothnageVs Encyclopedia of Practical Medicine.
Amer. ed.
Dreschfeld (J.) & Smith (J. L.). Enteric fever. In: Syst. Med. (Allbutt & Rollestori).
8°. London, 1910, i, 1080-1167.
Kutscher (K. H.). Abdominally phus. In: Handb. d. pathogen. Mikroorg. (Kolle &
Wassermann). 2. Aufl. Jena, 1913 , Hi, 717-836.
McCrae (T.). Typhoid fever. In: Mod. Med. (Osier & McCrae}. 2d ed. Philadelphia &
New York, 1913, i, 67-201.
Schottmuller (H.). Die typhosen Erkrankungen. In: Handb. d. inn. Med. (Mohr &
Staehelin), Berlin, 1911, i, 369-577.
Thoinot (L.) & Ribierre (P.). Fievre typho'ide et infections paratyphoides. Paris, 1912,
J. B. Bailliere & fils. 312 p. 8°. [Nouv. traite de med. de therap., Hi.]
2. Symptoms and Complications
Brown (T. R.}. Cystitis due to the typhoid bacillus introduced by catheter in a patient not
having typhoid fever. Med. Rec., New York, 1900, Ivii, 405-411.
Camac (C. N. B.}. Gall-bladder complications of typhoid fever. Johns Hopkins Hosp.
Rep., Baltimore, 1900, viii, 339-361.
Cholecystitis complicating typhoid fever; tapping of gall-bladder; chole-
cystotomy; death. Am. J. M. Sc., Philadelphia & New York, 1899, cxvii,
275-285.
244 DIAGNOSIS OF INFECTIOUS DISEASES
Chapin (H. D.). A clinical study of typhoid fever in children. Tr. Pediat. Soc., Chicago,
1914, xxvi, 51-56.
Conner (L. A.}. A contribution to the symptomatology of thrombophlebitis in typhoid fever.
Arch. Int. Med., Chicago, 1912, x, 534-559. Also: Tr. Ass. Am. Phy-
sicians, Philadelphia, 1912, xxvii, 198-236.
Crile (G. W.). Diagnostic value of blood-pressure determinatibns in the diagnosis of typhoid
•perforation. J. Am. M. Ass., Chicago, 1903, xl,
Cumston (C. G.). The surgical aspects of typhoid fever. Internal. Clin., Philadelphia,
1911, 21s' s., ii, 125-138.
Gushing (H.}. Typhoidal cholecystitis and cholelithiasis. Report of a case withou1 pre-
vious history of typhoid fever, and discussion of a possible agglutinative
reaction in the bile and its relation to stone formation. Johns Hopkins
Hosp. Bull, Baltimore, 1898, ix, 91-95.
v. Eberts (E. M.}. Typhoid cholelithiasis and cholecystitis. Canad. M. Ass. J., Toronto,
1915, v, 913-914.
Finney (J. M. T.}. Surgical complications of typhoid fever. In: Handbook of Treatment
(Musser & Kelly), 1911, ii, 258-268.
Fitz (R.), Brigham (F. G.) & Minot (J. /.)• Bulbar paralysis in typhoid fever. Boston
M. & S. J., 1913, clxviii, 957-959.
Hare (H. A.) & Beardsley (E. J. G.). The medical complications, accidents and sequels
of typhoid fever and the other exanthemata. 2d ed. Philadelphia & New
York, 1909, Lea & Febiger. 406 p. 8°.
Lyall (H. W.). Meningitis in an infant caused by the typhoid bacillus. J. M. Research,
Boston, 1913, xxvii, 457-470.
McCrae (T.)» Typhoid and paratyphoid spondylitis, with bony changes in the vertcbrce.
Am. J. M. Sc., Philadelphia & New York, 1906, cxxxii, 878-889.
McPhedran (A.). Ascites in typhoid fever. Tr. Ass. Am. Physicians, Philadelphia,
1908, xxiii, 59-62.
Neuman (Lester) & Behrend (E. Z?.). A modification of Russo's urinary typhoid fever
test, with a report of its use in one thousand cases, and a complete bibli-
ography. Arch. Int. Med., Chicago, 1913, xi, 456 467.
Posselt (A.). Atypische Typhusinfektionen. In: Ergcbn. d. allgem. Pathol. [etc.] (Lubarsch-
Ostertag). Wiesbaden, 1912, xvi, Abth. i, 184-340.
Riesman (David). Entericoid fever— febris entericoides. J. Am. M. Ass., Chicago, 1913,
Ixi, 2205-2207.
Rogers (C. P.). The acute abdominal surgical complications of typhoid fever. Gulf States
J. M. & S. [etc.], Mobile, 1909, xv, 693-704.
Rudolf (R. D.}. Bleeding in typhoid fever. Am. J. M. Sc., Philadelphia & New York,
1914, cxlvii, 44-56.
Stille (A.). Table of comparison between typhus and typhoid fevers. [Transl. by Wm.
Pepper.] With an introductory note by Professor Osier. Univ. Penn. M.
Bull, Philadelphia, 1904-5, xvii, 63-74. [Read at the Sociele Medical
^Observation of Paris, Sept. 14 and 28, 1838.]
Thayer (W. £.)• Observations on the blood in typhoid fever. J. Bost. Soc. M. Sc., 1900-1,
v, 23-30.
On arteritis and arterial thrombosis in typhoid fever. N. Y. State J. M.,
1903, Hi, 15-33.
On the cardiac and vascular complications and sequels of typhoid fever.
The Jerome Cochran lecture. Johns Hopkins Hosp. Bull., Baltimore, 1904,
xv, 323-339.
Analysis of forty-two cases of venous thrombosis occurring in the course of
typhoid fever. Med. News, New York, 1904, Ixxxv, 637-^40.
DISEASES DUE TO BACILLI 245
Tileston (W.~). The occurrence of occult hemorrhages in typhoid fever. Boston M. & S. J.,
1906, civ, 30-32.
War field (L. M.). Typhoid fever. Report of a case with three relapses. Remarks. Johns
Hopkins Hosp. Bull., Baltimore, 1902, xiii, 173-176.
Wilcox (H. W.). Typhoid spine. Colorado Med., Denver, 1915, xii, 190-201.
Williss (B. C.)« Intestinal perforation in a case of ambulatory typhoid; operation with re-
covery. Old Dominion J. M. & S., Richmond, 1914, xviii, 193-196.
3. Metabolic
Barker (L. F.}. The diet in typhoid fever . J. Am. M. Ass., Chicago, 1914, Ixiii, 929-931.
Coleman (W.}. The high calory diet in typhoid fever: a study of one hundred and eleven
cases. Am. J. M. Sc., Philadelphia & New York, 1912, cxliii, 77-102.
Weight curves in typhoid fever. Am. J. M. Sc., Philadelphia & New
York, 1912, cxliv, 659-668.
Dubois (/?.)• The absorption of food in typhoid fever. Arch. Int. Med., Chicago, 1912,
x, 177-195.
Eustis (A.). Dietetics of typhoid fever. Pan-Am. S. & M. J., New Orleans, 1914, xix, 1L-
17.
Ewing (James] & Wolf (C. G. L.}. The clinical significance of the urinary nitrogen.
III. Nitrogenous metabolism in typhoid fever. Arch. Int. Med., Chicago,
1909, iv, 330-355.
Graves (M. L.}. Some clinical experiments in the treatment of typhoid fever with low-caloric
food values. Texas State J. M., Fort Worth,' 1912-13, 'ix, 4-6.
Shaffer (P. A.) & Coleman (Warren). Protein metabolism in typhoid fever. Arch. Int.
Med., Chicago, 1909, iv, 538-600.
4. Bacteriodiagnostic ; Experimental
Arima (R.). Ueber die Typhusloxine und ihre pathogene Wirkung. Centralbl. f. Bakteriol.
[etc.], I. Abt., Jena, 1912, Ixiii, Orig., 424-486.
Blackstein (A. G.). Intravenous inoculation of rabbits with Bacillus coli communis and
Bacillus lyphi abdominalis. Johns Hopkins Bull., Baltimore, 1891, ii,
96-103.
Dawson (G. D.}. The diagnosis of typhoid fever in inoculated subjects. Brit. M. J., London,
1915, ii, 137.
Metchnikoff (/?.) & Besredka (A.). Recherches sur la fievre typhoide experimentale. Ann.
de I'Inst. Pasteur, Paris, 1911, xxv, 193-221.
Patrick (A.). Remarks on typhoid bacilluria, with a description of certain atypical coli-
typhoid bacilli found in the urine in enteric fever. J. Path. & Bacteriol.,
Cambridge, 1914, xviii, 365-378.
Peabody (F. W.}. The diagnosis of typhoid fever by cultures from the blood of the ear.
Arch. Int. Med., Chicago, 1908, i, 149-153.
Richardson (M. W.). On the bacteriological examination of the stools in typhoid fever,
and its value in diagnosis. Boston M. & S, J., 1897, cxxxvii, 433-437.
On the cultivation of the typhoid bacillus from rose-spots. Philadelphia
M. J., 1900, v, 514-516.
Robinson (G. H.). Isolation, identification, and serum reactions of typhoid and para-
typhoid bacilli. J. Med. Research, Boston, 1915, xxxii, 399-418.
246 DIAGNOSIS OF INFECTIOUS DISEASES
Ruediger (E. //.)• Bacteriologic study of the blood in thirty cases of clinical typhoid fever,
two of which proved to be paratyphoid and one doubtful. Tr. Chicago Path.
Soc., 1901-3, v, 187-198.
Russell (F. F.). The isolation of typhoid bacilli from urine and feces, with the description
of a new double sugar tube medium. J. Med. Research, Boston, 1911-12,
xxv, 217-229.
5. Immunological
Denison (H. S.}. Amboceptors and complement in typhoid sera. Johns Hopkins Hosp.
Bull, Baltimore, 1908, xix, 262-268.
Gay (F. /*.)• Typhusimmunisierung. Ergebn. d. Immunitdtsforsch. exper. Ther., Bak-
teriol. u. Hyg., Berlin, 1914, i, 231-256.
Gay (F. P.) & Clay pole (E. J.). Induced variations in the agglutinability of bacillus
typhosus. J. Am. M. Ass., Chicago, 1913, Ix, 111+1.
An experimental study of methods of prophylactic immunization against
typhoid fever. Arch. Int. Med., Chicago, 1914, xiv, 671-705.
Gay (F. P.) & Force (J. N.}. A skin reaction indicative of immunity against typhoid
fever. Studies in typhoid immunization, III. Arch. Int. Med., Chicago,
1914, xiii, 471-479.
Lyons (/?.)• The clot culture in conjunction with the agglutination test in typhoid. Arch.
Int. Med., Chicago, 1909, iv, 64-68.
Moon (V. H.). Observations on antibody formation in typhoid. J. Infect. Dis., Chicago,
1914, xiv, 56-GO.
Wesbrook (F. F.) & Wilson (L. B.). The serum-diagnosis of typhoid fever from the public
health laboratory point of view. Phila. M. J., 1898, i, 549-553.
Wollstein (M.). The duration of immune bodies in the blood after antityphoid inoculation.
J. Exper. M., Lancaster, Pa., 1912, xvi, 315-324.
Zinsser (H.). On anaphylatoxins and endotoxins of the typhoid bacillus. J. Exper. M.t
Lancaster, Pa., 1913, xvii, 117-131.
C. Antityphoid Vaccination; Vaccine Treatment
Besredka (A.). Deux ans de vaccination antityphique avec du virus sensibilise vivant. Ann.
de I'Instit. Pasteur, Paris, 1913, xxvii, 607-319.
Gay (F. P.). Specific treatment in typhoid fever. J. Lab. & Clin. Med., St. Louis, 1915, i,
13-21.
Abortive treatment of typhoid fever by sensitized typhoid vaccine sediment.
J. Am. M. Ass., Chicago, 1915, Ixv, 322.
Mclntosh (/.) & McQueen (J. M.). The immunity reactions of an inagglutinable strain
ofB. typhosus. J. Hyg., Cambridge, 1914, xiii, 409.
Russell (F. F.). Antityphoid vaccination. Am. J. M. Sc., Philadelphia & New York,
1913, cxlvi, 803-833.
Antityphoid vaccination in the army and in civil life. Washington, 1913,
Gov. Print. Off. 8 p. Diag. 8°.
The prophylaxis of typhoid fever by means of vaccines. In: Therap. Int.
Dis. (Forchheimer). New York & London, 1914, v, 182-202.
Sawyer (W. A.). The efficiency of various antityphoid vaccines. J. Am. M. Ass., Chicago,
1915, Ixv, 1413-1418.
Stone (W. J.}. Bacterial and serum, therapy in typhoid and paratyphoid fevers. In : Therap.
Int. Dis. (Forchheimer) . New York & London, 1914, v, 203-235.
Zuebltn (Ernest). Is antityphoid vaccination harmless? American Medicine, Burling-
ton, Vt., & New York, 1914, ix, 484~4S9.
DISEASES DUE TO BACILLI 247
7. Epidemiological
Baetjer (W. A.). Study of a house epidemic of typhoid fever. Johns Hopkins Hosp. Bull.,
Baltimore, 1909, xx, 152.
Barker (L. F.). Recent progress in the study of typhoid fever. Charlotte [N. C.] M.J.,
1908, xxxii, 245-252.
Brannan (J. W.}. Hospitals and typhoid carriers. Am. J. M. Sc., Philadelphia & New
York, 1912, cxliv, 347-350.
Calvert (W. J.}. Prevention of typhoid fever. Columbia, Mo., 1913. 35 p. 8°.
Cook (F. C.}, Hutchinson (R. H.) & Scales (F. M.}. Further experiments in the destruc-
tion of fly larvae in horse manure. Washington, 1915. 22 p. 8°.
U. S. Dep. Agric. Bull. No. 245.
Fitzsimons (F. W.}. The house fly: a slayer of men. New York, 1915, Longmans, Green
&Co.
Ford (W. W.}. The present status of the antityphoid campaign in Germany. Johns Hop-
kins Hosp. Bull, Baltimore, 1912, xxiii, 269-274.
Fornet (W.). Ergebnisse und Probleme der Typhusforschung. Ergebn. d. inn. Med. und
Kinderh., Berlin, 1913, xi, 167-218.
Freeman (A. W.}. The prevention of typhoid fever in the rural districts of Virginia. Am. J.
Pub. Health, New York, 1913, iii, 1322-1325.
The. present status of our knowledge regarding the transmission of typhoid
fever. Pub. Health Rep., Washington, 1913, xxviii, 64-68.
Kaiser (M.). Ueber ein einf aches Verfahren infektiose Stuhle zu desinflzieren. Arch. f.
Hyg., Berlin, 1913, Ixxviii, 129-162.
Sawyer (W. A.). The later history of the typhoid carrier H.O. J. Am. M. Ass., Chicago,
1915, Ixiv, 2051-2053.
Stokes (W. R.) & Hachtel (F. W.). The control of typhoid fever in city and country,
with a description oj the modified Hesse's medium for the detection of the
typhoid bacillus in excreta and fluid foods. Arch. Int. Med., Chicago,
1910, vi, 121-138.
Whipple (G. C.) & Freeman (A. W.} [et al.]. Second progress report of the committee on
standard methods of shellfish examination. Am. J. Pub. Health, New
York, 1912, ii, 84-42.
8. Pathological-Anatomical
Barker (L. F.). Area of necrosis in internal capsule in typhoid fever. Johns Hopkins
Hosp. Bull, Baltimore, 1900, xi, 72-73.
Hamman (Louis). The heart muscle in typhoid fever. Arch. Int. Med., Chicago, 1910,
vi, 339-879.
Messerschmidt (T7.). Bakteriologischer und histologischer Sektionsbefund bei einer chro-
nischen Typhusbacillustragerin. Ztschr. f. Hyg., Berlin, 1913, Ixxv,
411-423.
Opie (E. L.) & Bassett (V. H.}. Typhoid infection without lesion of the intestine. A case
of haemorrhagic typhoid fever with atypical intestinal lesions. Johns
Hopkins Hosp. Bull, Baltimore, 1901, xii, 198-202.
Rogers (M. #.)• Pathology of typhoid spine. Boston M. & S. J., 1913, clxviii, 348-350.
248 DIAGNOSIS OF INFECTIOUS DISEASES
11. Diseases Due to B. paratyphosus
Paratyphoid Bacilli. — The Bacillus paratyphosus has been studied care-
fully by Schottmiiller, and by Kayser. There are two forms, the Bacillus
paratyplwsus A (or acidumfaciens), and the Bacillus paratyphosus B (or
alkalifaciens) . Of these two, the second is much the more important as
the cause of disease in human beings, though either may be concerned.
Each of them is capable of setting up a disease that clinically (aside
from bacteriological examinations) is indistinguishable from ordinary
typhoid fever, but the same organism is capable of causing, in addition to
a disease like clinical typhoid fever, any one of several local diseases in
the body, viz:: (1) gastroenteritis paratyphosa, (2) pyelitis paratyphosa,
(3) endometritis paratyphosa, (4) cholecystitis paratyphosa, and (5)
meningitis paratyphosa. The cases may occur sporadically, or in epidemics.
The infections with paratyphoid bacilli are far less numerous than cases of
infection with the B. typkosus.
(a) Gastroenteritis paratyphosa B (Cholera nostras paratyphosa)
It turns out that a gastro-intestinal form of meat-poisoning, or food-
poisoning, is often due to the local action of paratyphoid bacilli, especially
of variety B upon the mucous membrane of the stomach and intestine.
Symptoms. — The onset is sudden, with violent abdominal pain. There
are frequent stools for one or two days, after which there may be constipa-
tion. The fever is, as a rule, not high. Sometimes nausea and vomiting
accompany the attack. Recovery usually follows in a few days. In severer
cases of summer diarrhea (cholera nostras), the symptoms may last
longer. Herpes and rose spots may appear. In fatal cases, delirium and
convulsions are not uncommon. Cramps in the calves of the legs may
occur. There is outspoken thirst.
Diagnosis. — The clinical picture indicates the presence of a gastroen-
teritis. The demonstration of the causal agent depends upon cultures from
the stools (smears on Endo's agar, on Drigalski-Conradi medium, or on
malachite-green-agar), with subsequent identification of the bacillus
through fermentation tests and by agglutinative or bacteriologic tests with
a known immune serum (q. v.).
(b) Paratyphus abdominalis B
(Typhoid Form of Meat-,, or Food-poisoning)
Here, clinically, the picture is that of ordinary typhoid fever. The
fever is usually milder, however, rarely remaining continuous for more
than a short time; the average duration is briefer (21 days). The rose
spots are indistinguishable from those of typhoid. Herpes occurs in 50
per cent of the cases (in marked contrast with typhoid). Intestinal hemor-
DISEASES DUE TO BACILLI 249
rhage is much rarer than in typhoid. Perforation occasionally occurs.
The spleen is enlarged. The pulse is dicrotic and relatively infrequent, as
in typhoid, and there is leukopenia with relative lymphocytosis. The
agglutination titer of the serum is usually higher for Bacillus paraiyphosus
B than for Bacillus typliosus. The Bacillus paraiyphosus B can he ob-
tained hy blood culture, early in the disease. Relapses are less common
than in typhoid, though they sometimes occur.
Most patients recover. In fatal cases, the intestinal lesions may
resemble those of typhoid, but thus far only a few autopsies are on record ;
sometimes there are no lesions in Peyer's patches, as in Longcope's case.
Diagnosis. — A clinical picture resembling that of typhoid fever, but
beginning with a chill and associated with diarrhea, abdominal pain and
herpes, speaks for paratyphoid. The exact diagnosis depends upon the
demonstration of the B. paraiyphosus in the blood culture, and of specific
agglutinins and other immune bodies in the serum, later on.
(c) Gastroenteritis paratyphosa A and Paratyphus abdominalis A
This organism, also, can cause (1) a disease resembling typhoid fever
(paralhyphus abdominalis A), and also (2) a gastroenteritis (gastroenter-
itis paralyphosa A).
(d) Typhus manchuricus
Comparatively recently, Russian physicians have studied the typhoid
fevor of Manchuria (typhus manchuricus). The blood contains a bacillus
belonging to the typhoid-paratyphoid group. Whether it is a bacillus
already known, or a new variety, has yet to be determined.
A table based upon Schottmiiller's findings and contrasting the mor-
phological and cultural properties of bacteria of the typhoid-colon group is
here appended. (See next page.)
References
Achard (C.) & Leblanc (A.}. Fievre paratypho'ide du type A. Arch. d. med. exper., etc.,
Pans, 1914, xxvi, 264-276.
Bonhoff (F.). Ueber Paratyphusbacillenbefunde an der Leiche. Arch. f. Path., Anat.,
etc., Berlin, 1914, ccxvi, 321-331.
Coleman (W.). Types of infection produced in man by intermediate members of the typhoid-
colon group of bacilli. Amer. Med., Philadelphia, 1902, iv, 498; 578; 622.
Irons (E. E.} & Jordan (E. O.). An infection with the paratyphoid bacillus (B. paratypho-
sus B). J. Infect. Dis., Chicago, 1915, xvi, 234-240.
Proescher (B. F.} & Roddy (J. A.}. Bacteriological studies on paratyphoid A and para-
typhoid B. Arch. Int. Med., Chicago, 1910, v, 263-312.
Torrey (J. C.). Brilliant green broth as a specific enrichment medium for the paratyphoid-
enteritidis group of bacteria. J. Infect. Dis., Chicago, 1913, xiii, 263-272.
Uhlenhuth (P.) & Hiibener (E.}. ' Infektiose Darmbakterien der Paralyphus- und Gartner-
gruppe einschl. Immunitdt. In: Handb. d. pathogen. Mikroorg. (Kolle &
Wassermann). 2. Aufl. Jena, 1913, Hi, 1005-1156.
250
DIAGNOSIS OF INFECTIOUS DISEASES
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3
o
1
1
DISEASES DUE TO BACILLI 251
12. Diseases Due to the Colon Bacillus
Colon Bacillus. — The colon bacillus Bacterium coli commune (Esch-
erich) is a short, plump rod, constantly present in the normal intestine of
man and of animals. Morphologically and tinctorially, it resembles the ty-
phoid bacillus, though it is less motile, having fewer nagella. Its distin-
guishing characters are given in the table preceding. It is Gram-negative,
and is only slightly pathogenic for animals.
(a) Local Infections
It not infrequently causes local inflammations and suppurations
(cholangitis, cholecystitis, hepatic abscess, peritonitis, appendicitis, pye-
litis, and cystitis). See especially Part X.
(b) Coli-sepsis
Definition. — This is a septicemia due to the B. coli, the infection-atrium
being usually the biliary passages or the intestine, more rarely, the uro-
genital passages.
Symptoms. — The temperature is markedly intermittent, and chills are
common. The pulse rate corresponds to the height of the temperature.
Suppurative metastases are very common (spleen ; lungs ; kidneys). Endo-
carditis is a frequent accompaniment. A leukocytosis of 7,000-12,000 or
higher is present. The bacilli are quickly removed from the blood, and
thus often escape detection by blood culture.
References
Conradi (JET.) & Bierast (TF.). Bacterium coli commune als Krankheitserreger. In:
Handb. d. pathogen. Mikroorg. (Kolle & Wassermann}. 2. Aufl. Jena,
1913, vi, 483-514.
Jacob (L.). Uber Allgemeininfektion durch Bacterium coli commune. Deutsches Arch. f.
klin. Med., Leipzig, 1909, xcvii, 303-347.
Jochmann (G.). Zur Kenntnis der von den Harnwegen ausgehenden Sepsisformen: a.
Katheterfieber durch Staphylococcus pyogenes albus. b. Allgemeininfec-
lionen mit Bakterium coli. Deutsches Arch. f. klin. Med., Leipzig, 1906,
Ixxxvii, 479-498.
Kolisepsis. In: Handb. d. inn. Med. (Mohr & Staehelin). Berlin.
1911, i, 700-716.
Jordan (E. O.). The inhibitive action of bile on B. coli. J. Infect. Dis., Chicago, 1913,
xii, 326-334.
Liebermeister (G.). Ueber die Bedeutung des Bacterium coli fur die menschliche Patho-
logie mit besonderer Beriicksichtigung der Infektion der Harnwege u. der
seplischen Erkrankungen. Ztschr. f. klin. Med., Berlin, 1906, lix, 473-489.
Rogers (L. A.}, Clark (W. M.} & Davis (B. J.). The colon group of bacteria. J. Infect.
Dis., Chicago, 1914, xiv, 411-475.
Ruediger (E. H.}. The occurrence of bacillus coli communis in the peripheral blood of man
during life. Philippine J. Sc., Manila, 1915, B, x, 25-28.
Widal (F.) & Lemierre (A.}. Septicemies colibacillaires. Gaz. d. hop., Paris, 1904,
Ixxvii, 801-805.
Widal (F.) & Nobecourt (P.). Seroreaction dans une infection d paracolibacille. Semaine
med., Paris, 1897, xvii, 285-287.
252 DIAGNOSIS OF INFECTIOUS DISEASES
13. Diseases Due to the Dysentery Bacillus
Dysentery Bacillus. — The Bacillus dysenterice is met with in several
forms (type Shiga, type Flexner, type Strong, type Y or His, etc.). The
differential characters are shown in the table given on page 250.
(a) Bacillary Dysentery (Epidemic Dysentery)
Definition. — This is an infectious inflammation of the large intestine,
and is accompanied by diarrhea, with blood, mucus, and dysentery bacilli
in the stools. The disease is not accompanied by a bacteriemia as a rule,
though occasionally the bacillus can be isolated from the blood as well as
from the stools; the bacilli are localized in the intestinal mucous mem-
brane and in the mesenteric lymph glands whence the toxins pass to the
blood and give rise to a general intoxication.
The different types of dysentery bacilli are best distinguished, according to
Lentz, by growth on 3 forms of litmus agar (mannite, maltose, saccharose).
Agglutination tests with immune sera are also helpful.
Epidemiology. — Like typhoid, cases of epidemic dysentery arise from
some sick individual, directly or indirectly. Fingers and flies play a role
in the contamination. Mild infections, in ambulant patients, are especially
dangerous to other individuals. Healthy bacillus carriers are often
observed, and have been proven to be the starting point of epidemics in
recent years. Direct contact infection is more common than infection by
polluted water, though water, milk, and foods are sometimes a source. The
disease prevails in the summer months, and is especially common among
large aggregations of people (army camps, festivals, etc.).
Symptoms. — An acute and a chronic form of epidemic dysentery occur.
In the ACUTE FOKM the onset is insidious (digestive disturbances) after an
incubation period of a few days. There is anorexia, coated tongue, ten-
dency to diarrhea, and to colicky pains in the abdomen. After two or
three days, the abdominal pains become more severe, the diarrhea becomes
worse (8-30-100 stools per day). The feces, at first soft, like those of
simple diarrhea, undergo a change, and come to consist of pure mucus, or
of blood-stained mucus. There is burning and pain in the rectum on defe-
cation (tenesimis). The feces are not foul, but they have a stale odor.
The patients emaciate rapidly, the eyes become sunken, and the voice
grows feeble ; the tongue is dry and coated ; the abdomen is retracted and
tender on pressure; the urine is scanty; and there is slight elevation of
temperature ; sometimes, however, the temperature is subnormal.
The majority of patients begin to recover after 1 to 3 weeks ; the stools
regain their fecal consistency, the number lessens, and the appetite and
DISEASES DUE TO BACILLI 253
strength begin to return. Relapses are common (dietetic errors, cold
drinks). In severer cases, death occurs at the end of 2 or 3 weeks.
Complications. — Polyarthritis ; peripheral neuritis ; conjunctivitis.
Liver abscess is rare (contrast with amebic dysentery).
In the severer cases, type Shiga is usually found, in the milder cases, type
Flexner, or type Y. The mortality in the severer forms amounts to from 10 to
15 per cent; in the milder forms it may be only 0.5 per cent (Jochmann).
In the CHRONIC FORM OF BACILLARY DYSENTERY there is emaciation,
anemia, and weakness ; the bowels are irregular ; recurring abdominal pains
are complained of; the stools contain small masses of blood-stained mucus,
crowded with dysentery bacilli. In this form, the disease may continue
for months or years. Many patients are unaware of the infection, and
thus form the starting point of epidemics.
Diagnosis of Bacillary Dysentery. — The clinical diagnosis of dysentery
is easy : diarrhea ; tenesmus ; blood and mucus in the stools. Microscopic
examination of the feces rules out amebic dysentery. Cultures, from
washed mucus, on litmus-lactose agar, and on litmus-mannite agar, followed
by agglutination tests, reveal the bacillus and its type.
Amebic Dysentery is described further on.
References
Charlton (G. A.) & Jehle (L.). On the etiology of bacillary dysentery and of catarrhal
enteritis in children. Tr. Ass. Am. Physicians, Philadelphia, 1904, xix,
405-420.
Davidson (A.} & Flexner (S.). Dysentery. In: Syst. Med. (Allbutt & Rolleston). 8°.
London, 1910, ii, pt. 2, 477-545.
DeSautelle (W. T.). A case of bacillus dysenteries septicemia. J. Am. M. Ass., Chicago,
1914, Ixiii, 1853.
Flexner (S.). On the etiology of tropical dysentery. Johns Hopkins Hosp. Bull., Balti-
more, 1900, xi, 231-242.
Hiss (P. £T.). On fermentative and agglutinative characters of bacilli of the "dysentery group."
J. Med. Research, Boston, 1904-05, xiii, 1-51.
Kraus (R.) & Dorr (O.). Ueber experimentelle Therapie der Dysenterie. Wien. klin.
Wchnschr., 1905, xviii, 1077-1079.
Lentz (O.). Dysenterie. In: Handb. d. Mikroorg. (Kolle & Wassermann). 2. Aufl.
Jena, 1913, Hi, 899-1004.
Major (R. H.) & Nobel (E.). Ueber die Empfindlichkeit der kindlichen Haul gegenuber
Dysenterietoxin und Tuberkulin. Ztschr. f. d. ges. exper. Med., Berl.,
1913, ii, 9-18.
Raubitschek (H.}. Die bazilldre Dysenterie. In:Ergebn. d. allgem. Pathol., etc. (Lubarsch-
Ostertag). Wiesb., 1912, xvi, Abth. i, 66-133.
Shiga (K.). Bacillary dysentery. Mod. Med. (Osier). 8°. Philadelphia & New York,
2d ed., 1914, i, 766-782.
Strong (R. S.). Bacillary dysentery. In: Therap. Int. Dis. (Forchheimer). New York &
London, 1914, v, 253-269.
Strong (R, ?,) & Musgrave (W. E.). The bacillus of Philippine dysentery. J. Am. M.
Ass., Chicago, 1900, xxxv, 498-500.
254 DIAGNOSIS OF INFECTIOUS DISEASES
14. Diseases Due to the Bacillus of Ducrey
Ducrey's Bacillus. — The bacillus of soft chancre (Unna-Ducrey) is a
Gram-negative, non-motile, fairly thick bacillus, with rounded ends ; it
is often seen in chains. It stains well with methylene blue (polar stain-
ing) . It grows well on blood agar, and is pathogenic for man and monkeys,
reproducing soft chancre (ulcus molle). Smears from a soft chancre, or
from the juice of a bubo secondary thereto, contain large numbers of the
bacilli.
(a) Soft Chancre (Ulcus molle)
This lesion may be single or multiple. It appears within a few days
after exposure (coitus). An ulcer, with sharp margins, secreting pus,
soon forms. Under treatment, it usually heals quickly ; neglected, it lasts
longer, and often causes suppurative metastases (unilateral, or bilateral)
in the inguinal lymph glands (suppurative bubo). Soft chancre may
multiply locally, by auto-inoculation.
Sites. — Frenulum praiputii, sulcus coronarius, and glans; also, in
females, at the introitus vaginsr.
Nature. — The disease has nothing to do with syphilis, but occasionally a
syphilitic infection (with Treponema pallidum) is contracted at the same
exposure, and the sore, beginning as a soft chancre, later (3 weeks) under-
goes hardening, due to the initial sclerosis of a hard chancre (chancre
mixte of the French).
References
Ducrey (A.). Recherches experimentales sur la nature intime du prindpe contagieux du
chancre mou. Cong, internal, de dermal, et de syph., C. r., 1889, Paris,
1890, 229-250.
Also [abstr.]: Ann. de dermat. et syph., Paris, 1890, 3e s., i, 56.
Stein (R. O.). Ulcus molle. In: Handb. d. pathogen. Mikroorg. (Kolle & Wassermann).
2. Aufl. Jena, 1913, v, 1218-1236.
15. Diseases Due to the Diphtheria Bacillus
Diphtheria Bacillus. — The Bacillus diphtheria? (Klebs-Loeffler) is a
slender, non-motile, often somewhat curved bacillus, slightly swollen at the
ends, and of very variable morphology. One often sees these bacilli in
pairs, more or less parallel to one another, and occasionally in threes.
Involution forms (clubs, dumb-bells, spindles), staining irregularly in
Loeffler's alkaline methylene blue, are common. Diphtheria bacilli stain
with ordinary anilin dyes best with Loeffler's blue. (Plate IV, Fig. 4.)
They are Gram-positive.
Cultures on Loeffler's serum, 6 to 20 hours old, stained by the method
of M. Neisser, show fine points at the ends of the bacilli — the so-called
Babes-Ernst polar bodies.
DISEASES DUE TO BACILLI 255
NEISSER'S METHOD OF STAINING POLAR BODIES. — 1. Smears are stained- 1
second in a mixture of 2 parts of Solution A and 1 part of Solution B.
Solution A: Methylene blue (Hb'chst) 1.0.
Absolute alcohol 20.0.
Distilled water 1000.
Glacial acetic acid 50.0.
Solution B: Crystal violet (Hochst) 1.0.
Absolute alcohol 10.0.
Distilled water 300.0.
2. Wash with water.
3. Counterstain in chrysoidin solution (1 part of dye, dissolved in 300 parts
hot water and filtered) for 3 seconds.
4. Wash with water.
The bodies of the bacilli are stained brown, while at each pole a minute blue
granule is visible (Plate IV, Fig. 5). The bacilli resembling B. diphtheria? do not
show these granules.
CULTURES OF B. DIPHTHERIA. — The diphtheria bacillus grows best on
Loeffler's blood serum in tubes or Petri dishes, at the body temperature,
or a little lower.
Special nutrient media like Deycke's alkali-albuminate agar, or Tochtermann's
serum agar, yield good growths, but are unnecessary.
On Loeffler's blood serum (3 parts blood serum, 1 part peptone bouillon, with
2 per cent glucose) the diphtheria bacilli grow somewhat more luxuriantly than
do pseudodiphtheria bacilli or xerosis bacilli. Glycerin-ascites agar is an excellent
medium, if Loeffler's blood serum be not available.
Pathogenicityv — Inoculated into the trachea of rabbits and pigeons,
pseudomembranes are produced and fatal intoxications may follow. Pure
cultures of the bacilli yield diphtheria toxin, which, injected into animals,
causes intoxication and death. If sublethal doses be injected at intervals, a
specific diphtheria antitoxin is formed. Applying this principle, enormous
amounts of diphtheria antitoxin (Behring) are now prepared, in horses,
and used in the treatment of diphtheria (passive immunization).
Genuine diphtheria bacilli can be distinguished from the xerosis bacilli of
the conjunctiva, and from the pseudodiphtheria bacilli sometimes met with in the
oral or nasal cavity, in that the true diphtheria bacilli (1) in bouillon culture,
give rise first to acid production, and later to a strong alkaline reaction; (2) are
virulent for guinea-pigs, but, when mixed with diphtheria antitoxin before injec-
tion, lose this virulence; (3) kill animals on injection, while the others do not.
Mixed Infections. — In diphtheria infections, besides the diphtheria
bacilli, there are often present also streptococci, staphylococci or pneumo-
cocci (mixed infections), of great importance clinically, since the antitoxin
antagonizes only the toxin produced by the B. diphtheria.
Carriers. — Many healthy individuals harbor diphtheria bacilli (bacillus
carriers). These bacilli are sometimes virulent, sometimes avirulent;
256 DIAGNOSIS OF INFECTIOUS DISEASES
in the former instance, they are probably of importance in the starting
of epidemics (Moss and Guthrie).
Forms of Diphtheria. — In human beings, the diphtheria bacillus may
cause (1) a pharyngeal diphtheria, (2) a nasal diphtheria, or (3) a laryn-
geal diphtheria; more rarely, it sets up (4) a cutaneous diphtheria, (5) a
conjunctival diphtheria, (6) a vulval diphtheria, or (7) a wound-infection
diphtheria. In all instances, the incubation period seems to vary (2 to 8
days).
Susceptibility to Diphtheria. — It has recently been shown that the
blood of many normal individuals contains diphtheria antitoxin, in demon-
strable quantities. Thus some 80 per cent of the newborn, 90 per cent of
adults, and 50 to 60 per cent of children are so protected. Such individuals
are not susceptible to diphtheritic infection, and in cases of epidemics, or
in instances of single exposure, the prophylactic injection of diphtheria
antitoxin ordinarily given may be omitted. This new knowledge has
resulted from the introduction of the intracutaneous test of Schick.
SCHICK'S TEST. — 1/50 of the minimum lethal dose of diphtheria toxin for the
guinea-pig is diluted to make 0.1 c.c. of fluid. This is injected intracutaneously,
and the site of injection examined at the end of 24 hours. Those who are
susceptible to diphtheritic infection show a definite inflammatory reaction. Those
who are insusceptible, owing to the presence of diphtheria antitoxin in the blood,
show no inflammatory reaction. (See the work of W. H. Park and his colleagues
in New York, with this test.) The simple outfit devised by A. Zingher for the test
will be found convenient by practitioners.
(a) Pharyngeal Diphtheria
This is the commonest form of diphtheritic infection. The bacilli
multiply on the mucous membrane, and in its superficial layers, causing
extensive necrosis, with formation of fibrinous membranes. Though a few
bacilli may get over into the blood, the general phenomena are due to the
toxins produced by the bacilli in loco, rather than to a bacillemia.
In the membranous form, a grayish white deposit is seen on the uvula,
the soft palate, and tonsils (unilateral or bilateral).
In the lacunar form, there is redness and swelling of the uvula, soft
palate, and tonsils, but no visible membrane except whitish plugs in the
fossulse (crypts) of the tonsils. These cases are often mistaken for
streptococcus angina.
In the severer forms of diphtheria, black areas may appear in the
membrane (gangrenous form), or the membrane formation may extend
from the throat upward to the nose, or downward to the larynx, trachea,
and bronchi (progressive or spreading form).
Symptoms. — The onset may be insidious, with fever, malaise, headache,
sore throat, and foul breath. The pulse and the respiration are acceler-
ated. Children, when infected, are apt to be dull and sleepy. If the
PLATE IV
Fig. 1. — Smear from Nasal Secretion in
Leprosy. (After C. Mense, "Handb. d.
Tropenkrankh.," published by J. A.
Earth, Leipzig.)
Fig. 2. — Smear from Sputum in Primary
Plague-pneumonia. (After C. Mense,
"Handb. d. Tropenkrankh.," published by
J. A. Earth, Leipzig.)
Fig. 3. — Cholera Bacillus, Pure Culture Stained
with Carbolfuchsin. After L. Mohr u. R.
Staehelin, "Handb. d. inner. Med.," published
by J. Springer, Berlin.)
Fig. 4.— Bacillus diphtheriae— 36-
Hour Pure Culture. (After P.
Krause, "Lehrb. d. klin. Diag-
nostik d. inner. Krankh.," pub-
lished by G. Fischer, Jena.)
Fig. 5. — Bacillus diphtheriae —
Pure Culture — Neisser's Stain.
(After P. Krause, "Lehrb. d.
klin. Diagnostik d. inner.
Krankh.," published by G.
Fischer, Jena.)
DISEASES DUE TO BACILLI 257
condition be recognized early (inspection, throat culture), and antitoxin
be given promptly, the membrane disappears in a day or two, the tempera-
ture becomes normal, and, in a week, the patient is usually well. If anti-
toxin be not given, the membrane spreads, the lymph glands at the angle
of the jaw become large and tender, the tachycardia and fever persist, and
albuminuria appears. Many of the patients, without antitoxin, die ; others,
after a week or two, gradually recover, though in convalescence post-
diphtheritic paralyses or death from heart failure may occur. In all
cases there is a leukocytosis.
(6) Nasal Diphtheria
This may occur as a primary infection, or it may be secondary, through
extension of diphtheria of the throat. The nose is obstructed and a thin
bloody discharge runs down over the upper lip. On rhinoscopic examina-
tion, the membrane is visible, and diphtheria bacilli are demonstrable
in smears and in cultures.
(c) Laryngeal Diphtheria
This, too, may be primary, though it is more often secondary to pharyn-
geal, or to nasal, diphtheria. The primary cases are frequently over-
looked by physicians until it is too late to save the patient.
The child is, at first, a little hoarse, and has a croupy cough, with
slight fever ; nothing more malign than simple "croup" may be suspected !
Later, signs of laryngeal stenosis appear, with long-drawn-out, noisy in-
spiration, and retraction in the jugular fossa and in the epigastrium. In
such cases, unless intubation, or tracheotomy, is promptly resorted to,
the issue is nearly always fatal. I have, however, known patients, given
up as hopeless, to expectorate a cast of the larynx and trachea, and go
on to recovery.
(d) Cutaneous Diphtheria
This is due, usually, to infection of a scratch, or of a minute skin
lesion (rhagades, intertrigonous eczema) ; it is most often seen in the
groin, or about the anus. It may or may not be associated with pharyngeal
diphtheria. Irregular ulcers appear, covered by a diphtheritic membrane,
containing the bacilli. The condition may be confused with infantile
ecthyma, or with a drug dermatosis (iodids, bromids).
(e) Vulval Diphtheria
This is usually a puerperal infection; rarely it may follow other
traumata. The membrane may extend to the vagina, and may even in-
volve the whole extent of the vaginal cavity.
258 DIAGNOSIS OF INFECTIOUS DISEASES
(/) Conjunctival Diphtheria
Diphtheria of the conjunctiva is rare; it is usually an extension from
the nose, though it may occasionally occur as a primary infection. En-
largement of the lymph glands in front of the ear quickly follows, and slight
fever develops. If neglected, the eye may be lost.
Complications and Sequela? of Diphtheria
The most important are (1) acute nephritis, (2) heart failure, (3)
postdiphtheritic paralyses. In addition, (4) otitis media, (5) broncho-
pneumonia, or (6) polyarthritis may occur.
Nephropathies. — Though most diphtheritic patients show albuminuria
and a few casts, a few have an outspoken acute nephropathy, which not
infrequently goes over into chronic renal disease.
Cardiopathies. — Sudden heart failure after diphtheria is not uncom-
mon and is greatly feared as a complication (myocardial degeneration?).
It may appear early in the disease, but is more often met with in the second
or the third week.
A child, apparently almost well, may, on sitting up, drop back dead.
In some cases, symptoms of severe myocardial insufficiency appear (dilata-
tion, feeble sounds, tachycardia or bradycardia, gallop rhythm) ; many
of these patients die, but a few recover. Occasionally a partial heart block
is observed.
Neuropathies. — Postdiphtheritic paralyses may appear, in 1-3-6 weeks
after the infection. Most often the soft palate is paralyzed (nasal voice ;
regurgitation of fluids through the nose). If this occur early, it is usually
due to the local inflammation ; later cases are due to nerve degeneration.
Another common form is postdiphtheritic paralysis of the M. ciliaris
(accommodation paralysis). Children find that they cannot read, and may
be punished in school therefor. In a few instances, a multiple neuritis
occurs with eye muscle paralysis, along with weakness of the arms and
legs, with ataxia. Sensation is usually but little affected. The paralyses
may occur, even when antitoxin has been used. The patients recover as a
rule, though the disability may be prolonged.
Diagnosis of Diphtheria
The membranous cases of pharyngeal diphtheria can usually be
recognized at once by inspection, though streptococcus anginas are occa-
sionally accompanied by membrane formation. The lacunar cases can only
be distinguished with certainty, by bacteriological examination. On ac-
count of the danger of overlooking a diphtheritic angina, it is a good rule to
make a smear preparation, and a culture on Loeffler's serum, in every case
of sore throat. The utensils for the purpose can be obtained at any corner
drug store, and if the physician does not care to make the examination
DISEASES DUE TO BACILLI 259
himself, he may send the materials to the laboratory of the Board of
Health and receive a telephonic report within 20 hours. • In outspoken
cases, the report need not be awaited before giving antitoxin.
Differential Diagnosis. — The pharyngeal form of diphtheria must be
distinguished (by smears and cultures) from other forms of angina (strep-
tococcus angina, Plant-Vincent's angina, syphilitic angina, angina scarlati-
nosa).
References
1. General
Blumenthal (J. Af.) & Lipskerow (A/.). Vergleichende Bewertung der differentiellen
Methoden zur Fdrbung des Diphtheriebacillus. Centralbl. f. Bakteriol.
[etc.], 1. Abt., Jena, 1905, xxxviii, Orig., 359-366.
von Jurgensen (77i.). Diphtheria, measles, scarlatina, German measles. Edited, with
additions, by William P. Northrup. Authorized translation from the
German, under the editorial supervision of Alfred Stengel. Philadelphia &
London, 1902, W. B. Saunders Co. 672 p. 8°. [Nothnagel's Encyclo-
pedia of Practical Medicine. Amer. ed.]
Krause (P.). Diphtherie. In: Handb. d. inn. Med. (Mohr & Staehelin), Berlin, 1911, i.
240-278.
McCollum (J. H.} & Place (E. H.). Diphtheria. Mod. Med. (Osier). 8°. Philadel-
phia & New York, 2d ed., 1914, i, 689-732.
Neisser (M.) & Gins (H. A.). Ueber Diphtherie. In: Handb. d. pathogen. Mikrodrg.
(Kolle & Wassermann). 2. Aufl. Jena, 1913, v, 931-1002.
Wernicke (E.). Die Immunitdt bei Diphtherie. In: Handb. d. pathogen. Mikrodrg. (Kolle
& Wassermann). 2. Aufl. Jena, 1913, v, 1011-1062.
2. Etiological
Abbott (A. C.)« Etiology of membranous rhinitis (rhinitis fibrinosa) . Med. News, Phila-
delphia, 1893, Ixii, 503-509.
Ford (W. W.}. The recent epidemic of diphtheria in the Johns Hopkins Hospital and
Medical School. General procedures adopted. Johns Hopkins Hosp.
Bull., Baltimore, 1911, xxii, 357-361.
Frosch (P.). Die Verbreitung des Diphtheriebacillus im Korper des Menschert. Ztschr. f.
Hyg., Leipzig, 1893, xiii, 49-53.
Klebs (E.). Ueber Diphtherie. Verhandl. d. Cong. f. innere Med., Wiesbaden, 1883, ii,
139-174.
Loffler (F.). Untersuc,hungen iiber die Bedeutung der Mikroorganismen fur-die Entstehung
der Diphtherie beim Menschen, bei der Taube und beim Kalbe. Mitth. a.
d. k. Gsndhtsamte., Berlin, 1884, ii, 451-499.
Nuttall (G. H. F.) & Graham-Smith (G. S.). The bacteriology of diphtheria. Cam-
bridge, 1913, Cambridge University Press.
Roux {E.} & Yersin (A.). Contribution a V etude de la diphtherie. Ann. de I'Inst. Pasteur,
Paris, 1888, ii, 629-661.
Teague (O.). Some experiments bearing upon droplet infection in diphtheria. J. Infect.
Dis., Chicago, 1913, xii, 398-414.'
Welch (W. H.) & Abbott (A. C.). The etiology of diphtheria. Johns Hopkins Hosp.
Bull, Baltimore, 1891, ii, 25-31.
Welch (W. H.) & Flexner (5.). The histological lesions produced by the toxalbumen of
diphtheria. Johns Hopkins Hosp. Bull, Baltimore, 1892, Hi, 17-18.
Wesbrook (F. F.). Problems in the laboratory study of diphtheria. Medicine, Detroit,
1903, ix, 125-129,
260 DIAGNOSIS OF INFECTIOUS DISEASES
3. Diphtheria-Bacillus Carriers
Alden (A. M.). The staphylococcus-spr&y treatment of diphtheria carriers. J. Am. M.
Ass., Chicago, 1913, Ix, 1876-1878.
Moss (W. L.), Guthrie (C. G.) & Gelien (/.)• Diphtheria bacillus carriers. Tr. XV
Internal. Cong. Hyg. & Demog., Washington (1912), 1913, iv, 156-170.
Weichardt (W.) & Pape (Martin). Dauertrdger und Dauertrdgerbehandlung bei Diph-
theric. Ergebn. d. inn. Med. u. Kinderh., Berlin, 1913, xi, 754-813.
4. Schick Reaction
Bundesen (H. N.~). Schick reaction, with a report of eight hundred tests. J. Am. M. Ass.,
Chicago, 1915, Ixiv, 1203-1205.
Graef (C.) & Ginsberg (G.). Some observations of the Schick test. J. Am. M. Ass.,
Chicago, 1915, Ixiv, 1205-1206.
Kolmer (J. A.) & Moshage (Emily L.)« A note on the occurrence of pseudoreactions on
the skin, with special reference to the Schick toxin test. J. Am. M. Ass.,
Chicago, 1915, Ixv, 144-146.
Moody (E. E.}. The intradermic diphtheria toxin test. J. Am. M. Ass., Chicago, 1915 ,
Ixiv, 1206-1208.
Park (W. H.), Zing her (A.) & Scrota (H. M.}. The Schick reaction and its practical
applications. Arch. Pediat., New York, 1914, xxxi, 481-487.
Schick (#.)• Die Diphtherietoxin-Hautreaktion des Menschen als Vorprobe der prophy-
laktischen Diphlherieheilseruminjektion. Munch, med. Wchnschr., 1913,
Ix, 2608-2610. Also: J. Am. M. Ass., 1914, Ixii, 1176.
Zingher (A."). A simple outfit for the distribution of toxin for the Schick test. J. Am. M.
Ass., Chicago, 1915, Ixv, 329.
5. Clinical
Behring (E. v.}, Boer (O.) & Kossel (H.}. Zur Behandlung diphtheriekranker Menschen
mit Diphtherieheilserum. Deutsche med. Wchnschr., Leipzig u. Berlin,
1893, xix, 889, 415.
Elliott (J. B.). The heart in diphtheria. N. Orl. M. & S. J., 1912-13, Ixv, 706-708.
Guillain (G.) & Laroche (G.). Note sur la physiologic pathologique des paralysies diph-
theriques. Bull, et mem. Soc. med. d. hop., Paris, 1913, xxix, 4~8-
Hume (W. E.). A poly graphic study of four cases of diphtheria, with a pathological ex-
amination of three cases. Heart, London, 1913, v, 25-44-
Kinyoun (J. /.)• The serum therapy of diphtheria. Rep. Superv. Surg.-Gen. Mar. Hosp.,
Washington, 1895, 311-343.
Lind (S. C.). Atypical pharyngeal diphtheria. J. Am. M. Ass., Chicago, 1913, Ix, 1412-
1413.
Morgan (E.}. Diphtheria septicaemia, with report of a case. Am. J. Dis. Child., Chicago,
1913, v, 317-321.
Moss (W. L.}. A cutaneous anaphylactic reaction as a contraindication to the adminis-
tration of antitoxin. J. Am. M. Ass., Chicago, 1910, Iv, 776-777.
Nicoll (M.) & Wilcox (H. £,.)• /« diphtheria frequently a bacteremia? Am. J. Dis. Child.,
Chicago, 1913, vi, 23-27.
Plaut (H. C.). Studien zur bacteriellen Diagnostik der Diphtheric und der Anginen. Deutsche
med. Wchnschr., Leipzig u. Berlin, 1894, xx, 920-923.
Porter (W. T.) & Pratt (J. H.}. The state of the vasomotor centre in diphtheria intoxica-
tion. Am. J. Physiol, Boston, 1914, xxxiii, 431-440.
Rolleston (J. D.). Diphtheritic paralysis. Arch. Pediat., New York, 1913, xxx, 335-345.
Some aspects of the serum treatment of diphtheria. Practitioner, London,
1905, Ixxiv, 660-674.
DISEASES DUE TO BACILLI 261
Schick (#.), Kassowitz (K.) & Busacchi (P.)« Experimentelle Diphtherieserumtherapie
beim Menschen. Ztschr. f. d. ges. exper. Med., Berlin, 1914, iv, 88-148.
Tylecote (F. E.}. Diphtheria of the stomach, with a note on diphtherial onychia. Brit. J.
Child. Dis., 1913, x, 211-216.
16. Diseases Due to the Bacillus pyocyaneus
Bacillus pyocyaneus. — The Bacillus pyocyaneus is a slender motile rod
with a flagellum at one end. It is Gram-negative. * In cultures, it lique-
fies gelatin • grows, in the presence of oxygen, with a greenish fluorescence
on agar; and coagulates milk. It produces a proteolytic ferment (pyocy-
anase) and a soluble toxin. It is pathogenic for guinea-pigs.
Human Infections. — In 1897, I described a series of human infections
due to this bacillus. In America, Blumer has also studied these infections,
while in Europe they have been met with by many observers.
Most often, this '"bacillus of green pus" is seen in mixed infections
along with the pyogenic cocci, but it is entirely capable of setting up
pathological processes by itself. It usually causes local inflammations,
especially of the alimentary tract (esophagus, intestine), of the umbilicus
in the new-born, of the pelvis of the kidney, etc. A general pyocyaneus
sepsis is also known, associated with high fever, diarrhea, and a hemor-
rhagic or pustulo-hemorrhagic exanthem ; sometimes there is also an endo-
carditis.
References
Barker (L. F»). The clinical symptoms, bacteriologic findings and postmortem appearances
in cases of infection of human beings with the bacillus pyocyaneus. J. Am.
M. Ass., Chicago, 1897, xxix, 213-216.
Brown (T. R.}. Cystitis caused by the bacillus pyocyaneus. Maryland M. J., Baltimore,
1899-1900, xliii, 221-224.
Heiman (H.). A case of bilateral hydroureter. Chronic pyocyaneus infection. Arch.
Pediat., New York, 1913, xxx, 814-819.
Heller (O.) & Lepere (E.). Bacillus pyocyaneus. In: Handb. d. pathogen. Mikroorg.
(Kolle & Wassermann). 2. Aufl. Jena, 1913, v, 1185-1217.
Krannhals (H.). Ueber Pyocyaneusinfectionen. Deutsche Ztschr. f. Chir., Leipzig, 1893,
xxxvii, 181-200.
Lagriffoul, Bousquet & Roger. La typhopyocyanie (pyocyanie generalisee d forme
typhoide). Compt. rend. Soc. de biol., Paris, 1910, Ixviii, 1019.
Wollstein (Martha) & Meltzer (S. J.). The pulmonary reaction to B. pyocyaneus.
Proc. Soc. Exper. Biol. & Med., New York, 1913-14, xi, 97.
17. Diseases Due to the Bacillus mallei
Glanders Bacillus. — The Bacillus mallei (Loeffler and Schutz) is a slen-
der rod, about as long as the tubercle bacillus, but thicker. It is non-
motile. It stains irregularly with Loeffler's methylene blue, and is Gram-
negative. It is easily grown on ordinary media like agar, blood serum,
262 DIAGNOSIS OF INFECTIOUS DISEASES
and potato, but it is best isolated by means of animal inoculation (intra-
peritoneal injection of male guinea-pig, with recovery after two days from
the testicle). Infection due to this bacillus is rare in man, and when
met with, it has usually been contracted from the horse, an animal in
which glanders is a contagious and fatal disease. Among human beings, it
is stable-men, soldiers (cavalry), cab-drivers, and veterinarians that are
most often infected.
(a) Glanders and Farcy
Definition. — An infectious disease, common in horses, rare in man, due
to the Bacillus mallei, which gives rise to nodules (infectious granulomata)
in the nose (glanders) and beneath the skin (farcy).
Man is most often infected by inoculation of the skin, occasionally,
through the mucous membranes. Laboratory workers may be accidentally
infected ; among the pathogenic bacteria, the B. mallei, the B. pestis,
the B. anthracis, and the Nicrococcus melitensis are among the most dan-
gerous to work with.
Symptoms. — The disease may be acute or chronic. It is believed that
the incubation period is from 3 to 5 days.
In the acute cases, always fatal, the symptoms are those of septic infec-
tion starting from a cutaneous wound. After slight prodromala (head-
ache, fever, malaise,) there is local infiltration and ulceration, with
lymphangitis, and swelling of adjacent lymph glands. In less than a
week, the signs of general sepsis, and of metastases appear. Painless
swellings, quickly leading to suppuration and ulceration, appear in the
skin (farcy). In addition, a red papular eruption, becoming pustular,
appears between the 6th and the 12th day. A bloody discharge from
the nose appears; abscesses develop in the muscles and in other organs;
there is marked sweating ; the patient loses strength ; finally there is cir-
culatory failure and death.
Occasionally, an acute nasal infection (glanders) is seen, causing nasal
obstruction, with sanguineo-purulent discharge, dysphagia, hoarseness, and
foul breath. Bronchitis and bronchopneumonia develop, and later general
sepsis with metastases. The disease is accompanied by leukopenia.
In the chronic form, the onset is insidious, with pains in the limbs
and joints, and slow development of local abscesses, followed by ulcers
and cicatrization. This chronic form may last for years.
Diagnosis. — The anamnesis is helpful. In the acute cases, typhus
abdominalis, acute rheumatic fever or general sepsis due to other bacteria
may be simulated. The cutaneous lesions help to distinguish the disease
from these, and the bacteriological examination, with guinea-pig inocula-
tion, is decisive.
In the chronic cases, a mallein test (similar to the tuberculin test) may
DISEASES DUE TO BACILLI 263
be employed; a complement-fixation test has also been worked out (Schultz
and Schubert), the antigen being made from the Bacillus mallei. An
agglutination test has been much used in recognizing the disease in animals.
References
Frothingham (L.) & O'Toole (5.). Notes on complement-fixation in glanders. J. M.
Research, Boston, 1913, xxviii, 333-844.
Hoke (E.). Ein Fall von akuten Rotz. (Laboratoriumsinfektion.) Prag. med. Wchnschr.,
1907, xxxii, 351-353.
Irons (E. E.). Glanders. In: Therap. Int. Dis. (Forchheimer). New York & London,
1914, v, 659.
MacCallum (W. G.}. Beitrag zur pathologischen Anatomie des Lungenrotzes. Beitr. z.
path. Anat. u. z. allg. Path., Jena, 1902, xxxi, 440-451.
M'Fadyean (/.). Preliminary notes on the sero-diagnosis of glanders. J. Comp. Path. &
Therap., Edinburgh & London, 1896, ix, 322.
Mohler (John R.}. Ophthalmic malleinfor the diagnosis of glanders. Washington, 1915.
11 p.
Musgrave (W. E.} & Sison (A. G.}. Acute malignant glanders in man. Philippine J.
Sc., Manila, Sect. B, 1913, viii, 385-395.
Rayer (P.). De la morve et du farcin chez Vhomme. Paris, J. B. Bailliere, 1837. 251 p.
Schultz & Schubert. Die Ermittelung der Rotzkrankheit mit Hilfe der Komplementablen-
kungsmethode. Arch. f. wissensch. u. prakt. Tierh., Berlin, 1909, xxxv,
44-83.
Wade (E. M.}. The laboratory diagnosis of glanders. J. Infect. Dis., Chicago, 1913, xii,
7-H.
Wladimiroff (A.}. Malleus. In: Handb. d. pathogen. Mikroorg. (Kolle & Wassermann) ,
2. Aufl. Jena, 1913, v, 1063-1184.
Woodhead (G. S.}. Glanders and farcy. In: Syst. Med. (Allbutt & Rolleston). 8°.
London, 1909, U, pt. 1, 201-227.
18. Diseases Due to the Tubercle Bacillus
Tubercle Bacillus. — The Bacillus tuberculosis (Koch, 1882) occurs in
four varieties, or races:
1. The human bacillus (typus humanus).
2. The bovine bacillus (typus bovinus).
3. The bacillus of avian tuberculosis (chicken, pheasant, pigeon,
parrot).
4. The bacillus of cold-blooded animals (turtle bacillus, etc.). Morpho-
logically, these races resemble one another closely. The 4th variety appears
to be harmless for man.
Human beings are infected most commonly with the first, occasionally
with the second, and very rarely with the third variety.
The tubercle bacillus is a long slender bacillus (Plate I, Fig. 1), often
slightly curved and occasionally showing branching forms. In smear prep-
arations, made from sputum containing tubercle bacilli, one sees usually
groups of a few bacilli, lying parallel to one another, at an angle, or
264 DIAGNOSIS OF INFECTIOUS DISEASES
across one another. The bacillus is non-motile, and does not form spores.
It does not stain easily with the ordinary anilin dyes ; it is Gram-positive
and is acid- fast (like lepra bacilli, smegma bacilli and butter bacilli)
owing to its content in wax.
The human type is not easily cultivated; it grows only at the body
temperature, preferably on blood serum, glycerin agar, or bouillon or on
Dorset's egg-medium; a dry scaly growth appears, taking several weeks
to develop. For staining methods, see page 143. The tubercle bacillus
occurs in the sputum in pulmonary tuberculosis, in the feces in intestinal
tuberculosis, in the urine in urogenital tuberculosis, in the pus from carious
bones and scrofulous glands, in the skin in lupus, and, sometimes, in the
blood in general miliary tuberculosis.
Pathogenicity of the Tubercle Bacillus. — The guinea-pig is the most
susceptible animal. Human beings are relatively insusceptible, even to the
iypus humanus. Though the majority of human beings are infected at
some time or another, most people have sufficient resistance to prevent
serious disease. For tuberculin tests, see page 172.
Cultures of the human type of the bacillus have but little virulence
for cattle or for rabbits, producing no lesion, only a local lesion, or a
mild and chronic disease; whereas cultures of the bovine type, inoculated
into cattle or rabbits, cause a generalized, and rapidly fatal, tuberculosis.
Inoculation of a guinea-pig is a most important method for determin-
ing the presence or absence of tubercle bacilli, when they cannot be
demonstrated by ordinary tests, or even by the antiformin method.
If a guinea-pig be inoculated subcutaneously in the lower abdominal
region, or, preferably, in the groin, the adjacent lymph glands can be
extirpated at the end of 2 weeks and examined for tubercle bacilli in
paraffin sections or in smears ; moreover, if the injected material contains
tubercle bacilli, the animal will die, and will show typical tuberculous
lesions at autopsy.
Portals of Entry and Paths of Infection in Tuberculosis. — Human
beings may be infected through the most different portals of entry, but the
spread, in each case, from the infection atrium to other parts of the body,
occurs through the lymph paths (lymphogenous tuberculosis). A few ba-
cilli may enter the blood and reach distant organs (hematogenous infec-
tion). In some cases, large numbers break through a vein into the blood
and cause general miliary tuberculosis.
In considering the paths of infection in human tuberculosis, we try to
determine: (1) how the tubercle bacillus entered the body to cause the
oldest focal lesion, and (2) how, thence, the bacilli reached other organs,
and caused the clinical symptoms.
An individual may be infected before birth (congenital tuberculosis ', or
intra-uterine infection) ; a majority, however, are infected after birth
(extra-uterine infection), either from some other tuberculous human being
DISEASES DUE TO BACILLI 265
(directly or indirectly), or from tuberculous cattle. There is much dis-
pute as to whether infection occurs most often through the digestive tract,
or through the respiratory apparatus. In the former, the primary infec-
tion may involve the throat (tonsils) and the cervical lymph glands, or the
intestinal mucous membrane and the mesenteric lymph glands, and thence
spread through the lymphatics or through the blood to other parts of the
body. In case of infection by the respiratory path, the bacilli are taken
up by inhalation,, infecting the mucous membrane of the bronchi and lungs,
and extending to the bronchial lymph glands.
In human beings, tuberculous infections cause, as a rule, exquisitely
chronic diseases, especially at first. In certain special conditions, acute,
rapidly progressive forms appear (galloping phthisis, miliary tuberculosis).
The tubercle bacillus may become disseminated in the body (1) by con-
tinuity, (2) by the lymph paths (e. g., in polyserositis), (3) by auto-in-
oculation (e. g.? infection of the larynx, or of the intestine, by tuberculous
sputum from lungs), (4) by way of the urine (e. g., infection of the blad-
der from a tuberculous kidney), and (5) by way of the blood (hematogen-
ous infection), as in chronic metastatic tuberculosis, and especially in acute
general miliary tuberculosis.
Wherever the tubercle bacilli lodge in the body, there is a peculiar
inflammatory reaction, with production of a nodule (tubercle), gray at first,
later becoming white, and, after central caseation, yellow. A miliary
tubercle is about the size of a hemp seed, and histologically consists of one
or more giant cells near the center, surrounded by a layer of epithelioid
cells, or fibroblasts, outside of which is a layer of small mononuclear cells ;
the bacilli are often demonstrable in such nodules. Adjacent miliary
tubercles often become confluent, to form later a single caseous mass
(conglomerate tubercles). As a result of caseation, and of softening,
tuberculous cavities, tuberculous ulcers, and tuberculous fistulce, arise.
Any organ of the body may become tuberculous, though the thyroid
gland and the muscles are rarely attacked. Tuberculosis shows a pre-
dilection, however, for certain organs (lungs, meninges, serous membranes,
kidneys, urogenital system, bones). This selective affinity is sometimes
a help in differentiating tuberculous from syphilitic lesions ; thus, in bone,
tuberculosis attacks most often the marrow (caries), especially that of the
epiphyses, while syphilis frequently causes subperiosteal lesions and new
formation of bone ; in the male genitals, tuberculosis more often involves
the epididymis, while syphilis is prone to attack the testicle itself.
(a) Pulmonary Tuberculosis
(Pulmonary Phthisis, Tuberculosis pulmonum, Pulmonary Consumption)
Only a brief epitome will be given here; for a fuller account see
Part V, Diseases of the Respiratory Apparatus.
266 DIAGNOSIS OF INFECTIOUS DISEASES
Three clinical groups of pulmonary tuberculosis may, for practical
purposes, be considered (Osier) :
1. Acute phthisis.
2. Chronic ulcerative phthisis.
3. Chronic fibroid phthisis.
i. Acute Phthisis
(Galloping Consumption, Phthisis florida)
A pneumonic form and a bronchopneumonic form are distinguishable.
In the pneumonic form, we deal with caseous pneumonia, involving usually
a whole lobe, or more. In the bronchopneumonic form, there is an acute
caseous bronchopneumonia ; it is especially common in children.
Symptoms. — The symptoms in the PNEUMONIC FORM are, at first, those
of a frank lobar pneumonia, but no crisis occurs ; the temperature contin-
ues elevated and the pulse accelerated. . The sputum becomes mucopuru-
lent and greenish in color (Traube). Signs of softening appear, and elastic
tissue and tubercle bacilli become demonstrable in the sputum. Death may
occur in a week, but some patients drag on for three months or more.
Absence of breath sounds in the consolidated area is common, but there
may be outspoken tubular breathing. The fever is more remittent than
in lobar pneumonia.
In the BRONCHOPNEUMONIC FORM, there is high fever, tachycardia,
tachypnea, with chills and sweating. Signs of bronchopneumonia gradu-
ally become demonstrable in the lungs. The disease is, in children, often
preceded by measles, or by whooping-cough.
ii. Chronic Ulcerative Phthisis
This is the commonest form of pulmonary tuberculosis. It occurs most
frequently in individuals with the so-called habitus phthisicus (pallor,
emaciation, poor muscular development, small bones, paralytic type of
thorax). On examining these patients, one often sees the brown dis-
coloration of pityriasis versicolor on the chest.
Anamnesis. — The patient usually gives a family history of tuberculosis
(parents, sibs, conjugal partner, children), stating that one or more mem-
bers have suffered from consumption, pleurisy, scrofula, or meningitis.
The patient himself may have earlier suffered from enlarged cervical
glands, corneal lesions, or bone troubles (scrofula), or he may give
a history of cough, of hemoptysis, of hoarseness, or of one or two attacks
of pleurisy earlier in life. On questioning the patient, his general cir-
cumstances and mode of living should be gone into; his occupation (dust,
exposure) and habits (alcoholism, work, sleep) should be asked about.
Recent loss of weight is an important symptom, and, in following a case,
DISEASES DUE TO BACILLI
267
the keeping of a body-weight chart may be more important than a tempera-
ture chart.
Physical Findings in the Lungs. — In the first stage (PHTHISIS INCJP-
IENS) one finds signs of apical bronchitis (moist or dry rales, especially
after coughing), with enfeebled, roughened, or cogwheel-like, respiratory
Lee M. aet. 25.
Fig. 81. — Pulmonary Tuberculosis. (Personal Observation.)
murmur. Expiration is often prolonged. There may or may not be slight
dullness on percussion. A slight delay in expansion of the affected side
can often be made out. In such patients there is usually a little morn-
ing cough, with scanty sputum, and this may contain tubercle bacilli
268 DIAGNOSIS OF INFECTIOUS DISEASES
("open case"), or they may yet be absent ("closed case"). A hemoptysis
may have been the first symptom noticed.
In the second stage (PHTHISIS CON FIRM ATA) the physical signs of
infiltration can be made out in the upper part of one upper lobe; there
is dullness in front and behind -with bronchial breathing, consonating
crackles, and lessened expansion. The sputum is more abundant, is
mucopurulent, and contains tubercle bacilli. The rontgenogram taken
after a deep inspiration, the patient holding his breath, shows infiltration
in areas corresponding to the dullness on percussion, and often beginning
infiltration in the other lung.
Instantaneous rontgenography with use of an intensifying screen gives the
best negatives, as regards details; in women the breasts should be pressed lateral-
ward as far as possible by the plate holder. It is well to make special small plates
of the apices with the aid of a diaphragm; the anticathode should be placed close
to the first intercostal space, for otherwise this space is likely to be hidden by the
second rib; the normal radiation should be adjusted for the jugulum, the head
being bent well back. Good rontgenograms of the upper aperture of the thorax
can be taken by the method of Hart and Harras (1908). Stereoscopic plates are
very valuable for exact diagnosis. (See Part V.)
In the third stage (PHTHISIS CONSUMMATA) there are signs of wide-
spread infiltration in both lungs, and of cavity formation. The cavities
are recognizable on physical examination by the loud bronchial, or amphoric
sounds audible over them, with tympany and changes of pitch in different
positions (Wintrich, Friedreich, Gerhardt). (See examination of the
lungs.) The sputum is often nummular and crowded with tubercle bacilli,
often in large masses from the walls of cavities; it may contain elastic
fibers also.
In most cases there is fever, often of HECTIC type, especially in the
third stage. The patients suffer from night sweats, and, sooner or later,
become emaciated. Digestive disturbances are troublesome ; it is often of
these that the patient complains when he first consults his physician. Not a
few of the cases present signs of Graves's disease (tachycardia, tremor,
palpitation, nervous symptoms).
iii. Chronic Fibroid Phthisis
This is a very common form of pulmonary tuberculosis, the duration
of which may be 10 to 20 years, or more. The patients are usually
afebrile, much ,of the time, but they suffer from paroxysmal cough, and
from dyspnea on exertion. The sputum is purulent, and contains tubercle
bacilli. Complicating bronchiectasis is common, with fetid bronchitis.
The physical signs of shrinking of the lung (retraction of the affected
side); dislocation of adjacent organs; vicarious emphysema of unaffected
lung, enlargement of the right heart and hippocratic fingers are demon-
DISEASES DUE TO BACILLI 269
strable. The cases are sometimes confused with pulmonary cirrhosis,
due to anthracosis, etc.
Complications of Pulmonary Tuberculosis
The more important are (1) hemoptysis, (2) tuberculous pleuritis,
(3) mixed infections (pyogenic cocci, influenza bacilli), (4) laryngeal
tuberculosis, (5) intestinal tuberculosis (swallowing of sputum), (6)
pneumothorax, and (7) amyloid disease.
(b) Lymphadenoid Tuberculosis
(Tuberculosis of the Lymph Glands, Scrofula}
This may occur at any age, but is most common in children, affecting
most often the bronchial, though, also often, the cervical, the mediastinal,
or the mesenteric glands (tabes mesenterica) , or, occasionally, all the
lymph glands of the body simultaneously (generalized tuberculous lympha-
denitis).
Scrofulous children are usually pale and delicate, and are very subject
to chronic catarrhal inflammations. Thus they often have nasal catarrh,
with thickening of the nose and of the upper lip. They are often victims
of ozena, of hypertrophied tonsils, of suppurative otitis media, of phlycten-
ular conjunctivitis, and of recurring blepharitis. Many of them suffer
from chronic skin eruptions (eczema, prurigo, lupus, lichen scrofulosorum,
etc.). In addition to the enlargement of the lymph glands, they frequently
suffer from tuberculous diseases of the bones and joints (hip- joint disease,
white swelling of the knee, caries of the spine), and from that form of
chronic osteomyelitis of the phalanges of the fingers and toes, with spindle--
shaped expansion of the compact substance known as spina ventosa. (See
also Lymph Glands, under Diseases of the Blood and of the Blood-Building
Organs. )
Diagnosis and Differential Diagnosis. — This is usually easy, but
enlarged lymph glands, especially in the neck, may be due to causes other
than tuberculosis, for example, long standing pediculosis causing eczema
of the head, swelling of the cervical lymph glands, blepharitis and coryza.
Hereditary syphilis should be ruled out (Hutchinsonian teeth, keratitis
syphilitica, Wassermann reaction, etc.). In tuberculosis of the bronchial
glands, the cough may resemble that of whooping-cough, though the stridor
is more often expiratory than inspiratory. The percussion sounds and the
x-ray findings are characteristic.
In tabes mesenterica with enlarged and tympanitic abdomen and with
diarrhea, marked emaciation and anemia, the diagnosis can usually be
easily made.
In generalized tuberculous lymphadenitis, the affection may be mis-
taken for HodgMns disease. Cultures from, and histological examination
of, an excised gland, and the differential count of the leukocytes will decide.
270 DIAGNOSIS OF INFECTIOUS DISEASES
(c) Tuberculosis of the Serous Membranes
( Tuberculous Serositis)
Acute or chronic tuberculosis of any one of the serous membranes may
occur (pleuritis, pericarditis, peritonitis), or two or more cavities may be
simultaneously involved (polyserositis, polyorrhomenitis).
The diagnosis depends upon the family history, the physical signs, the
presence or absence of signs of tuberculosis elsewhere in the body, the
examination of the exudate (cytodiagnosis, tubercle bacilli, animal inocu-
lation, q. v.), rontgenoscopy and rontgenography, and tuberculin tests.
These diseases are described more fully under Pleuritis and Perito-
nitis.
(d) Tuberculosis of the Joints
(Arthritis tuberculosa)
This was formerly known, especially in the knee, as "white swelling'
(tumor albus). The joints most frequently affected are the hip and the
knee, though the elbow, wrist, shoulder, or ankle may be involved. (See
also Part XL)
Tuberculosis of the Hip-Joint
(Coxitis tuberculosa)
A child complains of tiring easily, begins to limp on walking and to
complain of the leg hurting. On examination, the gluteal fold 011 the
affected side may be obliterated, and the musculature on that side some-
what atrophic. Sometimes the child complains more of the knee than of the
hip, but physical examination shows that the knee joint is normal. If the
child be undressed and laid upon a flat table, with both legs outstretched,
there is found to be lordosis of the lumbar spine, so that the hand can be
thrust underneath. If, next, the back be laid flat upon the table, the knee
on the affected side will be somewhat lifted, oAving to slight flexion of the
hip. Sometimes, along with this, there is abduction and lateral rotation,
sometimes adduction and medial rotation.
The movements of flexion, extension, adduction, abduction, and rota-
tion of the affected joint are limited. The child tries to use the lumbar
spine instead of the hip, keeping the hip rigid. He thus moves his pelvis
without his thigh. Such rigidity of the hip may be due either to muscle
spasm or to changes inside the joint itself (ankylosis). The earliest
movements to be limited are, as a rule, abduction and rotation. If one try
to abduct the lower extremity rather quickly, and this cause adductor
spasm, it is strong evidence of coxitis, even though movements in other
directions are normal.
In some instances, a cold abscess beneath the anterior superior iliac
DISEASES DUE TO BACILLI 271
spine is palpable. The inguinal lymph glands may be enlarged. There is
often tenderness on pressure on the anterior surface of the joint, just
below the middle of Poupart's ligament. If the knee be held stiff, a sudden
blow on the heel, shoving the femur upwards, or a blow over the trochanter,
may cause pain in the hip-joint.
Differential Diagnosis. — 1. From a non-tuberculous arthritis — more
acute onset, in the acute cases ; in the chronic cases, the older the patient,
the less probable tuberculosis ; x-ray examinations are often decisive.
2. In the painful stage, from coxa vara — Jimping due to shortening,
not to pain ; foot strongly rotated lateralward ; high position of trochanter ;
rontgenogram.
3. From congenital luxation of hip — shortening of spinomalleolar
distance ; abnormal mobility of thigh ; high position of trochanter ; head of
femur palpable near trochanter ; lumbar lordosis ; rontgenogram.
4. From diseases independent of the hip-joint — old abscess from spon-
dylitis ; peri nephritic abscess ; appendiceal abscess ; hy drops of iliac bursa ;
sciatica; hysteria.
In any of these, there may be a flexion-contracture of the hip, or pains
in the region of the hip, with painful limping.
ii. Tuberculosis of the Knee-Joint
( White Swelling, Tumor albus, Gonitis tuberculosa)
(a) Simple Effusion. — This is most common in children, in whom it is
the commonest form of serous gonitis. From the beginning the capsule is
thickened at the upper recess of the joint and over the two condyles of the
femur, and the joint always feels hot, even when the disease has lasted for
months. Movements of the joint may be only slightly, if at all, limited,
and muscular atrophy comes late.
DIFFERENTIAL DIAGNOSIS. — In the differential diagnosis, we must dis-
tinguish it: (1) from chronic infectious arthritis (periarticular) ; (2)
from congenital lues (choroiditis, teeth, Wassermann) ; (3) from hemoph-
illc joint (blood on aspiration, typical rontgenogram, family of bleeders).
(1)) Fungous Gonitis. — In this form, the capsule is diffusely thickened.
In the differential diagnosis we must consider (1) luetic arthritis, (2)
sarcoma, and (3) lipoma arborescens.
(e) Tuberculosis of the Bones (Caries)
The process begins in the bone-marrow. The bones most' frequently
affected are (1) those of the spine, (2) the bones of the pelvis; but other
bwif'N Cos calcis, humerus, jaw, femur, ribs, skull, sternum, tibia) may be
affected.
272
DIAGNOSIS OF INFECTIOUS DISEASES
I
i. Spondylitis tuberculosa (Caries of the Spine)
In caries of the spine, or Pott's disease of the spine (spondylitis tuber-
culosa), the diagnosis is easy when the vertebra has softened enough to give
rise to a projecting angle or gibbus. One has, then, only to look at the
back to make a diagnosis, as the angular bend of the spondylitic kyphosis is
very characteristic. If a projecting portion of the spine involve more than
one spinous process, we think of
rachitic deformity rather than of
tuberculosis. Ordinary scoliosis
and kyphoscoliosis are easily dis-
tinguishable.
In adults, there may be no gib-
bus and no cold abscess. Some-
times the diagnosis can be made
in a child before a gibbus or a cold
abscess has appeared (stiffness of
the spine, crying when lifted from
the bed, x-ray examination, tuber-
culin test).
In adultSy pain referred to the
umbilical region, to the back of the
neck, or along the sciatic nerve, or
a pain in the back on descending
stairs, or on hitting the boot against
a stone in the street, should make
one think of spondylitis. In be-
ginning spondylitis of the cervical
spine, a sudden movement of the
head may cause pain in the lower
extremities.
On examining the movements
of the spine, the patient should al-
ways be wholly undressed. Flex-
ion, extension, and the lateral Fig>
movements of the spine should be
tested.
Pressure in the long axis may cause pain,
upon the individual spines of the vertabrae
though this is not usually found.
The application of a hot sponge over the individual spines may cause
pain in the affected area.
In looking for cold abscess., which sooner or later appears in 25 per
cent to 50 per cent of the cases, and may be the first tangible symptom, we
examine the following localities: (1) posterior pharyngeal wall, (2) the
82. — Caries of Spine. (Pott's Disease.)
Note the Gibbus in the Thoracic Spine.
(Med. Service, J. H. II.)
Pressure with the thumb
may elicit a tender spot,
DISEASES DUE TO BACILLI 273
side of the neck, (3) axilla and infraclavicular fossa, (4) the back, (5)
between the last rib and the crest of the ilium in the lumbar region, (6)
above and below Poupart's ligament (psoas abscess), (7) beneath the
muscles of the buttock, (8) in the iliac fossa (iliac abscess), (9) in the
perineum, and (10) in the mediastinum.
Differential Diagnosis of Cold Abscess. — Such cold abscesses must be
differentiated: in the cervical region, from (1) lipomata, (2) bronchial
cysts, (3) esophageal diverticula, and (4) strumata; in the lumbar region,
from (1) lipomata, (2) lumbar hernia, and (3) perinephritic abscess;
in the iliac fossa, from (1) ileocecal tumors, (2) appendiceal abscess, (3)
abscess from osteomyelitis, and (4) parametritis ; in the inguinal region,
from (1) hernias, (2) hydroceleof the spermatic cord, and (3) hygroma of
the subiliac bursa; in the perineum, from (1) dermoid cysts, and (2) peri-
proctitic abscess.
The origin of a cold abscess with fistula formation can often be traced
by Beck's method (rontgenogram after injection with vaselin containing
20 per cent bismuth carbonate, or 30 per cent zirconium oxide [Caution !] ).
The differential diagnosis from non-tuberculous spondylitis is usually
easy by means of the constitutional symptoms, the x-ray, and immunological
tests.
(f) Tuberculosis of the Skin
Clinically, this may assume any one of several different forms, the
etiological unity of which is shown by the demonstration of the tubercle
bacilli in the lesions by microscopical examination, culture or animal
experiment, by the histological structure, and by focal reactions on injection
of old tuberculin. Whether or not there are also skin lesions due only to
the toxins of bacilli (so-called tuberculides) is still disputed. The forms of
skin disease absolutely established as local lesions due to the tubercle bacilli
are (1) lupus vulgar is, (2) scrofuloderma, and (3) ulcerative acute mil-
iary tuberculosis of the skin (tuberculosis cutis propria). It seems prob-
able that (4) lichen scrofulosorum (tuberculosis maculo-papulosa aggre-
gata) belongs hore also.
Tuberculosis of the skin may be primary or secondary to tuberculosfs
of internal organs.
i. Lupus vulgaris
Definition. — A chronic form of tuberculosis of the skin, characterized
by a peculiar primary efflorescence known as the lupus nodule.
Symptoms. — A lupus nodule is a conglomerate of miliary tubercles,
appearing as a sharply circumscribed, transparent, yellowish or brownish-
red maeule, varying in size from the head of a pin to a pea, which
does not disappear when pressed upon by a glass slide but becomes even
more distinct. Such spots may be the only sign at the beginning (lupus
274 DIAGNOSIS OF INFECTIOUS DISEASES
maculosus) ; later, the epidermis on the surface may desquamate (lupus
exfolialivus). Later still, there may be irregular central scarring (lupus
serpiginosus) . Sometimes the infiltration rises above the level of the skin/
and flat brownish-red thickenings appear (lupus tuberosus). If there be
marked proliferation of the connective tissue beneath, tumor-like nodules
arise (lupus hypertrophicus). Lupus most often attacks the face (nose,
cheeks, upper lip). If the neck, trunk, and extremities are affected, a ser-
piginous lupus is usually seen. In the hand, whole phalanges may be lost
in the older cases (lupus mutilans), as in leprosy. Occasionally, the
mucous membranes are attacked.
The disease begins usually in childhood, is extremely chronic, 'and
shows periods of improvement followed by exacerbation.
ii. Scrofuloderma
Definition. — A tuberculosis of the skin, beginning in the subcutaneous
layers, or in the deeper layer of the cutis.
Symptoms. — Two forms are met with, one giving the impression of a
direct infection of the skin from without or through the blood, the other
secondary (by extension) from tuberculosis of bones, lymph vessels and
glands. It is a disease of youth. The course is chronic and painless.
Differential Diagnosis. — It is distinguished (1) from acute inflamma-
tory processes (furuncles) by its chronicity and its painlessness ; (2) from
gumma (therapeutic test, Wassermann reaction, negative local reaction
to old tuberculin, no tubercle bacilli in tissues on histological exami-
nation).
iii. Ulcerative Miliary Tuberculosis of the Skin
This is a rare condition, seen in connection with advanced tuberculosis
of the internal organs; it appears usually around one of the orifices
(mouth, nose, anus) as shallow, granulating, painful ulcers, in which,
often, miliary tubercles are visible. It may be mistaken for soft chancre,
or for syphilitic ulcer. The disease appears to be due to auto-inoculation
from the neighboring orifice.
iv. Lichen scrofulosum
This also is a rare disease met with in children who suffer from tuber-
culosis of the lymph glands, bones, or cornea. The disease presents itself in
the form of minute nodules, the size of a hemp-seed, arranged in groups,
or in circles. They are of a pale yellow, or brownish-red, color, and early
show superficial desquamation. The trunk is most often affected (sacral
region, lateral wall of thorax) ; occasionally, the face or the extremities
may be involved.
DISEASES DUE TO BACILLI 275
The course is chronic. Tubercle bacilli have been demonstrated in the
lesions microscopically and by animal inoculation. There are no sub-
jective symptoms.
The disease must not be confused (1) with lichen pilaris (no grouping,
extensor surfaces), (2) with lichen ruber, or (3) with lichen syphiliticus
(Wassermann test).
(</) Tuberculosis of the Urogenital System
Any one of the urogenital organs in the male or female may be affected.
After one organ is infected, others frequently become involved by exten-
sion, and in late stages it may be difficult to determine the primary site.
Acid-fast bacilli in the urinary sediment (when urine has been drawn
by catheter to avoid the smegma bacillus) give positive evidence of infec-
tion. If infection be suspected and the bacilli are not discoverable micro-
scopically, inoculation of guinea-pigs should be resorted to.
Chronic Renal Tuberculosis (Phthisis renum). — The infection is of
hematogenous origin in 90 per cent of the cases (George Walker). Clini-
cally the signs are those of pyelonephritis. The urine contains albumin
and pus, sometimes blood and tissue shreds, elastic fibers, and tubercle ba-
cilli, and there usually is fever and emaciation. In urethral tuberculosis,
the thickened urethra can sometimes be felt through the rectum, or in
women through the vagina. Catheterization of the ureters should be done,
to see whether both sides are affected, or only one. In renal tuberculosis,
bladder tenesmus may be most troublesome, and frequency of urination is
an early and constant symptom. Dull aching pain in the lumbar region is
frequently complained of and a tender enlarged kidney may be palpable.
Hematuria frequently occurs, and x-ray examinations may show irregular
enlargement of the kidney. (See also Part X.)
Tuberculosis of the bladder, prostate, seminal vesicles and testes is compara-
tively rare, though tuberculous epididymilis is fairly common.
Tuberculosis of the Fallopian Tubes (Salpingitis tuberculosa) . — This
is a common disease in women, usually bilateral. The masses are easily
felt on bimanual palpation, especially under an anesthetic. The differen-
tial diagnosis must be made from gonorrheal salpingitis and from t'ubal
pregnancy.
Tuberculosis of the ovary and uterus are rare.
Tuberculosis of the placenta in pregnant women is not uncommon when pul-
monary tuberculosis exists.
Tuberculosis of the mammary gland sometimes occurs at the menopause and
later, in women. There is irregular induration, sometimes retraction of the nipple,
and frequently ulcers and fistulae, following cold abscess. The course is chronic.
The axillary glands are enlarged.
276 DIAGNOSIS OF INFECTIOUS DISEASES
(h) Tuberculosis of the Meninges (Meningitis tuberculosa)
This disease occurs most often in children (2-5 years), but is not infre-
quent in young adults.
Symptoms. — The onset is insidious, often following a period of poor
health, or an attack of measles, or whooping-cough. The child emaciates,
looks badly, seems apathetic, suffers from constipation, and is restless in its
sleep. Later the temperature begins to rise, and there is vomiting. The
pulse is slow and irregular (though often very rapid at onset). After com-
plaining of pain in the head for a variable period, the child becomes dull,
sleepy, delirious, often gritting its teeth in its sleep. The neck becomes
rigid, there is often general hypertonicity of the muscles; and there is gen-
Fig. 83.— Tuberculous Meningitis. Universal Tonic Spasm ; Automatic Movements of the Left
Half of the Body; Scaphoid Abdomen; Extreme Emaciation. (After J. Ibrahim, in E.
Feer's "Lehrb. d. Kinderheilkunde," published by G. Fischer, Jena.)
eral cutaneous hyperesthesia (period of irritation). The pupils mav be
unequal and sluggish in reaction; choked disk is common. Boat-shaped
retraction of the abdomen is an important sign.'
In the paralytic stage, the child becomes comatose, the pupils are
dilated ; facial paralysis, eye muscle paralysis, or hemiplegia may develop.
The pulse becomes rapid; Cheyne-Stokes breathing may appear. Leuko-
cytosis is not uncommon. Death in convulsions commonly occurs in the
third week. In the more chronic cases of the disease, convulsions may or
may not be present. (For a further description, see Diagnosis of Diseases
of the Nervous System. )
Diagnosis. — Tuberculous (bacillary) meningitis should always be
thought of when a child predisposed to tuberculosis (heredity, scrofula,
preceding attack of whooping-cough, or measles) becomes apathetic, vomits
without apparent cause, and develops a slow, irregular pulse. Whenever
the disease is suspected, lumbar puncture should be done. A turbid fluid
under heightened pressure, with increased lymphocytes rather than poly-
.morphonuclear leukocytes, speaks for tuberculous meningitis, (See Exaini-
DISEASES DUE TO BACILLI 277
nation of Cerebrospinal Fluid.) On careful' search, tubercle bacilli can
usually be demonstrated in the fluid, either by staining a smear of the
fibrin-film that frequently forms on standing, or by animal inoculation
(J. Hemenway). Sometimes the cerebrospinal fluid is clear in tubercu-
lous meningitis, and still tubercle bacilli may be demonstrable in it.
Differential Diagnosis. — (1) From epidemic cerebrospinal meningitis
— polymorphonuclear cells and meiiingococci in spinal fluid ; sudden onset ;
(2) from typhoid fever with meningismus — blood culture; lumbar punc-
ture; (3) from uremia — urinary examination; phenolsulphonephthalein
test ; lumbar puncture.
(i) Acute General Miliary Tuberculosis
Definition. — A disease due to the sudden overwhelming of the blood witli
tubercle bacilli, with formation of innumerable miliary tubercles in the
organs. The bacilli enter the blood through an eroded vein, or through
the thoracic duct (caseous lymph gland; caseous pulmonary tuberculosis).
More rarely, miliary tuberculosis follows tuberculosis of the intestine and
mesenteric lymph glands, of the medulla of the adrenal, or of the genito-
urinary system.
Symptoms. — Jhese are partly due to the multiple tubercles in the
organs, partly to the toxins of the tubercle bacilli.
Three principal types are distinguished: (l)'the typhoid form; (2)
the meningeal form, and (3) the pulmonary form.
(1) The Typhoid Form.— Here the toxic effect dominates the clinical
picture. The onset is often acute, with chill, vomiting, and high fever,
which may be continuous or slightly remittent. In addition, one sees
tachycardia, tachypnea, cyanosis or pallor, delirium, often splenic tumor,
meteorism, and diarrhea; occasionally rose spots and sometimes herpes.
Death usually occurs in the third week, in coma. The absence of the B.
typhosus in the blood culture, the small rapid pulse, the cyanosis, and the
tachypnea distinguish it from typhoid. Sometimes a focus of tuberculosis
is demonstrable in the body, and occasionally the bacilli are demonstrable
in the blood by the \method of Jessen and Rabinowicz.
These authors draw 5-10 c.c. of blood into an equal amount of 2.5 per cent
citric acid. The mixture is carefully shaken, avoiding foam formation, allowed
to stand in the ice-box for several hours, and then thoroughly centrifugalized.
Smears are made from the sediment and stained for tubercle bacilli.
I have often looked for tubercles in the choroid, a much vaunted
pathognomonic sign, but in my experience it is not easy to find them.
(2) Meningeal Form. — Here the symptoms are largely due to the
metastatic infection of the meninges and of the brain. The signs are
those of tuberculous meningitis (q. v.).
278 DIAGNOSIS OF INFECTIOUS DISEASES
(3) Pulmonary Form.— If the symptoms of toxin effect, or of menin-
geal infection, be not marked, the patient's appearance may call attention
rather to the pulmonary disturbances. The principal symptoms then are
fever, cough, pain in the chest, tachycardia and tachypnea, cyanosis, signs
of a diffuse general bronchitis in the lungs, or a wide-spread bronchopneu-
monia ; occasionally, there is blood-tinged sputum. Death occurs in from 3
to 5 weeks, the approach to death resembling that in acute bronchopneu-
monia".
Differential Diagnosis of Miliary Tuberculosis. — Besides excluding (1)
typhoid fever, (2) epidemic cerebrospinal meningitis, (3) bronchopneu-
monia, and (4) pneumonia of pyogenic origin, the following diseases
should be ruled out: (5) septicemia, especially in the puerperal period
(blood culture, leukocytosis) ; and (6) malaria (parasites; temperature
curve; therapy).
Occasionally miliary tuberculosis is combined with typhoid fever, or
with sepsis, in which event the elect may be deceived.
The tuberculin reactions are rarely of any assistance in the diagnosis of
these acute types of tuberculosis. (See Tuberculin Reactions.)
Some of the Factors Influencing the Course of Tuberculosis
We shall now discuss some of the factors 'influencing the course of tuberculosis,
referring briefly to the relations of tuberculosis (1) to pregnancy, (2) to mar-
riage, and (3) to the use of alcohol.
Tuberculosis and Pregnancy. — The unfavorable influence of pregnancy upon
the course of tuberculosis has long been recognized, though now and then one
hears a report of a favorable influence being exerted. Thanks to the studies of
Rosthorn and Fraenkel, we have data concerning this point derived from exact
observation of a large number of cases. These authors assert that, in apical
processes that are not very extensive, or in cirrhotic processes in the lungs,
whether accompanied by fever and emaciation or not, provided other complica-
tions are absent, there is no indication for the interruption of pregnancy. In
such cases, a waiting attitude should be assumed, the tuberculous process in the
lung being closely watched and the patient, of course, being given every hygienic
and dietetic advantage. In case, despite careful treatment, there should be no
improvement in the condition, no increase in the body weight or diminution of the
fever, the question of interruption of the pregnancy, even in apparently mild
cases, may be considered.
In patients in whom the tuberculous process is progressive, and especially
when it is florid, with signs of high fever, rapid emaciation, and complications,
especially if there be tuberculosis of the larynx, the interruption of pregnancy is
distinctly indicated.
Artificial abortion, if it is to be done, should be carried out as early as possible,
after which it may sometimes be possible to arrest the tuberculous process.
Every tuberculous woman who becomes pregnant should be kept under the
strictest medical supervision, for if pregnancy is to be interrupted it should be
done early in its course. Interruption of an advanced pregnancy is a serious
matter and may be even as dangerous for the tuberculous woman as to allow the
pregnancy to proceed to its natural termination.
DISEASES DUE TO BACILLI 279
Laryngologists and obstetricians have frequently emphasized the important rela-
tions existing between pregnancy and laryngeal^phthisis ; the majority agree that
tuberculosis of the larynx is a definite indication for artificial abortion (Kuttner),
though Rosthorn suggests that no general rule be set up, each case being rather
considered and solved for itself. There can be no doubt that laryngeal tuberculosis,
even in its early stages, is a highly dangerous complication in pregnancy, since
even a mild, and otherwise relatively benign, tuberculous process in the larynx
may, under the influence of pregnancy, assume a malignant and progressive char-
acter (Glas and Kraus). The symptoms rapidly increase, owing to the increased
burden thrown upon the body as a whole, and to the interference with respiration,
due to the high position of the diaphragm. The air exchange in the lungs and
the expectoration are interfered with; everything that favors the extension of a
pulmonary tuberculosis also exercises a deleterious influence upon the laryngeal
tuberculosis.
Any pregnant woman who complains of hoarseness, or of difficulty in swallow-
ing, should be examined by a laryngological specialist, and be kept under close
observation, in order that any exacerbation of the local process may be recognized
as soon as possible.
Tuberculosis and Marriage. — Conjugal tuberculosis is, as is well known, quite
common ; it is stated, variably, to exist in from 3.4 per cent to 39 per cent of the
cases, the different statistics depending probably upon the difference in social
classes studied. Of the two partners, it is the healthy wife who is the more
endangered, since she, in caring for a sick husband, is more closely tied to the
house than the husband who, having a sick wife, continues his work outside and
leaves the care of her to others.
Both pulmonary and urogenital tuberculosis are common in conjugal tuber-
culosis, the urogenital tuberculosis being usually secondary to a primary pulmonary
or to peritoneal tuberculosis, though it may sometimes be primary (q. v.).
The family practitioner has often to decide the question of marriage for a
tuberculous person. No absolute rule dare be laid down; each single case must
be considered for itself, and the decision entails a heavy responsibility. Per-
sons suffering from fresh, progressive, tuberculous changes certainly should not
marry, no matter how slight the process is; only after the condition has become
stationary and the general state favorable, and after a period of at least three
years has elapsed since the beginning of the disease, dare we, except in very
unusual instances, consent to a marriage. Several other factors have to be borne
in mind: First, whether it is a love-match, or a manage de convenance; if the
former be forbidden, the depressing mental effect will be greater than in the
latter instance, while permission to marry when a suitable condition has been
reached may be a strong spur to the patient to do everything possible for recovery.
Again, the age of the patient should be considered; the younger the patient, the
more prone is the tuberculous process to revival; moreover, excesses coincident to
marriage and the bearing of children are less likely to occur in older persons1
than in the young.
Certainly no marriage should be contracted by a tuberculous person unless the
healthy prospective partner has been previously fully informed regarding the
infection in the other, and its dangers as well as the necessary modifications of
life have been discussed.
Pecuniary circumstances have also to be considered. Among people of means
who can command the best hygienic and dietetic conditions and who will not be
compelled to engage in the struggle for existence, marriage may be permitted,
when in opposite conditions it might be highly dangerous.
The question as to whether the marriage of two persons who are both tuber-
280 DIAGNOSIS OF INFECTIOUS DISEASES
culous may be permitted, sometimes comes up. Obviously, should such a marrinirc
take place, an agreement to a childless marriage should be arrived at beforehand.
From a eugenic standpoint, it would seem wrong to burden offspring with a
double tuberculous heredity.
Alcoholism and Tuberculosis. — The question as to whether alcohol plays any
role in the origin of tuberculosis has been much discussed. Statistical studies
indicate that it plays no important part; thus females are seldom the subject
of alcoholism, according to statistics 16 times less than men, but tuberculosis is
half as common in women as in men; moreover, many human beings sicken of
tuberculosis at a period in life in which alcoholism plays no part (lymph gland
tuberculosis in children). In as far as alcoholism leads to poverty, and to bad
hygienic, dietetic and social conditions, it can of course contribute to the causa-
tion of tuberculosis.
The question as to whether the tuberculous patient shall, or shall not, use
alcohol as a therapeutic agent, as a food, or as a luxury, has also been much
discussed. Here again, the answer must be an individual, not a general one.
Moderate amounts of alcohol seem to be no more harmful to tuberculous persons
than to healthy people. Highly nervous people, or those who have a tendency
to hemoptysis, should, of course, avoid alcohol. As a remedial agent, alcohol
sometimes finds a place in tuberculosis as a stimulant, just as in other infectious
diseases. It is also used by many physicians for patients who suffer from night
sweats, or who have much fever. Finally, the pleasurable effects of a glass of
wine, or of other substances containing alcohol, in moderation, may be argued as
an advantage; especially in patients with a tendency to emaciation, the property
of alcohol as a protein-sparer and fat-sparer is emphasized by many authorities.
Sometimes, a patient who suffers from anorexia may eat better if a little wine,
or beer, be given with his food. Certainly, all excess is to be avoided. There are
many physicians who believe that alcohol should be strictly prohibited in tuber-
culosis and in all other diseases; it is not my purpose, however, to enter here
upon a discussion of the advisability of total abstinence.
i. General Remarks on the Early Diagnosis of Pulmonary Tuberculosis in Adults
The general practitioner must depend, in the first place, upon the time-
honored methods of examination, though in doubtful cases he may call
upon accessory aids. The anamnesis is of very great importance, special
attention being paid to the family history, the history of previous disease,
the social and hygienic conditions under which the patient has lived, and
the opportunities for contact-infection.
On inspection, the general "size-up" of the patient is important, though,
in making an early diagnosis, it must be remembered that persons in
apparently blooming health and of robust constitution may have the dis-
ease. It is, of course, much more common in people with the habitus
phthisicus (see above). The thorax should be examined for stenosis of the
superior aperture (W. A. Freund), due to calcification of the first costal
cartilage. Delayed expansion at one apex on inspiration or a retraction as
the result of a pleuritic exudate will also be manifest on inspection.
On palpation, the state of tension of the tissues in the supraclavicular
and supraspinous fossae on both sides should be tested, since, as Diinges has
DISEASES DUE TO BACILLI 281
pointed out, a diminished tonus points to a beginning retraction on that
side.
The more important findings are to be made out on percussion- and on
auscultation, especially the latter. We cannot expect changes in the per-
cussion note before the lesion has reached a certain grade. The infiltration
must involve an area measuring 4-6 cm. by 2 cm. to cause dullness on per-
cussion. I am inclined not to lay much weight on very slight differences in
the percussion note at the two apices, since those who have most experience
in the early diagnosis of tuberculosis may be in error regarding the signifi-
cance of a slight apical dullness (L. Hamman). Still, careful percussion
of the apices should be undertaken, and we pay attention not only to the
sound produced, but also to the resistance felt by the pleximeter finger. It
is well to compare also the note on percussion on both sides at the end of
inspiration and at the end of expiration. The first percussion signs of
infiltration are (1) a shortening of the percussion sound, and (2) an
enfeeblemcnt of the normal lung resonance. Only later, when the infiltra-
tion has become more marked, or the pleura thickened, can we expect to
find dullness or flatness.
It has long been known that the right apex may occupy a little lower
position than the left, even in entirely healthy people, and that, in pa-
tients with chronic nasal obstruction, there may be a non-tuberculous col-
lapse-induration of the right apex (Baumann). Aside from this, a depres-
sion of the upper limit of lung resonance points to infiltration or retraction.
Normally, the lung resonance should extend for from 3-5 cm. above the
clavicle, and behind to the level of the 7th cervical spine.
The exact determination of the lower lung limits is also important,
since, in most cases of incipient phthisis, the diaphragm on the affected
side moves sluggishly or not at all during respiration, owing to diffuse
adhesions of the costal pleura with the diaphragmatic pleura. Rontgeno-
scopy is a help here.
On auscultation, change, in the breath sounds, especially a roughening
or a weakening of inspiration, or a prolonged and roughened expiration at
one apex, is very suggestive of a tuberculous process, especially if these
findings be confirmed on repeated comparative auscultation of both
apices.
The presence of rales at one opex, especially after coughing, is a most
important auscultatory sign. Such rales may be present even when the
breath sounds are as yet unaltered. Their presence, on repeated examina-
tions, is pathognomonic for "apex catarrh."
At first, these rales consist of a few fine crackles, or crepitations.
Later, coarser rales may be heard, and when infiltration has begun, they
become consonating. As soon as the infiltration has reached a certain
grade, the breathing loses its vesicular character and becomes bronchial.
In older persons, a pulmonary tuberculosis may be masked by an asthma or
282 DIAGNOSIS OF INFECTIOUS DISEASES
by an emphysema and then the diagnosis is hard to make, on account of
the rarity of the association of tuberculosis with these conditions.
The vocal resonance is increased over infiltrated areas and especially
over cavities, but enfeebled behind pleuritic exudates. Increased vocal
resonance may appear at a period before auscultation of the breath sounds
or percussion can demonstrate an infiltration. Later on, as the process
advances, the voice sounds may diminish in intensity.
A circumscribed pleurisy with friction rub may be the first sign of
early tuberculosis, especially in the upper lateral regions of the thorax.
It is unusual to find beginning tuberculosis associated with arterial
hypertension. Usually, the blood pressure is lower than normal in tuber-
culous patients.
Among the conditions suggestive of a nearly latent, or larvate, form of
tuberculosis may be mentioned: (1) a chlorotic blood state with the
symptoms of chlorosis, (2) unexplained digestive disturbances (anorexia,
acid eructations, meteorism, hyperacidity, atony), (3) neurasthenic states,
(4) unexplained pleurisy, especially of insidious type, with recurrences,
(5) loss of weight, and (G) low fever. In the so-called active-latent form
of early tuberculosis the cardinal symptoms are fever, emaciation and
sweats.
In all the forms of early tuberculosis mentioned above, the oplithalmo-
tuberculin reaction is a great help in arriving at a decision.
In pulmonary tuberculosis with demonstrable local lesion, the diag-
nosis is easier. The patients now have cough, dyspnea, pains in the chest,
and sometimes hemoptysis.
The coiujh may be a "dry cough/' characterized by its short, non-
resonant sound and by the absence of sputum, and of rales; it is usually
worse at night. In another form of cough, there is associated vomiting of
unaltered food. These two forms of cough are sometimes supposed to be
"nervous cough." The patients are often hoarse. In a third form of
cough, the so-called "catarrhal cough/' there is mucous expectoration, some-
times tinged with blood.
Not so much stress can be laid upon dyspnea, or upon pains in the
chest, as signs of tuberculosis, since they occur in the most different varie-
ties of intrathoracic disease.
Hemoptysis may be the first symptom of incipient pulmonary tubercu-
losis, and it may recur at different stages of the. process. Hemoptysis
alone does not permit of the diagnosis of pulmonary tuberculosis, however,
since it may occur in bronchiectasis, in neoplasm, in lung syphilis, in
cardiac disease, in aortic aneurism, in throat affections, in vicarious men-
struation, etc. ; but if hemoptysis be associated with other signs of tuber-
culosis, or occur in persons with the habitus phthisicus, or with a tuber-
culous family history, it speaks strongly in favor of a tuberculous infection.
It may or may not be associated with fever.
DISEASES DUE TO BACILLI 283
Whenever there is any sputum in a patient with signs suggestive of
tuberculosis, it should be repeatedly examined by the Ziehl-Neelsen method
for tubercle bacilli. If persistently negative by this method, it may be
examined by the antiformin method, or be sent to a laboratory with the
request that a guinea-pig be inoculated.
ii. General Remarks on the Early Diagnosis of Tuberculosis in Children
Von Behring (1903) believed that the pulmonary tuberculosis of
adults is simply "the end of a song which was sung by a candidate for
tuberculosis when in the cradle." In other words, he believes that tubercu-
lous infection occurs during the suckling period, through milk.
The introduction of von Pirquet's test and of the ophthalmo-reaction
for the study of tuberculosis in children has, as a matter of fact, opened
our eyes to the frequency of childhood infection, and the clinical findings
have been confirmed by the pathological anatomists.
At present, the supporters of two views are fighting for ascendency
regarding the mode of infection: (1) that of aerogenous infection and
(2) that of enterogenous or alimentary infection. While congenital in-
fection may occur, it is now generally considered that it plays but little,
if any, role in the origin of human tuberculosis.
There can be no doubt that children become infected from some human
being (phthisical father, mother, sib, servant, playmate, neighbor) who
distributes bacilli in their neighborhood. The younger the child, the
greater the danger of infection ; hence, in taking the family history, it is
very important to inquire into the associates of the infant up to the time it
was two years old (Hamburger). After infancy, the child may be exposed
at the kindergarten or 'in the schools.
Judging by tuberculin tests of children between 7 and 10 years of age,
64 per cent yield a positive reaction; between 11 and 14 years, 77 per
cent. It seems therefore probable that the majority of children, especially
among the poor, are infected with tuberculosis, though not sick with tu-
berculosis. According to Naegeli, 97 per cent of the individuals coming
to autopsy in Zurich show the signs of a healed tuberculosis. In other
words, practically every human being is at some time or another infected
with tuberculosis.
It would seem that the disposition to tuberculous infection is very pro-
nounced in the suckling period, and less pronounced later on.
It goes without saying that material and social factors are of great
importance in diminishing, or in increasing the disposition to tuberculosis ;
children who are abundantly nourished, and who live in favorable hygienic
surroundings, are far less predisposed to tuberculosis than the poor.
Of the diseases of childhood which increase the disposition to tubercu-
lous disease, measles and whooping-cough occupy the first place.
284 DIAGNOSIS OF INFECTIOUS DISEASES
Children with exudative diathesis (Czerny) possess a peculiar predis-
position to scrofulosis or tuberculosis of the lymph glands.
The course of tuberculosis in children varies much in different in-
stances, depending (1) upon disposition, as above discussed, (2) on the
grade of infection, and (3) on the age of the child. The differences in the
manifestations of the disease in children from those in adults is explained
by the lower capacity for resistance in the infantile. organism, the tissues
having very little tendency to localize or to heal tuberculous processes. It
is therefore common to find a generalization of the process in young
children. The bacilli invade a whole series of organs (lymph glands,
spleen, kidney, liver, bones, etc.). The predilection site of infantile
tuberculosis is, however, the bronchial lymph glands, and it is thence that
the other organs, like the lungs, spleen, bones, joints and brain, most often
become infected. This is in marked contrast with what is met with in
adults, in whom the predilection site is the apex of one lung. As children
approach puberty, the tendency to the adult form of localization of the
tuberculous process begins to appear.
Rapid generalization of the tuberculous process with fatal termination
is characteristic of the first year of life (Engel). In children attacked at
this age, we observe a general nutritional disturbance, often otorrhea, ec-
zema of the head, swelling of the lymph glands, tuberculous abscesses in iho
subcutaneous tissue and in the lungs, signs of a diffuse bronchial catarrh,
or of bronchopneumonic foci in the lower lobes, with irregular fever and
digestive disturbances. Every practitioner has been surprised to see a
small child, apparently fairly healthy, suddenly attacked by a fatal tuber-
culous meningitis. During the suckling period, tuberculosis, once well
started, runs a stormy course, always terminating fatally, usually with a
picture of general miliary tuberculosis.
In older children, tuberculosis is less malign; there is less tendency to
generalization, and an increased tendency to localization in certain organs,
especially the bronchial lymph glands, the other lymph glands, the bones
and the joints.
Pathological-histological studies of tuberculosis in childhood indicate
that the tubercle bacilli^, on entrance, may or may not at once produce
tuberculous disease. In the latter case, it may remain latent, without
undergoing multiplication, at some spot in the body, and cause no signs of
disease (so-called lai'.ni stage). Later, under the influence of trauma or
of some infection (measles, whooping-cough, influenza), the latent tubercu-
losis is transformed into a manifest tuberculosis; the tuberculosis
spreads, (1) directly, by continuity, or (2) by carriage in secretions or
excretions, as when the bladder becomes tuberculous secondary to tubercu-
losis of the kidney, or (3) through the lymph channels, or the blood vessels.
When acute miliary tuberculosis appears in childhood it presents the
features of an acute infectious disease, usually beginning suddenly, with
DISEASES DUE TO BACILLI 285
quick rise of temperature, irregular pulse, dyspnea, cyanosis, usually dry
cough, enlargement of the spleen, and marked cerebral symptoms due to
miliary tubercles in the meiiinges. There may be no bacilli in the sputum
or in the urine ; sometimes bacilli will be found in the cerebrospinal fluid
on lumbar puncture, or, on ophthalmoscopic examination choroidal tu-
bercles may be visible. The disease is often confused with typhoid fever,
with cryptogenetio sepsis, with capillary bronchitis, or with influenza.
In the broncliial-gland tuberculosis of children, the onset of the disease
is usually insidious, with loss of appetite, pallor, emaciation, and slight
atypical pyrexia ; sometimes, the disease sets in acutely, with high fever
and rapid emaciation. In such cases, the absence of outspoken objective
signs elsewhere in the body should make one very suspicious of the
existence of bronchial-gland tuberculosis. Two symptoms are, however,
usually present to facilitate the diagnosis, namely: (1) a high-pitched
cough and (2) an expiratory dyspnea, both of which are the result of
a compression of the bronchi by the swollen glands. These, symptoms, will
often permit of a positive diagnosis, even at a stage when the children
are still well nourished. Sometimes the cough is more like that of
whooping-cough, in which case it is probably due to vagal irritation. A
tuberculin test, however, will often distinguish between whooping-cough
and tuberculosis.
The course of bronchial-gland tuberculosis varies much in different
cases. It may be benign, becoming stationary through encapsulation of the
focus and calcification of the glands. In malign cases, it extends from the
lymph glands through the lymph vessels or the blood vessels, and gives rise
to an acute general miliary tuberculosis. Sometimes a bronchial-gland
tuberculosis that has long been stationary (encapsulation, calcification)
is lighted up again by trauma, • measles, or whooping-cough, and gives
rise to an acute diffuse process. In the more advanced cases, rontgen-
ogniphy is very helpful in differential diagnosis, but it is desirable to make
the diagnosis at an earlier stage.
In early pulmonary tuberculosis in children,, the disease may take the
form either of tuberculous pneumonia, or of chronic ulcerative tuber-
culosis (phthisis).
Tnhcirulous pneumonia in children is usually secondary, represent-
ing an acute process following upon a disease previously chronic. The
clinical signs resemble those of a catarrhal, or of a lobar, pneumoifia,
which, however, is prolonged beyond the period characteristic of benign
forms of these discuses. The nature of the process may be entirely obscure
at first, but the existence of tuberculosis in the child, the family history,
the delayed resolution of the pneumonic process, and the presence of
tubercle bacilli in the sputum clear up the diagnosis.
('liraiiir ulcerative tuberculosis, like that of adults, is not very
common in children before puberty, though it may occasionally appear
286 DIAGNOSIS OF INFECTIOUS DISEASES
after the 4th or 5th year of life. At the beginning, the little patient
ceases to gain in weight, grows pale, emaciates, tires easily, and becomes
irritable and capricious. A morning cough appears, though there may
be no sputum at first. At the beginning the physical examination of the
lungs may be negative, though later on small foci of infiltration appear.
It is important to remember that in children with the signs of pulmonary
tuberculosis we must direct our attention to the lower lobes of the lungs
rather than to the apices ; though, as children approach the age of puberty,
the tendency to an apical localization becomes manifest, just as in adults.
As the disease advances, rontgenoscopy, and especially stereoscopic
rontgenography, afford important help in diagnosis. At this time outspoken
infiltrations become demonstrable, and, later on, cavity formation and the
signs of mixed infection with pyogenic cocci (hectic fever, profound ema-
ciation) are met with.
Among the complications of pulmonary tuberculosis in children, tuber-
culous pleuritis, laryngeal tuberculosis, and tuberculous -u I re ration of the
intestines are common, while hemoptysis is rare.
A systematic procedure should be followed for purposes 'of diagnosis
when one suspects a beginning pulmonary tuberculosis in childhood. The
regular routine should include: (1) a carefully taken anamnesis, (2)
repeated precise examinations of the lungs, (3) the keeping of a two-
hourly temperature chart for two weeks, (4) the keeping of a body-
wciglii, chart, (5) frequent examinations of the sputum (microscopically,
and by animal inoculation), (6) cautiously undertaken tuberculin tests
during afebrile periods, (7) stereoscopic rontgenogyaphy.
It is important, further, that the practitioner should be more or less
familiar with the local lesions of the skin that occur in tuberculosis
in childhood. These include (1) the tuberculids and (2) the scrofulids
( Hamburger, Escherich ) .
Among the TUBERCULIDS may be mentioned: (a) Gumma scrofulosorum, in
which there are indolent subcutaneous infiltrations of the skin of firm consistence,
varying in size from that of a hemp-seed to that of a small cherry, often showing
through the skin as bluish red nodules. They are sometimes attached to the skin
and may, after softening, break through to the outside. They are most common
in the lower extremities. In number, there may be only a single nodule taken by
the family to be a boil, but in furunculosis there are usually many nodules, whereas
a small number speaks in favor of gumma scrofulosorum. (b) Lichen scrofu-
losorum, with small lesions about the size of grains of wheat, or smaller, arranged in
groups ; they are of a bluish red color, or may be pale grayish white. They occur
most commonly on the lateral part of the trunk, (c) The tuberculids proper
include the papulosquamous and the papulonecrotic tuberculids. All these varieties
follow a very chronic course and, on account of the scanty number of the lesions,
must be sought for if they are to be observed.
Among the SCROFULIDS may be mentioned: (a) Phlyctenular conjunctivitis,
sometimes called conjunctival tuberculids. These are small, scarcely visible, grayish
white nodules in the conjunctiva. They are surrounded by a markedly hyperemic
DISEASES DUE TO BACILLI 287
zone. On superficial examination, the process may be taken to be a simple form
of conjunctivitis with photophobia, (b) Chronic blepharitis. (c) Scrofulous
rhinitis, (d) Thickening of the upper lip. (e) Moist eczema, (f) Catarrhal
inflammations of the throat, ear, air passages and digestive tract, (g) Multiple
indolent enlargements of the lymph glands.
In all these children with signs of scrofulosis, a positive tuberculin reaction can
be obtained. In other words, scrofulosis falls within the domain of tuberculosis.
One must differentiate these scrofulous lesions, especially those involving the
lymph glands, from (1) Pfeiffer's glandular fever, (2) Schick's postscarlatinal
lymphadenitis, and (3) lymph/adenoid leukemia and aleukemic lymphadenosis.
The diagnosis of tuberculous serositis and of tuberculous meningitis
is described elsewhere, as are the methods of using the tuberculin tests,
and of making x-ray examinations in tuberculosis of tlie lungs and of
the bronchial glands. Here, however, may be mentioned the contra-indi-
cations to a diagnostic tuberculin test'. (1) In cases in wrhich the clinical
diagnosis is clear, especially when tubercle bacilli are present in the
sputum or urine, a tuberculin test is superfluous. (2) In advanced in-
filtrative processes in the lung, a tuberculin test need not be made. (3)
In cases in which the mouth temperature is above 37° C., a tuberculin
test should not be made. (4) During hemoptysis, and for a short time
after, the test should be avoided. (5) In outspoken nephropathy, no
tuberculin test should be made. (6) In very neurotic patients, a positive
tuberculin test is of doubtful value, owing to the fact that such patients
often react with fever to a hypodermic injection even of water. (7) In
epileptic patients, a tuberculin test may call forth an attack. (8) In
suspected tuberculosis along with severe constitutional disease (diabetes
mellitus, typhoid fever, pneumonia) it is best to avoid a diagnostic tuber-
culin test.
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Czerny (A.}. Die exsudative Diathese. Jahrb.f. Kinderh., Berlin, 1905, Ixi, 199-221.
Exsudative Diathese, Skrophulose und Tuberculose. Jahrb. f. Kinderh.,
Berlin, 1909, n.F., Ixx, 6 29-538.
Engel. Die Pathologic der Kindertuberkulose. Beihefte z. med. Klin., Berlin, 1909, v,
233-260.
Escherich (T.). Was nennen wir Skrofulose? Wien. klin. Wchnschr., 1909, xxii, 224-228.
d'Espine (A.). Le diagnostic precoce de la tuberculose des ganglions bronchiques chez les
enfants. Bull. Acad. de med., Paris, 1907, 3 s., Ivii, 167-174.
Fraser (./.)• An experimental study of bone and joint tuberculosis. J. Exper. M., Lan-
caster, Pa., 1913, xvii, 3
Hamburger (F.). Allgemeine Pathologic und Diagnostik der Kindertuberkulose. Leip-
zig u. Wien, 1910, F. Deuticke. 153 p. 8°.
Hemenway (/.)• The constant presence of tubercle bacilli in the cerebrospinal fluid of
tuberculous meningitis, with observations on the cerebrospinal fluid in
other forms of acute meningitis. Am. J. Dis. Child., Chicago, 1911, i,
37-41.
DISEASES DUE TO BACILLI 291
Landis (H. R. M.) & Kaufmann (/.). The diagnosis of tuberculosis in early life. Am.
J. M. Sc., Philadelphia, 1914, cxlviii, 530-539.
v Pirquet (C.). Tuberculosis in childhood. In: Tuberculosis, etc. (Klebs). New York
& London, 1909. 141-148.
Priestley (J.). Tuberculosis during school life: its prevalence; the means of detection In-
ternal. Arch. f. Schulhyg., 1913, ix, 244-258.
Salge (#.). Skrofulose. In: Handb. d. Kinderheilk. (Pfaundler & Schlossmann). Leip-
zig. 2. Aufl., 1910, ii, 569-583. 1 pi.
Schlossmann (A.}. Tuberculosis. In: Diseases of children (Pfaundler & Schlossmann).
English translation. Philadelphia c£ London, 1908, ii, 568-611.
Shennan (T.). Tuberculosis in children, especially with reference to tuberculosis of lym-
phatic glands, and its importance in the invasion and dissemination of the
disease. Lancet, London, 1909, i, 315.-318.
Speder (E.) & Dubourg (E.}. L'adenopathie tracheo-bronchique latente chez V enfant.
Comparaison du radio diagnostic et du diagnostic clinique. Arch, d'electr.
med., Paris, 1914, xxii, 529-547.
Tileston (Wilder). Disseminated miliary tuberculosis of the skin. An important sign in
general miliary tuberculosis oj infancy. Arch. Int. Med., Chicago, 1909,
iv, 21-31.
Walker (G.}. Studies in the experimental production of tuberculosis in the genito-urinary
organs. Johns Hopkins Hosp. Rep., Baltimore, 1911, xvi, 1-222.
Weinberg (Wilhelm). Die Kinder der Tuberkulosen. Leipzig, 1913, S. Hirzel. 160 p.
7. Epidemiological; Statistical
Bardswell (Noel D.}. The expectation of life of the consumptive after sanatorium treatment.
Edinburgh, 1910, H. Frowde & H odder & Stoughton. 135 p. 8°.
Billings (J. S.), Jr. The registration and sanitary supervision of pulmonary tuberculosis in
New York City by the Department of Health. New York, 1912. 104 P-
8°. Monogr. senes No. 1.
The tuberculosis clinics and day camps of the Department of Health,
New York, 1912, Dep. Health. 123 p. 8°. Monogr. series No. 2.
Bulloch (William}. The problem of pulmonary tuberculosis considered from the stand-
point of infection. London, 1911, School Press. 19 p. 8°.
Carrington (Thomas Specs}. Fresh air and how to use it. New York, 1912, Nat. Ass.
Study & Prey. Tuberc. 250 p. Front. 8°.
Dispensary control of tuberculosis; fourth annual report of the Association of Tuberculosis
Clinics of the City of New York, 1911. [New York], 1911. 8°.
Elliott (J. H.}. TJic anti-tuberculosis movement in Canada. Brit. J. Tuberculosis, London,
1910, iv, 73-89.
Flick (Lawrence F.}. The crusade against tuberculosis. Consumption a curable and pre-
ventable disease. Philadelphia, 1903, D. McKay. 295 p. 12°.
Journal of the Outdoor Life. Published monthly at Adirondack Cottage Sanitarium,
1905-15, Saranac Lake, New York.
Lapham (Mary E.}. The prevention of tuberculosis from an economic standpoint. Inter-
state M. J., St. Louis, 1914, xxi, 463-469.
Field work in tuberculosis. J. Am. M. Ass., Chicago, 1914, Ixii,
122-125.
Latham (A.} & Garland (C. H.). The conquest of consumption; an economic study.
London, 1910. 8°.
National Association for the Study and Prevention of Tuberculosis. A tuberculosis directory
containing a list of institutions [etc.], in the United States and Canada.
Compiled by Philip P. Jacobs. New York, 1911. 331 p. 8°.
Newsholme (Arthur). The prevention of tuberculosis. London, 1908, Methuen & Co.
429 p. 3 pi. 8°.
292 DIAGNOSIS OF INFECTIOUS DISEASES
Pearson (Karl). A first study of the statistics of pulmonary tuberculosis. London, 1907. 4°-
Pope (E. G.}. A second study of the statistics of pulmonary tuberculosis: Marital infection.
Edited and revised by Karl Pearson, with an appendix on assortative mating
from data reduced by Ethel M. Elderton. London, 1908. 4°.
Thomson (Henry Hyslop). Consumption in general practice. London, 1912, H. Frowde
[etc.]. 350 p. 8°.
Trudeau (E. L.}. Sanitaria for the treatment of incipient tuberculosis. N. York M. J.,
1897, Ixv, 276-281.
United States. Department of Commerce and Labor. Bureau of the Census. Tuberculosis
in the United States. Washington [1909]. 8°.
Walters (F. Rufenacht}. Sanatoria for consumptives in various parts of the world (France,
Germany, Norway, Russia, Switzerland, the United States and the British
possessions). A critical and detailed description, together with an exposi-
tion of the open-air or hygienic treatment of phthisis. With an introduc-
tion by Sir Richard Douglas Powell. 3d ed. London, 1905, S. Sonnen-
schein & Co. 406 p. 69 pi. 8°.
Warren (B. S.)* Open-air schools for the prevention and cure of tuberculosis among children.
Washington, 1912. 8°.
Welcker (H.). Die Volkheilstdtten fur Lungenkranke in ihrer socialpolitischen Bedeutung.
Koln, 1895. 8°.
(For other references to tuberculosis, see Part IV, Tuberculin, and Part V, Pulmonary
Tuberculosis.)
19. Diseases Due to the Leprosy Bacillus
Leprosy Bacillus. — The Bacillus leprce (Hansen, 1872), studied care-
fully by Neisser (1879), is a slender, non-motile, acid-fast, rod, 4-6 ju,
long by 0.3-0.5 /* broad, present in enormous numbers inside the cells, or
within the lymph spaces of the lesion. Both ends of the bacilli are often
pointed. The bacilli show a strong tendency to grow in masses, in which
the individual bacilli are parallel to one another — so-called cigar-bundle
masses of bacilli — or glcea of Unna, or globl. Many of these lepra-globi
are bacillary thrombi in the lymph vessels. On staining by Gram's
method, each bacillus is seen to contain rows of granules (Lutz and Un-
na) ; they correspond to the Babes-Ernst granules of other bacteria. Many
of the granular forms will not stain at all in carbol-fuchsin, but are
beautifully demonstrable by Much's modification of the Gram stain.
Diphtherioid, partially acid-fast bacilli have occasionally been grown from
leprous lesions (Bordoni-Uffreduzzi, 1886; Babes, 1901; Duval; and Ked-
rowsky). According to Keitschewsky and Bierger (1913), complement-
fixation tests indicate that Kedrowsky's strain is identical with Hanson's
bacillus, and Duval's is not. Acid-fast streptothrix forms have been grown
from leprous lesions by several observers (G. Deycke, 1903; Williams,
1911; Bayon, 1912). Thus far, the actual proof of a causal relationship
between either the diphtherioid bacilli, or the streptothrix forms, has not
been brought forward. (Plate IV, Fig. 1.)
Experimental Leprosy. — Attempts to produce leprosy in experimental
animals have been made by many workers (Melcher and Ortmann, 1885;
DISEASES DUE TO BACILLI 293
Kedrowsky; Bayon; Nicolle; Much), but have not been satisfactory. At-
tempts to inoculate healthy human beings have also been made (Daniellsen
and Boeck), but have failed, except in the single instance of the criminal
Keanu, condemned to death in Hawaii, but pardoned on condition that he
would submit to inoculation of leprous material as a scientific experiment.
He was inoculated by Arning and two years later was manifestly leprous,
but as certain distant relatives were leprous, the case is not wholly free
from objection.
In infected human beings, leprosy bacilli are almost always present
in the nasal secretions ( Sticker) . They are sometimes present in the saliva,
in the sputum, in the milk, in the feces, and in the blood.
In about TO per cent of the cases of the tuberous form of leprosy, the
Wassermann reaction is positive (Meier), and complement fixation for
tuberculin is said to be positive in a very large percentage. Mollers (1913),
out of 32 sera, from 20 patients with tuberous, 8 with nervous, and 4 with
mixed lepra found complement-binding antibodies to tuberculin prepara-
tions in no less than 25. This probably points to a "group-reaction," due
to the biological relationships of the bacilli of leprosy and the bacilli of
tuberculosis.
(a) Human Leprosy (Lepra)
Epidemiology. — The disease is transferred directly from the patient to
other human beings, though the degree of contagiosity must be very low
and the possibility of an intermediate change in the virus has to be con-
sidered. Just how the transmission occurs is disputed. Close relation-
ship, as in families and sleeping in the same bed, or sexual intercourse,
seem to be responsible, and, recently, Honeij and Parker have shown that
a species of fly (Stomoxys calcitrans) may carry the bacillus. Insects, how-
ever, play no part in the actual transfer of the disease, as far as is known.
The anesthetic form is but little, if at all, contagious. The tuberous form
is the most dangerous, probably because the patients give off bacilli on
coughing, or through open wounds.
Congenital infection is exceedingly uncommon. The Commission of
the National Leprosy Fund in India collected 1,564 instances of leprous
parents who had 2,915 children, of whom only 75 had leprosy. Sand
(1910), in Norway, reported 512 leprous parents with 1,835 children,
of whom 1,710 (93.2 per cent) were healthy, and 125 (6.8 per cent) were
leprous. In 17 instances, both parents were leprous and had 55 children,
of whom 8 (i. e., 12.7 per cent) were leprous.
The disease is very widely distributed over the earth's surface. For-
tunately, the northern parts of America are relatively free from the
disease; autochthonous leprosy does not occur in Canada, nor in the
United States, except perhaps in Minnesota and in Louisiana. In Mexico,
Central America, and the West Indies, the disease is common; about 1 in
294 DIAGNOSIS OF INFECTIOUS DISEASES
every 1,000 of the population is affected. The countries in the northern
part of South America suffer still more. In Colombia there are over 4,000
lepers (Montaya y Florez) ; in British Guiana, 1 out of every 250 or 300
of the population has leprosy (Hillis; Deycke). Brazil and Argentina
are less affected; Chili is relatively free from the disease. The nodular
form is most common in countries in which the disease has been newly
introduced, the nervous form in countries in which the disease has long
existed. The disease is widespread in Asia, Africa, and certain parts
of Europe.
Symptoms. — The incubation period is very long, 3-5-10-20 years elaps-
ing after exposure before symptoms develop. In the early stages, sub-
jective disturbances of sensation (hyperesthesia, itching, formication) are
common; other early signs include falling out of the hair, dry rhinitis
with epistaxis, and hypersecretion of sweat and of sebum. The first visible
signs of general infection are skin lesions (maculae, vesicles, nodules).
The mucous membranes of the larynx and of the nose may be early in-
fected.
Three principal clinical forms are distinguished: (1) nodular, or tuber-
cular, leprosy (lepra nodosa), (2) nervous, or anesthetic, leprosy (le/>ra
nervorum), (3) mixed leprosy (lepra md.i-ta). There would seem to be
no good reason to set up a paralepra, analogous to paralues, as Zambaco
has attempted to do.
i. Lepra nodosa (Lepra tuberosa)
The characteristic nodules appear in the skin, usually on the extensor
surfaces of the extremities, sometimes symmetrically arranged; they are
not rare 011 the face and back. The color is at first carmine red; the
center gradually grows darker, becoming brown or brownish-red. The
hairs fall out and the skin becomes infiltrated. The face is usually involved
and ulcers and cicatrization follow, the face assuming a peculiar appearance
(fades Icon! itnt ), in which there is loss of skin pigment, and loss of the eye-
brows, eyelashes, and beard.
ii. Lepra nervorum
Here the sensory and trophic disturbances due to disease of the
peripheral nerves are most marked, but there are also leprous changes in
the skin, mucous membranes, and internal organs. The onset is insidious,
with erythemas and macular eruptions (symmetrical). There may be pains
or cutaneous hyperesthesia at first. The thickened nerves can be felt
through the skin in both lepra nodosa and lepra nervorum, especially the
nervus auricularis magnus in the neck. I palpated this nerve in a number
of lepers in the Philippine Islands and was surprised to find how fre-
quently it was thickened. The N. ulnaris is also often palpable, but since
DISEASES DUE TO BACILLI 295
this can often be felt in normal persons, palpation of this nerve is
less helpful in diagnosis. Islands of anesthesia develop; sometimes the
anesthesias are widespread.
On rontgenography, the trophic lesions in the bones, especially of the
Fig. 84.— Middle and Distal Phalanges of a Normal Finger Compared with Those of a Case
of Leprosy. Note in Diseased Finger Beginning Absorption of Bulbous Tip of the Distal
Phalanx, and an Associated Narrowing of Shaft. (After A. B. Herrick and T. W.
Earhart, Arch. Int. Med.)
fingers may be pronounced; in Tokio, in 1899, K. Miura showed me
interesting negatives illustrating these changes.
iii. Lepra mixta
Most cases of leprosy are more or less "mixed," but usually the nodular,
or nervous, lesions markedly predominate. In some cases, they appear in
about equal numbers.
Complications of Leprosy. — Pyogenic infections ; carcinoma.
Diagnosis. — If leprosy be suspected, the signs are usually so distinct, or
the bacilli can be so easily demonstrated in the lesions (carbol-fuchsin
method, or, better, Much's modification of Gram's method), that doubt
is soon dissipated. This is especially true of the tuberous form; the
296 DIAGNOSIS OF INFECTIOUS DISEASES
maculo-anesthetic form may give more difficulty. We should rule out
(1) syphilis, (2) lupus, (3) syringomyelia (Morvan type), (4) sclero-
derma, and (5) Raynaud's disease. (See the diagnosis of these diseases.)
References
Abraham (P. S.). Leprosy. In: Syst. Med. (Allbutt & Rolleston). 8°. London, 1910,
ii, pt. 2, 648-694-
Babes (V.). Die Lepra. Jn: NothnageVs Spezielle Pathologic und Therapie.. Wien, 1901,
A. Holder, xxiv, 1-338.
Brown (P. K.). The study of the blood in leprosy. Occidental M. Times, Sacramento,
1897 ', xi, 537-539.
Chapman (E. />.)• The etiology and treatment of leprosy. J. Am. M. Ass., Chicago, 1915,
Ixv, 934-939.
Deycke (G.). Die Lepra. In: Spez. Path. u. Therap. inner. Krankh. (Kraus & Brugsch).
Berlin, 1913, ii, 1, 469-597.
Duval (C. W.) & Couret (M.}. A further note upon the experimental production of kprosi/
in the monkey (Macacus rhesus), with a critical study of the culture em-
ployed. J. Exper. M., Lancaster, Pa., 1912, xv, 292-306.
Duval (C. W.) & Harris (W. //.)• Further studies upon the leprosy bacillus. Its culti-
vation and differentiation from other acid-fast species. J. M. Research,
Boston, 1913, xxviii, 165-198.
Dyer (Isadore). Leprosy. Mod. Med. (Osier). 8°. Philadelphia & New York, 2d ed..
1914, i, 522-533.
Harbitz (Francis). Trophoneurotic changes in bones and joints in leprosy. Arch. Int.
Med., Chicago, 1910, vi, 147-169.
Herrick (A.B.}& Ear hart (T. W.). The value of trophic bone changes in the diagnosis of
leprosy. Arch. Int. Med., Chicago, 1911 , vii, 801-811.
Jadassohn (J.). Lepra. In: Handb. d. pathogen. Mikroorg. (Kolle & Wassermann).
2. Aufl. Jena, 1913, v, 791-930.
Marchoux (E.). La lepre. Rev. d'hyg., Par., 1913, xxxv, 883-939.
Montgomery (D. W.). Illustrations of the history of leprosy. J. Am. M. Ass., Chicago.
1915, Ixv, 927-931.
Morrow (//.) & Lee (A. W.). Symptoms and diagnosis of leprosy. J. Am. M. Ass.,
Chicago, 1915, Ixv, 931-934.
Pautrier (L. M.). Le diagnostic de la lepre par les methodes de laboratoire. Presse mcd.,
Paris, 1914, xxii, 203-204.
Smith (A. J.), Lynch (K. M.) & Rivas (D.). The transmissibility of the lepra bacillus
by the bed-bug (Cimex lectularius L.). Am. J. M. Sc., Philadelphia &
New York, 1913, cxlvi, 671-681.
Sticker (G.). Lepra. In: Mense's Handbuch der Tropenkrankheiten. Leipzig, 1905, J.
A. Earth. Bd. ii, 175-210.
Wolbach (S. B.) & Honeij (J. A.). A critical review of the bacteriology of human and
rat leprosy. J. M. Research, Boston, 1914, xxix, 367-423.
The diphtheroid bacillus from leprosy lesions. J. M. Research, Boston,
1914, xxx, 1-8.
20. Diseases Due to the Cholera Bacillus
Cholera Bacillus. — The Vibrio cholera? asiaiicce, or comma bacillus of
Koch (1883), is a curved rod, the ends of which do not lie in the same
plane. It is motile, having a long, tortuous flagellum at one end. It does
not form spores. This bacillus stains in ordinary dyes (best in con-
DISEASES DUE TO BACILLI 297
centrated aqueous fuchsin solution) ; it is Gram-negative. Aerobic cultures
on ordinary alkaline agar grow best at 37° C. The bacillus liquefies
gelatin (funnel-formation), peptonizes blood serum and forms indol in
pepton solutions ("cholera red reaction"). The bacillus is extremely
sensitive to dry heat, and to disinfectants. Its virulence is variable.
Rabbits, injected in the ear vein, develop diarrhea and die. Accidental
infection with pure cultures of cholera bacilli have occurred in human
beings (laboratory infection). Prof. Pettenkofer of Munich, who denied
the relation of the- bacillus to the disease, intentionally swallowed a cholera
culture after making the stomach juice alkaline with bicarbonate of soda.
He developed cholera, but recovered. Prof. Emmerich is also said to have
swallowed a culture, along with an excess of beer, and he, too, had a severe
attack of typical Asiatic cholera as a result. (Plate IV, Fig. 3.)
(a) Asiatic Cholera
Definition. — An acute infection of the surface of the intestine, due to
Bacillus cholenv asiaticce (Koch) and characterized by violent purging
and speedy collapse.
Epidemiology. — The disease occurs (1) in great epidemics breaking
out suddenly (water-borne infection), and (2) sporadically (contact infec-
tion; bacillus carriers).
Symptoms. — There may be slight premonitory symptoms (diarrhea,
abdominal pains, headache, malaise) ; more often, there is a sudden attack,
with vomiting arid profuse diarrhea ; the diarrheal defecation is painless.
The discharges, at first feculent, soon become watery, colorless, and
odorless — the so-cabled rice-ivater stools — and contain the comma bacilli
in great numbers with flecks of mucus, detritus and sometimes blood.
Extreme prostration quickly follows, with small rapid pulse, cyanosis, and
cold extremities (stadium algidum). Nothing can be retained in the
stomach ; there is boat-shaped retraction of the abdomen ; the voice becomes
feeble and hoarse (vox cliolerica^) ; the tissues are dehydrated, the skin
being wrinkled, dry and devoid of elasticity, and the urine scanty or
absent. Cramps in the calves of the legs develop. Though the extremities
and integument may feel cold to the touch the rectal temperature is usually
elevated. Death may ensue in a few hours.
In milder cases, the symptoms gradually decrease, the skin becoming
warm and moist (stadium reactionis). The kidneys begin to secrete again,
the urine containing albumin and casts.
Relapses are not uncommon, the extremities becoming again cold and
cyanosed, the patient feeble and apathetic, with renewal of the fever,
delirium ;md muscular cramps. The diarrhea and vomiting recur, and the
patient sinks into coma (stadium comatosum, or cholera typhoid}, which
usually ends fatally, though occasionally a patient recovers.
In the algid stage, the leukocytes may number over 40,000, owing
298 DIAGNOSIS OF INFECTIOUS DISEASES
to concentration of the blood ; during the stage of reaction, they rapidly
decrease in number.
Sellards has shown that a marked acidosis accompanies the dehydra-
tion in cholera, and constitutes one of the dangerous features of the dis-
ease.
When the attack is not severe, but resembles an ordinary catarrh al
gastro-enteritis, even though -comma bacilli are demonstrable, the condition
is known as cholerine.
The average mortality in Asiatic cholera is 50 per cent to 60 per cent ;
the death-rate varies in different epidemics.
Diagnosis. — It is all important to recognize the first oases, which must
be differentiated from (1) cholera nostras, or paral uphold infection, and
(2) arsenical poisoning.
Where cholera is suspected, an expert bacteriologist should make a
systematic examination of a particle of mucus from the feces, or from the
vomitus: (1) Microscopically (many vibrios in smears stained in carbol-
fuchsin; motility in hanging-drop, in peptone solution); (2) By cultural
methods (gelatin and aiiar plates, after enrichment by planting an oese
of the mucus in several tubes of Schottmiiller's slightly alkaline, salt- and
nitrite-containing peptone solution, and iucubat ing at 37° C. for 6 hours,
when enormous numbers <>f vibrios owing to their affinity for oxygen will
have accumulated near the surface of the medium ; from this surface layer,
plate cultures on gelatin, on agar and on Dieudonne's blood-alkali a^a-
are made); (3) By testing pure cultures (a) for agglutination with im-
mune serum, (b) by Pfeiffer's experiment (q. v.) and (c) for the nitroso-
indol-reaction (red color on addition of II2SO4 to the growth in nitrite-
containing peptone water).
Special cholera courses should be given in the bacteriological labora-
tories at the time of cholera epidemics, so that the local health officers
can learn to act promptly and with certainty.
Prophylaxis. — All water used in times of cholera should be boiled and
no uncooked food should be eaten. Great care should be taken to avoid
dietetic errors. Every digestive disturbance should be met promptly (rest
in bed ; bismuth). All suspects should be isolated. The drinking of acidu-
lated water (lime juice, citric acid, muriatic acid) i» recommended,
References
Anderson (J. F.) & Stimson (A. M.). Bacteriological procedure in suspected cholera,
with report of a positive case. Pub. Health Rep., U. S. Mar. Hosp. Serv.,
Washington, 1910, xxv, 1477-1479.
Armstrong (S. T.) & Kinyoun (J. J.). Observations on the cholera bacillus as a means of
positive diagnosis. New York M. J., 1887, xlvi, 646-547.
Aumann. Ueber die Maassnahmen bei der Bekdmpfung der Cholera in Serbien, 1913.
Berl. klin. Wchnschr., 1914, li, 589-592.
Dunbar (W. P.). Asiatica cholera. Mod. Med. (Osier). 8°. Philadelphia & New
York, 2d ed., 1914, i, 672-688.
DISEASES DUE TO BACILLI 299
Haffkine (M. M. W.}. Lecture on anlicholera inoculation. Referred to in Brit. M. J.,
London, 1895, ii, 1509.
Hetsch (H.). Choleraimmunitdt. In: Handb. d. pathogen. Mikroorg. (Kolle & Wasser-
mann). 2. Aufl. Jena, 1912, iv, 110-154.
Koch (/?.)- Ueber die Cholerabakterien. Deutsche med. Wchnschr., Berlin, 1884, x, 725-
728.
Also: Wien. med. Wchnschr., 1884, xxxiv, 1361.
Wasser filtration und Cholera. Ztschr. f. Hyg. u. Infektionskr., Leipzig,
1893, xiv, 393-426.
Kolle (W.} & Schurmann (W.}. Cholera Asiatica. In: Handb. d. pathogen. Mikroorg.
(Kolle & Wassermanri). 2. Aufl. Jena, 1912, iv, 1-109.
Krause (P.) & Rumpf (T.). Cholera Asiatica. In: Handb. d. Tropenkrankheiten (Mense},
Leipzig, 1905, ii, 293-346.
Krumwiede (C., Jr.) & Pratt (J. 5.). Dahlia-Agar als Unterscheidungsmittel zwischen
Cholera- und anderen Vibrionen. Zentralbl. f. BakterioL, etc., Orig., 1913,
Ixviii, 562-566.
Munson (E. L.). Cholera carriers in relation to cholera control. Philippine J. Sc., Manila,
1915, B. x, 1-9.
Pfeiffer (/2.) & Issaeff. Ueber die specifische Bedeulung der Choleraimmunitdt. Ztschr.
f. Hyg. u. I nfectionskrankh., Leipzig, 1894, xvii, 355-400.
Pfeiffer (jR.) & Marx. Untersuchungen uber die Bildungsstdtte der C holer aantikorper.
Deutsche med. Wchnschr., Leipzig u. Berlin, 1898, xxiv, 47-48-
Ueber Schutzimpfungen gegen Cholera und Typhus mit conservirtem 'Impf-
stoff. Deutsche med. Wchnschr., Leipzig u. Berlin, 1898, xxiv, 489-491.
Rogers (L.). Cholera and its treatment. London, 1911, H. Frowde. 236 p. 8°.
Schobl (O.). Observations concerning cholera carriers. Philippine J. Sc., Manila, 1915,
B. x, 11-17.
Sellards (A. W.}. Tolerance for alkalies in Asiatic cholera. Philippine J. Sc., Manila,
1910, v, (B.) 363-390.
Stokes (W. R.) & Hachtel (F. W.}. The use of a modified Hesse's medium for isolating
the typhoid bacillus and the cholera spirillum from stools. Zentralbl. /.
BakterioL, etc., Orig., 1913, Ixix, 346-349.
Strong (R. P.}. Protective inoculation against Asiatic cholera (an experimental study).
Manila, 1904. 52 p. 8°.
Forms No. 16 of Dept. Interior, Bur. Gov't Laborat. Biol. Laborat.
21. Disease Due to the Bacillus of Milk Sickness
Bacillus of Milk Sickness. — The Bacillus lactomorbi (Jordan and Har-
ris) was isolated from cases of milk sickness in an epidemic in New Mexico
(1908), and grown in pure culture. Inoculation of animals with the
culture reproduces the disease.
(a) Milk Sickness
Symptoms. — The symptoms consist of nausea, vomiting, intense thirst,
fever, and abdominal pains, with constipation. The breath is foul, the
tongue swollen and tremulous ; mental symptoms are often marked. Death
may occur in from 3 to 21 days.
300 DIAGNOSIS OF INFECTIOUS DISEASES
In cattle, the disease known as the trembles appears to have the same
etiology. Man is presumably infected through meat, milk, butter or
cheese.
Reference
Jordan (E. O.) & Harris (N. M.). The cause of milksickness or trembles (Bacillus lac-
tomorbi). J. Am. M. Ass., Chicago, 1908, i, 1665-1673.
22. Disease Due to the Bacillus proteus vulgaris
Bacillus proteus vulgaris. — This bacillus has been isolated from the
liver, and from the kidney, in cases of acute infectious jaundice, sometimes
known as epidemic catarrhal jaundice or WEIL'S DISEASE. A similar
disease is often due to infection with the paratyphoid bacillus. (See
Part VIII.)
23. Diseases Due to Bacillus typhi-exanthematici
(a) Typhus Fever
(Typhus exantltematicus, Spotted Fever, Camp Fever, Brill's Disease)
Definition. — Typhus fever is an acute, specific, febrile, infectious dis-
ease, with characteristic macular, often hemorrhagic, exanthem, and ac-
companied by severe nervous and mental symptoms, occurring generally
in epidemics, though occasionally sporadically; it was definitely differen-
tiated from typhoid fever by Gerhard (1829).
Occurrence. — Formerly the disease was very prevalent ; now it is rare,
except in countries or in communities in which there are notoriously
bad hygienic conditions. In 1815-1818, the disease was epidemic in
England and Ireland; one-eighth of the Irish population died of it. In
1846-1848 over a million people in England suffered from the disease.
In the Eusso-Turkish war (1877-78), no less than 32,451 Kussian soldiers
died of typhus exanthematicus. The disease still occurs, occasionally in
epidemics, and sporadically, in different parts of the United States and
Europe. Thus the fever, not uncommon in New York, and known as
Brill's disease, has been shown to be typhus fever (Anderson and Gold-
berger), as has also the tabardillo of Mexico. A young scientist, Dr. H.
T. Ricketts of Chicago, died from this disease, contracted while investi-
gating it in Mexico.
Etiology. — The nature of the virus was, until recently, unknown,
though it is present in the blood during the febrile stage, and can be
transmitted, by blood inoculations, to monkeys and to guinea-pigs. The
virus does not lose virulence on heating for 15 minutes at 55° C. One
attack of the disease appears to yield permanent immunity.
Ricketts and Wilder were the first to show that the disease could be
DISEASES DUE TO BACILLI
301
transmitted by the bite of the louse. On this discovery are based all the
prophylactic measures that are now so successfully used.
The disease can be transmitted from man to man by the body-louse
(Pediculus vestimenti'), and by the head-louse (Pediculus capitis), which
probably explains its prevalence in epidemic form in over-crowded, filthy
surroundings ("camp fever"). Lousiness, formerly common, is rapidly
disappearing; the same is true of typhus fever. The most cleanly or
fastidious person, compelled to work in certain surroundings, may occa-
sionally be bitten by lice, and if the lice carry the virus, contract the
disease.
Recently, Plotz, Olitsky and Baehr have reported the discovery of B. typhi-exan-
thematici as the cause of typhus fever. The organism was recovered from the
blood of several cases of European epidemic typhus fever and also from cases
of the mild endemic form of the disease known in the United States as Brill's dis-
ease. Moczutkowski had proved that the virus is present in the circulating blood
during the febrile period; he inoculated
himself with blood from a typhus patient,
and typical symptoms of the disease de-
veloped at the end of an incubation pe-
riod of eighteen days. Nicolle ( 1909 ) , by
injecting the blood of patients into chim-
panzees, reproduced the disease. He was
able to transmit the disease from monkey
to monkey by the bite of the body-louse.
The studies of Nicolle, of Ricketts and
Wilder, and of Anderson and Goldberg-
er, had shown that the virus is non-fil-
trable. Ricketts and Wilder then point-
ed out that typhus fever is an acute, self-
limited disease, one attack of which con-
fers immunity, and they emphasized the
fact that these features favor a bacterial
rather than a protozoal origin.
Cultures made by aerobic methods by
many investigators have been negative.
In 1914, Plotz, under Libman's direction,
first isolated a bacillus by anaerobic
methods. He used first Noguchi's meth-
od for the cultivation of spirochaetes,but
later found the Liborius-Veillon method
more satisfactory. Colonies of the bacil-
lus appear in the tubes in from three to
sixteen days. "The organism is a small,
pleomorphic, Gram-positive bacillus, not
motile, not encapsulated, and not acid- Fig 8R_(A) Tube Showing Growth (Seven
fast. Its length varies from 0.9 to Days) of Bacillus typhi-exanthematic on
1.93 p, its breadth being from one-fifth Serum Glucose Agar. Note Whitening of
-,„,, ., . £„ T, , Medium (Precipitation). (B) Control
fths its length." It does not Tube of Glucose Serum Agar. (After
produce spores. It is an obligatory an- Plotz, Olitsky and Baehr, J. of inf. Dis.)
302
DIAGNOSIS OF INFECTIOUS DISEASES
V ,
aerobe. The bacteriemia is more marked in the epidemic than in the endemic cases.
Owing to the slow development of the colonies in the culture media, the results of
the blood cultures are, as a rule, not determinable, until after the end of the illness,
but it is maintained that the
cultures are of value for con-
firming the clinical diagnosis.
Plotz reports that, in 87.5 per
cent of 51 cases studied, the
clinical diagnosis was confirmed
by blood culture, agglutination
or complement-fixation tests.
In two cases in which the diag-
nosis had been overlooked, a
positive blood culture first
called attention to the nature
of the condition.
It is asserted that the dis-
ease can be typically repro-
duced in animals by inocula-
tion with pure cultures of the
bacillus, and that from these
animals the identical organism
can be recovered from the cir-
culating blood.
Olitsky, who made the im-
munological studies, found that
complement -fixing antibodies against the bacillus occur in typhus fever, and not in
other conditions. Specific agglutinins, specific precipitins and specific immune opso-
nins are also present, but specific bacteriolysins or baeteriocidins are not demon-
strable. The results of further studies upon this bacillus will be awaited with inter-
est. In personal communications from Serbia, I am told that investigators there
have thus far had difficulty in confirming the findings of Plotz, Olitsky and Baehr.
Prophylaxis. — This consists chiefly in a campaign against lice. If con-
taminated clothing be soaked in a 1 :500 solution of bichloride of mercury,
Fig. 86. — Bacillus typhi-exanthematici — Gram's Stain,
x 1,000. (After Plotz, Olitsky and Baehr, J. of
Inf. Dis.)
(A) | (B)
Fig. 87. — (A) Pediculus capitus (Kuchenmeister) ; (B) Ova of Pediculus capitus (Kaposi)
(C) Pediculus pubis (Schmarda),
DISEASES DUE TO BACILLI
303
the lice and their eggs will be destroyed. After closely clipping the
patient's hair, the head should be thoroughly sponged in bichloride solu-
tion (1:2,000) to destroy lice eggs. The lice in a bedroom can be killed
by sulphur fumigation. Doctors and nurses attending typhus patients
should take especial care to avoid louse bites. Many distinguished mem-
bers of both professions have succumbed to typhus fever, contracted at
the bedside. According to Osier, "in a period of 25 years in Ireland,
among 1,230 attached to in-
stitutions, 550 died of this
disease."
Symptoms. — The incuba-
tion period lasts from 5 to
20 days, averaging 12 days.
The onset is usually sudden,
with chill, or chills, and fe-
ver, headache, severe pros-
tration, pain in the back and
legs, tachycardia, coated
tongue, suffusion of the face
and eyes, mental dullness,
often delirium, and vomit-
ing.
The exanthem appears on
the 4th and 5th day, first up-
on the lower abdomen and
the shoulders, later upon the
back, chest and upper abdo-
men, and lastly upon the face
and extremities, the whole
rash appearing within 2 or 3
days; it lasts a few days, in
the severer cases for a week
or longer. The rash consists
of pale red spots the size of
a pin's head, or of a pea
(macular, not papular) ; in a
few days it assumes a dirty
red or copper-colored tint and
ceases to disappear on pressure ; some of the spots become definitely hemor-
rhagic (petechial). The spots are often very abundant in the inguinal
regions. In addition, there is usually a dusky red, subcuticular mottling.
In the cases known as Brill's disease, the rash may resemble the rose
spots of typhoid fever, or may be absent altogether. Toward the close
of the first week and during the second week, the symptoms are more
Fig. 88.— Typhus exanthematicus. (Mod. Service,
J. H. H.)
304 DIAGNOSIS OF INFECTIOUS DISEASES
pronounced, especially the fever, prostration, the delirium and stupor.
Urinary retention and coma-vigil are common. The tachycardia and
tachypnea are marked.
The fever, in contrast with that of typhoid, rises suddenly, rather than
by steplike ascent. The remissions during the first week are slight
(ahout half a degree). Defervescence occurs about the end of the second
or beginning of the third week either by crisis, or by rather rapid lysis,
the fall being often preceded by a critical perturbation, or by a pseudo-
crisis. Instead of the slow lytic fall seen in typhoid fever, the fall of
the temperature in typhus exanthematicus occurs within 12-24 hours to
subnormal. Hyperpyrexia is not rare.
The blood usually shows a slight leukocytosis (12,000-15,000), with
a relative increase in the lymphocytes; in severe cases, anemia may de-
velop rapidly in the later stages.
The spleen is occasionally palpable at first, but diminishes in size dur-
ing the fever. The urine is scanty and contains a trace of albumin ; the
diazo-reaction is positive. Blood cultures made in the ordinary aerobic
way and Widal reactions are negative. Bronchopneumonia is the com-
monest complication met with.
Diagnosis. — The very sudden onset, the course of the fever and of the
pulse and the appearance of the exanthem make the diagnosis easy at
times of epidemic. Sporadic cases are often wrongly diagnosed.
The disease should be differentiated: (1) From typhoid fever (posi-
tive blood culture in the first week, leukopenia, rose-spots and their dis-
tribution, palpable spleen, dicrotic pulse, more insidious onset, longer
course, Austrian's ophthalmic test). (2) From smallpox (eruption dif-
ferent in character with definite cycle of evolution, the distribution of the
initial exanthem, the fall of temperature before the outbreak of the main
exanthem). In purpura variolosa, the differentiation in a sporadic case
from typhus exanthematicus may be impossible, though subsequently the
corneal experiment (q. v.) may reveal the true nature of the case. (3)
From malaria (intermittent fever, parasites in the blood, leukopenia, large
firm spleen). (4) From relapsing fever (blood examination). (5) From
sepsis with Jiemorrhagic eruption (leukocytosis, cocci in blood culture,
primary focus). A most useful diagnostic test in doubtful cases is the
test of Anderson and Goldberger (injection of patient's blood into peri-
toneal cavity of guinea-pig; if the disease be typhus exanthematicus, or
Brill's disease, a typical temperature curve will be obtained).
From now on anaerobic cultures by Plotz's method should be under-
taken when the disease is suspected to exist.
References
Anderson (F. A. ). Collected studies on typhus. Washington, D. C., 1912, Gov't Print. Office.
143 p. 8°.
U.S. Treas. Dep., Pub. Health Serv., U.S. Hyg. Lab. Bull. No. 86
DISEASES DUE TO BACILLI 305
Anderson (J. F.). Typhus fever. Its etiology and the methods of its prevention. Pub.
Health Rep., Washington, 1915, xxx, 1803-1311.
The reaction of the guinea pig to the virus of typhus fever. J. Med. Re-
search, Boston, 1914, xxx, 467-473.
Anderson (J. F.) & Goldberger (/.)• On the etiology of tabardillo or Mexican typhus.
An experimental investigation. J. Med. Research, Boston, 1910, xxii.
469-481.
The relation of so-called BrilVs disease to typhus fever. An experimental
demonstration of their identity. Pub. Health Rep., U. S. Mar. Hosp.
Serv., Washington, 1912, xxvii, 149-160.
Brill (N. E.). An acute infectious disease of unknown origin. A clinical study based on
221 cases. Am. J. M. Sc., Philadelphia & New York, 1910, cxxxix,
484-502.
Doty (A. H.). Typhus fever. In: Therap. Int. Dis. (Forchheimer) . New York & London,
1913, ii, 31-39.
Foster, Jr. (G. B.}. Endemic typhus fever in the Philippine Islands. Observations based
on a study of twenty-three cases occurring among Filipinos at Camp Keith-
ley, Mindanao, P. I., with the results of animal inoculations. Arch. Int.
M., Chicago, 1915, xvi, 363-381.
Friedman (G. A.). Brill's symptom-complex; typhus fever; Manchurian typhus. Arch.
Int. Med., Chicago, 1911, viii, 427-439.
Lee (R. /.)• Typhus fever (Brill's disease) at the Massachusetts General Hospital in ten
years (Oct. 1, 1902, to Oct. 1, 1912). Boston M. & S. J., 1913, clxviii,
122-127.
Lewis (M. /.)• So-called Brill's disease: a study based upon thirteen cases treated at the
Pennsylvania Hospital. Tr. Ass. Am. Physicians, Philadelphia, 1911,
xxvi, 234-245.
Louria (£.)• Brill's disease. Report of cases. Med. Rec., New York, 1911, Ixxx, 424~427.
McCampbell (E. F.}. Observations on typhus exanthematicus (tabardillo) in Mexico
(Feb. 7, 1910}. J. Med. Research, Boston, 1910, xxiii, 71-83.
McCrae (T7.). Typhus fever. Mod. Med. (Osier). 8°. Philadelphia & New York, 2d
ed., 1914, i, 924-935.
Moczutkowski (O. O.). Ueber die Im.pfbarkeit des Typhus exanthematicus. Allg. med.
Centr.-Ztg., Berlin, 1900, Ixix, 1055-1057.
Ueber die Ueberimpfung des Flecktyphus. St. Petersb. med. Wchnschr.,
1900, Beilage, xxv, 30.
Moore (Sir J.). Typhus fever. In: Syst. Med. (Allbutt & Rolleston). 8°. London, 1909 ,
ii, pt. 1, 538-564.
Newell (L. /?.) & Allan (W.). Typhus fever: a report of four cases. South. M. J., Nash-
ville, 1914, vii, 564-568.
Nicolle (C.). Recherches experimentales sur le typhus exanthematique, entreprises a Vln-
stitut Pasteur de Tunis pendant Vannee 1909. Ann. de VInst. Pasteur,
Paris, 1910, xxiv, 243-275.
Nicolle (C.), Conor (A.}, Conseil (E.} & Jaeggy (E.}. Recherches experimentales sur
le typhus exanthematique entreprises a VInstitut Pasteur de Tunis pendant
Vannee 1910. Ann. de VInst. Pasteur, Paris, 1911, xxv, 1-55, 97-144-
Nicolle (C.), Comte (C.) & Conseil (E.). Transmission experimental du typhus ex-
anthematique par le pou du corps. Compt. rend. Acad. d. Sc.f Paris,
1909, cxlix, 486-489.
Plotz (H.). L'etiologie du typhus, note preliminaire. Presse med., Paris, 1914, xxii, 411.
The etiology of typhus fever (and of BrilVs disease). Preliminary com-
munication. J. Am. M. Ass., Chicago, 1914, Ixii, 1556.
Plotz (H.}, Olitsky (P. K.) & Baehr (G.). The etiology of typhus exanthematicus. J.
Infect. Dis., Chicago, 1915, xvii, 1-68. 1 pi.
Rabinowitsch (M.). Ueber den Flecktyphuserreger. Berl. klin. Wchnschr., 1914, Ka
1458-1459...
306 DIAGNOSIS 'OF INFECTIOUS DISEASES
Ricketts (H. T.) & Wilder (R. M.). The typhus fever of Mexico (tabardillo) . Prelimi-
nary observations. J. Am. M. Ass., Chicago, 1910, liv, 463-467.
The transmission of the typhus fever of Mexico (tabardillo) by means of
the louse (pediculus veslimenti). J. Am. M. Ass., Chicago, 1910, liv,
1304-1307.
The etiology of the typhus fever (tabardillo) of Mexico City. A further
preliminary report. J. Am. M. Ass., Chicago, 1910, liv, 1373-1375.
Further investigations regarding the etiology of tabardillo, Mexican typhus
fever. J. Am. M. Ass., Chicago, 1910, Iv, 309-311.
Wenckebach (K. F.). Ueber die Klinik des Flecktyphus. Wien. klin. Wchnschr., 1915,
xxviii, 539-544.
Wilder (R. M.}. The problem of transmission in typhus fever. J. Infect. Dis., Chicago,
1911, ix, 9-10 L
The bacteriology of typhus fever. J. Am. M. Ass., Chicago, 1914, Ixiiij
937-939.
Wilson (W. /.). The etiology of typhus fever. J. Hyg., Cambridge, 1910, x, 155-176.
C. Diseases Due to the Coarser Fungi
(The Mycoses)
Formerly, only actinomycosis and thrush were adequately described in
text-books of internal medicine. In recent years, a whole series of dis-
eases, due to different kinds of fungi, have become recognized and the
chapter on the mycoses is one of the most interesting in internal medicine.
It is a worthy field, also, to work in, since the early recognition of certain
forms, especially of the sporotrichoses, permits of the rapid cure of a
disease that otherwise may be very serious. Many of the mycoses stand
in the borderland between internal medicine and surgery. Like so many
borderland diseases, they are apt to be neglected. For this reason, I am
dealing more fully with them than is perhaps customary.
Definition. — The mycoses include a group of external and internal dis-
eases of human beings and animals, due to the coarser forms of parasitic
fungi, thus differing from forms of infectious disease due to bacteria
or to protozoa.
Varieties of Mycoses. — Among these mycoses, we include the diseases
due to (1) ordinary HYPIIOMYCETES (mucor, aspergillus, penicillium,
achorion, trichophyton, etc. ) , in which a genuine mycelium is formed and
which propagate by spore formation, or by the production of higher forms
of fructification organs; (2) the BI.ASTOMYCETES or yeast fungi, which
multiply by budding and by spore formation (saccharomyces, yeasts), and
only exceptionally give rise to mycelium (blastomyces, oidiomyces, thrush
fungi, etc.), and, finally, (3) the STREPTOTHKICES, which consist of
branched threads, breaking up into short rods, and propagate by fission
(streptothrix actinomyces, streptothrix of madura foot, nocardia forms,
leptothrix, etc.).
These different varieties of the coarser fungi are not yet entirely
satisfactorily placed from the botanical standpoint, though the French in-
DISEASES DUE TO THE COAESEE FUNGI 307
vestigators, especially, have gone far toward giving us a purely botanical
classification. Thus, in the recent valuable volume on parasitic diseases
in Gilbert and Thoinot separate chapters are devoted to (1) sporotrichoses,
(2) botrytimy coses, (3) hemisporoses, (4) exascoses, (5) oidiomycoses,
(6) mucormycoses, (7) oosporoses, (8) aspergilloses, and (9) actino-
mycoses.
Such a botanical classification, however, is, I fear, for practical pur-
poses, a little premature, and, with Plant, I am inclined to adopt a simpler
grouping, as follows: (1) mycoses due to hyphomycetes, (2) mycoses due
to blastomycetes, (3) mycoses due to thrush fungi, (4) mycoses due to
sporotrichum and related fungi, (5) mycoses due to the different varieties
of streptothrix (actinomyces, madura foot, nocardoses, leptotrichomycosis,
etc.).
References
i ford (B. /if.). Notes on sprue in Porto Rico and the results of treatment by yellowed
santonin. Am. J. Trop. Dis., etc., New Orleans, 1913, i, 146-158.
Beurmann (C. L.) & Gougerot (H.). Les mycoses. Traite de mededne et de thera-
peut. Paris, A. Gilbert & Thoinot; Paris, Bailliere et fils.
Boggs (T. R.) & Pincoffs (M. C.). A method for the study of morphology and reproduction
in filamentous organisms. (Illustrated.) Johns Hopkins Hosp. Bull,
Baltimore, 1915, xxri, 854-365.
tuschke (A.). Die Sprosspilze. Handb. d. path. Mikroorg. 2. Aufl. (Kolle & Wasser-
mann), Jena, 1913, v, 157-210.
Vuillemin (P.). La classification des mycoses. Rev. gen. d. sc. pures et appliq., Paris,
1910, xxi, 148-157.
Widal (F.) & Abrami (P.) \et al.]. Serodiagnostic mycosique. Ann. de I'Inst. Pasteur,
Paris, 1910, xxiv, 1-83.
Wright (J. II.}. Actinomycosis ; streptothricosis ; mycetoma; oidiomycosis ; blastomycosis;
sporotrichosis ; pulmonary aspergillosis ; mycosis; mucorina. Mod. Med.
(Osier). 8°. Philadelphia & New York, 2d ed., 1914, i, 1033-1060.
1. Mycoses Due to the Hyphomycetes
Hyphomycetes. — These are fungi that form whitish, greenish, yellow-
ish, brownish or blackish deposits on organic substances like fruit, bread,
carpets, preserves, straw, manure, etc. Botanically, these hyphomycetes in-
clude several species (e. g., aspergillus, mucor, penicillium, botyris, achor-
ion, tricophyton and microsporon). Many of them are pathogenic for man
and for animals, the more important belonging to aspergillus and mucor.
Aspergillus belongs to the my corny cetes, sub-variety, ascomycetes. It is
an asexual form of eurotium, in which the more complex form of fructifi-
cation, known as ascus formation, occurs also. The conidiophore is strong,
and presents a flask-like swelling at its end, upon which sit short, wedge-
like pedicles, the so-called sterigmata, in stellate arrangement. From
these sterigmata, the spores, or conidia, are pinched off in chains; the
color of these varies according to the variety (black, yellow, etc.). The
pathogenic varieties include (a) Aspergillus fumigatus, (b) Aspergillus
308 DIAGNOSIS OF INFECTIOUS DISEASES
niger, (c) Aspergillus flavus, and (d) Aspergillus nidulans. Infections
with aspergillus fumigatns are by far the most common.
In testing aspergillus for its pathogenicity, it is best to use guinea-pigs
and birds. After intravenous injection of the spores, the animals die in
from 48 to 72 hours.
Mucor belongs to the phy corny cetes, or algae-fungi. Its mycelium is
either free from septa, or poor in septa ; it gives rise both to sexual and to
asexual spores, which form in sporangia that rest upon conidiophores,
easily distinguished from the rest of the mycelium by their length and
thickness. During the spore formation, the conidiophore undergoes club-
like swelling at its end, the septum immediately beneath giving rise to
the so-called columella. The asexual spores are formed from the proto-
plasm that lies beneath the columella and the surface of the club. The
whole structure is known as a sporangium. The membrane of the spo-
rangium bursts when the spores are ripe and they are scattered through
the air. Of the pathogenic forms, the commonest are (a) Mucor corymbifer
(lung, ear) ; (b) Mucor rhizopodiformis, and (c) Mucor septatus (ear).
In testing the pathogenicity of a mucor, it is best to use rabbits (intra-
venous injection).
Penicillium is the commonest of all the hyphomycetes. It is the asexual
form of an ascus-forming perisporiacea. Asci, however, are seldom seen.
This fungus is distinguished from aspergillus by the fact that the conidio-
phore does not undergo bulbous enlargement and is subdivided at its apex.
From the tips of these subdivisions, the sterigmata give off chains of spores
by budding.
Pathogenic varieties have been found in the ear.
Fungi Affecting the Skin. — Here belong Achorion schoenleinii (favus),
Trichophyton in its different forms, Microsporon furfur (of pityriasis),
and Microsporon minutissimum (of erythrasma).
Reference
Plant (H. C.). Die Hyphenpilze oder Ewnyceten. In: Handb. d. pathogen. Mikroorg.
(Kolle & Wassermanri). 2. Aufl. Jena, 1913, v, 1-154-
(a) Human Aspergillosis
The infection is met with in diabetes and in cachexias. The fungus may
invade the skin (dermatomycosis), the ear (otomycosis), the nose (rhino-
mycosis, the lungs (pneumonomycosis aspergillina). A very interesting
case of the pulmonary form has been described by Osier. Persons ex-
posed to vegetable dust (millers, gardeners) are frequently affected. In
France, the so-called pig eon- fancier's disease or pseudo tuberculosis asper-
gillina is due to aspergillus, the infected persons allowing the birds to take
masticated food directly out of their mouths ; these birds often suffer from
spontaneous aspergillosis. Hair-sorters who comb out hair with the use of
DISEASES DUE TO THE COARSER FUNGI 309
meal containing fungi, and sponge-cleaners, through the dust from the dry
sponges, may also contract the disease.
Pinta. — A parasitic skin affection found only in the tropical regions of the
Western Hemisphere and characterized by the appearance of black, red, violet, and
white patches on the skin. These patches have been shown to be due to various
fungi, of which Aspergillus pictor, Penicillium montayai, Montoyella, and Monilia
are the best known. The patches are usually first noted on the hands; itching
is marked; and apparently by scratching the process is spread over the body.
The diagnosis can be made from the examination of scrapings in liquor potassa3;
and by the cultivation of the fungus on Sabouraud's medium.
References
Bodin (E.} & Gautier (L.). Note sur une toxine produile par I' Aspergillus fumigatus.
Ann. de I'Inst. Pasteur, Paris, 1906, xx, 209-224-
Renon (L-.). Etude sur Vaspergillose chez les animaux et chez Vhomme. Paris, 1897,
Masson et Cie. 312 p. 8°.
(b) Human Mucormycoses
Fungi belonging to mucor have been found in infections of the lung
and of the ear ; also in enteritis. In one case there was a generalization of
infection from the intestinal lesions with multiple abscesses in the brain,
lungs and elsewhere (Mucor corymbifer).
Reference
Paltauf (A.). Mycosis mucorina; ein Beitrag zur Kenntnis der menschlichen Fadenpilzer-
krankungen. Arch. f. path. Anat., etc., Berlin, 1885, cii, 543-564-
(c) Human Achorion-mycosis or Favus
This is a disease of the hairy scalp, due to invasion by Achorion schoen-
leinii. The Achorion schoenleinii belongs to the hyphomycetes. It is
rich in mycelium and shows only a few gonidia. A scraping, treated with
NaOH, examined under a cover-slip shows it well. Yellowish, disklike
scales (scutula) having a peculiar earthlike odor, and perforated in the
middle by a hair, appear. If a scutulum be raised, one sees a red, moist
surface underneath and in chronic cases atrophy of the underlying skin.
Later, the encrusted areas enlarge and become confluent, forming thick,
yellow encrusted areas. Suppuration is not uncommon at the edges of
the lesions. The hairs are involved early, becoming dull, brittle and often
splitting or falling out, so that one may find atrophic almost hairless areas,,
with crust formation at the borders.
In one case, reported by Kundrath, there was an intestinal f avus and
a general favus-sepsis !
The diagnosis is made by examining a scutulum, in NaOH, under the
microscope, and looking for the typical fungus. The presence of this differ-
entiates the disease from a sehorrheic eczema resembling it.
310 DIAGNOSIS OF INFECTIOUS DISEASES
(d) Human Mycoses Due to Trichophyton tonsurans
The Trichophyton tonsurans met with in the human skin is seen in
delicate thread-forms in a mycelium, with roundish or oval gonidia,
arranged usually in chains. The threads are often tortuous and curved,
but rarely branched.
Scales, hairs and crusts containing the fungus, cleared in NaOH or
KOH, reveal it distinctly, on microscopic examination, though sometimes a
number of specimens must be examined before the fungus is found. It
causes several different forms of disease in man.
i. Superficial Ringworm (Trichophytia superficialis)
This is an inflammation in the most superficial part of the skin, due
to the lodging and growth of Trichophyton tonsurans in the stratum cor-
neum. It is a dermatitis, and, according to its intensity, gives rise to the
clinical pictures known as herpes tonsurans maculosquamosus and herpes
tonsurans vesiculosus. This is the ordinary superficial "ringworm" of
non-hairy parts. A sub-variety is known as pityriasis rosea (Gibert).
ii. Eczematous Ringworm (Epidermophytia cruris)
The skin affection, variously known as eczema marginatum, dhobie
itch, and washerman's itch, has been shown to be due to various species
of Epidermophyton. This fungus varies somewhat from Trichophyton
in that it never invades the hair or hair follicles. The skin affected is
usually that of the crotch, or of the axilla, though the process may be
localized between the toes and on the feet where it gives rise to a very
chronic form of dyshydrosis. It is prone to attack parts of the body rich
in glands, e. g., the genitals, scrotum, crena ani, and axilla. When the
process is acute the affected skin is red and swollen ; the margin of the
area is sharply delimited and may be marked by many small vesicles.
The itching is extremely severe. Subsidence and recurrence of the infec-
tion are characteristic.
The diagnosis can readily be made by cutting off the cap of one of the
vesicles with a razor and examining it microscopically in 10 per cent
KOH under a cover-slip. The mycelium and spores are usually readily
made out. The organism may be grown upon Sabouraud's maltose-agar.
Many such cases of years' standing can be readily cured if the parasitic
character of the lesion be recognized and parasiticidal remedies applied.
iii. Barber's Itch or Ringworm of the Hairy Scalp and Beard
(Trichophytia tonsurans capillatii)
In this form, circles of parasitic invasion appear in the scalp or beard,
interfering with the growth of hair, and giving it a "stubbly" appear-
ance, in contrast with the smooth circles devoid of hair in alopecia areata.
DISEASES DUE TO THE COAESEE FUNGI
311
The hairs are not killed for they will grow again if the infection be
overcome.
iv. Parasitic Sycosis (Trichophytia profunda)
In this disease, the fungus penetrates the follicles and sets up a suppu-
rating folliculitis and perifolliculitis. Abscesses of considerable size may
develop. In the region of the beard the disease is sometimes called sycosis
parasitaria, while on the hairy scalp it is called kerion celsi. The disease
gives rise to a repugnant sweetish smell.
v. Ringworm of the Nails (Trichophytia unguium)
The fungus here attacks the finger-nails. It is most common in those
who have their nails well cared for by manicurists. It rarely occurs
among the farming population. The nails lose all their gloss, become
rough and nodular, and look splintered; the lateral margins may be
elevated. Shavings from the nails, treated with KOH, reveal the fungus,
which differentiates the affection from trophic disturbances, syphilis, etc.
Reference
Morris (Sir M.). Parasitic diseases of the skin. In: Syst. Med. (Allbutt & Rollestori).
8°. London, 1911, ix, 117-161.
.'
(e) Human Microsporon Mycoses
These include (a) pityriasis versicolor and (b) erythrasma.
i. Pityriasis versicolor
This is due to the fungus Microsporon furfur, which has characteristic
large gonidia, in grapelike ar-
rangement. None of the other
pathogenic fungi of the skin
show such large masses of fruc-
tification elements (Fig. 89).
A yellowish, or brownish,
discoloration of the skin occurs,
due to its invasion with this
Microsporon furfur. It may
cover the whole front of the
trunk, and is sometimes seen on
the arms. Occasionally, only
small 'areas are affected. The
disease is accompanied by bran-
like desquamation, especially
when the skin is neglected. It
is rarely seen in parts of the
skin not covered by clothing.
Fig. 89.— Microsporon Furfur from a Scraping
in Pityriasis Versicolor. From Jesionek's
Article in Riecke's "Lehrbuch," published
by G. Fischer. Jena.)
312 DIAGNOSIS OF INFECTIOUS DISEASES
It causes no subjective sensation except, sometimes, slight itching. It
occurs most often in persons who sweat freely (flannel underclothing).
Tuberculous patients are peculiarly subject to it. It is practically never
seen in children nor in the aged.
The diagnosis is easy from the characteristic appearance, and can be
confirmed by examining a scraping in KOH under the microscope.
(f) Erythrasama (Baerensprung)
This is an invasion of the skin, by the fungus Microsporon minutis-
simum, which looks like Microsporon furfur, except that the threads are
much smaller and more delicate. The spores consist of minute granules
lying in loose heaps. The sites of predilection in the skin are the scrotum,
Scarpa's triangle, the perineum, the folds between the buttocks, the infra-
mammary region, and the axilla.
The infection gives rise to round, yellowish-brown spots, of a reddish
tint. These have a pronounced tendency to become confluent, giving rise
to areas as large as a silver dollar, or even as large as the palm of the
hand.
The diagnosis can be confirmed by examining a scraping, microscopic-
ally, in NaOH. The disease should not be confused with eczema margina-
tum (see above) though this name has sometimes been applied to it.
Reference
p. Baerensprung (F. W.F.). Die Gurtelkrankheit. Annal. d.Charite-Krankenh., Berlin,
1857, Bd. ix, Hft. 2, 40-128.
2. Mycoses Due to Yeasts and Yeastlike Fungi
The blastomycetes or yeast fungi are round or oval, unicellular, nucle-
ated organisms, which propagate by budding. A projection appears on
the wall of a cell, and gradually grows larger; the daughter-cell soon
assumes the shape of the mother-cell. It then becomes pinched off, or it
may remain for a time in connection with it.
Some varieties give rise to endogenous spores (ascospores). Others
do not form spores, or have lost the power to do so ("imperfect fungi'7).
Among the latter, there are varieties that form genuine mycelia and
resemble morphologically the eumycetes; they have been called crypto-
cocci, zymonema, monilia, oidia, dematia, etc. In other words, the term
blastomycetes is an omnium gatherum for fungi of wholly different origin,
propagation by budding alone being common to them all. Botanically,
the name and the group are very unsatisfactory, so that the botanists
urge that we do away entirely with the term Blastomyces, and replace it
DISEASES DUE TO THE COAKSEK FtHSTGI 313
by terms technically more satisfactory. Thus, Yuillemin, a distinguished
French investigator, instead of using the term "blastomycoses" for the
diseases produced by these fungi, suggests that we call the diseases pro-
duced by the spore-formers exascoses, and the diseases produced by
budding fungi, like oidia, oidiomy coses. If the fungus turns out to be a
variety of endomyces, the disease it causes is known as an endomycosis.
As Plaut points out, however, such a classification, while more correct, is
difficult for the clinician to apply; thus, for example, the same clinical
affection (thrush), when it is produced by yeasts that form ascospores,
would have to be designated an endomycosis, or saccharomycosis, but if
produced by yeasts not forming such spores would be called a parasac-
charomycosis or moniliomycosis. If in place of these terms we use the
single word thrush-mycosis, every physician knows immediately what we
mean.
It is therefore convenient for the present to retain the term blastomy-
cosis, meaning by it a disease caused by budding fungi, which as a rule
have no mycelium, and possess the capacity of forming endogenous spores.
Mycoses due to similar fungi that produce mycelium may be called
oidiomy cosis, if they morphologically resemble the well-known oidium
lactis. Should the fungi belong to the thrush-fungus group, we can
separate these out as a special group — the thrush-mycoses, notwithstand-
ing the fact that this group may include different species belonging either'
to endomyces or to monilia. When the fungi are not closely related to
the budding fungi, but are characteristic in their morphology, we give them
names based upon their form (e. g., sporotrichosis, hemisporosis, etc.).
It may be convenient to have the French classification of this group o£
diseases. That used by de Beurmann and Gougerot is as follows :
EXASCOSES
(A) Saccharomy coses and Atelosaccharomy coses. — These give rise ta
the ordinary blastomycoses. In this group belong monospora, saccharo-
myces, cryptococcus, and endomyces. These species, as a rule, do not give
rise to mycelium.
(B) Parasaccharomy coses. — This group of diseases stands between
those in A and in C. The fungi form mycelia.
(C) Zymonematoses ("Yeast Threads"). — This group includes the
oidiomycoses (e.g., Gilchrist's disease). The fungi form mycelia in
growths on culture media, and multiplication by budding can be made out
in the pus and in the tissues. No endosporulation is seen.
(D) Parendomy coses. — The fungi causing these diseases stand mid-
way between C and E in their morphological behavior. Here belong the
fungi causing remarkable diseases in horses (Tokishige's disease, and the
epizootic lymphangitis of Rivolta and Micellone). The fungus of the
314 DIAGNOSIS OF INFECTIOUS DISEASES
coccidioidal granuloma of the San Joaquin valley probably belongs here ;
in the pus, endosporulation occurs but no budding forms are seen.
(E) Endomy coses. — These include the diseases due to thrush fungi
of the endomyces type, whereas the thrush fungi of the monilia type
would, by the French, be excluded from the exascoses.
(a) The Blastomycoses and Coccidioidal Granuloma
These affections of human beings and animals are due to yeast-like
organisms (see above).
i. Blastomycetic Dermatitis and Systemic Blastomycosis
Definition and Etiology. — Blastomycosis is a disease due to a budding
fungus — Cryptococcus gilchristii. Obtained from the lesions in which it
occurs, it appears as a spherical cell surrounded by a refractive membrane,
the diameter of the yeast varying between
ten and sixteen microns. In the pus one
often sees a pair of cells, one larger and
one smaller, the smaller one having been
budded off from the larger. The fungi
are often enclosed within the bodies of
phagocytes (giant cells). They are easily
demonstrable in fresh pus or fresh tissue
by treatment with a solution of caustic
soda. No endosporulation is seen in the
fungus in tissues or in pus. The fungus
grows well on acid media, but the initial
Fig. 90.— Sediment from Tissue Dis- growth is slow, requiring from ten days
integrated in 50 per cent Alcohol, -, /? j n •, i i
Showing Biastomyces in Various to two weeks for definite development,
stages of Budding. (After F. H. though after prolonged cultivation it may
Montgomery and O. S. Ormsby, , . ,. -, m1 ... -, ,
Arch. int. Med.) grow out in a few days. The optimal tem-
perature for growth is 20° C. Rabbits
and guinea-pigs are susceptible to infection with this fungus, but less so
than for the fungus of coccidioidal granuloma (see below).
Forms of the Disease. — Two main forms have been distinguished: (1)
blastomycetic dermatitis and (2) systemic blastomycosis.
Blastomycosis of the skin is usually primary. It appears as an acne-
like process, later giving rise to ulcers and cauliflowerlike excrescences.
It often begins about the nose or the eye, or the side of the neck. Me-
tastases in the internal organs (lungs, brain, bone) are not uncommon.
In systemic blastomycosis the infection probably occurs by inhalation,
as the respiratory tract seems to be first infected, and the early symptoms
are referable to the lungs in which signs of a bronchopneumonia develop.
Later the infection becomes generalized, and small or large abscesses occur
DISEASES DUE TO THE COABSEB FUNGI
315
in the skin, subcutaneous tissue, lymph glands, muscles, bones, nervous
tissues and viscera. The abscesses may range in size from minute areas to
large cavities containing a quart of pus.
Symptoms. — In blastomycetic dermatitis pustules and local ulcera-
tions or subcutaneous abscesses appear in the skin. The lesions are mul-
tiple and may occur successively or in crops. An ulcer may be primary,
or it may develop at the site of a ruptured abscess. The chronic ulcers
f
Fig. 91.— Skin Lesions in a Case of Blastomycosis. (After B. W. Fontaine, M. Haase and!
R. H. Mitchell, Arch. Int. Med.)
often present a fungoid appearance, the surface being nodular or papillo-
matous. Blastomycetes can be found in the pus by mounting a little of it
fresh or by mixing some of it with a 20 per cent solution of NaOII.
In systemic blastomycosis the patients usually report that their ill-
ness began with a cold or some acute respiratory infection, often with a
chill, pain in the chest, fever, shortness of breath, cough and expectora-
tion. Later on, characteristic subcutaneous abscesses appear. In some
instances, no acute stage is reported, but small subcutaneous abscesses or
local ulcerations of the skin first attract the patient's attention. Once
the disease is well established, the symptoms of a chronic infection become
evident. The patients emaciate, grow weak, and complain of pain in the
affected part; the pulse is accelerated, there is irregular fever, and occa-
sionally there are chills and sweats. In most cases signs of pulmonary
involvement are demonstrable. Often the blastomycetes can be demon-
316 DIAGNOSIS OF INFECTIOUS DISEASES
strated in the sputum ; occasionally they can be isolated in blood cultures
or in cultures made from the urinary sediment. Pains in the bones
and joints may herald a localization in these structures. Paralyses may
occur owing to the presence of lesions in the spinal cord or brain. A sec-
ondary anemia develops, usually with a marked leukocytosis, sometimes
Pig. 92. — Characteristic Lesions of Cutaneous Blastomycosis. (After P. H. Montgomery and
O. S. Ormsby, Arch. Int. Med.)
as high as 30,000 w. b. c. per c.mm. In Stober's series the average leuko-
cytosis was 16,800. When the bones are involved, there may be an irrita-
tion myelocytosis.
In Gilchrist's form the parasite appears in the tissue only as a yeast,
though, in cultures, it forms threads and conidia, like oidium. With Dr.
H. C. Buswell, of Buffalo, I saw a remarkable instance of infection with
this organism. There were multiple, small, subcutaneous abscesses pres-
ent in the pus from which Dr. Clough isolated the fungus. Later the
DISEASES DUE TO THE COAESEE FUNGI 317
patient developed a nodule on his tongue, suggestive of carcinoma ; a piece
was excised for diagnosis, and, on examination, Dr. Welch found that it
was a granuloma due to the same fungus !
Diagnosis. — When multiple subcutaneous nodules or abscesses appear
in a patient, some of the pus, or a piece of the tissue, should always be
examined in a solution of NaOH for the fungus. In obscure pulmonary
infections and in atypical lesions of bones and joints, systemic blastomy-
cosis should be kept in mind as a possibility. The diagnosis is rendered
certain by the demonstration of the blastomycetes in the pus, sputum, urine,
or blood, or in histological sections of infected tissues excised for diag-
nostic purposes. With such a simple method at our command there is
now no excuse for not recognizing the disease when it exists. Fresh
material is far better than stained preparations, since in the latter the
fungi are easily overlooked.
Differential Diagnosis. — Blastomycetic dermatitis and systemic blasto-
mycosis must be differentiated: (1) from coccidioidal granuloma (closer
resemblance to tuberculosis; involvement of lymph nodes more common;
cutaneous lesions more ulcerative ; disease fatal and not amenable to treat-
ment with KI; fungus shows endosporulation and not budding in pus
and tissues; initial growth of fungus in cultures more rapid; fungus more
pathogenic for rabbits and guinea-pigs) ; (2) from tuberculosis (cavity
formation and hemoptysis more common; tubercle bacilli in sputum;
cutaneous lesions uncommon, except when lupus is present; Calmette re-
action positive); (3) from syphilis (Wassermann reaction; absence of
blastomycetes) ; (4) from sporotrichosis (q. v.) ; (5) from epithelioma
(slower growth; greater induration; absence of fungus; histology).
ii. Goccidioidal Granuloma
(California disease; San Joaquin Valley disease; Mycoderma immite)
Definition and Etiology. — A disease due to a peculiar fungus that
has received various names O'idium protozonide; O'idium coccidioide;
Coccidioides pyogenes; Posadasia esseriforme, etc.
The fungus was discovered by Wernicke, in 1892, in a Brazilian soldier affected
with a peculiar cutaneous lesion. A careful study of the condition was made by
Posadas, who inoculated animals with fragments of the diseased tissue. In the
lesion, the fungus occurs in the form of spherical cells, varying from 3 to 80 mi-
crons in diameter, and surrounded by a thick refractive membrane. Spores are
formed inside the cells (endosporulation). In cultures, though not in tissues, the
fungus grows out into mycelial filaments, just as does the blastomycetic fungus.
The initial growth is more rapid than for blastomycetes, some growth being noted
at the end of twenty-four hours. The optimal temperature for growth is 37° C.
Animal inoculation yields well-defined endosporulating organisms. Budding forms
do not appear. Rabbits and guinea-pigs are susceptible to infection, as are also
monkeys and mice. Like blastomyces this coccidioidal fungus can give rise either
318 DIAGNOSIS OF INFECTIOUS DISEASES
to an inflammation and ulceration of the skin (coccidioidal dermatitis), or to a
general systemic involvement with lesions in the lungs, kidneys, liver, spleen, supra-
renal capsule, bones and jonts (systemic coccidioidal granuloma).
Symptoms. — As met with in California, the disease is nearly always,
and often rapidly, fatal. The symptoms closely resemble those of tuber-
culosis. The infective agent shows a greater predilection for the lym-
phatic system than in blastomycosis, and the cutaneous lesions of coccidio-
idal granuloma tend to be more ulcerative. The iodides, so efficacious
in blastomycosis, seem to be without effect in coccidioidal granuloma.
The disease occurs most often in males, and in foreigners living in this
country. Occasionally, a female is attacked.
Diagnosis. — This depends upon the demonstration of the peculiar
fungus in the lesion. Fresh specimens treated with from 4 per cent to
20 per cent NaOH should be examined. The absence of budding and
the existence of endosporulation distinguish this fungus from the blasto-
myces (see above).
The frequent occurrence of yeast-like fungi in carcinoma, and in other
tumors, has been the subject of especial study by Sanfelice ; for a time, it
was thought that the fungi were etiologically related to the neoplasms, but
this view is no longer held.
References
Adamson (H. G.). Blastomycosis. In: Syst. Med. (Allbutt & Rolleston). 8°. London,
1911, ix, 516-524.
Brown (P. K.). A fatal case of coccidioidal granuloma. J. Am. M. Ass., Chicago, 1913,
Ixi, 770-771.
Brown (P. K.) & Cummins (W. T.}. A differential study of coccidioidal granuloma and
blastomycosis. I. Pathology and bacteriology. II. Report of two addi-
tional cases of coccidioidal disease. Arch. Int. Med., Chicago, 1915, xv,
608-627.
Buschke (A.}. Die Sprosspilze. .In: Handb. d. pathogen. Mikroorg. (Kolle & Wasser-
mann). 2. Aufl. Jena, 1913, v, 155-210.
Cooke (Jean F.)» Immunity tests in coccidioidal granuloma. Arch. Int. Med., Chicago,
1915, xv, 479-486.
Fontaine (B. IF.), Haase (M.) & Mitchell (R. H.). Systemic blastomycosis. Arch.
Int. Med., Chicago, 1909, iv, 101-117.
Gilchrist (T. C.)« A case of blastomycetic dermatitis in man. Johns Hopkins Hosp.
Rept., Baltimore, 1896, i, 269-283.
Comparisons of the two varieties of protozoa, and the blastomyces found
in the preceding cases, with the so-called parasites found in various lesions
of the skin, viz., Psorospermosis Follicularis Vegetans (Darier), Carci-
noma, Herpes Zoster, Molluscum Contagiosum, Varicella. Johns Hop-
kins Hosp. Repts.. Baltimore, 1896, i, 2917347.
Blastomycetic dermatitis in the negro. Brit. M. J., Lond., 1902, ii, 1321-
Harter (Andre G.}. De la blastomycose humaine. Nancy, 1909. 222 p. 6 pi. 8°.
Hektoen (L.). Systemic blastomycosis and coccidioidal granuloma. J. Am. M. Ass.,
Chicago, 1907, xlix, 1071-1077.
DISEASES DUE TO THE COAKSER FUNGI 319
Irons (E. E.) & Graham (E. A.}. Generalized blastomycosis: report of a case with miliary
and ulcer -alive blastomycosis of the lungs; miliary blastomycosis of the spleen
and multiple superficial and deep abscesses. J. Infect. Dis., Chicago 1906
in, 666-682.
Laederich (L.) & Duval (H. 12.) • La mycose de Gilchrist; blastomycose ou oidiomycose des
Americains. Rev. de med., Paris, 1909, xxix, 673; 721.
MacNeal (W. G.) & Taylor (R. M.}. Coccidioides immitis and coccidioidal granuloma
J. Med. Research, Boston, 1914, xxx, 261-274.
Montgomery (F. H.) & Ormsby (O. £.)• Systemic blastomycosis. Its etiologic, path-
ologic and clinical features as established by a critical survey and summary
of twenty-two cases, seven previously unpublished, the relation of blasto-
mycosis to coccidioidal granuloma. Arch. Int. Med., Chicago, 1908, ii,
Montgomery (F. H.} & Ricketts (H. T.}. Three cases of blastomycetic infection, of the
skin. J. Cutan. & Genito- Urin. Dis., New York, 1901, xix, 26-48.
Powers (C. A.). Systemic blastomycosis. Ann. Surg., Philadelphia, 1914, lix, 815-820.
[Discussion] Ix, 110.
Ricketts (H. T.}. Oidiomycosis (blastomycosis) of the skin and its fungi. J. M. Research,
Boston, 1901, n. s., i, 877-546.
Rusk (G. F.) & Farnell (F. J.). Systemic oidiomycosis ; a study of two cases developing
terminal oidiomycetic meningitis. Berkeley, 1912, Univ. ofCal. 58 p.
Ryerson (E. W.). Blastomycosis: a report of two cases resembling bone tuberculosis. Am. J.
Orthop. Surg., Philadelphia, 1908-09, vi, 79-88.
Stober (A. M.). Systemic blastomycosis. A report of its pathological, bacteriological and
clinical features. Arch. Int. Med., Chicago, 1914, xiii, 509-556.
(6) Diseases Due to Thrush Fungi
i. Thrush
This disease is described under Stomatitis in the section on Diseases
of the Digestive Apparatus.
The Thrush Fungi. — We have come to learn that many different, though
probably related, fungi may cause what is known, clinically, as thrush.
Part of these fungi are "imperfect fungi/' and cannot be classified, other-
wise, botanically. Some forms, however, belong definitely among the
Ascomycetes. The most common form met with in the thrush of children
is a thread-fungus, which not only produces mycelia, but also multiplies
by budding. It grows easily, on all nutrient media, though preferably in
acid media containing sugar ; it ferments sugar and will grow either
aerobically or anaerobically ; in the presence of oxygen, the budding forms
are prominent; on exclusion of oxygen, mycelia with conidia develop. In
addition to the 'forms of propagation just mentioned, one sometimes sees
chlamydospore formation, and ascospores.
The variety that forms true ascospores in the pseudomembrane is
called Endomyces albicans. Still oftener, the disease is due to Monilia
Candida Bonorden; thrush is sometimes due, also, to a pure budding form.
320
DIAGNOSIS OF INFECTIOUS DISEASES
CHARACTERISTICS OF ENDOMYCES ALBICANS. — In cultures, mycelia
develop, which show oidium-formation at the ends; spherical chlamydo-
spores may be seen singly, or in pairs, at the tips of the mycelia. Endo-
conidia are formed in the mycelia, and also outside them, on the lateral
Fig. 93. — The Thrush Fungus — 94-96=Spores ; 97-102=Mycelium ; 104-105=Chlamydospores ;
110-lll=Ascospores. (After Vuillemin, in H. C. Plaut's "Spez. Path. u. Ther. inn.
Krankh.," puolished by Urban & Schwarzenberg, Berlin.)
surface of the mycelium threads. The asci may be located either at the
tip of a thread, or in its course ; they are elliptical, or oval, and contain 4
spores in a delicate membrane, which quickly disappears. -
CHARACTERISTICS OF MONILIA CANDIDA BONORDEN. — Two varieties
may be distinguished, a large-spored variety, the Oidium albicans of
Robin, and a small-spored variety, the Saccharomyces non-liquefaciens of
Fischer.
DISEASES DUE TO THE COARSER FUNGI
321
The large-spored variety is the commoner. It differs from the Endo-
myces albicans chiefly in the fact that no asci are formed. In cultures, it
multiplies by budding, like
the yeasts, but it may grow
like monilia with myce-
1 i u m formation. The
chains of conidia from the
sides of the threads and
from the ends of the my-
celia, are prominent fea-
tures. Mycelium forma-
tion is favored by anae-
robic conditions, by an
alkaline medium, and by
scarcity of carbohydrate
in the medium; the bud-
ding process is favored by
a medium rich in sugar,
by an acid medium, and
by aerobic conditions.
Fig. 94.-Oidium albicans. (After N. D. Jagic and H. K. On gelatin, or On agar,
Barrenscheen, "Atlas u. Grund. d. Klin, d Mikro- the thrush fungUS grOWS
superficially as a snow-
white hemispherical layer; in deep colonies, fine feathery threads grow
out from the periphery.
For a full account of these different varieties of thrush fungi, see
Plaut's article in Kolle and Wassermann, V, 50.
References
Fischer (B.) & Brebeck (C.). Zur Morphologic, Biologic und Systematik der Kahnpilze,
des Monilia Candida Hansen und des Soorerregers. Jena, G. Fischer,
1894. 52 p.
Plant (H. C.). Neue Beitrage zur systcmatischen Stellung des Soorpilzes in der Botanik.
Leipzig, 1887, H. Voigt. 32 p. 8°.
Vuillemin (P.). Les caracteres specifiques du champignon du muguet (Endomyces albicans).
Compt. rend. Acad. d. Sc., Paris, 1898, cxxvii, 630-633.
Les formes du champignon du muguet. Rev. mycol., Toulouse, 1899, xxi,
43-55.
Difference fondamentale entre le genre Monilia et les genres Scopulariopsis
Acmosporium et Catenularia. Bull. Soc. mycol. de France, 1911 , xxvii,
137-152.
322 DIAGNOSIS OF INFECTIOUS DISEASES
3. Mycoses Due to Sporotrichum and Related Fungi
(a) Sporotrichoses (Schenck's Disease)
Sporotrichum. — This is a fungus belonging to the Hyphomycetes; fam-
ily, Nucedinacce; sub-group, Botrytidce, and is closely related, botanic-
ally, to the fungi that cause favus, ring-worm and pityriasis. No less
than 120 varieties of Sporotrichum are already known. The fungus grows
in nature on rotten wood, decaying plants, old walls, etc. The hyphae are
branched. Oval or spherical conidia arise at the ends of short sterigmata.
HISTORICAL. — This disease was discovered in Baltimore. A patient; suffering
from a peculiar ulceration of the hand, with induration of the forearm, applied
for treatment in the surgical out-patient department at the Johns Hopkins Hos-
pital, in November, 1896. It was made the object of especial study by Dr.
Schenck, now the gynecologist of Detroit, who isolated, in cultures, a branching
fungus, giving rise to mycelium and spores; it was submitted to Dr. Ervin F.
Smith of Washington, who identified it and gave it the name Sporotrichum
schenckii. The case was reported in the Johns Hopkins Hospital Bulletin, in 1898.
Two years later, a careful study of the same fungus from a second case, was
reported by Hektoen and Perkins, in the Journal of Experimental Medicine, under
the title "Refractory Subcutaneous Abscesses Caused by Sporothrix schenckii."
In both cases, a nodular lymphangitis of the arm had followed an infection of the
finger. Since this discovery, the disease has been found in various parts of the
world; it seems to be especially prevalent in France.
In 1903, de Beurmann, of Paris, reported a number of cases of sporotrichosis.
While the credit of the discovery of the disease undoubtedly belongs to American
observers, great credit is also due to the French physicians, for having shown,
(1) the frequency of the disease, (2) its resemblance in many cases to tubercu-
losis and to syphilis, and (3) the importance of separating it from these diseases,
since it can be speedily and completely cured by medical measures, namely, by
large doses of potassium iodid. Many individuals, falsely held to be luetic or
tuberculous, have been freed from their disease, in a remarkably short time,
through the making of a correct diagnosis of sporotrichosis and the institution of
an appropriate therapy.
PKOPERTIES OF THE FUNGUS. — The Sporotrichum, when examined in
the tissues affected, may lie either outside of cells, or inclosed within
macrophages. It is a rod-shaped, oblong, somewhat granular body, 3-5 /*
long and 2-3 i*> broad. It is surrounded by a pale membrane, which re-
mains unstained in ordinary dyes, while the protoplasm is basophilic. It
is very difficult to find the fungus in the disease focus, so difficult that
there is but little use in looking for it as a diagnostic measure. It can,
however, be easily grown from the lesions, on culture media. In cultures,
it is a genuine mycelial fungus, divided by septa ; it shows round or
oval ectospores, which, pedicellate or unpedicellate, may form large
groups, or may be seen singly, surrounded by threads of mycelium. The
DISEASES DUE TO THE COAESEK FUNGI
323
microscopic examination of the culture alone will not suffice for diagnosis ;
one has to rely upon the macroscopic appearance. The growth begins as
Fig. 95. — Sporotrichosls beurmanni, Smear from Lesion. Parasites are of Unequal Size, 2-5 /«.
Long and 2-3 /u- Broad. (After H. C. Plaut, "Spez. Path. u. Ther. inn. Krankh.," pub-
lished by Urban & Schwarzenberg, Berlin.)
a fine mycelial star, colorless, or waxy-looking. As the growth proceeds
it forms a folded membrane, resembling the appearance of a walnut, or
the gyri of a cerebral hemisphere. Gradually the culture becomes dis-
B
Pig. 96.— Sporotrichosis. (A) Young Thread-forming and Spore-bearing Hyphae, (B) Older
Hyphae with Numerous Spores. (After Gougerot, in H. C. Plaut's "Spez. Path. u. Ther.
inn. Krankh.," published by Urban & Schwarzenberg, Berlin.)
tinctly yellowish-brown in color. Later on, the center presents a blackish,
rusty appearance, due to spore formation.; at this time, the appearance of
the culture is very characteristic, and suffices for diagnosis,.
324
DIAGNOSIS OF INFECTIOUS DISEASES
Thus far, five distinct pathogenic varieties of sporotrichum have been
described, depending upon the optimal temperature for growth, poly-
morphism, pathogenicity, toxin formation and cultural properties. The
details of the differentiation of these different varieties will be found in
the excellent article by Gougerot (Die Sporotrichose, in Kolle and Was-
sermann, 2te Aufl., V, 236).
Symptoms of Sporotrichosis. — Any tissue of the body may be affected,
though the skin is most often involved. Nodules like gummata appear,
but show a marked tendency to soften, and to
break down. These nodules may be single
or multiple. Sometimes the ulcers resemble
tuberculous ulcers, or they may suggest ec-
tliyma. Large subcutaneous abscesses, difficult
to heal, were observed in the cases described
by the discoverer, Schenck and by Hektoen and
Perkins. In some cases, papillomalike, warty
efflorescences appear. The condition is often
diagnosed "warty tuberculosis" of the skin,
or as "gumma." Most of these cases are seen
first by the dermatologist. The internist is
more likely to see the cases of sporotrichous
sore throat, or sporotrichous affections of the
bones, joints, and synovial sheaths. In some
cases, the disease runs the course of a broncho-
pneumonia, in others, of a pyelonephritis.
Some of the most puzzling cases are first seen
by the surgeon, and are taken to be gummata, or
tuberculosis of the bones or of the joints. Sporotrichosis of the larynx,
and of the eye, are also known.
The following characteristics are emphasized by Gougerot: (1) numerous
lesions, without marked impairment of the general condition; (2) beginning in
the form of painless nodules, with partial softening, and gradual abscess forma-
tion; (3) jagged margins to the ulcerations, violet color of the margins of abscesses,
pigmentation and undermining of the margins of ulcers; (4) contrast between
the slight extent of the ulceration and the distribution of the softening; (5) pres-
ence of several openings, or of two ulcers lying opposite one another for one
infiltrated area, and union of the ulcerated areas by a narrow bridge of violet
colored skin; (6) mucoid or citron-yellow fluid; (7) ease of auto-inoculations;
(8) cold, indolent swellings; (9) cicatrization, with persistence of the abscess
beneath the skin; (10) flat, narrow, or broad, soft scars, with jagged and pigmented
edges. Lymph glands not enlarged.
Prognosis. — If recognized in time, and a vigorous iodin therapy insti'
$uted, the prognosis is favorable,
Fig. 97. — Sporotrichotic
Gumma ; Multiple Fistulae,
Separated by Bridges of
Non-ulcerated Skin. (Aft-
er de Beurmann and Gou-
gerot, in H. C. Plaut's
inn.
by
Urban & Schwarzenberg,
Berlin.)
DISEASES DUE TO THE COARSER FUNGI 325
(b) Other Mycoses Resembling Schenck's Sporotrichosis
Clinical phenomena, exactly like typical Sporotrichosis, can be due to
other fungi. Of these, several varieties are already known (hemisporosis,
acremoniosis, bothrytimycosis, cladiosis., etc.).
References
Adamson (H. G.). Sporotrichosis. In: Syst. Med. (Allbutt & Rollestori). 8°. London,
1911, ix, 525-531.
de Beurmann (C. L.) & Gougerot (JET.). Les sporotrichoses. Paris, 1912, F. Alcan.
856 p. Roy. 8°.
Les nouvelles mycoses: exascoses (exblastomycoses) , o'idiomy coses, sporo-
trichoses, botrytimycose, oosporoses hemisporose. Paris, 1912, Masson
& Cie. [etc.]. 165 p. 8°.
Davis (D. /.). Inter agglutination experiments with various strains of sporothrix. J. In-
fect. Dis., Chicago, 1913, xii, 140-143.
Gougerot (#.)• Die Sporotrichosen. Die pathogenen Sporotrichen und die Sporotrichosen.
Handb. d. path. Mikroorg. 2. Aufl. (Kolle & Wassermann). Jena,
1913, v, 211-266.
Hektoen (L.) & Perkins (C. F.). Refractory subcutaneous abscesses caused by Sporo-
thrix schenckii. A new pathogenic fungus. J. Exper. Med., New York,
1900, v, 77-89.
Schenck (B. /£.)• On refractory subcutaneous abscesses caused by a fungus possibly re-
lated to the sporotricha. Johns Hopkins Hosp. Bull., Baltimore, 1898,
ix, 286-290.
4. Mycoses Due to the Different Varieties of
Streptothrix
(The Sireptotriclwses, Cladioses, Nocardoses, etc.)
Streptothrix. — This term was originally used, by Corda, for a micro-
organism different from that to which the name is now applied. What is
now known as Streptothrix was described first by F. Cohn as Streptothrix
foersteri, and was the name given to a fungus first found in the lachrymal
duct. On account of the previous use of the name by Corda, French
botanists prefer to use some name other than Streptothrix for the organism
we are now considering. Vuillemin, for example, calls it microsipho-
myces, and de Toni and Trevisan suggest that the whole class be included
under the name Nocardia, in honor of the French veterinarian Nocard,
who investigated these fungi in animals. Accordingly, in the French
literature the diseases due to Streptothrix are spoken of as nocardoses.
It may be convenient to have the classification followed by the French and
German schools before us:
326
DIAGNOSIS OF INFECTIOUS DISEASES
1. Group.
Actinomyces.
2. Group.
Mycetoma.
3. Group.
Nocardia
Eppinger.
French Classification
Nocardoses, Granules
with clublikes well-
ings.
Actinomyces Harz.
Actinomyces bovis.
Actinomyces Israeli,
Ravaut et Piney, Thi-
bergi.
German and American
Classification
Typical actinomycosis.
Nocardoses, with [Actinomyces Moorhof, )
white or yellowish I Poncet-Dor, Hesse, ^Atypical actinomycosis.
granules, without ] Garten, Doepke.
club formation.
[Mycetoma blanc. Vincent Nocardia Madurse.
J " actinomycosique " bovis.
| " " " Eppinger.
\ " " " Carougeau.
Nocardia asteroides Eppinger.
« « " Var. Rivieri
« « « Var. Japonica
" " " Var. Ferrei
4. Group. Nocardosis of Carougeau.
5. Group. Erysipeloid of Rosenbach.
Madura foot.
Ipseudoactinomy coses .
Streptotrichomycoses.
Discomyces Carougeaui.
Rotlauf bacilli.
References
Block (B.) & Vischer (A.). Die Kladiose. Arch. f. Dermatol. u. Syph., Wien & Leipzig,
1911, cviii, 477-512.
Eppinger (#.)• Ueber eine neue pathogene Cladothrix und eine durch sie hervorgerufene
Pseudotuberculosis. (Cladothrichica.) Beitr. z. path. Anat. u. z. allg.
Path., Jena, 1891, ix, 287-329.
Gougerot (H.). Oosporoses ou nocardoses cutanees. Gaz. d. hop., Paris, 1913, Ixxxvi,
149, 197.
Petruschky (/.)• Di<e pathogenen Trichomyceten und Trichobakterien, Slreptoihrix, Clado-
thrix, Leptolhrix. Handb. d. path. Mikroorg. 2. Aufl. (Kolle & Wasser-
mann), Jena, 1913, v, 267-300.
Schottmiiller (#.)• Zur Aetiologie und Klinik der Bisskrankheit (Ratten-, Katzen-, Eich-
hornchen-BisskrankheiC) . Dermatol. Wchnschr., Leipzig u. Hamburg,
1914, Iviii, Erganz.-H., 77-103.
Steele (A. E.) & Lee (R. /.)• A case of infection with nocardia. Boston M. & S. J., 1913,
clxix, 502-503.
(a) Typical Actinomycosis in Human Beings
Streptothrix actinomyces. — The ray-fungus, or Streptothrix actinomyces,
occurs as a spore-bearing mycelium. In the human body, peculiar whitish-yellow
granules, or "glands," are thrown off. They may be visible to the naked eye in
sputum, so-called "sulphur granules"; on microscopic examination, flasklike
enlargements of the threads may be seen at the margin.
The fungus is not easy to grow in culture-media; out of about 60 tubes inocu-
lated, one is lucky to get 4 or 5 cultures. Some varieties grow aerobically, others
anaerobically. The best medium is coagulated blood serum to which glycerin has
been added; glucose-bouillon (1 per cent), and potato, are also satisfactory media.
The fungus is common in cattle (Bollinger, 1877), horses, goats, pigs, and
sheep. It is the cause of the "lumpy jaw" of cattle. In order that human beings
may be infected, some irritating foreign body (barley grain, splinter) must
DISEASES DUE TO THE COAKSEE FUNGI 327
accompany the germ. The fungus was found in a disease of the human spine by
Langenbeck in 1845, and the mycosis in human beings was very exactly described
by J. Israel in 1878. A good review of the bibliography up to 1911 will be found
in the article by M. Schlegel. The portal of entry in human beings is usually the
mucous membrane of the mouth, the tongue, or the tonsils; sometimes the primary
focus is in a carious tooth.
Symptoms. — These are variable, according to the portal of entry.
In ORAL, ACTINOMYCOSIS, swelling of the submaxillary and of the
submental regions or of the margin of the gum appear ; hard at first, these
later undergo softening, with pustule formation. Infection through
carious teeth causes subperiosteal growth, with swelling and tumor
formation.
The subcutaneous tissue is sometimes involved (DERM-ACTINOMY-
cosis). Actinomycosis of the skin involves most often that of the neck
and head, leading to the formation of nodular masses that soften, ulcerate,
and discharge characteristic pus. The course is extremely chronic.
In PULMONARY ACTINOMYCOSIS, the infection may arise through aspi-
ration of the fungus in dust, or, secondarily, by extension from the neck.
The yellow actinomyces particles are coughed up, and appear in the
sputum. The inflammation may extend to the pleura. The symptoms
include irregular fever, cough, and expectoration, the clinical picture
closely resembling that of pulmonary tuberculosis. The physical signs
may he those of bronchitis, of bronchopneumonia, or of pulmonary ex-
cavation.
INTESTINAL ACTINOMYCOSIS also occurs, especially in parts in which
there is often fecal stasis (cecum, vermiform appendix, colonic flexures,
rectum). It gives rise sometimes to diarrhea, sometimes to chronic
peritonitis, often to symptoms resembling chronic appendicitis. A GEN-
ERALIZED ACTINOMYCOSIS, or septicemic form has also been described.
Diagnosis of Actinomycosis. — The disease often goes long unrecognized,
until the characteristic "sulphur" granules are found. Still, in the well
developed stage, the condition is very characteristic; the chronic inflam-
mation of low grade, the insidious course, the slight discomfort to the
patient at the beginning, the combination of tough connective tissue masses
with softened areas, the fistula-formation giving rise to a coarse-sieve-like
appearance to the skin, are striking features.
Actinomycosis must be distinguished in the skin: (1) from lupus,
(2) from gumma, and (3) from tuberculosis; in the tongue, (4) from
carcinoma, and (5) from blastomyces; in the lung, (6) from tubercu-
losis, (7) from syphilis, and (8) from neoplasm; in the intestine, (9)
from appendicitis, and (10) from periproctitis, etc.
It is well to follow the advice of Poncet and Thevenot, who suggest
that whenever one thinks of tuberculosis, cancer, or syphilis, he should
also think of the possibility of actinomycosis.
328 DIAGNOSIS OF INFECTIOUS DISEASES
If typical, club-shaped swellings are not present, one can try by culture
to determine whether he is dealing with (1) a true or typical actinomy-
cosis, (2) an atypical actinomycosis, or (3) apseudo-actinomycosis (actino-
bacillosis, or streptotrichomycosis).
References
Cohn (T.). Die Aklinomykose der Harnorgane. Verhandl. d. deutsch. Gesellsch. f. Urol.
Wien, 1911. Berlin & Leipzig, 1912, Hi, 236.
Erving (W. G.)« Actinomycosis hominis in America, with report of six cases. Johns
Hopkins Hosp. Bull, Baltimore, 1902, xiii, 261.
Israel (/.)• Klinische Beitrdge zur Kentniss der Aktinomykose des Menschen. Berlin,
1885, A. Hirschwald. 152 p.
Schlegel (M.)« Aktinomykose. In: Handb. d. path. Mikroorganismen. (Kolle &
Wassermann.) 2. Aufl. Jena, 1913, v, 801-364.
(b) Mycetoma (Madura Foot)
Definition. — A chronic infectious process, characterized by the forma-
tion of multiple granulomatous nodules, beginning usually on the plantar
surface of the foot. The tumors soften, and sinuses are formed that can
often be traced between the bones of the enormously enlarged and greatly
deformed foot. Characteristic streptothrix forms may be found in the
mucopurulent discharge. The disease is sometimes mistaken for syphilis
or for sarcoma. Occasionally, parts of the body other than the foot are
invaded ; thus involvements of the abdomen, of the head, and of the hand
are known. The disease was first described, in 1712, by Kampfer.
The disease is common in India, but occurs also in Africa, in South
America, and in the Philippines; it has been observed also in Italy, in
Roumania, and in Greece. In India, Carter recognized the similarity to
actinomycosis. Boyce and Surveyor (1894) pointed to the clinical differ-
ences between the two diseases. Vincent (1894) was probably the first
to isolate a fungus in pure culture from Madura foot, but now no less than
11 different fungi have been separated from different forms of the disease ;
6 of these are associated with "yellow granules," 5 of them with "black
granules."
The Mycetoma Fungi. — The fungi occur in the pus, and in the tissues, either
as yellow granules, or, less commonly, as black or melanoid granules, according
to the variety. Each granule consists of masses of a hyaline, brownish, brittle
substance, which has a matrix, in which is imbedded the mycelium. The fungi
from yellow granules grow like streptothrix, or Indiella; those from black granules
do not, but seem to be forms of aspergillus, and of Madurella. One of the fungi,
Streptothrix freeri, has been grown in Manila by Musgrave and Clegg; successful
cultures have also been made from Madura foot by J. H. Wright of Boston.
Mycetoma differs from actinomyces in several important respects: (1)
it attacks, by preference, the foot, which is hardly ever attacked by actino-
DISEASES DUE TO THE COARSER FUNGI 329
myces; (2) a generalization of the fungus does not occur; (3) the course
is more chronic than in actinomycosis, extending over decades ; (4) spon-
taneous cure does not occur; and (5) the iodin treatment, so beneficial in
actinomycosis, is not efficacious in mycetoma.
References
Babes (F.). Der Madurafuss. (Aktinomyces des Fusses, Perical, Mycetom.) In: Handb.
d. path. Mikroorganismen. (Kolle & Wassermann.) 2. Aufl. Jena,
1913, v, 365-390.
Boyce (R. W.) & Surveyor (N. F.). The fungus-foot disease of India. Brit. M. J., Lon-
don, 1894, ii, 638.
Brault (/.). Mycetome a grains noirs observe en Algerie; isolement du Madurella mycetomi.
Ann. de dermal, et syph., Paris, 1912, 5th s., Hi, 333-343.
Carter (H. F.)« On mycetoma, or the fungus disease of India. London, 1874, J. & A.
Churchill. 118 p. 4°-
Musgrave (W. E.) & Clegg (M. T.). The etiology of mycetoma. Report of a case of the
ochroid variety occurring in the Philippine Islands and caused by a new
species of streptothrix (Streptothrix freeri). Philippine J. Sc., Manila,
1907, ii, 477-510.
Remlinger (P.). Contribution d V etude de Discomyces madurae Vincent. Compt. rend.
Soc. de Biol., Paris, 1913, Ixxiv, 516-518.
Vincent (H.). Etude sur le parasite du " pied de Madura." Ann. de I'Inst. Pasteur,
Paris, 1894, viii, 129-151.
(c) The Pseudo-Actinomy coses or Streptotrichomycoses
The lungs, the brain, the skin, the digestive tract, and 'the eye may be
invaded by streptothrix forms. According to Foulerton, of 78 cases col-
lected from the literature 65.4 per cent were in men, 34.6 per cent in
women; 51.2 per cent of the cases were primary in the mouth and neck,
25.6 per cent in the appendix, 18.1 per cent in the lungs, and 5.1 per cent
in the eye, kidney or bladder.
Lungs. — The Streptotrichomycoses of the lungs closely resemble pulmonary
tuberculosis clinically and pathologically. Thus S. Flexner has described the
process as Pseudotuberculosis hominis streptotricha. The streptothrix can be
found sometimes in the sputum; it can be distinguished from the tubercle bacillus
by the fact that (1) it is longer, (2) the individual members of the chains are
of equal length, while the granules of tubercle bacilli are irregularly arrayed, and
(3) the streptothrix is somewhat less acid-fast.
The streptothrix shows branching forms. The varieties of pathogenic strepto-
triches and their group relationships to other acid-fast organisms have been espe-
cially well studied in this country by Edith Claypole.
Digestive Tract. — Stomatitis, tonsillar abscess, pyorrhea, noma, esophagitis,
enteritis, and appendicitis are among the conditions in which streptothrix may be
found as a causative agent.
Skin. — Cutaneous infections are fairly common, and may give rise to metastatic
infection of the organs. In one case, reported by Frankel and Schottmiiller
(1912), in which a laboratory worker became infected after a rat-bite, a septic
330 DIAGNOSIS OF INFECTIOUS DISEASES
process developed and ended fatally; large colonies of strep tothrix grew in plate-
cultures made from the blood during life.
Brain. — Metastatic abscess of the brain may thus arise, and simulate tubercu-
losis. In the well-known case, reported by Eppinger (1890), a chronic abscess
of the brain broke into the ventricle, and caused purulent meningitis. At autopsy,
foci were found in the lungs, supraclavicular lymph glands, and in the brain;
all of them contained streptothrix-threads, reported by Eppinger as a pathogenic
cladothrix — Nocardia asteroides. The organism was pathogenic for rabbits and
guinea-pigs but not for mice. In the experimental animals, lesions like those of
miliary tuberculosis were produced (pseudotuberculosis). Similar streptothricoses
have been studied by Sabrazes and Riosere and by Ferre and Faguet.
Eye. — The first streptothrix ( Streptothrix forsteri) was obtained from the
lachrymal duct. Keratitis and conjunctivitis sometimes occur, due to the same
fungus.
References
Caminiti (/?.)• Ueber die allgemeinen Strcptothrixinfektionen, unter besonderer Bctrach-
tung der Streptothrix-Pydmie. Centralbl f. Bakteriol. [etc.]. 1 Abt.
Jena, 1912, Ixv, Orig., 4%3~458.
Clay pole (Edith ,/.)• Human streptothricosis and its differentiation from tuberculosis.
Arch. Int. Med., Chicago, 1914, xiv, 104-119.
Davis (D. J.}. An acid-fast streptothrix (nocardia). Arch. Int. Med., Chicago, 1914, xiv,
1-7.
Flexner (S.). Pseudotuberculosis hominis streptotricha. J. Exper. M., New York, 1898,
Hi, 435-450.
Foulerton (A. G. R.). The pathology of streptothrix infections. In: Syst. Med. (Allbutt
& Rolleston). 8°. London, 1909, ii, pt. 1, 302-324. Also: The strepto-
thricoses and tuberculosis. The Milroy Lectures for 1910. Lancet, Lon-
don, 1910, i, 551; 626; 769, 1 pi.
Lee (R. /.)• A case of infection with nocardia. Boston M. & 8. J., 1913, clxix, 502-503.
Musser (J. //.), Pearce (R. M.) & Gwynn (N.). Abscess of the brain due to a streptothrix.
Tr. Ass. Am. Physicians, Philadelphia, 1901, xvi, 211-216.
Poppe (K.). Pseudotuberkulose. In: Handb. d. pathogen. Mikroorg. (Kolle & Wasser-
mann). 2. Aufl. Jena, 1913, v, 775-790.
Topley (W. C. C.). A case of generalized streptothricosis with extensive lesions in the cen-
tral nervous system. Brain, London, 1912-13, xxxv, 26-37.
Tuttle (G. A.}. A case of general streptothrix infection; with a study of the micro-organism.
M. & Surg. Rep. Presbyterian Hosp., New York, 1904, vi, 147-169.
Welch (D. A.} & Barling (J. E. F.). A note on the frequency of streptothrix infection in
man. Australas. M. Cong. Tr., 1905, Adelaide, 1907, vii, 383.
Wynn (W. //.)• A case of actinomycosis (streptothricosis) of the lung and liver successfully
treated with vaccine. Brit. M. J., London, 1908, i, 554-557.
(d) Discomyces Mycoses
In the tropics, Jeanselme has described a disease resembling somewhat Madura
foot but not identical with it. Nodules of the size of a hazel-nut or larger develop
in the subcutaneous tissue about the large joints. It is painless, disturbs the
patient but little, but is a protracted disease. The lesions are exceedingly like
tubercles, containing giant-cells and undergoing caseation in the center. The
disease is due to a discomyces (Gougerot, 1909; Fontoynont and Carougeau,
1910) ; it is sometimes called the nocardosis of Carougeau.
DISEASES DUE TO THE GOAESEE FUNGI 331
Reference
Fontoynont & Carougeau (J.}. Nodosites juxta-articulaires, mycose due au Discomyces
Carougeaui. Arch, de parasitol., Paris, 1908-10, xiii, 583-620.
II. DISEASES DUE TO ANIMAL MICEOOEGANISMS
(PEOTOZOA)
References
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pt. 2, 169-186.
A handbook of the tsetse flies (genus Glossina). London, 1911, 120 p. 8°.
Calkins (G. N.}. A textbook of protozoology. Philadelphia & New York. Lea & Febiger.
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Castellani (A.) & Chalmers (A. J.). Manual of tropical medicine. 2d ed. London,
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Jeanselme (E.} & Rist (E.}. Precis de pathologic exotique. Paris, 1909, Maison & Cie.
821 p. 8°.
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Le Dantec (A.). Precis de pathologic exotique (Malades des pays chauds et des pays froids).
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Mense (Carl}. Handbuch der Tropenkrankheiten, unter Mitwirkung von A. Baelz, P.
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Nuttall (G. H. F.). Lectures on the Herter Foundation: I. Spirochaetosis. II. Trypan-
osomiasis. III. Piroplasmosis. Johns Hopkins Hosp. Bull., Baltimore,
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Patton (W. S.) & Cragg (F. W.). A text-book of medical entomology. London [etc.],
1913, Christian Literature ~Soc. for India. 764 p. 4°.
Prowazek (S. von). Handbuch der pathogenen Protozoen. Unter Mitwirkung von P.
Ehrlich, Fr. Fulleborn [et al.}. I. Bd. Leipzig, 1912, J. A. Barth. 523 p.
Ruge (R.) & Zur Verth (A/.). Tropenkrankheiten und Tropenhygiene. Leipzig, 1912,
W. Klinckhardt. 471 p. 8°.
Scheube (B.}. The diseases of warm countries. Transl. from the German by Pauline
Falcke. Ed. by James Cantlie. 2d revised ed. Phila., 1903, P. Blakis-
ton's Son & Co. 604 P- 8°.
Ticks. A monograph of the ixodoidea. By G. H. F, Nuttall, Cecil Warburton, W. F. Cooper
and L. E. Robinson. Part I. Afgdsidae. Cambridge, 1908. 8°.
Wurtz (R.) & Thiroux (A.}. Diagnostic et semeiologie des maladies tropicales. Paris,
1905, Masson & Cie. 553 p. 8°.
332 DIAGNOSIS OF INFECTIOUS DISEASES
A. Diseases Due to Pathogenic Rhizopoda
Under this heading will be described the diseases due to pathogenic
amebae. The rhizopoda are characterized by the fact that they have pseu-
dopodia but no flagella.
Amebae. — The amebae are cells usually somewhat larger than white blood cor-
puscles, with strongly refractive protoplasm. On a warm stage, they show lively
ameboid movements. Often a clear hyaline ectoplasm can be distinguished from
a granular endoplasm. The protoplasm contains vacuoles, and sometimes bacteria
and red blood corpuscles. The nucleus is vesicular. Vegetative forms are distin-
guished from the encysted forms.
Amebae are difficult to cultivate, but cultures have been made in symbiosis with
bacteria. Amebae were first seen in dysenteric stools by Loesch (1875), who named
the organism Ameba coli. Kartulis first produced experimental infection in cats.
Kruse and Pasquale ruled out bacteria as the cause of the disease. Councilman
and Lafleur showed that besides the pathogenic Ameba dysenterice a harmless
ameba may be present in the stools. This harmless Entameba coli may occur in
normal persons, but it is seen more often in chronic diarrhea. The pathogenic
Entameba histolytica (Schaudinn, 1903) is the cause of amebic dysentery and
of tropical liver abscess. The disease can be produced in cats by experimental
inoculation of the rectal mucous membrane. Sellards and Baetjer (1914) have
kept the disease going for more than 10 passages through cats by injection into
the large intestine after laparotomy. In the stools, the amebae are best looked for
in flecks of mucus, or blood.
Viereck (1907) endeavored to distinguish an additional species, Entameba
tetragena (nucleus visible during life, always spherical, and possessing a definite
limiting membrane; 4 nuclei in the mature cyst); this view was supported by
Hartmann, but more recent studies (Craig; Sellards and Baetjer) indicate that
E. histolytica (of East Asia and Egypt) and E. tetragena (of Africa and S. Amer-
ica) may be one and the same species. In both forms, the formation of chromidia
and of cysts has been carefully followed.
In certain cases of mild dysentery, an actively motile flagellate is sometimes
present which is neither cercomonas nor Entameba histolytica. An especial species
has been described by Craig as Parameba hominis and afterwards renamed by
others Craigia hominis. Marlowe has described about thirty cases of craigiasis in
Honduras.
1. Human Amebiasis
Under this heading, we include Amebic Dysentery, Amebic Abscess
of the Liver, and Amebic Pyorrhea.
(a) Amebic Dysentery
Occurrence. — This disease, very common in the tropics, is widespread,
also, in the Southern United States. We meet with it frequently in the
clinic in Baltimore.
Symptoms. — The symptoms are usually those of a chronic dysentery
DISEASES DUE TO PATHOGENIC KHIZOPODA 333
(alternating periods of constipation and diarrhea with tenesmus ; mucus
and blood in the stools ; abdominal pain and frequently symptoms of dis-
turbed digestion). During the exacerbations of diarrhea, there is often
slight elevation of the temperature, tachycardia, colic, lassitude, headache,
prostration, dry skin, and scanty urine and saliva. The general state of
nutrition is good, at first, in contrast with that seen in acute and subacute
types of the disease. Rarely a perforative peritonitis or a hemorrhage
from the bowel occurs.
The disease is frequently overlooked, simply from failure to examine
the feces, microscopically, in cases of chronic diarrhea. The mucus
accumulated in the "eye" of a rectal tube is particularly suitable for
examination (warm stage).
Some cases of amebiasis have an acute onset with (1) abdominal pain,
often intense, (2) tenesmus constant and severe, (3) a marked intestinal
flux with very frequent evacuations of blood and mucus, and (4)' rarely,
the passage of large amounts of blood, or sloughs from ulcers. There may
be (5) slight pyrexia. There is usually (6) eosinophilia. The prolonged
diarrhea may lead to (7) extreme emaciation. Death may occur in from
one week to three months from inanition and exhaustion. Some of the
cases of this type pass over into the chronic form of the disease.
Diagnosis. — This is easy, if one thinks of the possibility of the diarrhea
being due to amebiasis, and examines the stool microscopically for amebae.
A proctoscopic examination may reveal the characteristic undermined
ulcers in the rectum. The therapeutic test confirms the diagnosis, for the
amebae quickly disappear under the use of salol coated pills containing
ipecac (70 grains per day), or under hypodermic injection of emetin
hydrochlorid (Rogers). (For a further description of amebae in feces,
see Part VIII.)
(6) Amebic Abscess of the Liver
This is common in hot countries (tropical liver abscess). It is really
not an abscess, but a widespread necrosis, with softening, often without
marked leukocytosis. It is one of the most frequent complications of
amebic dysentery, occurring in about 20 per cent of the cases at the Johns
Hopkins Hospital.
The abscess may be single, or multiple. It most often involves the
right lobe of the liver, especially at its convexity (x-ray examination ;
increase in dullness on percussion). The disease may be entirely latent;
more often it is accompanied by irregular fever, sweats, chills, local pains,
and enlargement of the liver. Leukocytosis, 15,000-16,000, with eosino-
philia, is common. Amebic abscesses of the liver sometimes break through
into the lung, and the diagnosis is first made by finding amebae in the
anchovy-sauce sputum. (See also Hepatic Abscess in Part VIII.)
334 DIAGNOSIS OF INFECTIOUS DISEASES
(c) Amebic Pyorrhea
This disease, known also as Riggs' disease, and associated with the pres-
ence of Entameba buccalis, will be described in Part VIII under Pyorrhea
alveolaris.
References
Baetjer (W. A.} & Sellards (A. W.). Continuous propagation of amebic dysentery in
animals. Johns Hopkins Hosp. Bull., Baltimore, 1914, xxv, 165-173.
The behavior of amebic dysentery in lower animals and its bearing upon
the interpretation of the clinical symptoms of the disease in man. Johns
Hopkins Hosp. Bull., Baltimore, 1914, xxv, 237-241.
Calkins (G. JV.)« Genera and species of amoeba. Tr. XV. Internal. Cong. Hyg. & Demog.,
Washington (1912), 1913, ii, 287-306.
Chauffard (A.). La dysenterie amibienne chronique. Presse mid., Paris, xxi, SS9-391.
Councilman (W. T.) '& Lafleur (H. A.). Amebie dysentery. Johns Hopkins Hosp.
Rep., Baltimore, 1889, i.
Craig (C. F.}. Parasitic amebae of man. Philadelphia & London, 1911, J. B. Lippincott
Co. 268 p. 8°.
Observations upon the morphology of parasitic and cultural amebae. J. M.
Research, Boston, 1912, n. s., xxi, 1-87.
The classification of amebas, with observations on morphology and life
cycle of Entameba coli, Craigia hominis and Vahlkampfia lobospinosa.
Arch. Int. Med., Chicago, 1914, xiii, 737-769.
Decks (W. E.~). Treatment of dysentery due to infection with Entameba histolytica. J. Am.
M. Ass., Chicago, 1913, Ix, 38-42.
Fantham (H. B.). On the amebae parasitic in the human intestine, with remarks on the
life cycle of Entameba coli in cultures. Ann. Trop. M. & ParasitoL,
Liverpool, 1911, v, 111-123.
Hartmann (Af.). Die Dysenterie-Amoben. In: Handb. d. pathogen. Protoz. (Prowazek),
Leipzig, 1912, i, 50-66.
Unlcrsuchungen uber parasitische Amdben. II. Entameba tetragena
Viereck. Arch.f. Protistenk., Jena, 1912, xxiv, 163-181.
Hartmann (M.) & Withmore (E.). Untersuchungen uber parasitische Amdben. Ill,
Entameba coli em. Schaudinn. Arch. f. Protistenk., Jena, 1912, xxiv,
182-194.
Kartulis (S.). Die Amobendysenterie. In: Handb. d. pathogen. Mikroorg. (Kolle &
Wassermann). 2. Aufl. Jena, 1913, vii, 651-686.
Lynch (K. M.). Concerning endamebiasis of the mouth. Am. J. Trop. Dis. & Prevent. M.,
New Orleans, 1915, in, 231-242.
Musgrave (W. E.} & Clegg (M. T.). Amebas: their cultivation and etiologic significance.
Bureau Gov't Lab., Bull. 18, Manila, P. I., 1904, 8°.
Osier (W.). On the ameba coli in dysentery and in dysenteric liver abscess. Johns Hop-
kins Hosp. Bull., Baltimore, 1890, i, 53-54.
Patterson (H. S.). End.emic amebic dysentery in New York, with a review of the distril
tion in North America. Am. J. M. Sc., Philadelphia, 1909,-cxxxi
198-202.
v. Prowazek (S.). Entameba. Arch.f. Protistenk., Jena, 1912, xxv, 273.
Weitere Beitrage zur Kenntnis der Entameben, vi. Arch. f. Protistet
Jena, 1912, xxvi, 241-249.
Rogers (L.). Dysenteries; their differentiation and treatment. London, 1913, 1-336.
Amebic colitis in India: prevalence, diagnosis and emetine cure. Lam
London, 1912, ii, 1062-1067.
PATHOGENIC MASTIGOPHORA, OR FLAGELLATA 335
Schaudinn (F.). Untersuchungen uber die Fortpflanzung einiger Rhizop'oden. Arb. a. d. k.
Gsndhtsamte, Berlin, 1903, xix, 547-576.
Sellards (A. W.) & Baetjer (W. A.}. The experimental production of amebic dysentery
by direct inoculation into the cecum. Johns Hopkins Hosp. Bull., Bal-
timore, 1914, xxv, 323-328.
Immunity reactions with amebae. Philippine J. Sc., Manila, 1911, B.,
vi, 281-298.
Strong (R. P.}. Amebic dysentery. Mod. Med. (Osier & McCrae). 2d ed. 1914, ii,
17-53.
Viereck (H.). Sludien uber die in den Tropen erworbene Dysenteric. Leipzig, 1907, J. A.
Earth. 41 p. 8°.
Forms Hft. I of: Beihefte z. Arch. f. Schiffs- u. Tropenhyg.
Walker (E. //.)• A comparative study of the amebae in the Manila water supply, in the
intestinal tract of healthy persons and in amebic dysentery. Philippine
J. Sc., Manila, 1911. B. vi, 259-277.
Wells (R. T.)* Aerial contamination as a fallacy in the study of amebic infections by cul-
tural methods. Parasitology . Cambridge, 1911, iv, 204-211.
Werner (//.)• Entameba coli. In: Handb. d. pathogen. Protoz. (Prowazek), Leipzig, 1912,
i, 67-77.
Whitmore (E. R.). Vorldufige Bemerkungen uber Amoben aus Manila und Saign.
Centralbl.f.Bakteriol, 1. Abt., Jena, 1911, Iviii, Orig., 234-235.
B. Diseases Due to Pathogenic Masti-
gophora, or Flagellata
Several relatively unimportant flagellates are occasionally met with as
human parasites: (1) Tricliomonas vaginalis; (2) Tricliomonas intesti-
nalis; (3) Lamblia intestinalis (Megastoma entericum) ; (4) Cercomonas
hominis).
Certain very important human diseases are, however, due to the fol-
lowing pathogenic flagellates ; (5) Pathogenic Trypanosomidce (Trypano-
soma gambiense; Trypanosoma rhodesiense; Schizotrypanum cruzi) ; (6)
pathogenic Piroplasmidce (Leishmania donovani; Leichmania infantum;
Leishmania tropica) ; (7) pathogenic Plasmodidce (Malaria), 3 varieties;
(8) Spirocliceia obermeieri; and (9) Treponema pallidum.
According to Hartmann, the parasitic Flagellates can be classified as follows:
Phylum :
Protozoa.
Class: MASTIGOPHORA (= whip -bearing organisms).
Order: Binucleata.
1. Family: Trypanoplasmidas.
2. Family: Trypansosomidce.
(a) Leptomonas.
(b) Herpetomonas.
(c) Trypanosoma.
(d} Schizotrypanum.
(e) Endotrypanum.
3. Family: Halteridae.
336 DIAGNOSIS OF INFECTIOUS DISEASES
4. Family: Leukocytozoidae.
5. Family: Hemogregarinada3.
6. Family: Piroplasmidce.
(a) Leishmania.
(b) Toxoplasma.
(c) Babesia.
7. Family: Plasmodidce.
(a) Achromaticus.
(b) Polychromophilus.
(c) Proteosoma (Malaria of Birds).
(d) Plasmodium (Human Malaria).
1. Plasm, vivax (Tertian).
2. Plasm. malariaB Laveran (Quartan).
3. Plasm, immaculatum Grassi-Feletti (Estivo-
autumnal).
8. Spirochceta and Treponema.
Common to these parasitic Binucleates is (1) the complicated developmental
cycle, with usually an asexual multiplication (schizogony) , and a sexual multipli-
cation (gametogony] , and (2) the adaptation to life in different species of animals.
1. Diseases Due to Pathogenic Trypanosomidae
(Human Trypanosomiasis)
Trypanosomes. — These parasites are Protozoa, Class MASTIGOPHORA, Order
Binucleata, Family Trypanosomida?. In man, three main varieties cause disease:
(1) Trypanosoma gambiense, which causes sleeping-sickness; (2) Trypanosoma
rhodesiense, in a variety of sleeping-sickness; (3) Schizotrypanum cruzi, which
causes the thyreoiditis parasitaria, or Chagas' disease, in Brazil.
Many trypanosomes can be tolerably easily grown on artificial culture media
(Novy and McNeal) ; unfortunately the method is not so successful with the highly
pathogenic varieties as with the nonpathogenic forms.
Trypanosoma gambiense. — This parasite, the cause of sleeping sickness,
was described by Dutton (1901) in trypanosome fever (attention having
been earlier called by Forde to the presence of a parasite; it is a small
(16-30 ft), fish-shaped flagellate provided with an undulating membrane;
it is found in the blood plasma, where it shows active motility and multi-
plies by fission in the long axis. It is 3 times the length of a red blood
corpuscle. In the middle of its body is situated the principal nucleus, and
at the blunt end, a smaller nucleus (blepharoblast) , whence a long thread
runs along the body, helping to form the undulating membrane, and pass-
ing beyond the sharp end of the body as a free flagellum. Eesistant forms
and resting forms are now being studied; they are small round bodies
with two nuclei, and without flagellum (Moore and Breinle, 1907) ; these
forms are infectious (Fantham). Chemotherapeutic experiments indi-
cate that several races exist.
PATHOGENIC MASTIC OPHOKA, OR FLAGELLATA 337
Mode of Infection. — The parasite is transferred to man by the bite of
one of the tsetse flies, Glossina palpalis (Button and Todd) (Fig/ 98),
which is abundant on the banks of streams in Africa, and perhaps also by
the bite of Glossina morsitans — by the latter especially in high, dry places,
by the former in low, damp regions.
Fig. 98. — Glossina palpalis (Tsetse Fly). x5. (After Donitz.)
The trypanosomes taken up by the fly undergo a cycle of development in
the digestive tract of the insect (Gray and Tulloch, Bruce) ; sexual forms appear
and multiply, becoming infective for man about the third day, and they con-
tinue to be infective for at least 75 days (Bruce) ; it seems probable now, that
the fly, once infected, retains the capacity of transmitting the infection for the
rest of its life, that is for a year or longer. Only about 5 per cent of the flies
ingesting trypanosomes become infected. It is also asserted that the trypanosome
can be transferred from one human being to another by sexual intercourse (Koch,
Kudicke).
It has recently been found that trypanosomes give rise to specific agglutinins,
precipitins, trypanolysins, etc., and that these substances can be used for the
differentiation of varieties that closely resemble one another morphologically
(Laveran and Mesnil).
Other Trypanosomes. — A number of different species of trypanosomes
have been distinguished in animal infections (surra, dourine, nagana, etc.).
In the Brazilian trypanosomiasis, children suffer from thyroiditis para-
sitaria (Pereira) due to infection with Schizotrypanum cruzi (Chagas),
transmitted by the insect Conorrhinus megistus, or Triatoma; and in
Rhodesia (Stephens and Fantham), in Nyassaland (Bruce), and in Ger-
man East Africa (Taute), there is a form of trypanosomiasis, known as
, due tto tjie Trypanosomg, rhofasiertfe,, in which the principal
338 DIAGNOSIS OF INFECTIOUS DISEASES
nucleus lies at the posterior end of the body, "behind the hlepharoblast ; the
disease resembles that due to T. gambiense, and is transmitted by the fly
Glossina morsitans (Kinghorn and Yorke, 1912), perhaps also by Glossina
brevipalpalis ; 16 per cent of the antelopes in the district harbor the
parasite.
(a) Congo Trypanosome Fever and Sleeping -Sickness
Definition. — A disease common among the negroes in tropical Africa,
known since 1373, attacking also the whites, most prevalent in the region
of the Congo and its tributaries, and due to invasion by the Trypanosoma
gambiense (Dutton) (bite of the fly Glossina palpalis). (See above.)
In 1903, at the suggestion of Bruce, Castellani examined the cerebrospinal
fluid of negroes suffering from sleeping sickness and found the trypanosome that
Dutton had described in trypanosome fever. The disease can be spread only
where the tsetse fly exists; this fly can live in certain districts only (wooded
banks of streams). The disease is carried from one district to another by infected
negroes. Antelopes, cattle and dogs, as well as man, can harbor the Trypanosoma
gambiense (Bruce). It is possible that crocodiles also act as carriers of this
trypanosome (Koch).
Symptoms. — The incubation period is believed to be 10 to 20 days. The
onset is gradual with fever, chills, headache, and vomiting, suggesting a mild
malarial attack. Examination of the blood at this stage may reveal the
presence of the trypanosomes. The temperature falls in a few days, after
which there is a period of well-being lasting several days, or weeks, to be
followed by a second febrile attack. Such alternating periods of fever and
apyrexia may continue for months (so-callod TRYPANOSOME FEVER). An
early and peculiar symptom is hyperesthesia of the deep muscles on
pressure. After a time, the patients complain of headache and of pains
in the extremities, and the cervical lymph glands become enlarged but not
painful (Greig and Gray). In white people erythemas may come and
go. Edema of the ankles and about the eyes and cheeks is not uncom-
mon. There is no marked anemia at first, though later in the disease it
may be profound. The leukocyte count is low, with relative increase in
both the large and small mononuclear elements.
The trypanosome fever, after lasting for months, goes over into true
SLEEPING-SICKNESS (invasion of the central nervous system and the cere-
brospinal fluid by the trypanosomes). The cerebrospinal fluid shows also
an increase, in globulin-content. The patients become depressed, apa-
thetic, tremulous; mental defects appear, and sometimes epileptiform
attacks develop. The patients become lethargic and somnolent. In the
more advanced cases, they sleep all the time and can scarcely be awakened
for meals, some going to sleep with food in their mouths. Emaciation is
rapid ; decubitus develops ; and death occurs from a complicating terminal
streptococcus sepsis..
PATHOGENIC MASTIGOPHOKA, OE FLAGELLATA 339
The disease may last for years, but appears to be always fatal, once
the nervous system has been invaded.
Diagnosis. — This depends upon demonstrating the presence of the try-
panosomes in the cervical glands, the blood, or the cerebrospinal fluid. In
the stage of trypanosome fever they may be looked for in the fresh blood
slide, especially by the dark-field method; a "thick-drop" of blood (Ross,
Ruge) will, in stained smears, often show the trypanosomes. They are
not numerous, and should, therefore, be looked for repeatedly in many dif-
ferent preparations on successive days.
As soon as the cervical glands become enlarged, gland juice can be
obtained by hypodermic puncture, and in this the trypanosomes are often
found (Todd).
After the nervous system has become invaded, the trypanosomes can
be demonstrated in the cerebrospinal fluid. This fluid shows, as a rule, in
sleeping-sickness, an enormous number of lymphocytes (sometimes 1,000-
1,200 per c.mm.).
In the differential diagnosis, the disease must be distinguished (1)
from malaria, and (2) from relapsing fever; either of these may compli-
cate a trypanosomal infection.
F. W. Mott has kindly shown me specimens from the brain of patients
dead of African sleeping-sickness ; the perivascular infiltration with small
mononuclear cells is very striking.
(6) Rhodesian Trypanosomiasis (Kaodzera)
Definition. — A disease prevalent in Rhodesia, similar to the trypanosome fever
and sleeping-sickness due to Trypanosoma gambiense, but due to a different para-
site, Trypanosoma rhodesiense (Stephens and Fantham), and showing certain
epidemiological peculiarities.
Occurrence. — Discovered in Rhodesia (1910), the disease has also been observed
in Nyassaland (Bruce), in Portuguese East Africa, and in German East Africa
(Taute).
Symptoms. — These are similar to ordinary sleeping-sickness, but the disease is
more virulent and progresses more rapidly. The incubation period lasts 5-10
days, and the course is rapid, averaging 4J months. The parasites are often
present in large numbers in the blood. The lymph glands may not be enlarged.
The three stages of the disease are well described by Shircore.
(c) Brazilian Trypanosomiasis (Chagas' Disease; Thyroiditis
parasitaria; Careotrypanosis)
Definition. — An endemic, acute and chronic disease due to Schizotrypanum
cruzi, occurring among. children, in the interior of Brazil, apparently related to
the parasitic thyroiditis prevalent there; the parasite is introduced by the bite of
an insect (see above).
Symptoms. — In the acute forms, small children under 1 year are affected during
the hot months (October to March). They sicken with high fever and enlargement
of the lymph glands, spleen and liver. Trypanosomes can be demonstrated in
the blood, for from 10 to 30 days, after onset. The thyroid becomes enlarged and
340 DIAGNOSIS OF INFECTIOUS DISEASES
signs of infantile myxedema develop (skin, bradycardia) . In the severer cases
signs of meningo-encephalitis develop, and the patients die, or, if they recover,
suffer from organic nervous lesions.
In the chronic forms it may not be possible to demonstrate the parasites on
microscopic examination of the blood, except during exacerbations, though they
can be recovered by inoculating a guinea-pig with the blood of the patient. The
heart muscle is often invaded.
References
1. General
Bruce (Sir David). Trypanosomiasis. Mod. Med. (Osier). 8°. Philadelphia & New York.
2d ed. 1914, ii, 116-132.
Castellani (A.}. The history of the association of trypanosoma with sleeping sickness.
Brit. M. J., London, 1903, ii, 1565.
Laveran (A.) & Mesnil (F.). Trypanosomes and Trypanosomiasis. 1st ed. Trans, by
D. Nabarro. London, 1907, Bailliere, Tindall & Cox. 528 p. 8°.
Low (G. C.). Sleeping sickness. In: Syst. Med. (Allbutt & Rolleston). 8°. London,
1910, ii, pt. 2, 208-226.
Mayer (M.). Trypanosomiasis des Menschen. Ergebn. d. inn. Med. u. Kinderh., Berlin,
1908, ii, 1-29.
Newham (H. B.}. Trypanosomiasis. J.Lond. Sch. Trop. Med., 1913, ii, 144-146.
Stephens (J. W. W.). Trypanosomiasis. In: Syst. Med. (Allbutt & Rolleston). 8°.
London, 1910, ii, pt. 2, 207-208.
2. The Trypanosomes
Bruce (D.). The etiology of sleeping sickness. Brit. M. J., London, 1903, ii, 1343-1350.
Bruce (Sir D.), Harvey (D.), Hamerton (A. E.}, Davey (J. B.) & Bruce (Lady}. The
morphology of the trypanosome causing disease in man in Nyassaland.
J. Roy. Army M. Corps, 1913, xx, 542-552.
The Croonian lectures on trypanosomes causing disease in man and domes-
tic animals in central Africa. Lancet, London, 1915, i, 1823; ii, 1; 91;
109.
Bruce (Sir D.}, Harvey (/>.)» Hamerton (A. E.} & Bruce (Lady}. The trypanosome
causing disease in man in Nyassaland. Susceptibility of animals to the
human strain. Proc. Roy. Soc., London, 1913, (B) Ixxxvii, (b) 592, 85-45.
Castellani (A.). Some observations on the morphology of the trypanosoma found in sleeping
sickness. Brit. M. J., London, 1903, i, 1431-1432.
Graham (L. W.) & Hutchinson (R. //.)• The influence of experimental trypanosomiasis
upon the body temperature of white rats. Am. J. Trop. Dis. [etc.], New
Orleans, 1913-14, i, 760-775,
Beckenroth (F.) & Blanchard (M.). Recherches sur V existence des proprietes trypano-
lytique, attachante, agglutinante et protectrice dans le serum des malades
atteints de trypanosomiase au Congo frangais. Ann. de Vlnst. Pasteur,
Paris, 1913, xxvii, 750-764.
Kinghorn (A.), Lloyd (L.) & Yorke (W.). On the development of Trypanosoma rho-
desiense in Glossina morsitans. Ann. Trop. M. & ParasitoL, Liverpool*
• 1912-1913, vi, 495-503.
Kleine (F. K.) & Eckard (B.). Uber die Bedeutung der Haustiere und des Wildes fur
die Verbreitung der Schlafkrankheit. Ztschr. f. Hyg. u. Infektionskrankh.,
Berlin, 1913, Ixxv, 118-122.
Kolle (W.)t Hartoch (Q.) & Schurmann (W.). Chemotherapeutische Experimental-
studien bei Trypanosomeninfektionen. Mittlg. 2. Ztschr. f. Immunjr
tatsforscfy. u. exp. Therap., Orig., Jena, 1913, xx, 436-475.
PATHOGENIC MASTIGOPHOEA, OK FLAGELLATA 341
Kolmer (J. A.). A method of transmitting known numbers of trypanosomes , with a note on
the numeric relation of trypanosomes to infection. J. Infect. Dis., Chicago,
1915, xvi, 79-94.
Mac fie (J. W. S.). Trypanosomiasis of domestic animals in Northern Nigeria. Ann.
Trop. Med. and ParasitoL, London, 1913, vii, 1-26.
McNeal (W. C.) & Novy (F. G.). On the cultivation of trypanosoma Lewisi. Contrib.
Med. Research (Vaughan), Ann Arbor, Mich., 1903, 549-577.
MacNeal (W. J.). The life-history of trypanosoma Lewisi and trypanosoma Brucei. J.
Infect. Dis., Chicago, 1904, i, 517-543.
Mayer (M.). Trypanosomen als Krankheitserreger. In: Handb. d. pathogen. Mikroorg.
(Kolle & Wassermann). 2. Aufl. Jena, 1913, vii, 321-418.
Plimmer (H. G.) & Bradford (J. .)• A preliminary note on the morphology and distri-
bution of the organism found in the tsetse fly disease. Proc. Roy. /Soc.,
Lond., 1899, Ixv, 274-281.
v. Prowazek (5.). Uber reine Trypanosomenstamme. Zentralbl. f. Bakteriol., Orig., Jena,
1913, Ixviii, 498-501.
Stephens (J. W. W.} & Fantham (H. /?.). Trypanosoma rhodesiense. A second species
of African trypanosome producing sleeping sickness in man. Brit. M. J.,
London, 1912, ii, 1182.
Taute (M.). Zur Morphologic der Erreger der Schlafkrankheit am Rowennafluss (Deutsch-
Ostafrika). Ztschr. f. Hyg., Leipzig, 1913, Ixxiii, 556-560.
Vrijburg (A.). Trypanosomen. Folia microbioL, Berlin, 1913, ii, 79-94-
Yorke (W.) & Blacklock (/?.)• The differentiation of the more important mammalian
trypanosomes. Ann. Trop. M. & Parasitol., Liverpool, 1914-15, viii, 1-12.
3. African Sleeping Sickness
Bruce (D.} & Nabarro (/>.)• Progress report on sleeping sickness in Uganda. Roy. Soc.
Rep. Sleep.-Sick. Com., London, 1903, i, 11-88.
Camac (C. N. B.}. Human trypanosomiasis. Report of a case, with special reference to
the treatment. Am. J. M. Sc., Philadelphia, 1911, n. s. cxlii, 658-674.
Castellani (A.). On the discovery of a species of trypanosoma in the cerebrospinal fluid of
cases of sleeping sickness. Proc. Roy. Soc. Lond., 1902-03. Ixxi, 501.
Chalard (J. H.} & Guthrie (C. G.). Human trypanosomiasis: report oj a case observed
in Baltimore. Am. J. Trop. Dis. [etc.], New Orleans, 1913-14, i, 493-503.
Dutton (J. E.). Preliminary note upon a trypanosome occurring in the blood of man.
[T. gambiense.] Thompson Yates Lab. Rep., Liverpool, 1902, iv, pt. 2t
455-470.
Also: Brit. M. J., London, 1902, ii, 881; 1680.
Dutton (J. E.) & Todd (J. L.}. First report of the trypanosomiasis expedition to Sene-
gambia (1902}. With notes by H. E. Annett and appendix by F. V.
Theobald. Liverpool, 1903. 4°.
Hoffmann (W. H.). Ueber Wesen und Ursache der Afrikanischen Schlafkrankheit. In:
Ergebn. d. allgem. Pathol. [etc.] (Lubarsch & Ostertag). Wiesbaden, 1912,
xvi, Abth. i, 341-453.
Kinghorn (A.}, Yorke (W.} & Lloyd (L.)» Final report of theLuangwa Sleeping Sickness
Commission of the British South Africa Company, 1911 to 1912. Ann.
Trop. Med. and ParasitoL, London, 1913, vii, 183-302.
Oswald (F.). Alone in the sleeping-sickness country. New York, 1915. 231 p. 8°.
Schilling (C.). Beobachtungen uber die Schlafkrankheit in Uganda. Deutsche med.
Wchnschr., Leipzig u. Berlin, 1913, xxxix, 2094-2096.
Shircore (J. O.). Nyassaland Trypanosome fever. Tr. Soc. Trop. Med. & Hyg.,Londonf
1913, vi, 131-142.
Todd (J. L.). The duration of trypanosome infections. Arch. Int. Med., Chicago, 1911,
vii, 500-505.
342 DIAGNOSIS OF INFECTIOUS DISEASES
Todd (J. L.) Concerning the age and sex of Africans suffering from trypanosomiasis.
Ann. Trop. M. & Parasilol, Liverp , 1913, vii, 309-319.
Todd (J. L.) & Wolbach (S. B.}. The diagnosis and distribution of human trypanosomia-
sis in the colony and protectorate of the Gambia. Ann. Trop. M. &
Parasitol, Liverpool, 1911, v, 245-286.
4. Brazilian Trypanosomiasis
Brumpt (E.}. Le Trypanosoma Cruzi evolue chez Conorhinus magistus, Cimex lectularius.
Cimex Boueti et Ornithodorus moubata; cycle evolutif de ce parasite. Bull.
Soc. path, exot., Paris; 1912, v, 360-367, 723.
Immunite partielle dans les infections a Trypanosoma Cruzi, transmission
de ce trypanosoma par Cimex rotundatus; role regulateur des holes inter-
mediares; passage a travers le peaux. Butt. Soc. path, exot., Paris, 1913,
vi, 172-176, 382.
Brumpt (E.) & Pirajoa da Silva. Existence du " Schizotrypanum Cruzi," Chagas, 1909,
a Bahia (Malta de Sao Joao); biologie du " Conorhinus megislus." Bull.
Soc. path, exot., Paris, 1912, v, 22-26.
Chagas (C.). Thireoidite parasitaria. Rev. med. de S. Paulo, 1912, xv} 337-350.
Les formes nerveuses d'une nouvelle trypanosomiase (Trypanosoma Cruzi
in'tcule par Triatoma magista) (Maladie de Chagas). J\ouv. iconogr. <lc
la Salpetr., Paris. 1913, xxvi, 1-9.
Franck (A. J. //.)• La nouvelle trypanosomiase humaine ou trypanosomiase americaine.
[T. cruzi.] Bordeaux, 1910. 8°.
Vianna (C.). Contribuicao para estudo da anatomia palalojica da " Molestia de Carlos
Chagas." (Esquizotripanose humana ou tireoidite parazitaria.) Mem.
do Inst. Oslwaldo Cruz, Rio de Janiero, 1911, Hi, 276-294.
2. Diseases Due to Varieties of Leishmania
(Human Leishmaniasis)
Varieties of Leishmania. — These parasites are Protozoa, class Masti-
gophora, order Binudeata, family Piroplasmidce, species Leishmania.
Three varieties are known to invade human beings: (1) Leishmania dono-
vanif causing kala-azar ; (2) Leishmania infantum, causing infantile leish-
maniasis; and (3) Leishmania furunculosa sive tropica, causing oriental
sore, or cutaneous leishmaniasis.
Leishmania donovani. — This protozoon appears in the form of small
ovoid corpuscles (2-4 /A) with two characteristic nuclei, one main nucleus,
rounded, the other, accessory nucleus, oblong or rod-shaped (Plate VIII,
Fig. 2). These corpuscles are usually enclosed in macrophages (endo-
thelial cells, large mononuclear leukocytes) ; they are occasionally seen in
polymorphonuclear neutrophils and in eosinophils but never in lymphocytes
or in erythrocytes (Patton).
They undergo bipartite subdivision occasionally, dividing into four. Close to
the accessory nucleus, can sometimes be seen a rhizoplast, or flagellum-root. In
isotonic solutions of sodium citrate, or on McNeal-Novy-Nicolle agar-medium, these
corpuscles grow out, in a few days, into small club-shaped flagellates (L. Rogers,
1904). These parasites differ from trypanosomes, in that the flagellum is formed
at the posterior end directly from the blepharoplast (accessory nucleus) out of the
rhizoplast, and no undulating membrane is formed. In nature, a similar develop-
ment into flagellates appears in the intestinal canal, in the bed-bug, and perhaps
PATHOGENIC MASTIGOPHORA, OE FLAGELLATA 343
in other insects (fleas, flies). The parasite is pathogenic for monkeys (Row).
Spontaneous infection of cats and dogs rarely, if ever, occurs (in contrast with
L. infantum).
(a) Kala-Azar
(Tropical Splenomegaly, Dum-Dum Fever, Cachectic Fever)
Definition. — A tropical disease, characterized by enlargement of the
spleen and liver, progressive anemia, and outspoken cachexia, due to
invasion with Leishmania donovani (R. Ross).
It is common in India, having been known there since the English observed it
in 1869, but occurs also in China, Arabia, Egypt, Algiers, Italy, Greece, and
Portugal. In Assam, over 26 per cent of the population is infected before the
tenth year, 50 per cent or more by the twentieth year (Clarke and McNaught; L.
Rogers). The disease was supposed to be a form of malaria until Leishman
(1903) discovered the parasite in spleen cells. His observation was confirmed by
Donovan and others, and soon examinations for the parasite were used for the
diagnosis of clinical kala-azar (Bentley, Christophers, L. Rogers). The disease
is probably transmitted by an insect, Clinocoris rotundatus (Patton, 1907, 1912),
or, possibly, by Conorrhinus rnbrofasciatus (Donovan).
Symptoms. — The incubation period lasts about 20 days, but may be
longer. The disease is -characterized by (1) splenic tumor, the spleen often
extending to the umbilicus; (2) irregular fever (two elevations every 24
hours); (3) progressive anemia; and (4) an extraordinary leukopenia
(L. Rogers). In 90 per cent of cases, there are less than 3,000 W. B. C. ;
in 40 per cent less than 1,000. Leishman described three stages of the
disease: (1) initial stage; (2) febrile stage with splenomegaly; and (3)
cachectic stage.
The course is chronic (6-18 months) ; more acute and more chronic
forms also occur (3 months; 10 years). %The mortality is about 98 per
cent without treatment ; with treatment it can be reduced to 70 per cent.
Diagnosis. — The parasites can sometimes be demonstrated (Leishman's,
Wilson's, or Giemsa's stains) in the leukocytes in blood smears; 5-30 are
present in a smear from 73.2 per cent (Donovan) to 86.8 per cent (Mar-
shall) of advanced cases; in one instance, Patton found 1,043 in a single
smear. Diagnosis by the blood smear, however, is often difficult. It is
much easier to demonstrate the parasites in smears of splenic juice (dry,
sterile syringe !), but great care should be taken in splenic puncture (q. v.).
Some puncture the liver for diagnosis, as there is less danger of hemor-
rhage. Others examine the bone-marrow of a rib or trephine the tibia.
Occasionally, a cutaneous ulcer is present, and smears from it reveal the
parasites. The parasites occur in ulcers of the intestine (Manson and
Low) ; in one instance they were found in mucus in the feces (Rach and
Zarfl). ^"ovy recommends blood cultures (10 c.c. blood) on N. N. N".
agar, for diagnostic purposes.
In advanced cases, the cachexia, the earthy color, the splenomegaly, and
344
DIAGNOSIS OF INFECTIOUS DISEASES
the enlargement of the liver are-characteristic. In early cases, the marked
leukopenia should excite suspicion.
Differential Diagnosis. — The disease has to be differentiated (1) from
malaria; (2) from Banti's disease; (3) from oilier forms of splenomegaly
(q. v.) ; (4) from Malta fever; and (5) from typhoid and paratyphoid.
The important thing is to think of the possibility of kala-azar.
(6) Infantile Kala-Azar or Infantile Leishmaniasis
The Leishmania infantum of Nicolle, which causes infantile kala-azar of Tunis,
Southern Italy, and the shores of the Mediterranean Sea generally, attacks chil-
dren rather than adults, causing anemia and splenomegaly. Dogs, cats and monkeys
are susceptible. Fleas (Pulex irritans, Pulex serraticeps) appear to transmit the
disease ("Basile, Visentini). The parasite differs somewhat from that of the
kala-azar of adults; it grows much more easily on N. N. N. agar (Nicolle). Dogs
can be infected experimentally (Novy). Clinically, there is enormous enlarge-
ment of the spleen, emaciation and cachexia; there may be severe diarrhea at the
beginning. There is leukopenia and moderate anemia (Jemma, Cannata, di Chris-
tina). It is much more difficult to find the parasites in blood smears than in
kala-azar of adults, though by long search they are found; Cannata demonstrated
them in 7 out of 8 cases.
(c) Cutaneous Leishmaniasis or
Oriental Sore
(Leishmaniasis cutanea, Bouton
d' Orient, Delhi Boil, Bouba, Utah)
Leishmania tropica. — This flagellate,
discovered by J. Homer Wright (1902),
differs slightly from the parasites of ka-
la-azar. Nicolle first grew it on N.N.N.
agar. It is the cause of Delhi boil.
The disease can be transferred to
man by inoculation (Deperer and Boinot,
1884), and to dogs and monkeys (Nic-
olle and Manceaux).
The disease has been given various
names, including Aleppo boil, Bagdad
sore, tropical sore, etc. This skin lesion
is widely distributed throughout the
world ; recently it has been shown to ex-
ist in a severe form in Brazil, Peru, and
Paraguay. The lesions are often mul-
tiple as in the "Espundia" of Peru, the
"Bouba" of Brazil and Paraguay, the
"Utah" of Peru (Strong, Tyzzer and
Sellards). Ulcers on the exposed parts
of the body appear, most often at the
end of summer, and in the early autumn
(insects.). Sections and smears of the
ulcer show the presence of Leishmania
99.— Oriental Sore. (After g, T,
Darling, Arch. Int. Med.)
PATHOGENIC MASTIGOPHOKA, OK FLAGELLATA 345
tropica. Occasionally, the parasites can be seen in the blood, or in regional lymph
glands. The disease is a less virulent type of leishmaniasis than the two pre-
ceding varieties. In the South American form, a severe buccopharyngeal local-
ization is sometimes seen. The disease in South America is often confused with
framboesia (yaws).
References
Caronia (6?.). Spezifische Agglutinine und Prddpitine bei der infantilen Leishmaniasis.
Ztschr. f. Immunitatsforsch. u. exp. Therap., Orig., Jena, 1913, xx,
174-177.
Castellani (A.}. Indian oro-pharyngeal Leishmaniasis. J. Trop. M. & Hyg., London,
1913, xvi, 49-50.
Concetti (//.)• II primo caso di Kala-azar constalo in Roma. II Policlinico, Roma, 1911,
xviii., 837-338.
Di Cristina (G.) & Caronia (G.). Ueber die Therapie der inneren Leishmaniasis.
Deutsches Arch. f. klin. Med., Leipzig, 1915, cxvii, 263-277.
Darling (S. r.)» Histoplasmosis: a fatal infectious disease resembling kala-azar among
natives of tropical America. Arch. Int. Med., Chicago, 1908, ii, 107-123.
Oriental sore in Panama. Arch. Int. Med., Chicago, 1911, vii, 581-597.
Gabbi (U.}. Uber den Ur sprung der Leishmaniasis interna (Kala-azar) vom Hunde-
Centralb. f. Bakteriol., Orig., Jena, 1913, Ixix, 504-516.
Jacquet (L.). Tropic ulcers of the hand and forearm. Pict. Atlas Skin Dis. & Syph.,
St. Louis Hosp., Land. Philadelphia, 1895-97, 233-236, 1 pi.
Jemma (U.)» L'anemie par leishmania. Arch, de med. des enfants., Paris, 1913, xvi,
721-766.
Leishman (Sir W. B.). Kala-azar. In: Syst. Med. (Allbutt & Rolleston). 8°. Lon-
don, 1910, ii, pt. 2, 226-241.
Critical review: Kala-azar and tropical sore. Quart. J. Med., Oxford,
1911-12, v, 109-152.
Mackie (F. P.}. The experimental transmission of Indian kala-azar to animals. Indian
J. M. Research, Calcutta, 1914-15, ii, 934-941.
Mayer (M.). Leishmanien. In: Handb. d. pathogen. Mikroorg. (Kolle & Wassermann).
2. Aufl. Jena, 1913, vii, 419-466.
Novy (F. G.)» Successful canine infection with cultures of Leishmania infantum (C. Nicolle).
Preliminary note. J. Am. M. Ass., Chicago, 1908, Ii, 1423-1424.
Sur Leishmania infantum. Bull. Soc. path, exot., Paris, 1909, ii, 385.
Patlon (W. S.). The parasite of kala-azar an<l allied organisms. Tr. Soc. Trop. Med. &
Hyg., London, 1908-09, ii, 113.
Also: Lancet, London, 1909, i, 306-309.
Rach (E.) u. Zarft (M.). Ueber den kulturellen Befund bei dem in Wien beobachteten Fall
von Kala-azar. Deutsches Arch. f. klin. Med., Leipzig, 1909, xcvi, 387-
396. 1 pi.
Rogers (L.). Kala-azar, its differentiation and its epidemiology. Lancet, London, 1907, i,
486, 568, 643. 1 pi.
Sluka (E.} & Zarft (M.). Ein Fall von Kala-azar aus Taschkent in Wien. Deutsches Arch,
f. klin. Med., Leipzig, 1909 , xcvi, 356-386.
Smith (T.). Preliminary observations on the microorganism of Texas fever. Med. News,
Philadelphia, 1889, Iv, 689-693.
Smith (T.) & Kilborne (F. L.). Investigations into the nature, causation and prevention
of Texas or Southern cattle fever. Rep. Bureau Animal Indust., 1891-92,
viii-ix, 177-304.
346 DIAGNOSIS OF INFECTIOUS DISEASES
Thomson (J. G.) & Pant ham (H. 1?.). The culture of Babesia (piroplasma) cam's in
vitro. Ann. Trop. Med. & ParasitoL, London, 1913, mi, 621 -532.
Wolbach (S. B.) & Todd (J. L.). A study of chronic ulcers (ulcus tropicum), from 1*>e
Gambia; third report of the Liverpool School of Tropical Medicine to the
Gambia in 1911. J. M. Research, Boston, 1912-13, xxvii, 27-43. 3 pi.
Woolley (P. G.). Tropical febrile splenomegaly. Philippine J. Sc., Manila, 1906, i,
533-545.
Some tropical cutaneous ulcerative conditions. J. Am. M. Ass., Chicago,
1907, xlviii, 789-792.
Wright (J. H.}. Protozoa in a case of tropical ulcer (Delhi sore). J. M. Research, Boston,
1903, x, 472-482. 4 pi.
3. Human Malaria
Parasites of Malaria. — These plasmodia lead their vegetative existence
upon red blood corpuscles. They show nn alternation of generations, the
ASEXUAL PROPAGATION (schizogony) being carried on in the blood of the
intermediate host (man), the SEXUAL PROPAGATION (gamogony or sporog-
ony) being carried on in the gastro-intestinal canal of the definitive host
(mosquito). The malarial diseases, as Laveran discovered, are due to
such parasites (malarial parasites), of which there are at least three
varieties (vide infra). These malarial parasites belong to the Family
Plasmodidw, of the Order Bmucleata, of the Class Mastigophora, which is
one of the great groups of Protozoa (cf. Prowazek).
LIFE HISTORY OP MALARIAL PARASITES. — In the accompanying figure (Fig. 100),
the development of these parasites is schematically illustrated. According to the
description given by Glaus Schilling, the youngest forms, or the merozoites (1)
penetrate the red corpuscles and begin to grow there. In the plasmodium, a
nutritive vacuole soon appears which gives the protoplasm a ring-shaped appear-
ance. As the plasmodia grow larger (2, 3, 4) pigment is formed. In the full-
grown parasite, the red corpuscle may be almost entirely filled by the plasmodium
(5). The vacuole disappears; the pigment increases. The parasite is now ready
to undergo segmentation, the whole period of growth requiring, for the tertian
and for the estivo-autumnal parasites, about 48 hours, and for the quartan
parasite about 72 hours. A "segmenter" (6) is a parasite undergoing subdivision
into a large number of merozoites. In the case of a tertian parasite, there are
15-25 segments; in the quartan parasite, 6-14, usually 8; and in the estivo-
autumnal parasite, 8-25. These small merezoites invade as yet unaffected red
corpuscles (1) and the cycle (schizogony) is gone through again. The pigment
is engulfed by phagocytes and is carried to the spleen and liver.
In addition to the schizontic forms, sexual forms, or gametes, also appear
(7, 12). They are distinguishable from schizonts in that they contain no vacuoles,
and in that, even when very small, they contain pigment. The male gametes, or
so-called microgametocytes (12, 13, 14) possess a rather homogeneous protoplasm
and abundant nuclear material, in contrast with the female gametes, or macro-
gametocytes (7, 8, 9), in which the protoplasm is granular and the nuclear material
less evident. These sexual forms grow more slowly than the schizonts. In the
estivo-autumnal form, they assume the form of "ovals" and "crescents."
PATHOGENIC MASTIGOPHOBA, OR FLAGELLATA 347
The female sexual forms (maerogametocytes) are capable of undergoing, with-
out fertilization, a process of segmentation (11) following upon nuclear reduction
(10), with formation of merozoites, which again start a new schizogonic cycle (1).
Fig. 100.— Cycle of Development of the Malarial Parasites. (After C. Schilling, in Mohr
& Staehelin's Handbuch.)
t is such parthenogenetic reproduction, by maerogametocytes that accounts for
latent infections with malaria, and, under certain circumstances relapses may be
thus started, especially in the spring of the year, or on removal of the patient from
one climate to another. The gametes are resistant, latent forms.
348
DIAGNOSIS OF INFECTIOUS DISEASES
Now it is the gametocytes (micro and macro) which start the sexual cycle
(sporogony) in the gastro-intestinal canal of mosquitoes. The Anopheles appears
to be the only species of mosquito in which this cycle occurs. But not every
species of Anopheles acts as a carrier. Thus in India, it has been found that
Anopheles rossi is unimportant, while Anopheles christopheri is a very important
host.
It is the "female of the species" which is concerned. Biting a patient whose
blood contains male and female gametes, remarkable changes take place in the
swallowed blood. The microgametocytes undergo what was formerly called
flag 'ella- formation. The pigment becomes concentrated, the nucleus divides into
8-10 parts, which become arranged in the periphery of the plasmodium. Sud-
denly, threadlike projections emerge from the surface (so-called flagella; in
Fig. 101.— Mosquitoes. (A) Resting Position of Culex on Vertical Surface, (B) Resting Posi-
tion of Anopheles on Vertical Surface, (C) Diagram of Typical Anophelina. (After
C. F. Craig, "Malarial Fevers," published by Wm. Wood & Co., N. Y.)
reality, micro gametes] . They consist chiefly of nuclear substance with a little
protoplasm (15), are actively motile, and become separated from the parent body,
which retains the pigment. They migrate as minute, snakelike bodies, among
the red blood corpuscles, until they find a macrogamete (9) that has undergone
reduction division and is ready for fertilization. A minute spermatozoonlike
microgamete penetrates the macrogamete at an elevated spot, the so-called fer-
tilization hillock (16) and fertilization (anisogamia) takes place. The fertilized
macrogamete, or zygote, soon changes into a wormlike structure called an ookinete
(17). This casts off the pigment, penetrates the wall of the stomach of the
mosquito, passing between the epithelial cells (18), and comes to lie in the
outer wall of the stomach (19), where it grows into a larger vesicle known as
an oocyst (20). In this, there gradually develop a large number of extremely
minute, spindle-shaped germs, each containing chromatin material (21). The
cyst wall ruptures and the minute germs are emptied into the body cavity of the
mosquito (22). These small sickle-shaped germs are known as sporozoites. They
PLATE V
Fig I
4
) xi
Fig II
< ;;
Fig III
9
Fig. 1. — Parasites of Tertian Fever: (1) Young Hyaline Form, (2) Beginning Pigmentation,
(3) Full Grown Body, (4 and 5) Segmenting Bodies.
Fig. 2. — Parasites of Quartan Fever: (1) Young Hyaline Form, (2 and 3) Developing Within
the Corpuscle, (4 and 5) Segmenting Bodies.
g< 3. — Parasites of Aestivo-autumnal Fever: (1) Small Refractive Ring-like Body, (2 and
3) Larger Disk-like and Ameboid Form, (4) Similar Pigmented Body, (5) Segmenting
Body, (6) Segmenting Parasite, (7) Crescent Form, (8) Ovoid Form, (9) Flagellating
Form. (After Thayer & Hewetson's "Malarial Fevers of Baltimore," ,T. H. H. Rep.)
PATHOGENIC MASTIGOPHOEA, OR FLAGELLATA 349
now wander through the body to the salivary gland in the neck of the mosquito,
penetrate the gland cells, and appear in large numbers in the ducts of this gland
(23). When a mosquito so infected bites a human being, the contents of the
salivary gland are injected into the wound, and the human being becomes inoculated
with the sporozoites. These enter the red corpuscles and start a schizogonic
cycle. The alternation of generations is thus completed, the asexual cycle in the
human body (schizogony), and the sexual cycle (gamogony, or sporogony) in the
body of the definitive host, the Anopheles mosquito.
(a) Tertian Malaria
Plasmodium vivax (Grassi and Feletti). — This parasite is best studied
in fresh blood, and in smears stained by Giemsa's or Wilson's stain. The
young forms appear as small rings, in diameter about £ that of a white
blood corpuscle. One-half of the ring is thicker than the other (seal-ring
form), but the red chromatin granule lies in the thinner half. At the end
of 24 hours, the rings fill about f of the corpuscle and contain dark brown
granules of pigment. The fresh blood slide, at this stage, shows active
ameboid movement and vacuolation of the parasite. The vacuole soon
grows smaller. At the end of 48 hours it has disappeared. The infected
red blood corpuscle is now markedly enlarged (1^ times its normal size),
the parasite containing actively dancing, yellowish-brown, pigment-gran-
ules. The red corpuscle shows a fine stippling of a brick-red color (Plate
VII, Fig. 1) in well-stained specimens (Schiiffner's stippling), not met
with in other malarial infections. Segmentation occurs at the end of 48
hours, each of the 15-25 segments containing nuclear material. (Plate VI,
Fig. 1.)
The gametocytes contain no nutritive vacuole, and are more pigmented
:han the schizonts. When half -grown, the male cells have a clear proto-
plasm and relatively little chromatin, while the female cells have a dark
granular protoplasm and relatively little loose-meshed chromatin. Wb^ix
full-grown, they are 1£ to 1| times the size of a red blood corpuscle.
(6) Quartan Malaria
Plasmodium malariaa (Grassi and Feletti). — During the first 24 hours
of its development, this parasite looks very much like the tertian parasite.
As it grows older, it tends to form an oblong band across the red blood
corpuscle. The pigment is blacker than that of the tertian parasite, and
the red blood corpuscle in which the parasite is contained, instead of
enlarging, contracts somewhat, is crenated, and has a brassy color. The
quartan parasite is less ameboid than the tertian, and soon loses its nutri-
tive vacuole. On segmentation, it gives rise to only 6-12 merozoites, which
arrange themselves in rosette-form around a pigmented center. At 60
hours, the quartan parasite is about the size of a red blood corpuscle. Seg-
mentation occurs at the end of 72 hours, (Plate VI, Fig. 2.)
350 DIAGNOSIS OF INFECTIOUS DISEASES
(c) Estivo-autumnal Malaria
(Tropical Malaria, Pernicious Malaria)
Plasmodium immaculatum sive precox (Grassi and Feletti). — This
differs from the parasite of tertian and quartan malaria, even in its young-
est stages. The protoplasm forms an extremely delicate ring, and two or
more parasites may be seen in a single red blood corpuscle. At the end of
40 hours, the ring is still delicate, and has a diameter f that of a red blood
corpuscle ; one-half of the ring is broader than the other, the thinner half
containing one or two nuclear particles. The pigment is extremely fine,
and is scattered, in the form of dust, throughout the protoplasm of the
parasite. The parasites are now largely withdrawn from the peripheral
blood, the further development going on in the internal organs (spleen,
bone-marrow). At the end of about 48 hours, segmentation occurs (8-25
merozoites). It is in this type of malaria that crescents and oval forms
are not infrequently seen in the blood. (Plate VI, Fig. 3.)
The infected corpuscles in estivo-autumnal cases are contracted (in
contrast with what happens in tertian malaria), and assume a dark-yellow,
brassy color. Stained intensely with Maurer's modification of the Roman-
owsky stain, the infected corpuscles exhibit dark, violet-red, irregular-
shaped spots of variable size (Maurer's spots, pernicious spots).
Epidemiology of Malaria. — Wherever malaria appears, an infected
human being, or an infected mosquito, must have introduced it. Human
beings with latent infection carry the parasites of the disease through
the winter. In spring, an attack of malaria may occur, owing to partheno-
genetic reproduction by a macrogamete. Anopheles mosquitoes bite the
patient, swallow blood containing gametes, and the spring crop of mos-
quitoes becomes infected. For the gamogenous cycle to develop in the
mosquito, external temperatures above 17° C. are necessary; the optimal
temperature lies between 20° and 30° C. (68°-86° F.). Malaria does not
occur in latitudes farther north than 60°, nor farther south than 40°.
The Anopheles multiplies in stagnant water (ditches, ponds, casks, tin
cans, etc.), not in larger bodies of water, nor in running streams nor above
a height of 5,000 feet. The parasites of human malaria, and of the Anoph-
eles mosquito do not, so far as is known, infect other animals. The ma-
larial parasites of birds, monkeys, horses and cattle are of entirely differ-
ent species.
Where there is no Anopheles, there is no malaria (excepting imported
cases). Thus in Barbadoes, the disease does not occur; there are no
Anopheles mosquitoes there, probably owing to destruction of the larvae
by a minnow known as Baricudos (Phoxinno).
In malarial countries, there are strange, unexplained epidemics of
very fatal malaria. Thus in India, in 1908, there were 100 million cases
PLATE VI
• •'"•'-.
Fig. 1. — Tertian Schizontes showing Schiifner's Stippling of the Red Cells.
After L. Mohr u. R. Staehelin, "Ilandb. d. inner. Med.," published by J.
Springer, Berlin.)
j.
Fig. 2.
Small and Middle Size Tropical Ring Large Tropical Ring Forms Stained with
Forms; Beginning Segmentation. Maurer's Modification of the Romanow-
ski Stain Showing the Pernicious Spots.
(After L. Mohr u. R. Staehelin, "Handb. d. inner. Med.," published by J. Springer, Berlin.)
PATHOGENIC MASTIGOPHORA, OR FLAGELLATA 351
of malaria, with 2 million deaths, at least double the yearly average. Dr.
Edwin C. Cort tells me that he has observed similar fatal epidemics in
Northern Siam.
Symptoms. — The incubation period lasts from 1 to 3 weeks. The onset
is sudden, after slight premonitory symptoms, with severe CHILL, chatter-
Fig. 102.— Tertian Malaria.
ing of the teeth, headache, palpitation, cyanosis, goose-skin, livid nails,
sometimes nausea and vomiting, small, frequent hard pulse, and rapid rise
of temperature, often to 105° or 106° F. The chill lasts for from 1 to 3
352
DIAGNOSIS OF INFECTIOUS DISEASES
hours. The feeling of cold then gives way to a feeling of burning HEAT
(2 to 4 hours), during which the face is red, the skin hot and dry, the res-
piration rapid and superficial, the pulse large and soft. The patient is
restless, thirsty, nauseated, complains of headache, and perhaps is slightly
106
105
104
103
101
100
99
96
Q
Fig. 103. — Two-Hourly Chart of Tertian Malaria.
delirious ; after this the temperature falls suddenly to normal or subnormal,
and the patient breaks out into a profuse SWEAT. Such an attack (malarial
paroxysm) lasts altogether from 7 to 10 hours, and corresponds to the
time of maturation and segmentation of a generation of parasites in the
blood. After the sweating, say from 12 to 18 hours after the onset of the
PATHOGENIC MASTIGOPHOBA, Oft FLAGELLATA 353
attack, the patient is greatly relieved and says that he feels well again,
though he may be weak.
In a single infection with tertian malaria, a generation ripens every
3rd day (TERTIAN FEVER). In a single infection with quartan malaria, a
generation ripens every 4th day (QUARTAN FEVER). In single infections
a 6 10 1 2. 6 10 I a
or i fe 10 a,
to z \ <o I 10
Fig. 104. — Two-Hourly Chart. Double Tertian Malaria.
with the estivo-autumnal malaria, the attacks usually occur every 3rd day.
In double tertian or triple quartan infections, a generation of parasites may
mature daily (QUOTIDIAN FEVER). In estivo-autumnal fever, there are
often many generations of parasites so that some segmentation is going on
all the time (CONTINUOUS MALARIAL FEVER) ; in the latter instance, the
course of the fever may resemble that of typhoid. Chills are often absent,
the paroxysms of fever are longer than in tertian fever, lasting usually
354
DIAGNOSIS OF INFECTIOUS DISEASES
over 20 hours, frequently with a more gradual ascent and descent of the
temperature than in the other forms.
The spleen soon becomes palpable and increases in size if the attacks
continue. The liver is sometimes enlarged. Herpes labialis is common,
T La.,. ./».*«;«. S. ffct: 1C,
Fig. 105.— Quartan Malaria.
as is also miliaria crystallina. Leukopenia is constant, except during the
paroxysm, when there is sometimes a slight leukocytosis. In latent infec-
tions, neuralgia may be a symptom.
In estivo-autumnal fever of the PERNICIOUS TYPE, severe and often
PATHOGENIC MASTIGOPHOKA, OE FLAGELLATA 355
fatal cerebral symptoms (malaria cerebri) or intestinal symptoms (choleri-
form malaria) may occur, due to thrombosis of capillaries with enormous
numbers of infected red corpuscles.
In long continued malaria the so-called MALARIAL CACHEXIA may
develop (grave anemia, pigmented skin, edema, enlarged firm spleen or
"ague-cake," hemorrhagic diathesis, secondary infections).
£l&k~U&!fA
Fig. 106. — Two-Hourly Chart Quartan Malaria.
Diagnosis of Malaria. — This is easy, if malaria be thought of and the
blood be searched for parasites (fresh, and stained, specimens). The
leukopenia helps to rule out ulcerative endocarditis and other septic proc-
esses, accompanied by intermittent fever. In the differential diagnosis, a
negative blood culture helps to rule out typhoid fever. The "therapeutic
test" with quinin rules out fevers oilier than those of malarial origin. The
absence of early jaundice, the presence of marked splenic enlargement, and
356
DIAGNOSIS OF INFECTIOUS DISEASES
-J-r-j-v-t--H---^-1-i- J*
.,r^...j.^..T...... .+ .£. ;,...;....j...,...j
H-H-H
msssmm
JEI
^
i • m
}
....._
IT/'
....
• .
:-
ill
4....
E:
Ff
:i
§ § § S S 5 | S S
Pig. 107.— Chart of Malarial Fever, Estivo-Autumnal Tertian.
(After W. S. Thayer, J. H. H. Bull.)
PATHOGENIC MASTIGOPHOEA, OE ELAGELLATA 357
the parasites in the blood rule out yellow fever. Dysentery, nephritis, and
in the tropics, sleeping-sickness, and relapsing fever may have to be con-
sidered in the differential diagnosis. In the United States the irregular
Fig. 108.— Estivo-Autumnal Malaria.
fever of tuberculosis is often supposed by patients, and even by physicians,
to be malarial ! The fever of syphilis is sometimes confused with malarial
fever.
Black-water fever is a malarial fever, associated with hemoglobinuria,
358
DIAGNOSIS OF INFECTIOUS DISEASES
and depending upon a hemolytic process, the exact nature of which is at
present obscure. (See Diseases of the Blood.) Some have thought that
quinin plays a part in giving rise to the hemolysin. (See Part VII.)
Considerable EXPERIENCE IN EXAMINING BLOOD is necessary for pro-
ficiency in malarial diagnosis. Unskilled observers often report a positive
Fig. 109.— Quotidian Malaria. (Double Tertian.)
finding when no parasites are present, and they often overlook parasites
when they are actually there. Occasionally, when no parasites are found,
the presence of pigment-containing leukocytes identifies the nature of the
infection.
PATHOGENIC MASTIGOPHOEA, OK FLAGELLATA 359
Pig. 110.— Temperature Chart of Malarial Fever. (Estivo- Autumnal Four-Hourly Chart.)
360
DIAGNOSIS OF INFECTIOUS DISEASES
ii
O 03
ert R
[5 "^
!l
01 a
5 a
II
PATHOGENIC MASTIGOPHOKA, OE FLAGELLATA 361
362 DIAGNOSIS OF INFECTIOUS DISEASES
References
1. General
Blanchard (JR.) & Langeron (M.). Le paludisme des macaques (Plasmodium cynomolgi,
Mayer, 1907). Arch, de parasitol, Paris, 1912-13, xv, 529-542. 2 pi.
Burnham (F. W. E.). Haemocytes and haemic infections. New York, 1913, E. B. Treat
& Co. 462 p. 226 pi.
Celli (A.). La Malaria secondo le nuove ricerche. 3d ed. Romae Milano, Societa Editrice
Dante Alighieri, 1903.
Craig (C. F.). The malarial fevers. Mod. Med. (Osier). 8°. Philadelphia & New
York, 2d ed., 1914, ii, 54-108.
The malarial fevers, haemoglobinuric fever and the blood protozoa of man.
New York, 1909, W. Wood & Co. 488 p. 4 pi. 8°.
Deaderick (W. H.}. A practical study of malaria. Philadelphia & London, 1909, W. B.
Saunders Co. 402 p. 8°.
Grassi (B.) et Feletti (R.). Malariaparasiten in den Vogeln. Centralbl. f. Bakteriol. u.
Parasitenk., Jena, 1891, ix, 403, 429, 461.
Ibid., 1891, x, 449, 481, 517.
Henson (G. E.). Malaria: etiology, pathology, diagnosis, prophylaxis and treatment, with
an introduction by C. C. Bass. St. Louis, 1913, C. V. Mosby Co. 190 p. 8°.
Laveran (A.}. Paludisme et Trypanosomiase. Paris, 1912, J. B. Bailliere & fils. 150 p.
8°. [Nouv. traite de med. de therap., v.]
MacCallum (W. G.). Notes on the pathological changes in the organs of birds infected
with haemocytozoa. J. Exper. M., New York, 1898, Hi, 103-116.
On the haematozoan infections of birds. J. Exper. M., New York, 1898,
iii, 117-136.
Mannaberg (/.)• Malarial diseases. Edited, with additions, by Ronald Ross, J. W. W.
Stephens and Albert S. Grunbaum. Authorized translation from the Ger-
man, under the editorial supervision of Alfred Stengel. Philadelphia &
London, 1905, W. B. Saunders Co. 517 p. 8°.
Nothnagel's Encyclopedia of Practical Medicine. Amer. ed.
Opie (E. L.). On the haemocytozoa of birds. J. Exper. M., New York, 1898 , Hi, 79-101.
Schilling (C.). Malaria. In: Handb. d. inn. Med. (Mohr & Staehelin), 1911, i, 925-967.
Thayer (William Sydney}. Lectures on the malarial fevers. New York, 1897, D. Apple-
ton & Co. 826 p. 9 pi. 8°.
Malaria. In: Syst. Med. (Allbutt & Rolleston). 8°. London, 1910 , ii,
pt. 2, 241-285.
Thayer (W. S.) & He wet son (John). The malarial fevers of Baltimore. Johns Hopkins
Hosp. Rep., Baltimore, 1895, v, 3-218.
Werner (H.). Neuere Ergebnisse der Malariaforschung. Ergebn. d. inn. Med. u. Kinderh.,
Berlin, 1911, vii, 1-21.
Ziemann (H.). Malaria. In: Handb. d. Tropenkrankh. (Mense). Leipzig, 1906 , in, 269-
657. 3 pi.
2. Epidemiological
Balfour (A.). A year's anti-malarial work at Khartoum. J. Trop. M. & Hyg., Lon-
don, 1913, xvi, 225-232.
Craig (C. F.). The prophylaxis of malaria, with special reference to the military service.
War Dept., Office of the Surgeon-General, Bull No. 6, Gov't Print. Office,
Washington, 1914. 116 p.
PATHOGENIC MASTIGOPHOKA, OE FLAGELLATA 363
Gor gas (W. C.). The sanitary organization of the Isthmian Canal as it bears upon anti-
malarial work. Military Surgeon, Richmond, 1909, xxiv, 261-267.
Some facts about malaria. Farmers' Butt. 450, U. S. Dept. Agri., 1911.
A preliminary report on the method for preventing the development of per-
nicious malaria. J. Trop. Med. & Hyg., London, 1911, xiv, 317-324.
King (A. F. A.). Insects and disease; mosquitoes and malaria. Pop. Sc. Month.. New
York, 1883, xxiii, 644-^58.
Legendre (/.)• La prophylaxie des affections causees par les moustiques et la destruction de
ces insectes a I'etat adulte. Bull. Soc. path, exot., Paris, 1913, vi, 205-209.
Le Prince (J. A.). Mosquito work in the Canal Zone. Internal. Clin., Philadelphia, 1911 ,
21st s., i, 186-198. 11 pi.
Mitzmain (M. B.). Anopheles as a winter carrier of plasmodium. Pub. Health Rep..
Washington, 1915, xxx, 2117-2121.
Ross (/?.)• Mosquito brigades and how to organize them. New York. 1902, Longmans,
Green & Co. 96 p. 8°.
Ross (Ronald). The prevention of malaria, with contributions by L. 0. Howard and W. C.
Gorgas [et al.]. New York, 1910, E. P. Dutton & Co. 669 p. 28 pi.
5ch. 8°.
Theobald (F. F.). Mosquitoes. In: Syst. Med. (Allbutt & Rolleston). 8°. London,
1910, ii, pt. 2, 122-168.
Walker (E. L.). The transmission of malaria in the Philippine Islands. Am. J. Trop. Dis.
& Prevent. M., New Orleans, 1915, in, 222-231.
3. Pathological
Barker (L. F.). A study of some fatal cases of malaria. Johns Hopkins Hosp. Rep.,
Baltimore, 1895, v, 221-279.
Bastianelli (G.) & Bignami (A.}. Studi sulla infezione malarica. Bull. d. r. Accad. med.
di Roma, 1894, xx, 151-237. 2 pi.
Councilman (W. T.} & Abbott (A. C.). A contribution to the pathology of malarial fever.
Am. J. M. Sc., Philadelphia, 1885, n. s., Ixxxix, 416-429.
Ewing (/.)• A case of malarial nephritis, with massing of parasites in the kidney. Am.
J. M. Sc., Philadelphia & New York, 1901, cxxii, 426-434.
4. Chemical
Brown (W. //".). Malarial pigment (hematin) as a factor in the production of the malarial
paroxysm. J. Exper. M., Lancaster, Pa., 1912, xv, 579-597.
Giemsa (G.). Biochemische Methoden bei Malariauntersuchungen. Handb. d. Biochem.
Arbeitsm. (Abderhalden) , 1912, vi, 193-222.
Simpson (G. C.) & Edie (E. £.). On hemoglobin metabolism in malarial fever. Ann.
Trop. M. & Parasitol, Liverpool, 1912, vi, 442-447.
5. The Malarial Parasites
ffass (C. C.). On the cultivation' of the malarial parasites in vitro by preventing the develop-
ment of complement in the human blood employed. J. Trop. Med. &
Hyg., London, 1911, xxv, 341,
364 DIAGNOSIS OF INFECTIOUS DISEASES
Bass (C. C.) & Johns (F. A/.). The cultivation of malarial plasmodia (Plasmodium vivax
and Plasmodium falciparum) in vitro. J. Exper. M., Lancaster, Pa..
1912, xvi, 567-579.
A method of concentrating malaria plasmodia for diagnostic and other pur-
poses. Am. J. Trop. Dis. [etc.], New Orleans, 1915, Hi, 298-303, 3 pi.
Craig (C. F.). The sexual forms of the malarial plasmodia occurring in the blood of man.
Arch. Int. Med., Chicago, 1910, v, 325-347.
Swing (/.)• Malarial parasitology . J. Exper. M., New York, 1901, v, 429-491.
Golgi (C.). Sull'infezione malarica. Arch, per le sc. med., Torino, 1886, x, 109-135. 1 pi.
Laveran (A.). Note sur un nouveau parasite trouve dans le sang de plusieurs malades
atteints de fievre palustre. Compt. rend. Acad. d. Sc., Paris, 1880, xciii,
$27.
Lavinder (C. HJ. A note on the cultivation of malarial plasmodia after the method of Bass
and Johns. J. Am. M. Ass., Chicago, 1913, Ix, 42.
Lawson (M. /?.)• The extracellular relation of the malarial parasite to the red corpuscle,
and its method of securing attachment to the external surface of the red
corpuscle. J. Exper. M., Lancaster, Pa., 1913, xvii, 324-843.
A stage in the migration of the adult tertian malarial parasite. Evidence
of the extracellular relation of the parasite to the red corpuscle. J. Exper.
M., Lancaster, Pa., 1914, xix, 450-458.
Free malarial parasites and the effect of the migration of the parasites of
tertian malarial infections. J. Exper. M., Lancaster, Pa., 1914, xix,
523-535.
MacCallum (W. G.}. On the haematozoan infections of birds. Johns Hopkins Hosp.
Bull., Baltimore, 1897, viii, 235-236.
Marchiafava (E.) & Celli (A.). Weitere Unlersuchungen uber Malariainfektion. Fort-
schr. d. Med., Berlin, 1885, Hi, 787-806.
Ruge (/?.)• Malariaparasiten. In: Handb. d. pathogen. Mikrodrg. (Kolle & Wasser-
mann). 2. Aufl. Jena, 1913, vii, 167-32G.
Stephens (/. W. W.) & Christophers (S. R.). The practical study of malaria and other
blood parasites. 3(1 ed. London, 1909, Williams & Norgate. 414 P-
6 pi. 8°.
Thomson (D.). The origin and development of gametes (crescents) in malignant tertian
malaria: some observations on flagellation, etc. (Being part 2 of the report
on the malarial expedition to Panama, 1912.} Ann. Trop. M. & Para-
sitol., Liverpool, 1914-15, viii, 85-104.
Thomson (J. G.) & Thomson (D. T.). The growth and sporulation of the benign and
malignant tertian malarial parasites in the culture lube and in the human
host. Ann. Trop. M. & Parasitol., Liverpool, 1913, vii, 509-524.
6. Briefer Clinical Articles
Bates (J. P.}. A review of a clinical study of malarial fever in Panama. J. Trop. M., etc.^
London, 1913, xvi, 145-153, 177-184, 209-213, 287-301.
James (W. M.). Notes on the etiology of relapses in malarial infections. J. Infect. Dis..
Chicago, 1913, xii, 227-235.
Rowley -Lawson (Mary}. The cause of malarial anemia, and the intravascular migrations
of the malarial parasite. Arch. Int. Med., Chicago, 1912, ix, 420-444.
Russell (W. W.). Malarial infection as a source of error in surgical diagnosis. Johns
Hopkins Hosp. Bull, Baltimore, 1896, vii, 204-206.
Tissier (L.) & Brumpt (E.). A propos d'un cas de paludisme congenital. Arch. wens.
d'obst. et de gynec., Paris, 1913, u, 166-174.
'
PATHOGENIC MASTIGOPHOBA, OK FLAGELLATA 365
4. Relapsing Fever
(Febris recurrens)
Spirochseta obermeieri. — In relapsing fever, a flagellate of spirochaeta form,
was first discovered by Obermeier
(1868). His publication on the sub-
ject (1873) was the first report demon-
strating the presence of a pathogenic
microorganism in human beings.
The Spirochceta obermeieri is a
corkscrew-shaped spirochaete (10-40 p
long), which undergoes screwlike
movements in the infected blood, shov-
ing the corpuscles about in the fresh
preparation. The spirochaetes can be
kept alive in blood serum for over 100
days. The disease can be transferred
from man to monkeys, and from mon-
keys to rats and mice.
In the relapsing fever of different
countries, somewhat different varieties
of spirochaetae have been found; thus
the European relapsing fever is due
to Spirochceta obermeieri, the African
to Spirochceta duttoni, the American
to Spirocliocta novyi, the Indian to
Spirochcela carteri.
Fig. 112.— Spirochetes of Relapsing Fever from
Blood of a Rat Seen at the Height of the
Infection, Showing One Normal Double
Form (A), One Stretched Out Form (B),
and One Recurved Form (C), in One Cover-
Slip Preparation. (After S. T. Darling,
Arch. Int. Med.)
Definition of Relapsing Fever.
—Relapsing fever is an infectious
disease characterized by periods of
fever separated from one another
by periods of apyrexia, and due to invasion of the blood by one of sev-
eral varieties of spirochaetae. The incubation period lasts about 7 days.
Mode of Infection. — Infection
^robably occurs through bloodsucking
insects, of which the louse (Pediculus
vestimenti). seems to be responsible in
Algiers, a tick (Ornithodorus mou-
bata) in equatorial Africa. Simple
contact infection seems improbable.
Symptoms. — The onset is with
fever, and usually with chill, head-
Fig, us. — Ornithodorus Moubata. 9 ache, pain in the back, tinnitus, gen-
Tho Tick that Transmits Reiaps- eral maiaise, pain in the calves and
mg I- ever. (After G. H. F. Nut- .-,,
tan, J. H. H. BUII.) in the extremities generally. I he
366
DIAGNOSIS OF INFECTIOUS DISEASES
tongue becomes coated. Herpes is not uncommon. Constipation, vomit-
ing, splenic tumor, moderate leukocytosis, with slight relative increase in
the polymorphonuclear elements, are also usually present.
The fever continues high for 5-7 days, and then falls hy crisis, with
sweating and diarrhea ; there is then rapid disappearance of the symptoms.
8 9 10 1 \I2 3 74/5/6
Fig. 114. — Relapsing Fever. (After P. Krause.)
In nearly all cases, after an interval averaging 5J days (hut sometimes as
great as 17 days), a RELAPSE, wholly similar to the first attack, except
that it is milder, occurs. The average duration of the first attack is 6f
days, of the second attack, 5^ days. In most cases, the disease is over at the
end of the second attack, but in about 7 per cent of the cases, a SECOND
PATHOGENIC MASTIGOPHOKA, OE FLAGELLATA 367
»-
Ul OOOOOO> COf-lO
h- ^ i- T- i- t- Ol O) O> O1
oJ **• co CM »- o o> oo i
E O OOOOO>CD
I ??°l§!sfsg£8S
•S ^:
tf a
i
368 DIAGNOSIS OF INFECTIOUS DISEASES
RELAPSE occurs 6 days later, lasting on the average 3^ days. In a few
cases, a THIRD RELAPSE comes after a 9 days' intermission and lasts 2 days,
and even a FOURTH RELAPSE (after 10 days' intermission) lasting 1 day,
has been observed.
In rare instances, during the apyretic period following the first attack,
an intense jaundice sets in (septic bilious recurrent fever, or bilious
typhoid). This appears to be a complication due to pyogenic sepsis. The
average mortality of relapsing fever is from 2 to 10 per cent. One attack
does not confer immunity to subsequent infection.
Diagnosis. — It is often difficult to demonstrate the spirochaetae in the
peripheral blood, especially at the height of the fever, though the thick-
drop method is helpful. Animal inoculation (monkeys) may be required
in doubtful cases.
References
Christian (H. A.}. Observations on the spirilla of relapsing fever. Arch. Int. Med., Chi-
cago, 1911, vii, 1-15.
Darling (S. 7\). The relapsing fever of Panama. Arch. Int. Med., Chicago, 1909, iv,
150-185.
Koch (/£.). Ueber afrikanischen Recurrens. Berl. klin. Wchnschr., 1906, xliii, 185-194-
Muhlens (P.}'. Spirochdten. In: Handb. d. pathogen. Mikroorg. (Kolle & Wassermann).
2. Aufl. Jena, 1913, vii, 864-920.
Nicolle (C.) & Blanc (G.). Les spirilles de laficvre recurrente sont-ils virulenle aux phases
successives de leur Evolution chez le pou? Demonstration de leur virulence
d une stade invisible. Compt. rend. Acad. Sc., Paris, 1914, clviii, 1815—
1817.
Nicolle (C.), Blaizot (L.) & Conseil (E.). fHiologie de la fievre recurrente, son mode de
transmission par les poux. Ann. de VInstit. Pasteur, Paris, 1913, xxvii,
204-225.
Novy (F. G.) & Knapp (R. E.). The cultivation of Spirillum obermeieri: a preliminary
note. J. Am. M. Ass., Chicago, 1906, xlvii, 2152-2154.
Studies on Spirillum obermeieri and related organisms. J. Infect. Dis.,
Chicago, 1906, Hi, 291-393.
Schilling (C.). Ruckfallfieber. In: Handb. d. Tropenkrankh. (Mense). Leipzig, 1906,
Hi, 668-688.
Sergent (E.), Foley (H.) & Villatte (C.). Transmission a Vhomme et au singe du typhus
exanthematique par les poux d'un malade atteint de fievre recurrente et par
des lentes et poux issus des precedents. Compt. rend. Acad. d. Sc., Paris,
1914, clviii, 964.
Smith (C. H.} & Graham (G. F.). Relapsing fever in Chitral, with an account of suc-
cessful animal inoculations. Indian M. Gaz., Calcutta, 1913, xlviii, 381-
382.
Sobernheim (G.) & Loewenthal (W.). Spirochdtenkrankheiten. In: Handb. d. pathogen.
Mikroorg. (Kolle & Wassermann}. 2. Aufl. Jena, 1913, vii, 724-744-
5. Syphilis, or Lues
Treponema pallidum. — The Treponema pallidum (or Spirocliceta pal-
lida, Schaudinn) is an extremely delicate, motile, corkscrewlike thread
(6-14 turns), at the end of which are extremely minute flagellalike ex-
tensions ; it is present in the lesions of syphilis at all stages. It is best seen
PLATE VII
Fig. 2. — Primary Lesion or "Hard
Chancre" of Syphilis in the Sulcus
retroglandularis. The Center is
Eroded. (From Buschke, in E.
Riecke's "Lehrb. d. Haut- u. Ge-
schlechtskrankheiten," published by
G. Fischer, Jena.)
Fig. 1. — Treponema pallidum in Section Through Tissue in
Hereditary Lues. Stained After Levaditi. (After W.
Kolle u. H. Hetsch, "Die experimented Bakteriologie,
etc.," published by Urban & Schwarzenberg, Berlin.)
Fig. 3. — Mucous Patches on the Un-
der Surface of the Tongue. Sec-
ondary Syphilis. (From Buschke,
in K. Riecke's "Lehrb. d. Haut-
u. Geschlechtskrankheiten," pub-
lished by G. Fischer, Jena.)
Fig. 4. — Tertiary Syphilis. Perforation
of the Hard and of the Soft Palate.
Destruction of the Uvula. Radial
Scar on Posterior Wall of Pharynx.
Healed Lesion. (After Buschke, in
E. Riecke's "Lehrb. d. Haut- u.
Geschlech tskrankheiten," published
by G. Fischer, Jena.)
PATHOGENIC MASTIGOPHOKA, OK FLAGELLATA 369
Fig. 117. — (5, 6 and 7) Treponema palli-
dum from a Ten-Day-Old Pure Cul-
ture in a Horse-Serum-Agar-Tissue
Medium. Giemsa Stain, xl,2SO. (8
and 9) Long Forms from a Pure Cul-
ture. Giemsa Stain, xl,2SO. (After
H. Noguchi, "Studies from the Rock-
feller Inst. for Med. Res.," Reprinted
from J. Exp. Med.)
in histological specimens prepared by Levaditi's silver-impregnation
method. The methods of demonstrating it by Giemsa's stain, by the
india-ink method, and by dark-field
illumination have already been re-
ferred to. It has been cultivated by
Noguchi in serum media containing
a little sterile rabbit's kidney. It can
also be cultivated by the modified
method of Schereschowsky.
It is pathogenic for human beings,
^^mm — — ^^ monkeys and rabbits.
Definition of Syphilis. — Syphilis
_, is a chronic infectious disease, due to
invasion of the body by the Treponema
pallidum. It is usually acquired
through coitus (GENITAL INFECTION),
though sometimes in other ways (EX-
TRAGENITAL INFECTION of lip, tongue,
tonsil, nipple, finger, eyelid, anus,
skin abrasion, etc. ) . Many physicians
suffer from syphilis "innocently'' acquired (gynecological examination,
surgical operations, autopsy infection, etc.). In contradistinction to
acquired syphilis, there is also a congenital syphilis, due either to fetal
infection from the mother (placental syphilis), or to germinal infection
(from the father).
(a) Acquired Syphilis
Four stages are distinguished: (1) a primary stage, (2) a secondary
stage, (3) a tertiary stage, and (4) a metasyphilitic, or parasyphilitic,
stage. It is well to remember that the primary, secondary and tertiary
stages often merge one into another, so that frequently no sharp line of
division can be drawn between them.
Primary Syphilis. — From 3 to 6 weeks after exposure, a pale, firm,
painless nodule appears at the site of infection (HUNTERIAN CHANCRE;
INITIAL SCLEROSIS). Under treatment, this may disappear without ulcera-
tion, but, usually, it breaks down, with the formation of an ulcer, which is
also known as a syphilitic chancre, with a hard, woodlike margin. It is
usually single, in contrast with soft chancre, which is most often multiple,
but the initial lesion of syphilis is occasionally multiple. It is most com-
mon on the glans penis, but may be situated on the prep'uce. Intraurethral
chancre may occur ; it probably often escapes observation. The chancre
usually disappears under mercurial. treatment in from 3 to 5 weeks after
its full development; under salvarsan treatment, it may disappear much
more quickly.
370 DIAGNOSIS OF INFECTIOUS DISEASES
PATHOGENIC MASTIGOPHOKA, OK FLAGELLATA 371
Before the primary lesion has disappeared, the inguinal glands and
the retrocervical lymph glands become enlarged and firm. About the
same time, the epitrochlear glands may also become palpable. The lymph
gland enlargement is always bilateral.
This general lymphadenoid hyperplasia reaches its height in from 7 to
9 weeks.
Secondary Syphilis. — From the 9th to the 12th week, the secondary
stage of syphilis is entered upon with the appearance of a macular, rose-
colored, or slightly copper-colored exanthem (ROSEOLA SYPHILITIC A, MAC-
ULAE SYPHILID).
This is often preceded by slight prodromal disturbances (fever, noctur-
nal headache, nocturnal pains in the limbs and bones (DOLORES OSTEO-
SCOPI). The syphilitic roseola appears first on the skin of the chest, abdo-
men, or back. It is rarely present on the face, or the extremities, though it
is sometimes visible on the uvula, tonsils, and soft palate. Later, whitish
areas appear in the mouth (margin of tongue, lips, tonsils, cheeks), the
so-called MUCOUS PATCHES and hypertrophic changes in the mucous mem-
branes, especially of the vulva and anus, may give rise to the syphilitic
excrescences known as CONDYLOMATA.
In this secondary stage, the patients feel ill (anorexia, progressive, ane-
mia, occasionally albuminuria, icterus, and palpable spleen). The hair
often falls out (defluvium capillorum), and the patients complain of sore
throat.
Instead of the macular syphilid, succeeding it, or mixed with it, there
may be a papular eruption (PAPULAR SYPHILID). These papules are
usually rather small, firm, and of a brownish red or copper color; they are
sharply circumscribed and rounded (lenticular syphilid, large papular
syphilid). On fading, they scale and become indented in the center, leav-
ing a brown pigmented area behind. In more malignant forms of syphilis,
the papules are very much smaller, about the size of the head of a pin,
brownish red, firm, and distinctly pointed (small papular syphilid, miliary
syphilid, lichen syphiliticus). The papules undergo slight desquamation,
similar to that seen in the larger form. In still other malignant cases, the
papules may take the form of quite large nodules that undergo ulceration,
simulating that of gummatous syphilids.
Instead of a macular, or a papular, syphilid, in the secondary stage, a
PUSTULAR SYPHILID or an ULCERATIVE SYPHILID form may be met with.
The pustules may be large and surrounded by a red areola. Crusts may
form over broken pustules, after which the ulcer may gradually extend at
its periphery. In these cases the older central crusts become gradually
elevated in oyster-shell-like laminations upon the crusts formed later
(RUPIA SYPHILITICA). The superficial form of pustular syphilid affecting
especially the scalp and beard is known as IMPETIGO SYPHILITICA. Some-
times small pustules arise on the bases of papular infiltrations, especially
372
DIAGNOSIS OF INFECTIOUS DISEASES
in hairy beards (ACNE SYPHILITICA). Again, in severe cases, the pustular
syphilid involves the deeper tissues (ECTHYMA).
Laryngeal catarrh is common in the secondary stage, with hoarseness
or aphonia, and laryngeal examination may reveal a papular eruption
or mucous patches, or
even ulcers of the mu-
cous membrane
The eruption of the
secondary stage often
recurs at intervals (re-
lapses, recidives). A
papular or papulo-
squamous exanthem on
the palms of the hands
or soles of the feet is
almost pathognomonic
of syphilis (= palmar
and plantar syphilitic
psoriasis). An ony-
chia or paronycliia
sypJiilitica is not un-
common in the sec-
ondary stage.
Falling out of the
hair has already been
mentioned. This may
be diffuse, or it may
occur in patches (alo-
pecia sypJiilitica). The hairs of the beard, axillae, eyebrows, eye-lashes
and pubic region may also fall out. Periostitis, occasionally arthritis,
peripheral neuritis, neuralgias (trigeminal, intercostal, sciatic), isolated
ptosis, diplopia, and optic neuritis are not uncommon. The periostitis
often gives rise to NODES on the tibia, ribs or skull.
Unilateral or bilateral iritis, with violent nocturnal pain, is often an
early symptom. Sudden deafness due to involvement of the labyrinth may
occur.
The lesions of secondary syphilis (at the beginning, and in its periodic
exacerbations) are extremely infectious, especially the mucous patches
and the condylomata on the genitals or about the anus.
In insufficiently treated cases, the recurrences may occur at regular
intervals (6 months) ; more often the intervals are irregular, going on for
from 3 to 5 years, to be followed by a latent period, before tertiary symp-
toms manifest themselves.
Fig. 119.— Scaling Syphilid of Palms. Conditions of Palms
Two Weeks After Treatment With "606." See Photo-
graph Before Treatment. (After H. J. Nichols and J. A.
Fordyce, "Studies from the Rockefeller Inst. for Med. Res.,"
Reprinted from J. Am. M. Ass.)
PATHOGENIC MASTIGOPHOKA, OK FLAGELLATA 373
Fig. 120. — Scaling Syphilid of Palms. Duration of Infection, Three Years ; of Palmar Lesions,
One Year. May 16, 1910, 0.3 gm. "606." Wassermann Before Treatment, + + ; June 10,
1910, Negative; Sept. 1, 1910, Still Negative. See Photograph After Treatment. (After
H. J. Nichols and J. A. Fordyce, "Studies from the Rockfeller Inst. for Med. Res., Re-
printed from J. Am. M. Ass.)
Two additional constitutional symptoms of the secondary stage deserve
especial mention:
1. The FEVER may be extremely variable in character. Thus it may
be slight and of brief duration. Some-
times it is continuous, simulating that
seen in the second week of typhoid fever.
Sometimes it is remittent over long peri-
ods of time, leading to a diagnosis of
tuberculosis. Or, again, it may be
paroxysmal and intermittent, simulating
the pyrexia of malarial fever.
2. The ANEMIA is often pronounced.
.It is of the secondary type (low color
index). A hematogenous jaundice, due
to rapid destruction of erythrocytes, may
develop. There is rarely a leukocytosis,
but a relative increase in the mono-
nuclear cells is the rule*
Fig. 121.— Alopecia Syphilitica. (After
Marschalko, from Torok's Article in
E. Riecke's Lehrbuch, published by
Cr, Fischer, Jena.)
374 DIAGNOSIS OF INFECTIOUS DISEASES
Tertiary Stage. — The characteristic lesion in this stage is the GUMMA
(aggregations of small mononuclear cells which tend to break down from
coagulation necrosis). The ulcer ation resulting heals with difficulty and
gives rise to dense scars, which cause marked deformity of parts affected.
The gummata may vary in size from that of a pin's head to that of a
child's head, or larger. They are very common in the skin, periosteum and
bones, less common in the muscles.
In some instances, the viscera (liver, lung, spleen, intestine, kidney,
heart) are predominantly involved (VISCERAL SYPHILIS). Gumma of the
brain may give rise to symptoms and signs of brain tumor. A gummatous
arteritis of the brain may cause hemiplegia, or aphasia. Gummatous
arteritis in the spinal cord is a frequent cause of paraplegia. Gummata of
bone are most often met with in the skull, clavicle, sternum and tibia. The
bones of the nose may break down (saddle-nose) ; the bony atrophy is
often followed by ozena. Perforation of the nasal septum is not uncom-
mon. Perforation of the palate may also occur; white scars on the hard
or soft palate are suspicious of preexisting luetic lesion. In the tongue, a
gumma may simulate carcinoma or actinomycosis.
Gumma of the liver is of great practical importance, sometimes being
mistaken for carcinoma. Syphilitic cirrhosis is multilobular.
In the intestine, syphilitic ulcers often cause strictures with stenosis,
especially in the rectum. Gummatous processes in the esophagus and tra-
chea, also, sometimes give rise to strictures.
Luetic arthritis is rather rare, being much less common than luetic
periostitis. A gummatous mesaortitis is the commonest cause of AORTIC
ANEURISM and of ISOLATED AORTIC INSUFFICIENCY. Amyloid disease is
not uncommon.
Paraluetic Stage. — Ten, fifteen, or more, years after infection, symp-
toms of parasyphilis may develop, giving rise to (1) the clinical picture
known as general paresis or DEMENTIA PARALYTICA, when the Treponema
pallidum invades the cerebral cortex itself, or (2) the picture of TABES
DORSALIS (locomotor ataxia) when the spinal meninges and roots of the
sensory nerves are involved, leading to degeneration of the posterior fu-
niculi of the spinal cord. (See Part XII.)
Diagnosis. — No reliance should be placed upon the anamnesis, unless it
is positive. The nature, site and appearance of the lesions are often charac-
teristic. In primary and secondary lesions, the presence of the Treponema
pallidum may be demonstrable. (See Methods.)
In all stages of syphilis, except in the early stage of the hard chancre,
and during and for two weeks after antiluetic treatment, the WASSERMANN
REACTION (q. v.) is positive in a large percentage of the cases.
In lues cerebrospinalis, the cell count of the cerebrospinal fluid, the
increase in globulin content, and the positive Wassermann reaction in this
fluid, aid in diagnosis.
PATHOGENIC MASTIGOPHOKA, OR FLAGELLATA 375
In the .paraluetic diseases, the neurological phenomena (q. v.), the lum-
bar puncture, and the Wassermann reaction make diagnosis, as a rule, easy.
Care should be taken not to confuse tertiary luetic lesions of the bones
and skin with (1) tuberculosis or (2) sporotrichosis (q. v.).
(6) Congenital Syphilis
The fetus may be infected through the placenta. In such cases the
mother is infected (positive Wassermann reaction), though the disease may
be entirely latent in her as far as symptoms are concerned. According to
COLLES' LAW, a child suffering from congenital syphilis may infect a
healthy nurse, but cannot infect its own mother, even though she suckle it.
Fig. 122. — Twins with Hereditary Syphilis. R = Diffuse Infiltration of the Skin, Very Marked,
Especially on Hands, Arms and Feet. Syphilitic Crusts About the Mouth and Chin.
L = Circumscribed Pustular Syphilide on the Face, Especially the Forehead. Rhagades at
the Edges of the Lips. (After Pfaundler, in E. Feer's "Lehrb. d. Kinderheilkunde," pub-
lished by G. Fischer, Jena.)
The reason is that the mother is already infected. Again, if a woman,
suffering from lues, bear a child that shows no symptoms of syphilis, the
child does not contract the disease if suckled by its mother (PROFETA'S
LAW). This may be due to the transference of a passive immunity to the
child in uiero, but is more likely due to the fact that the child is already the
bearer of latent infection (Diday).
Symptoms. — Many of the children are still-born, or die soon after birth
(feeble development, pemphigus neonatorum syphiliticus).
376
DIAGNOSIS OF INFECTIOUS DISEASES
Children may be born apparently healthy, and in one or two months
develop snuffles (syphilitic rhinitis), fissures and scabs at the angles of the
mouth (rhagades), syphilitic onychia, and enlargement of the spleen and
lymph glands. Violent, unmotived crying, during the early months of
life, should make one suspect the possibility of congenital syphilis.
In childhood, symptoms often reappear at the period of the second
dentition, or at puberty. Various dystrophic signs are more or less charac-
teristic; among these
are infantilism, sad-
dle-nose, scars of
rhagades, Hutchinso-
nian teeth (the upper
permanent central
incisors being peg-
shaped and crescent-
ically notched at the
cutting edge), inter-
stitial keratitis,
bosses on the frontal
bones, chronic gum-
matous periostitis.
A child may be
free from syphilis in
its early years, and
later on present defi-
nite symptoms (SYPH-
ILIS HEEEDITARIA TARDA). Whether or not the disease can be transmitted
to the third generation, is still in dispute.
Juvenile tabes and juvenile paresis occasionally occur.
References
1. General
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The prophylaxis of syphilis. Translation by C. F. Marshall. London,
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Hutchinson (J.). Syphilis. In: Syst. Med. (Allbutt & Rolleston). 8°. London, 1909,
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8 .
Fig. 123. — Hutchinson's Teeth in Hereditary Lines. Note the
Concave Defect in the Edges of the Medial Upper Incisors.
(From Buschke's Article in Eulenburg, Kolle and Wein-
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PATHOGENIC MASTIGOPHOEA, OR FLAGELLATA 377
2. Etiology ; Treponema pallidum
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The direct cultivation of Treponema pallidum pathogenic for the monkey.
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A method for cultivating Treponema pallidum in fluid media. J. Exper.
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378 DIAGNOSIS OF INFECTIOUS DISEASES
4. Clinical
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PATHOGENIC MASTIGOPHOKA, OR FLAGELLATA 379
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6. Yaws or Frambesia
Definition. — A disease of tropical countries characterized by papular, tuber-
cular and ulcerative skin lesions, and manifesting itself in a primary, secondary
and tertiary stage analogous to those of syphilis. The causative organism is the
Treponema pertenue.
Etiology. — By many authorities yaws was confused with syphilis until Cas-
tellani in 1905 demonstrated the presence in the skin lesions, lymph nodes, and
380 DIAGNOSIS OF INFECTIOUS DISEASES
spleen of the Treponema pertenue. This discovery has since been abundantly con-
firmed. The distinction between yaws and syphilis is likewise supported by the
fact that there have been many instances of the development of yaws naturally
and by inoculation in those affected with syphilis.
Symptoms. — After a period of incubation of from 2 to 5 weeks the initial lesion
appears at the point of inoculation as a small papule. The overlying skin soon
ulcerates, exposing a fungoid yellowish-red base from which seropurulent fluid
exudes. This mass of fungoid granulations may attain 1 to 2 inches in diameter.
The primary lesion is usually extragenital.
The secondary stage sets in in from six weeks to three months after the appear-
ance of the initial lesion. There is a generalized eruption of papules entirely
similar to the primary lesion. The face, neck, perineum and the extremities are
especially affected. Frequently the eruption is accompanied by marked itching.
The character of the lesions is very uniform in contrast to the pleomorphism that
is common in syphilis. The onset of the secondary stage is usually attended with
fever, headache and joint pains. There may be successive eruptions of yaws
tubercles prolonging the secondary stage for two to three years. More usually
it lasts only three or four months.
Certain cases of yaws exhibit a tertiary stage of which the characteristic lesions
are gummatous nodules and deep ulcerations (Castellani). It is possible that the
condition known as gangosa (q. v.) is simply tertiary yaws of the nose and palate.
There appears to be no tendency in tertiary yaws to involvement of the viscera or
of the central nervous system.
Prognosis. — The death-rate is very low — approximately \ of 1 per cent. Re-
covery does not yield complete immunity; reinfection may occur.
Diagnosis. — The juice from yaws tubercles should be stained by the India ink
method or with Giemsa's stain. The Treponema pertenue closely resembles the Tre-
ponema pallidum; it is, however, somewhat thicker, tin spirals are less regularly
formed, and the ends more blunt. In sections of the lesions, stained by Levaditi's
method, the treponema is found in the epidermal layer instead of in the corium,
as in syphilis.
Clinically the extragenital site of the primary lesion of yaws; the similarity of
the primary and secondary lesions; the uniformity in the appearance of these lat-
ter ; the rarity of involvement of mucous membranes in yaws help to differentiate
from syphilis. On the other hand salvarsan is more specific for yaws than for
syphilis, and the Wassermann reaction is more frequently positive in yaws.
Reference
Miihlens (P.). Treponema pertenue (Frambosieerreger) . In: Handb. d. pathogen. Mikroorg.
(Kolle & Wassermann). 2. Aufl. Jena, 1913, vii, 853-863.
7. Granuloma venereum
( Ulcerating Granuloma)
Definition. — A chronic superficial ulceration in the region of the genitals occur-
ring chiefly in tropical countries. A few cases have been reported in the United
States.
Etiology. — The causative organism has not been definitely ascertained. It is
probably a spirochete resembling Treponema pallidum (Wise).
The disease is transmitted by sexual intercourse. It is somewhat more common
in women.
PATHOGENIC MASTIGOPHOKA, OE FLAGELLATA 381
Symptoms. — The disease first manifests itself as a small painless papule or
nodule on the penis, the labia, or the perineum. This lesion ulcerates and the
ulceration then spreads by continuity to the groins and the inner surface of the
thighs. The margin of the ulcer is usually clean-cut and steep. The base of the
ulcer is often covered with a gray membrane. The granulations bleed easily. The
discharge is usually profuse and offensive. The process is very chronic. Healing
occurs with scar-tissue formation. The ulceration may involve the vagina, and
recto vaginal fistulae often result. The lymph glands are not affected. The process
is comparatively painless. The general health is impaired only when the area
of the ulceration is extensive.
Diagnosis. — The disease must be differentiated (1) from syphilis (secondary
symptoms; enlarged lymph nodes; Wassermann positive, response to specific treat-
ment) and (2) from tuberculosis (histology of excised material) .
8. Gangosa
Definition. — A destructive ulceration of the palate and nasal passages occur-
ring in tropical countries.
Etiology. — Gangosa is usually regarded as a tertiary manifestation of either
yaws or syphilis. The absence of other forms of syphilis in Guam, where gangosa
is prevalent, speaks strongly against the latter supposition. In 315 cases of gan-
gosa Kerr found only 18 in whom scars or a history of yaws were lacking.
Symptoms. — The disease usually begins with ulceration of the palate, which
very rapidly spreads upward destroying the bone and cartilage forming the tip
of the nose. The nasal ducts are frequently involved with consequent loss of one
or both eyes. The active process may subside in one or two years, leaving marked
deformations. Ozena is a common accompaniment.
Diagnosis. — Syphilis is hard to rule out, since entirely similar lesions may
occur in the malignant form of that disease. A large percentage of cases of gan-
gosa give a positive Wassermann test. Salvarsan is curative. The possibility that
the disease is a special form of either syphilis or yaws should be kept in mind.
9. Verrujja peruviana
Definition. — A tropical disease confined to certain valleys of Peru, apparently
an infectious granuloma.
Symptoms. — It is characterized by an eruption of vesicles and papules over the
extremities and face. Later on, subcutaneous nodules appear, which may reach
3-4 cm. in diameter. The skin over them frequently ulcerates and red fungous
masses result. Verruga nodules have also been found in the internal organs.
After several weeks or months the eruption disappears, but relapses are common.
As a result of the work of R. P. Strong, E. E. Tyzzer, A. W. Sellards and C. T.
Brues of the Expedition to South America from the Harvard School of Tropical
Medicine, verruga peruviana has been sharply separated from Oroya fever, which
had formerly been considered to constitute the febrile stage of verruga. The virus
of verruga peruviana is transmissible to monkeys, but has not been shown to be
filtrable.
References
Strong (R. P.). Etiology of some forms of tropical infective granulomata. Tr. Ass. Am.
Physicians, Philadelphia, 1914, xxix, 235-246.
Strong (R. P.) & Tyzzer (E. E.}. Experiments relating to the virus of verruga peruviana.
Fourth report. J. Am. M. Ass., Chicago, 1915, Ixiv, 1124-1127.
Etiology of Oroya fever and Verruga peruviana. New York M. J. letc.],
1914, xcix, 535-587.
382 DIAGNOSIS OP INFECTIOUS DISEASES
10. Oroya Fever
(La Maladie de Carrion)
Barton in 1909 and later Strong have reported as the etiological agent in this
fever a parasite of the red-blood corpuscles sufficiently distinct from the other
hematozoa previously described to permit it to be placed in a new genus. The
name Bartonia bacilliformis has been proposed for this organism. The disease
is characterized by high fever, a rapid and pernicious form of anemia, extreme
prostration and death. In Peru, where it is common, it is frequently combined
with verruga peruviana. In 1885 a young medical student, Daniel Carrion, in
an attempt to settle the question of the identity of the two diseases, allowed himself
to be inoculated with the blood of a patient with verruga peruviana. Within
thirty-nine days he succumbed to an apparently typical attack of Oroya fever.
The confusion of identity caused by this outcome may be compared to that follow-
ing the famous experiment of John Hunter with syphilis and gonorrhea.
References
Barton (A. L.). Description de elementos endoglobulares hallados en los enfermos de fiebre
verrucoca. Cron. Med., Lima, 1909, xxvi, 7-10.
Darling (S. T.). Verruca peruana. J. Am. M. Ass., Chicago, 1911, Ivii, 2071-2074.
Firth (R. H.). Verruga. In: Syst. Med. (Allbutt & Rollestori). 8°. London, 1910, ii,
pt. 2, 704-708.
C. Diseases Due to Pathogenic Sporozoa
The coccidia (coccidiosis), and the sarcosporidia (Miescher's tubes in striped
muscle), are, in this country, unimportant for human pathology; as hemosporidia,
the malarial parasites were formerly included under pathogenic sporozoa. They
have already been considered, above, in their new position, under the flagellata.
III. DISEASES DUE TO FILTKABLE OK "ULTKAMICKO-
SCOPIC" VIRUSES
Filtrable Viruses. — A number of diseases are due to forms of virus
that will pass through fine PORCELAIN FILTERS. The virus is therefore be-
lieved to be smaller than bacteria. The pores of the filter are, it is true,
larger than bacteria, but bacteria do not get through on account of the
tortuous passage. BerJcefeld filters, made of diatomaceous earth, are more
porous than Pasteur-Chamberland filters, made of unglazed porcelain
kaolin.
Studies of these viruses should be undertaken by the newer methods of study-
ing colloid particles of different sizes. Among these may be mentioned (1) the
observation of Tyndall's phenomenon (illuminated pyramid, on lateral observa-
tion, in a fluid, when a small bundle of light rays is projected through the
fluid) by the ULTRAMICROSCOPE, of which there are two main types: (a) the slit
DISEASE DUE TO PASTEUK'S VIEUS 383
ultramicroscope of Siedentopf and Zsigmondy, and (b) the cardioid-ultramicro-
scope of Siedentopf; and (2) the method of "ULTRAFILTRATION" OF BECHOLD, in
which the pores of the filter are covered with gels of different concentration, each
concentration permitting colloid particles of definite size to pass through but pre-
venting the passage of particles of larger size. So delicately do these filters work,
that it is possible by them to separate diphtheria toxin from toxon (Bechold), and
to separate the colloid particles of boiled milk from those of raw milk (Grosser).
References
Bechold (H.). Ultrafiltration. Biochem. Ztschr., Berlin, 1907, vi, 379-408.
Durchldssigkeit von Ultrafiltern. Ztschr. f. phys. Chemie, Leipzig. 1908,
Ixiv, 328-342.
Chauveau (A.). Les microbes pathogenes invisibles et les preuves physiques de leur existence.
Compt. rend. Acad. d. Sc., Paris, 1909, cxlviii, 1067-1073.
Cockayne (E. A.). Ultra-microscopic organisms in disease. St. Barth. Hosp. J., London,
1912, xix, 141-144.
Dorset (M.). Invisible microorganisms. Rep. Bureau Animal Indust., Washington, 1903,
xx, 139-156.
Gastou (/*.)• L' ultramicroscope dans le diagnostique clinique et les recherches de laboratoire.
Paris, 1910. 12°.
Herlitzka (A.). Eine Modifizierung und Vereinfachung des Ultrafiltrationsverfahrens.
Ztschr. f. biol. Tech. u. Method, Leipzig, 1912-13, Hi, 108-112.
Hewlett (R. T.). A lecture on ultra-microscopic causes of disease. Clin. J., London, 1912-
13, xl, 133-137.
Jobling (E.). The ultra-microscope and its application to the study of colloids. Scient. Am.
Suppl, New York, 1912, Ixxiv, 162.
Laird (A. T.). Ultramicroscopic studies. Albany M. Ann., 1905, xxvi, 758-767.
Lipschutz (/*.)• Filtrierbare Infektionserreger. In: Handb. d. pathogen. Mikroorg. (Kolle
& Wassermann). 2. Aufl. Jena, 1913, viii, 345-426.
Novy (F. G.). Ultramicroscopic organisms. Physician & Surg., Detroit & Ann Arbor,
1911, xxxiii, 241-246. [Discussion] 255.
A. Disease Due to Pasteur's Virus
Virus of Rabies. — The nature of the virus is unknown, unless it be the organism
recently described by Noguchi (see below) ; but it is present in the saliva of
animals suffering from rabies, and is concentrated in the tissues of their nervous
systems. To cause disease, it must be inoculated into the tissues; swallowed, it
is harmless. All mammals are susceptible, but the dog seems to be the animal
that keeps the disease going. Possibly healthy dogs may be chronic carriers.
1. Rabies
(Hydrophobia, Lyssa)
Definition. — An acute, fatal infection (after a long incubation period),
communicated to man, usually by a rabid dog, sometimes by other infected
animals (skunk, wolf , horse, cat, etc.).
Incubation Period; Immunity; Virus. — In this disease, which is always
fatal, once symptoms have developed, the incubation period is longer,
384 DIAGNOSIS OF INFECTIOUS DISEASES
and more variable, than in any other acute infection. It varies from 14
days to a year or more, the average, in man, being 40 days.
Active immunity can be produced in man by PASTEUR'S PREVENTIVE
INOCULATION in about 15 days. Since this is a much shorter period than
the incubation period, prompt action will nearly always, though not always,
prevent the disease, though in bites upon the face, the incubation period is
shorter, and rabies sometimes develops, despite preventive inoculation.
The virus appears in the saliva of the dog 3 to 8 days before the animal
shows symptoms. A dog kept under surveillance for 10 days after biting
a human being, or another animal, is probably free from rabies if no symp-
toms develop during that period.
A skin lesion is necessary for infection in human beings, and the virus,
like the tetanus toxin, appears to travel to the central nervous system along
the nerve trunks. Even when a person has been bitten by a mad dog,
and left untreated, rabies does not necessarily develop. Probably not over
10 to 15 per cent of people so bitten would develop the disease (Paltauf ).
The virus is killed by prolonged drying, by sunlight, and, quickly, by
heat and by disinfectant solutions. It is not injured by extreme cold
(liquid air) or by putrefaction. Glycerin preserves it, though it kills bac-
teria.
.Recently (1913) Noguchi reports that he has cultivated the virus of
rabies from the nervous system of infected rabbits, killed before the dis-
ease terminated naturally. He places the material in ascites fluid, along
with a small piece of sterile rabbit's kidney, just as in his method of cul-
tivation of the Treponema pallidum. After incubation, he found in some
of the tubes, on microscopic examination, granular chromatic corpuscles of
variable size. Some were on the limits of visibility ; others were as large
as 0.2-0.3 /A. He also saw groups of minute pleomorphic chromatoid par-
ticles, measuring 0.2-0.4 /A broad by 0.4-0.5 /* long. In Giemsa's stain,
these take a red or a bluish color. He was able to grow them for several
generations in the medium mentioned. Sometimes, he found in the cul-
tures larger corpuscles varying in size from 1 to 12 /A; the inner bodies
of these stained dark blue or violet, the outer part azure, and the mem-
brane reddish; some of these he asserts are identical with Negri bodies.
Injected into rabbits, guinea-pigs, and dogs, these minute corpuscles give
rise to typical rabies. Should this finding be confirmed, the micro-
organism might well be called Fasteuria negrii (Noguchi).
Symptoms. — In from 2 weeks to 6 months after the bite, the wound
begins to redden, and to become painful, and the bitten person becomes
depressed and restless, and complains of headache and of sleeplessness
(prodromal stage, or stadium melancholicum) . Two to 4 days later, the
stage of excitement (stadium hydrophobicum) begins; tonic spasms ap-
pear in the muscles of the pharynx and of the larynx. The respiratory
muscles also become involved ; the patient has difficulty in breathing, and
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DISEASE DUE TO PASTEUR'S VIRUS 385
feels as though, he were suffocating. There may be salivation and severe
thirst, with inability to swallow, attempts at swallowing causing pharyn-
geal spasm so that the patient fears to touch water (hydrophobia). The
patient becomes restless, jumps about in an excited way, cries out, strikes
at people and objects about him ; in other words, he is a "raving maniac."
This stage lasts li-3 days (v. Koranyi). He then enters upon the last, or
paralytic stage (stadium paralyticum) ; there is rapidly developing weak-
ness, and paralysis of various muscle groups (face, tongue, eye-muscles,
extremities). The temperature rises, and death occurs within 2 to 18
hours after the paralytic stage sets in. In the so-called "QUIET FORM" the
stage of excitement does not occur, the prodromal stage going directly over
into the paralytic stage. Recently, ABORTIVE CASES have begun to be rec-
ognized (Remlinger, Simon).
Diagnosis. — It is most important, after a dog-bite, to determine whether
or not the animal is really infected. It should be caught, immediately,
alive if possible. Formerly it was advised that it be kept under surveillance
for a few days. If one is fairly sure that the dog is not mad, this may be
permissible ; if there is strong suspicion, the dog should be killed at once,
the brain should be aseptically removed, and the medulla oblongata placed
in pure glycerin and sent to a bacteriological laboratory or to a Pasteur
Institute, for the experimental inoculation of rabbits ; further, a piece of
the horn of Ammon and a piece of the spinal cord and of a posterior root
ganglion should be fixed in formalin and sent to a histological laboratory
for examination (1) for NEGRI BODIES in Ammon's horn; (2) for the
NODULES RABIQUES OF BABES (collections of small pericellular foci of mo-
nonuclear cells around the nerve cells of the spinal cord), and (3) for THE
LESION OF VAN GEHuciiTEN AND NELIS, specific changes, revealed by
Nissl's methods, in the nerve cells of the sensory and sympathetic ganglia.
For INOCULATING THE RABBITS, an emulsion of the fresh or of the glyc-
erin-preserved medulla or spinal cord, is injected beneath the dura, after
trephining; or intracerebral injection may be employed. If the virus be
present, the animal injected will show signs of rabies, in most cases, before
the 21st day. At least two rabbits should be inoculated. In case the cord
is not aseptic, and especially if putrefaction has begun, it is better to
make intramuscular rather than subdural injections ; further, the material
may be rubbed up in 1 per cent carbolic acid solution and left in the ice-
box for 24 hours before injection (Marx), or the brain may be laid in
pure glycerin for 48 hours before injection (Nicolle), to kill any bacteria
present.
In EXAMINING FOR THE NEGRi BODIES, which can be found in 90 to 95
per cent of all infected animals, a piece of Ammon's horn is fixed in
formalin, quickly hardened in alcohol, and imbedded in celloidin or paraf-
fin, sectioned, and stained with Wilson's stain, or with eosin methylene
blue (Plate VIII, Fig. 4), or by van Giessen's method.
386 DIAGNOSIS OF INFECTIOUS DISEASES
A quicker method still is to make smears by crushing a small portion of
Ammon's horn between two slides, fixing, and proceeding to stain by the Mallory
eosin blue method as follows (Williams and Lowden) :
1. Treat with Zenker's solution for 15 minutes.
2. Wash in tepid water.
3. Place in 95 per cent alcohol tinged with iodin.
4. Dehydrate 5 minutes in absolute alcohol.
5. Stain 5 minutes in aqueous solution of eosin (Grubler, W. G.) 5-10 per cent.
6. Stain 2-3 minutes in Unna's polychrome methylene blue.
7. Wash in water.
8. Differentiate in 95 per cent alcohol, blot, dry, mount, and examine with
immersion lens.
Lentz's method is as follows:
1. Imbed in paraffin by the quick method of Henke-Zeller :
(a) 4 per cent formalin-fixation of piece \ cm. thick for 15 min.
(b) Pure acetone for \-\\ hours, changing 2-3 times.
(c) Xylol 15 minutes.
(d) Paraffins (several) £-l£ hours.
2. Stain section 1 minute in
Eosin extra a. B. (Hoechst) 0.5 g.
Alcohol (60 per cent) 100.0 c.c.
3. Wash in water.
4. Stain 1 minute in Loeffler's methylene blue.
5. Wash. Dry partially with filter paper.
6. Differentiate in:
Absolute alcohol 60 c.c.
NaOH (1 per cent) 10 drops
Leave in, until the color is pale red.
7. Differentiate further in:
Absolute alcohol 60 c.c.
Acetic acid (50 per cent) 2 drops
Leave in, until the ganglion cells are pale blue.
8. Dehydrate quickly in absolute alcohol; clear in xylol; mount in neutral
balsam.
The Negri bodies are carmine red; the inner bodies are blue; the red blood
corpuscles, brick red; cell-nuclei, dark blue; protoplasm, pale blue.
The Negri bodies are round or oval structures, situated inside the gan-
glion cells. They possess a membranous, capsulelike structure, and, in the
interior, show a differentiation, due probably to vacuoles ( ?). According
to Negri, they are protozoa (Neuroryctes hydrophobia?), and are the cause
of the disease. They are exclusively, and almost constantly, present in
rabies, but they cannot be found in some material that certainly contains
the virus (saliva, salivary glands), and they are present, in very small
numbers, in the spinal cord. Moreover, even in Ammon's horn, where
they are abundant later, they cannot be demonstrated in the incubation
DISEASE DUE TO PASTEUK'S VIKUS 387
period, though this tissue at the time is extremely infectious. The Negri
bodies do not pass through a Berkefeld filter, but a virus capable of pro-
ducing rabies does pass through.
In rabbits killed by virus fixe, Lentz finds peculiar structures between,
not in, the cells of Ammon's horn; they resemble Negri bodies, but are
not identical with them. These "passage-virus corpuscles" are not present
in rabbits killed by "street virus."
On EXAMINING FOR THE LESIONS OF VAN GEHUCHTEN AND NELIS, it is
best to section the ganglion on the vagus nerve or the Gasserian ganglion.
If the lesion be present, the endothelial cells surrounding the ganglion cells
will be found proliferated, the nerve cells being pushed aside and many of
them destroyed.
If a person has not been bitten, but simply licked on the hands or face
by a mad dog, there is probably no danger, unless there have been fissures
or abrasions on the skin at the time. Where any doubt exists, the pre-
ventive treatment should be taken.
Pasteur's Treatment for the Prevention of Rabies (1883). — A great
boon was conferred upon mankind l»y Pasteur's application of the principle
of producing an active immunity by means of an attenuated virus, in the
prevention of rabies. By passing the "street virus" (obtained from a dog
naturally infected) through a series of rabbits, the virulence is increased,
until the so-called "fixed virus" (of constant potency) is obtained. This
fixed virus causes rabies in rabbits by the 6th day, killing them on the 9th
or 10th day, but, strangely enough, has largely lost its virulence for dogs,
and is probably entirely avirulent for man (Proescher).
The spinal cord of a rabbit, chloroformed on the ninth day after inocu-
lation with fixed virus, is removed, and desiccated for 14 days. A segment
of the cord, cut off each day, is kept in pure glycerin. Glycerin emulsions
are made of the different segments. Two doses of the most attenuated
virus are given on the 1st day, and on each successive day a dose of pro-
gressively less attenuated virus is given until, by the 18th day, a virus
made from the cord that has been dried only 3 days- is given.
The treatment is best carried out at regularly established Pasteur Insti-
tutes, but emulsions of the cord in glycerin can now be sent to a distance
and the treatment can be carried out at home.
There is no longer any doubt about the value of this prophylactic
inoculation.
Neglect to begin the treatment early enough is often followed by the
most disastrous results. In Chicago, I saw 3 cases of human rabies. Half
an hour after I had shown one man, with beginning symptoms, in the
clinic at Kush Medical College, I was summoned to his room in the Pres-
byterian Hospital to find him violently insane, threatening all who came
near him. He had to be overpowered. One plucky interne rushed in
with a blanket in front of him, followed by a group of men, and together
388 DIAGNOSIS OF INFECTIOUS DISEASES
they secured the patient; he had to be kept under chloroform for a few
hours until the exitus !
References
1. General
Harris (D. L.). A method for the staining of Negri bodies. J. Infect. Dis., Chicago, 1908,
, v, 566-569.
ffetsch (H.). Lyssa. In: Spez. Path. u. Therap. inner. Krankh. (Kraus & Brugsch), Ber-
lin, 1913, ii, 2, 533-566.
Hbgyes (A.}. Lyssa. Spec. Path. u. Therap. Nothnagel, Wien, 1897, v, 5. Theil,2. Abt.t
1-240.
Maresch (R.}. Lyssa. In: Handb. d. pathogen. Protoz. (Prowazek). Leipzig, 1912, i,
196-218.
Ravenel (M. P.). Rabies. In: Mod. Med. (Osier & McCrae), 2d ed., Philadelphia & New
York, 1913, i, 956-973.
Stimson (A. M.). Facts and problems of rabies. Washington, 1910, Govt. Print. Office.
90 p. 8°.
Forms Bull. No. 65 ofTreas. Dep. Pub. Health & Mar.-Hosp. Serv., U. S.
Hyg. Lab.
Williams (A. W.) & Lowden (M. M.). The etiology and diagnosis of hydrophobia. J.
Infect. Dis., Chicago, 1906, Hi, 452-483.
'Hydrophobia. In: Therap. of Int. Dis. (Forchheimer). New York &
London, 1914, v, 707-748.
Woodhead (G. S.}. Hydrophobia. In: Syst. Med. (Allbutt & Rolleston). 8°. London,
1909, ii, pt. 1, 813-843.
2. Etiological
Bohne (A.}. Beitrag zur diagnostischen Verwertbarkeit der Negrischen Korperchen. Ztschr.
f. Hyg. u. Infektionskrankh., Leipzig, 1905-06, Hi, 87-96.
Negri (A.}. Beitrag zum Studium der Aetiologie der Tollwuth. Ztschr. f. Hyg. u. Infec-
tionskrankh., Leipzig, 1903, xliii, 507-527.
Zur Aetiologie der Tollwuth. Die Diagnose der Tollwuth auf Grund der
neuen Befunde. Ztschr. f. Hyg. u. Infectionskrankh. Leipzig, 1903,
xliv, 519-540.
Noguchi (H.}. Zuchtung der Erreger der Tollwuth. Berl. klin. Wchnschr., 1913, I, 1931-
1932.
Contribution to the cultivation of the parasite of rabies. J. Exper. M.,
Lancaster, Pa., 1913, xviii, 314-316.
Volpius (G.}. Ueber die histologische Diagnose der Wut. Ztschr. f. Hyg. u. Infections-
krankh., Leipzig, 1910, Ixv, 113-120.
Watson (E. M.}. The Negri bodies in rabies. J. Exper. M., Lancaster, Pa., 1913 , xvii,
29-42.
3. Briefer Clinical Articles
Babes (F.). Bemerkungen uber "Atypische Wutfalle." Ztschr. f. Hyg. u. Infections-
krankh., Leipzig, 1911 , Ixix, 397-404.
Simon (G.). Ueber Ldhmungen im Verlauf der Tollwutschutzimpfung. Centralbl. f. Bak-
teriol. (etc.), 1. Abt., Jena, 1913 , Ixviii, 72-112.
Wesson (M. #.)• Rabies: a pathognomic sign generally overlooked. J. Am. M. Ass.,
Chicago, 1913, Ix, 1069-1070.
KEED, CARROLL AND AGKAMONTE'S VIKUS 389
4. Prophylactic
Gumming (J. G.}. Rabies-hydrophobia: a study of fixed virus, determination of the M. L.
D., vaccine treatment (Hogyes, Pasteur and dialyzed vaccine), and im-
munity tests. J. Infect. Dis., Chicago, 1914, xiv, 33-52.
Harvey (W. F.) & McKendrick (A.}. The theory and practice of antirabic immunization.
Calcutta, 1907. 43 p. 4°.
Forms No. 30, n. s. ofScient. mem. med. off., India, Calcutta.
Heller (O.) & Rothermundt (M.}. Wutschutzimpfung und Wutimmuniidt. In: Handb.
d. pathogen. Mikroorg. (Kolle & Wassermann). 2. Aufl. Jena, 1913,
viii, 897-942.
Krause (R.)» Ueber Methoden der Schutzimpfung gegen Lyssa. Handb. d. Techn. u.
Methodik d. Immunitdtsforsch. (Kraus &Levaditi), Jena, 1908, i, 687-722.
Oshida (T.}. Eine neue Methode zur Einimpfung des Hundmvutgiftes und zum Herausnehmen
des Ruckenmarks. Centralbl. f. Bakteriol, Jena, 1901, xxix, 988-991 .
Ruediger (E. //.). Rabies in the Philippine Islands and a method available for controlling
it. Bull. Manila M. Soc., 1911, Hi, 64-70.
Pasteur (L.). Methode pour prevenir la rage apres morsure. Bull. Acad. de med., Paris,
1885, 2e s., xiv, 1431-1443.
Also: Compt. rend. Acad. d. Sc., Paris, 1885, ci, 765-774.
Nouvelle communication sur la rage. Compt. rend. Acad. d. Sc., Paris.
1886, ciii, 777-785.
Resultats de ^application de la methode pour prevenir la rage apres mor-
sure, Compt. rend. Acad. d. Sc., Paris, 1886, cii, 459-469.
B. Disease Due to Reed, Carroll and
Agramonte's Virus
Virus of Yellow Fever. — This virus, studied by Reed, Carroll, Lazear and Agra-
monte, is the cause of yellow fever. The virus is present in the blood during the
first 3 days of the fever only. If the infected human being be bitten, at this time,
by a particular variety of mosquito (Stegomyia calopus fasciata), the virus
undergoes some form of development within the body of the mosquito, and, after
about 2 weeks, if the same mosquito bite a healthy human being, the latter may
become infected. The findings of the United States Army Commission (Walter
Reed and his colleagues) have been confirmed by the French Expedition in Brazil
(Marchoux and Salimbeni).
It was shown that the blood of a patient in the first three days of the disease
would, if injected subcutaneously, produce the disease in a susceptible person.
Cutaneous vapcination with infected serum is without result. The virus in the
blood will pass through a Berkefeld filter. It has not as yet been cultivated.
1. Yellow Fever
Definition. — Yellow fever is an acute and severe infections disease,
transmitted by infected mosquitoes. It was formerly very prevalent in
Central America and the West Indies, and sometimes invades the Southern
United States. It is due to the filtrable virus of Keed, Carroll and Agra-
monte.
Epidemiology. — The disease was first described in Guadeloupe in 1635
390 DIAGNOSIS OF INFECTIOUS DISEASES
and has been endemic since then on the islands and on the coasts of the
Gulf of Mexico and the Caribbean Sea and on the West Coast of Africa.
The United States of America, Spain and Brazil have suffered from severe
epidemics. That in Philadelphia in 1793 was interestingly dealt with in
the medical writings of that day. The theory of transmission by fomites
was greatly stressed but the observation that the larger number of cases
developed in certain streets near the wharves led some authors to attribute
importance to "miasmatic vapors" from the water. We now know that the
Stegomyia calopus is preeminently "a house mosquito and a town mos-
quito" breeding in the water of cisterns, roof gutters, old tin-cans, etc.,
and rarely traveling further than 75 feet from the house in which it has
been feeding. The screening of all cases of yellow fever, and the drain-
ing, or oiling, of all standing water to eliminate the Stegomyia, have freed
Havana, Porto Rico, and the Panama Canal Zone of this dread disease.
Symptoms. — The incubation period is 3-5-13 days. The onset is sud-
den with chill, fever, tachycardia, severe pains in the small of the back and
in the extremities, congestion of the face and of the conjunctivae, and sore
throat. There is marked tenderness in the epigastrium on palpation, and
vomiting. The patients give off a "butcher-shop odor." The definite icte-
rus, which appears on the third day, is important for diagnosis. In from
2 to 4 days, there is a sudden fall of the temperature, to normal, often with
collapse and exitus ; in non-lethal cases, defervescence is usually by lysis.
The remission, in other cases, lasts only a few hours, and is generally
followed by a secondary fever of 1 to 3 days duration ; if the patient live,
gastric, cardiac, renal and hepatic symptoms appear. Albuminuria and
cylindruria are found more constantly and earlier in yellow fever than in
any other infectious disease. Among other phenomena often observed are
hematemesis (black vomit), enterorrhagia, and cardiac insufficiency. A
frequent finding is the presence of an increasingly marked bradycardia with
increasing febrile reaction. The patients generally appear bright men-
tally; occasionally deliria develop. The mortality is variable in different
epidemics (15 to 90 per cent). Even severe cases may recover. Re-
lapses are common. In times of epidemic mild and abortive cases are
often met with, especially in children. One attack gives complete im-
munity.
Diagnosis. — This may be very difficult, especially at the beginning of an
epidemic. The disease must be differentiated : (1) from malaria (para-
sites in stained smears or in fresh blood, absence of early jaundice, larger
spleen) ; (2) from relapsing fever (spirochaetes) ; (3) from phosphorus
poisoning (anamnesis^) ; (4) from acute yellow atrophy of the liver (con-
vulsions; deliria) ; (5) from dengue (absence of flushed facies of yellow
fever, of albuminuria and of the late bradycardia [Faget's sign in yellow
fever], and of the early jaundice).
DISEASE BITE TO ASHBURN AND CRAIG'S VIRUS 391
References
Augustin (George}. History of yellow fever. New Orleans, La., 1909, Searcy & Pfaff,
Balfour (A.). The wild monkey as a reservoir for the virus of yellow fever. Lancet, London.
1914, i, 1176-1178.
Carroll (James}. Yellow fever. Mod. Med. (Osier). 8°. Philadelphia & New York,
2d ed., 1914, i, 936-973. Revised by T. McCrae.
Carter (H. R.). Yellow fever. U. S. P. H. Reports, Supplement No. 19, Washington,
Gov't Print. Office, 1914. 29 p:
Davidson (A.). Yellow fever. In: Syst. Med. (Allbutt & Rollestori). 8°. London, 1910 >,
ii, pt. 2, 313-345.
Finlay (C.). El mosquito hipoteticamente considerado como agente de trasmision de la fiebre
amarilla. An. r. Acad. de cien med. de la Habana, 1881-82, xviii, 147-
Gorgas (W. C.}. The practical mosquito work done at Havana, Cuba, which residted in ifa
disappearance of yellow fever from that locality. Wash. M. Ann., 1903,
ii, 170-180.
Hunter (W.} & Spriags (E. /.). Acute yellow fever. In: Syst. Med. (Allbutt & Rolleston).
8°. London, 1908, iv, pt. 1, 115-129.
Kelly (H. A.}. Walter Reed, and yellow fever. Rev. ed. Baltimore, 1912, Medical and
Standard Book Co. 329 p. 12°.
Otto (M.). Gelbfieber. In: Handb. d. pathogen. Mikroorg. (Kolle & Wassermann).
2 Aufl. Jena, 1913, viii, 523-622.
Reed (W.), Carroll (J.) & Agramonte (A.}. Experimental yellow fever. Am. Med.,
Philadelphia, 1901, ii, 15-23.
White (J. H.}. The dissemination and prevention of yellow fever. Am. J. M. Sc., Phila-
delphia & New York, 1913, cxlv, 378-386.
C. Disease Due to Ashburn and Craig's Virus
Virus of Dengue Fever. — This filtrable virus, as shown by Ashburn and
Craig, who studied the disease in the Philippines, can be transmitted by mosqui-
toes (Culex fatigans), though no especial cycle seems to be gone through by the
parasite in the body of the mosquito. Contact infection may occur, but is prob-
ably rare.
1. Dengue Fever
Break-Bone Fever, Dandy Fever
Definition. — An acute, infectious, non-fatal, tropical fever, accompanied
by severe pains in the bones, joints and muscles, and by rashes at the begin-
ning and at the end of the disease; due to a filtrable virus, and occur-
ring, usually in the hot weather, in sharply circumscribed epidemics, or
occasionally, sporadically.
Symptoms. — After an incubation period of from 3 to 5 days, there is
sudden fever (105°-107° F.), with headache, chilly sensations, muscu-
lar and articular pains, and a skin exanthem (initial erythema). The
joint and bone pains are excruciating and may persist for many weeks.
392 DIAGNOSIS OF INFECTIOUS DISEASES
The fever is maximal by the 3rd or 4th day ; then there is apyrexia for
from 2 to 4 days, followed by a return of the fever and the pains. The
disease is associated with a leukopenia. The non-itching rash, which on
the 4th or 5th day usually appears on the palms and backs of the hands,
forearms, chest and back, consists of small red papules and macules, not
unlike the eruption of measles. There is generally lymphglandular en-
largement, which may persist long after recovery. On the Gth or the 7th
day, the temperature falls by crisis, and the disease is practically over,
though the skin eruption may disappear but slowly. In convalescence,
prostration of unusual .grade may be present. The immunity yielded by a
single attack does not last long (1 year).
Diagnosis. — Easy enough to recognize in epidemics, dengue may be dif-
ficult to diagnosticate in the first few cases. In the differential diagnosis
we have to distinguish it (1) from yellow fever (q. v.) ; and (2) from in-
fluenza, in which the pains in the muscles and joints are less severe, and the
respiratory catarrhal symptoms are more marked ; herpes is more com-
mon, and the B. influenzce is present in the sputum.
References
Ashburn (P. M.} & Craig (C. F.). Investigations regarding the etiology of dengue fever.
Philippine J. Sc., 1907, ii, 94-146.
Manson (Sir P.). Dengue. In: Syst. Med. (Allbutt & Rolleston). 8°. London, 1910, ii,
pt. 2, 345-354.
D. Diseases Due to Flexner and Noguchi's
Filtrable and Cultivable Virus
(Flexneria noguchii)
Flexner and Noguchi's Virus of the Heine-Medin Disease. — The virus of acute
poliomyelitis has been shown by Flexner to belong to the class of filtrable viruses.
Noguchi and Flexner have recently cultivated it (see below), and though supposed
to be ultramicroscopic, because filtrable, it is visible in stained preparations of
cultures and of infected tissue, being a small sub-coccoid body (0.2 /*), much smaller
than any known bacterium.
1. Heine-Medin Disease
Infantile Paralysis, Acute Anterior Poliomyelitis
Definition. — An acute, infectious disease occurring both in epidemics
and sporadically, due to the filtrable and cultivable virus Flexneria no-
guchii and involving different parts of the nervous system, often localizing
especially in the anterior horns of the gray matter of the spinal cord
FLEXNER AND NOGUCHFS FILTEABLE VIRUS 393
(poliomyelitis anterior), but also localizing in the cerebrum, in the medulla
oblongata, in the cerebellum, and in the meninges, to a variable extent in
different cases (cerebral, bulbar, cerebellar, polyneuritic, meningeal, and
abortive, types).
Historical. — Knowledge of the disease has been much increased since
the early clinical studies of Heine, of Cannstadt (1840), who called it "in-
fantile spinal paralysis." Striimpell later studied forms of cerebral paraly-
sis which he thought must have the same etiology as Heine's disease. A
great advance came through the studies of the Swedish observer Medin
(1890), who, in an epidemic, recognized that while spinal paralysis pre-
dominates, there occur also cerebral, bulbar, polyneuritic, and peculiar
ataxic forms of the disease evidently due to the same virus. The careful
studies of Wickmann (1905-6) in Sweden enlarged our views of the Heine-
Medin disease still further, as he demonstrated the existence also of a
meningitic form, of a form following the course of Landry's paralysis, and,
above all, of an abortive form. Wickmann must be regarded as the founder
of the epidemiology of the disease, since through his discovery of abortive
types, the explanation of the transmission from case to case begins to be
better understood. The study of the pathological anatomy of the disease
began with Charcot's observations on the anterior horns and has made
steady progress since, being contributed to in this country especially by
S. Flexner and his colleagues. In 1908 began the very important experi-
mental studies of the disease ; in that year, Landsteiner and Popper suc-
cessfully infected monkeys with the Heine-Medin disease by intraperitoneal
injection. In 1909, Flexner and Lewis showed that the disease could be
kept going in a series of monkeys, by passing it from monkey to monkey,
a fact also demonstrated by others (Leiner and v. Wiesner ; Romer ; Land-
steiner and Levaditi), the disease being most easily transmitted by intra-
cerebral injections, especially after a "passage virus" has been obtained
(Homer, Flexner). Other animals are not susceptible.
These findings gave an enormous spur to the study of the etiology of the
disease. It was soon shown that the juices of the nervous system of an
infected animal, when filtered through a porcelain, or other filter, are still
capable of infecting monkeys (Flexner and Lewis, Landsteiner and Leva-
diti) ; in other words, the disease is due to a so-called filtrable virus.
The virus is very resistant to glycerin ; it retains its virulence in diluted
glycerin 142 days (Romer) ; even in 33 per cent glycerin it may be fully
virulent after 202 days (Levaditi, Landsteiner and Pastia). In this
respect it resembles the virus of rabies and that of vaccinia. It stands
cold well, retaining its virulence when kept frozen for at least 11 days. It
is enfeebled by a temperature of 45° C. and is killed after heating for half
an hour at 55° C. It is not killed by drying. It can live for some time in
sterile water or sterile milk, apparently without multiplication. Recently,
Flexner and Noguchi (1913) have grown the virus outside the body, in
394 DIAGNOSIS OF INFECTIOUS DISEASES
ascites-fluid agar containing a piece of normal rabbit's kidney, the whole
culture being covered with a layer of paraffin. The anaerobic colonies
appear as a turbidity in the medium. On staining with one of the Ronia-
nowsky stains minute violet rounded-oval bodies, singly, in. pairs, and in
chains, can be seen ; they are Gram-positive ; examined fresh in the dark
field, they are non-motile. The average diameter is 0.2 /*. Monkeys
inoculated with the virus develop the disease, even when the virus used
has been grown for 20 generations on an artificial medium. The minute
parasite is visible in sections of the affected nervous tissue, on careful
search. Since the parasite of kala-azar has been named Leishmania dono-
vani, miglit we not do well to give to this virus of the Heine-Medin disease
the name Flexneria noguchii f Now that one filtrable virus has been culti-
vated in vitro, and has become visible on microscopic examination, there is
reason to hope that we are on the threshold of a new era as regards our
knowledge of diseases due to filtrable viruses. (See also Noguchi's studies
of rabies-virus.)
Transmission by insects has been suspected. That the virus may be
transmitted from one monkey to another through the bite of the stable-fly
(Stomoxys calcitrans) has been demonstrated by Rosenau.
The prevalence of the di-sease has been increased all over Europe and
America in recent years. The virus is concentrated in the central nervous
system (spinal cord) of infected persons and animals. One one-hundredth
of 1 c.c. of an emulsion of spinal cord will infect a monkey. In infected
persons and animals, the virus is present in (1) the nervous tissues, (2)
the mesenteric glands (Flexner and Lewis), (3) in the tonsils and throat
(Flexner and Clark, Landsteiner, Levaditi and Pastia) ; in one instance,
it has been possible to demonstrate it in washings of the mouth of the
healthy parents of a poliomyelitic child (Flexner, Clark and Eraser). It
may also be present in the feces. It is probable that the virus can be
carried for months,1 or perhaps for years, in a virulent state, in the throat
and tonsils. Such virus carriers must be a great menace to a community.
The blood and cerebrospinal fluid as a rule are free from the virus. The
virus appears to travel along the perineural lymph channels into the cen-
tral nervous system, rather than by way of the blood vessels ; here, again,
it is like rabies. The elective affinities of the virus for the nervous system
on the one hand and for the lymphatic system on the other are striking
features of the Heine-Medin disease.
Immunity. — A high degree of immunity is yielded by a single attack.
Areas in which the disease is epidemic in one year may be singularly free
from it during epidemics of the next succeeding years. T.he blood
serum of a person who has had the disease will neutralize fatal doses of
the virus (Anderson and Frost; Flexner and Lewis ; Landsteiner and
Levaditi ; Netter and Levaditi ; Homer) ; the principle can be used to cor-
roborate the clinical diagnosis (q. v.) in abortive cases. Monkeys that have
FLEXNER AND NOGUCHPS FILTRABLE VIRUS 395
had the disease and have recovered, with residual paralysis, cannot be
experimentally re-infected (Romer). Attempts to immunize by applying
the method used by Pasteur in rabies are not devoid of danger, since
drying the spinal cord does not always attenuate the virus. More can be
expected from attenuation by heating to* 50° C. (Romer; Landsteiner;
Levaditi and Pastia), or by treating the virus with 1 to 11/2 per cent
carbolic acid for 6 days (Kraus). The most hopeful experiments in the
direction of a prophylactic immunization for man would seem to be by
serovaccination ( Romer ) .
Human beings are probably infected by way of the upper respiratory
passages (nose and throat), possibly also by way of the digestive tract.
The possibility of infection by insect bites has been referred to above.
Occurrence in Epidemics. — Large epidemics apparently did not occur
until about 30 years ago, though sporadic cases of the disease have been
known for over a century. Up to 1907, the large epidemics were confined
to Scandinavian countries ; since 1907, large epidemics have occurred in
most civilized countries (United States, Canada, Cuba, Germany, Austria,
France, the British Isles, Russia and Australia.) In 1911, 6,000 cases
occurred in Sweden alone. Of all cases, 96 per cent occur before the 10th
year of life, 90 per cent before the 5th year, and over 75 per cent during
the first 3 years of life (Ed. Miiller). The well-to-do families are affected
just as often as the poor. Race has no effect on disposition.
Contagiosity. — The disease always comes from a preexisting human
case, either directly or indirectly. There is no evidence that it is spread
by water, milk, fruit or other foods. As the virus resists drying, it is pos-
sible that it may be spread by inanimate objects (fomites), that have been
contaminated by a person sick of the disease, or by a healthy carrier. It
is asserted that the dust from the sick-room injected into monkeys will
give rise to the disease (Neustadler and Throo, 1911). Again, it is said
that shoemakers or their children are often affected (Eichelberg).
Further, Hill, in Minnesota, found that cases of poliomyelitis were most
common on dusty streets; but Lovett and Sheppard (1914-) could make
out no relation to dust. Other points in favor of the possibility of infection
by fomites are (1) the infection of monkeys by extracts of handkerchiefs
used by poliomyelitis patients (Josef son) ; (2) the entrance of a new
family into a house in which there had been cases of poliomyelitis has
been followed by cases of the disease among the incomers.
As to transmission by insects, the frequency of the disease in August
and September, the proof that flies may be contaminated by the virus and
the latter retain its virulence for at least several days (Flexner and Clark ;
Howard and Clark), the experiment in which the stable flies (Stomoxys
calcitrans) were allowed to suck blood from paralyzed monkeys and to
bite healthy monkeys, transmitting the disease (Rosenau; Anderson and
Frost), are among the points of evidence adduced in its favor. But none
396 DIAGNOSIS OF INFECTIOUS DISEASES
of these is convincing. Against the view are the following facts: (1)
Lice and mosquitoes do not, on biting infected monkeys, become con-
taminated with the virus (Howard and Clark) ; (2) the virus is rarely
present in the blood; (3) epidemics, though commonest in autumn, may
also occur in mid-winter ; and (4) the disease may break out miles away
from any other case, and so must be brought by human intermediators
(Ed. Miiller).
Since (1) the portal of entry is, in all likelihood, the lymphatic tissue
of the mouth, throat, nose and pharynx (possibly, also, of the intestine),
(2) the virus remains for a long time virulent in the secretions from the
mouth and nasopharynx of patients, convalescents, and healthy contacts,
and (3) the disease undoubtedly develops in persons coming in contact
with those infected or near the infected, it seems probable that the trans-
mission is ordinarily direct from one human being to another, without
the intermediation of fomites, or of insects. Whether this occurs by
"droplet infection," or by immediate contact, or by both, we do not yet
know.
Certain points still remain to be cleared up : (1) the marked prevalence
of the disease in Northern climates; (2) the predominant prevalence in
August and September; (3) the greater predisposition of people in country
districts and in thinly populated areas; (4) the absence of tendency to
contact infection among monkeys, when diseased and healthy are permit-
ted to intermingle; and (5) the absence of tendency to infection among
doctors, nurses, and laboratory experimenters working with the disease.
It is probable that in every epidemic an enormous number of abortive
infections occur and give immunity.
Prophylaxis. — This must be very difficult, if the ideas regarding direct
transmission, above outlined, are correct. The danger from convalescents,
from abortive cases, and from healthy contacts who become carriers, must
be very great. The conditions seem to be similar .to those in epidemic
cerebrospinal meningitis.
Quarantine methods are worthless; the danger is less often from the
actually sick than from healthy people around them (Wickmann; Wern-
stadt, 1911). Similarly, compulsory disinfection of linen, clothing, etc.,
offers but little hope, and seems hardly worth while.
In epidemic times, the schools should be closed ; at any rate the sibs of
affected children should not be permitted to go to school, as they may act
as carriers. Children's parties should not be held. Funerals after deaths
from poliomyelitis should be private.
When the disease is prevalent, each child should have its own handker-
chief, and should never use the handkerchief of another child, or that of a
parent. Towels, handkerchiefs, etc., used by patients should be sterilized
by boiling. House disinfection is advisable after poliomyelitis, though it
is probable that the inmates have become carriers through contact.
FLEXKER AND NOGUCHrS FILTRABLE VIRUS 397
Mouth washes are of doubtful efficacy. If one is used at all, probably
a 1 per cent solution of hydrogen peroxid is best; if desired, 2 per cent
potassium permanganate may be added.
Symptoms. — The incubation period varies from 5 to 10 days, averaging
a week. Exceptionally it may be shorter, 1-3 days, or longer, 15 days.
In monkeys it averages about 10 days, but may last 33 days (Flexner and
Lewis), or even 46 days (Leiner and von Wiesner).
The children sicken with signs of an infection often taken to be ton-
sillitis or influenza. There may be vomiting, diarrhea, slight fever,
accelerated pulse, sweats, mental dullness, sometimes an exanthero, rarely
herpes labialis (in contrast with cerebrospinal meningitis), occasionally
herpes zoster, and, very rarely, convulsions; at first there may be signs
of meningeal irritation, with rigidity of the neck, and general cutaneous
hyperesthesia, suggestive of meningitis. Usually there is a leukopenia
(3,000-8,000 W.B.C.) ; occasionally, a leukocytosis (10,000-30,000). At
this time the cerebrospinal fluid shows but few changes ; it is clear ; the
pressure is increased ; the protein content is high ; there is slight lymphocy-
tosis/ and cultures are sterile — findings in marked contrast with those in
cerebrospinal meningitis.
In from 1 to 7 days later, the paralytic stage is entered upon ; in the
SPINAL FOEM, paralysis is noticed in one leg, or arm, or in two, three,
or four extremities simultaneously. The lower extremities are involved
in about four-fifths of the cases (E. Miiller). The M. quadriceps and the
Mm. peronei are most often involved, the muscles of the shoulder girdle
and the abdominal muscles frequently. Paralysis of the diaphragm and
of the intercostal muscles may occur. The muscles innervated by the cere-
bral nerves are sometimes, though rarely, paralyzed. Occasionally, there,
is paralysis of the muscles of the neck and back ; the child's head droops,
or he "falls together in a heap."
It is characteristic of the paralysis in the Heine-Medin disease that it
assumes its full development immediately, having its widest distribution,
usually, at the time of its first appearance. It is a lower motor neuron
paralysis (flaccid ; reaction of degeneration at the end of a week ; loss of
reflexes). The deep reflexes are lost, if the muscles concerned are para-
lyzed; otherwise they, and the cutaneous reflexes, are usually unaltered.
The sphincters are normal. The findings in the cerebrospinal fluid at
different stages of the disease, reported from the Hospital of the Rocke-
feller Institute, are interesting (-q. v.).
The stage of repair now sets in, and continues for 1-1-J years. Within
the first few weeks, there is usually a marked recovery from the paralysis,
with concentration of the residual paralyses in certain groups of muscles
(those in which the reaction of degeneration has been outspoken). In
these residual paralyses, the topography usually corresponds to the seg-
ments of the spinal cord in which the anterior horn cells have been injured.
398 DIAGNOSIS OF INFECTIOUS DISEASES
Later on, as a result of the degenerative atrophy, contractures develop in
the antagonists of the paralyzed muscles and cause paralytic club-foot,
flat-foot, etc. The bones remain backward in their development. Loose
joints develop. Scoliosis or kyphosis may result. The affected extremity
is cool, cyanotic, and often edematous for a time.
In the CEREBRAL FORM of the Heine-Medin disease, the clinical picture
is that of an infantile cerebral palsy ; undoubtedly some of the cases — not
all — of the Striimpell type of acute hemorrhagic encephalitis are examples
of the Heine-Medin disease. Occasionally a monkey manifests the
cerebral form after experimental infection; a typical meningoencepha-
litis is then found on histological examination, the lesions being simi-
lar in type to those found in the spinal cord in the spinal form of the
disease.
In the cases taking the FORM OF LANDRY'S PARALYSIS, we have to deal
with a peracute and fatal form of the Heine-Medin disease (Wickmann).
The paralysis begins in the lower extremities, quickly ascends, involving
the arms and the bulbar centers, ending in death in a few days. Should
the paralysis begin in the arms, it descends to the leg centers in the lumbar
cord and ascends to the medulla and pons. Similar cases are met with in
monkeys experimentally infected (Flexner and Lewis; Homer); in one
monkey the paralysis advanced with great rapidity, and death occurred
a few hours after the paralysis was first observed.
In the BULBAR AND TONTINE FORMS of the Heine-Medin disease, the
involvement of the cerebral nerves dominates the clinical picture. The
nucleus N". facialis is most often injured usually on one side only, and
frequently with simultaneous involvement of the nucleus N. hypoglossi — a
true polioencephalitis inferior. More rarely, the nucleus ~N. oculomotorii,
the nucleus !N". trochlearis, and the nucleus "N. abducentis are injured
(polioencephalitis superior). The motor nucleus of the "N: trigeminus
may be attacked ; the nuclei of the other motor cerebral nerves (N. vagus,
"N. glossopharyngeus, N. accessorius) are but rarely affected. In the
experimental disease in monkeys, the results resemble the disease in
human beings. In all the bulbar and pontine forms, there is usually some
simultaneous spinal paralysis.
In the ATAXIC FORM of the disease (Medin), the clinical picture
resembles that of Friedreich's ataxia (q. v.). It is due to lesions of the
cerebellum or of the cerebellar paths in the spinal cord, the medulla oblon-
gata, the pons or the mid-brain. As far as I know, this form has not yet
been reproduced in monkeys. It seems likely that some of the cases of
"acute ataxia in children" described by neurologists are instances of un-
suspected Heine-Medin disease.
In the so-called POLYNEURITIC FORM of the disease, the symptoms are
those of a multiple neuritis (pains, paresthesias, paralysis), but in cases
that come to autopsy, the actual lesions are found to be meningomyelitic.
FLEXJSTEE AND NOGUCHTS FILTEABLE VIEUS 399
I saw a remarkable example of this type in 1906 with Dr. G. H. Field of
Cobourg, Ontario. The patient, a young girl, after an attack resembling
influenza with sore throat, began to have excruciating pains all over the
body with extreme cutaneous hyperesthesia and sweats. She would cry
out when her bed was approached. After a few days there was paralysis
of both legs and partial paralysis of one arm. We made the diagnosis
of acute "anterior poliomyelitis, complicated by multiple neuritis." The
child recovered though there is considerable residual paralysis.
In the MENINGITIC FOKM, the symptoms due to the meningeal infiltra-
tion dominate the clinical picture. The rigidity of the neck, the pain in
the back, the tendency to opisthotonos, the positive Kernig's sign, the
headache and the vomiting all point to meningeal irritation. A meningitis
does exist but it is only a part of the general meningomyelitic process.
Cytodiagnostic and bacteriodiagnostic methods applied to the cerebrospinal
fluid (q. v.) quickly differentiate.
In the ABOKTIVE FORMS of the Heine-Medin disease, first recognized by
Wickmann, no outspoken paralyses occur, though the prodromal symptoms
may be present to a greater or less extent, (fever and sweating, with
symptoms suggesting a respiratory, a gastro-intestinal, a meningeal, or
a general influenzal infection). One sees every transition betweeri these
forms with no paralysis, through the forms in which there are transitory
slight pareses of one or of several muscle groups, or temporary loss of deep
reflexes — the so-called "rudimentary poliomyelitis" of E. Miiller — to the
outspoken monoplegias, paraplegias, and quadriplegias.
It is now believed that in large epidemics of the Heine-Medin disease
from -J to -J of all the infections are abortive forms ! These forms can
now often be recognized by the clinician, especially if he resort to sero-
diagnostic methods. (See Diagnosis.)
Prognosis. — The mortality varies much in different epidemics, accord-
ing to Wickmann from 10-42.3 per cent. It was formerly believed that
the disease is rarely fatal; that belief was due to a failure to recognize
the fatal cases as the Heine-Medin disease, physicians taking them to be
cerebrospinal meningitis, Landry's paralysis, etc. Death, when it occurs,
usually takes place on the 4th or 5th day. The mortality is greater in
adults (poliomyelitis acuta adultorum) than in children (2 or 3 to 1).
A great many patients recover without any residual paralysis. In children
this is true of nearly half the cases ; in patients over 11 years old, of about
-J. In Lovett and Sheppard's experience, 13.5 per cent of all the paralyzed
cases ultimately recovered completely, without residue. Wickmann assures
us that we can count on 20 per cent of complete recoveries without residue
in the cases suffering from paralysis.
The mortality is much greater among inoculated monkeys : With ordi-
nary virus f of the animals die; with passage-virus, the mortality ap-
proaches 100 per cent (Flexner and Lewis; Eomer). ^
400 DIAGNOSIS OF INFECTIOUS DISEASES
Pathology. — This has been carefully studied and described. In 1870, Char-
cot studied the after effects (loss of anterior horn cells). In 1888, Rissler
made a study of fresh cases, at autopsy Recently, human and monkey tissues
have been studied with great care, especially by Flexner and his co-workers, who
have shown that the process involves the organs of the body as a whole, and that
the involvement of the anterior horns is incidental to this general process. The
virus injures and destroys the ganglion cells of the anterior horns, partly by
direct intoxication, but chiefly through local perivascular, lymphangitic changes.
In the nervous system, the lesions are those of a widely disseminated meningo-
encephalomyelitis. Batten (1904) had attributed most of the paralyses to throm-
boses in the anterior spinal arteries.
A peculiarity of poliomyelitis lies in the fact that it is an acute perivascular
inflammation with lymphocytic infiltration, not limited to the anterior horns
(though predominant there), but involving also the arteries and veins in different
parts of the gray matter, including the posterior horns and the spinal ganglia;
in the nervous system, the lesions are those of a widely disseminated meningo-
encephalomyelitis. The infection, as we have seen, spreads through the perineural
and perivascular lymph vessels. Macroscopically, there may be but little to be
made out; but microscopically, the histological changes are so extensive that one
wonders that the clinical symptoms are not more pronounced than they are. The
infiltration of the pia, the dilatation of the veins in the gray matter, the peri-
vascular accumulations of small mononuclear cells, the neuronophagy of the ante-
rior horn cells, make a characteristic histological picture. The swelling of the
mesenteric lymph glands, of Peyer's patches and of the solitary follicles in the
intestine is emphasized by Flexner, Peabody and Draper, who have made a report
on the visceral lesions of human cases. It is remarkable that such a dissem-
inated infiltrative lymphocytic inflammation, involving so many tissues through-
out the body, should, in the majority of cases, give rise to a clinical picture
simulating a "system-disease" of the spinal cord (anterior horn cells). It is
probably simply owing to the richness of the anterior horns in blood-vessels ;m<l
in lymphatics that these cell-bodies of the lower motor neurons are picked out!
Diagnosis. — This is easy enough in the spinal form after the paralytic
symptoms have appeared, and it may be suspected, and made earlier in
epidemics, from the presence of fever, sweats, general hyperesthesia, and
the findings in the cerebrospinal fluid above described. The disease in its
earlier stages and in the atypical forms is most often mistaken for in-
fluenza, polyarthritis, polyneuritis, muscular rheumatism, tonsillitis, gastro-
enteritis, typhoid fever, or meningitis.
In the early stage, the general hyperesthesia is cbaracteristic. Tbere is
a tendency to profuse sweats. The leukopenia, or, at any rate, absence of
leukocytosis in spite of high fever, is helpful. The sleepiness in the day-
time, with restlessness at night, the diminished muscle tonus, and the early
loss of reflexes in limbs that later become paralyzed, and of the abdominal
reflexes, are important early signs. Tbe forms other than the spinal form
are very often incorrectly diagnosed.
Serodiagnosis of the Heine-Medin Disease.— In the blood of human beings,
and of monkeys that have had the disease and recovered from it, specific anti-
bodies are present, which neutralize the virus (Flexner and Lewis; Romer and
FLEXKEE AKD tfOGUCHFS FILTEABLE VIEUS 401
E. Miiller, et al) ; in the serum of human beings that have not had the disease,
these specific antibodies are not present (Kling and Levaditi). By serodiagnosis,
therefore, we have a method that permits us to decide whether a person has had
the Heine-Medin disease earlier or not, for the antibodies are very persistent,
remaining active in the blood certainly for many years after the infection, perhaps
through the whole of life. By serodiagnosis, it has been proved (1) that sporadic
cases that recover have the same antibodies as those that occur in epidemic cases,
the etiology of the two therefore being doubtless identical (Netter and Levaditi) ;
(2) that after abortive attacks, the antibodies are present in the blood, just as
after severer attacks, a fact of great importance for epidemiological studies
(Romer) ; (3) that among healthy contacts, the blood in many instances contains
the antibodies (Kling and Levaditi), thus supporting the view that in epidemics
a large number of people have a mild infection and acquire immunity without
knowing anything about it; and (4) that some cases of the Striimpell type of
acute encephalitis in children have been infections with the virus of Heine-Medin
disease (Miiller and Romer).
This method involves mixing some of the serum to be tested with an
amount of virus known to be capable of producing the disease in a monkey.
If on injection of the mixture into a susceptible animal the disease does
not develop it is assumed that the virus has been neutralized by immune
bodies in the serum.
Differential Diagnosis. — We differentiate the disease (1) from menin-
gitis, meningococcal, pneumococcal, influenzal, or tuberculous (cytodiag-
nosis and bacteriodiagnosis on lumbar puncture, greater rigidity of neck
and spine, severer headache, changes in eye grounds, greater disturbance
of consciousness) ; (2) from influenza (catarrhal phenomena more in the
foreground, rather than the pain and hyperesthesia ; sputum) ; (3) from
scarlatina with angina (may be impossible to differentiate early; later,
serodiagnosis). Later in the disease, we have to distinguish poliomyelitis
(4) from true poly neuritis (slower development, paralyses not complete
at beginning, edema occurs earlier, objective sensory disturbances usually
more marked and last longer, cerebral nerves more often involved, periph-
eral nerve topography rather than radicular topography of paralysis,
paralysis more distal in extremities and often bilaterally symmetrical) ;
(5) from other forms of acute myelitis (involvement of pyramidal tract
and sphincters, sensory disturbances) ; (6) from amyotonia congenita
(q. v.) ; (7) from paresis in rickets (slower onset, non-febrile) ; (8)
from hematomyelia (afebrile, dissociated anesthesias) ; .(9) from cerebro-
spinal lues; and (10) from progressive muscular atrophy.
References
1. General and Historical
Heine (/.)• Beobachtungen uber Lahmungszustdnde der unteren Extremitdten und deren
Behandlung. Stuttgart, 1840, F. H. Kohler. 78 p. 4°-
Spinale Kinderlahmung. 2. Aufl. Stuttgart, 1860, /. G, Cotta. 204 P- 8>»
402 DIAGNOSIS OF INFECTIOUS DISEASES
Landsteiner (K.). Poliomyelitis acuta. In: Handb. d. pathogen. Mikroorg. (Kolle &
Wassermann). 2. Aufl. Jena, 1913, viii, 427-462.
Medin (O.). Ueber eine Epidemie von spinaler Kinderldhmung. Verhandl. d.x. Internal.
Med. Cong., 1890. Berlin, 1891, ii, 6. Abth., 87-47.
Om den infantila paralysien, med. sdrskildhdnsyn till pess akuta stadium.
Nord. med. Ark., Stockholm, 1896, n.F., vi, hft. 1, No. 1, 1-84.
L'etat aigu de la paralysie infantile. Arch, de med. d. cnf., Paris, 1898*
t, 257-278.
Muller (E.). Die spindle Kinderldhmung; eine klinische und epidemiologische Studie.
Mil Unterstutzung von M. Windmuller. Berlin, 1910, J. Springer.
170 p. 8°.
Die epidemische Kinderldhmung (Heine-Medinsche Krankheit). In:
Handb. d. inn. Med. (Mohr & Staehelin). Berlin, 1911, i, 799-856.
Peabody (F. W.), Draper (G.) & Dochez (A. R.). A clinical study of acute poliomye-
litis. Monog. Rockefeller Inst. M. Research, New York, 1912, No. 4,
1-187.
Romer (P. II.). Epidemic infantile paralysis (Heine-Medin disease). Transl. by H.
Ridley Prentice. New York, 1913, W. Wood & Co. 220 p. 8°.
Starr (M. A.). Acute poliomyelitis. In: Syst. Med. (Allbutt & Rolleston). 8°. London,
1910, vii, 623-644.
Wickman (J.). Ueber die akute Poliomyelitis und verwandte Erkrankungen (Heine-
Medinsche Krankheit). Jahrb. f. Kinderh., Berlin, 1908, Ixvii, 182-196.
Poliomyelitis. New York, 1915, Nerv. & Ment. Dis. Pub. Co.
Zappert (J.), von Wiesner (R. R.) & Leiner (K.). Studien iiber die Heine-Medinsche
Krankheit (Poliomyelitis acuta). Leipzig u. Wien, 1911, F. Deuticke.
212 p. 8°.
2. Etiology and Epidemiology
Flexner (S.). The contribution of experimental to human poliomyelitis. J. Am. M. Ass.,
Chicago, 1910, Iv, 1105-1113.
The control of epidemic poliomyelitis. Am. J. Dis. Child., Chicago, 1911,
ii, 96-101.
Experimental poliomyelitis. Folia serolog. [etc.], Leipzig, 1911, vii, 1101-
1116.
The microbic cause and manner of infection of poliomyelitis. Johns
Hopkins Hosp. Bull., Baltimore, 1915, xxvi, 180-182.
Flexner (S.) & Amoss (H. L.). Penetration of the virus of poliomyelitis from the blood
into the cerebrospinal fluid. J. Exper. M., Lancaster, Pa., 1914, xix,
411-416.
Localization of the virus and pathogenesis of epidemic poliomyelitis. J. Ex-
per. M., Lancaster, Pa., 1914, xx, 249-268.
Penetration of the virus of poliomyelitis from the blood into the cerebrospinal
fluid. J. Exper. M., Lancaster, Pa., 1914, xix, 411-416.
Flexner (S.), Clark (P. F.) & Amoss (H. L.). A contribution to the epidemiology of
poliomyelitis. J. Exper. M., Lancaster, Pa., 1914, xix, 195-204-
Flexner (S.) & Noguchi (H.). Experiments on the cultivation of the- microorganism caus-
ing epidemic poliomyelitis. J. Exper. M., Lancaster, Pa., 1913, xviii,
461-485.
Kling (C.) & Levaditi (C.). Etudes sur la poliomyelite aigue epidemique. Ann. de VInst.
Pasteur, Paris, 1913, xxvii, 718; 839.
Landsteiner (K.) & Popper (E.). Uebertragung der Poliomyelitis acuta auf Affen.
Ztschr. f. Immunitdtsforsch. u. exper. Therap., Jena, 1909, ii, 1. Teil, 377-
390.
Romer (P. H.). Experimented Poliomyelitis. Ergebn. d. inn. Med. -u. Kinderh., Berlin,
1912, viii, 1-63.
FLEXNER AND NOGUCHI'S FILTRABLE VIRUS 403
3. Possibility of Transmission by Insects
Brues (C. T.} & Sheppard (P. A. E.). The possible etiological relation of certain biting
insects to the spread of infantile paralysis. Month. Bull. State Bd. Health,
Mass., Boston, 1911, vi, 338-340.
Howard (C. W.) & Clark (P. F.). Experiments on insect transmission of the virus of
poliomyelitis. J. Exper. M., Lancaster, Pa., 1912, xvi, 850-859.
Rosenau (M. /.)• The mode of transmission of poliomyelitis. J. Am. M. Ass., Chicago,
1913, Ix, 1612-1615.
4. Pathology
Flexner (S.). Contributions to the epidemiology and pathology of poliomyelitis. Berl. klin.
Wchnschr., 1914, li, 506-509.
Flexner (S.}, Clark (P. F.} & Amoss (H. L.}. A contribution to the pathology of epi-
demic poliomyelitis. J. Exper. M., Lancaster, Pa., 1914, xix, 205-211.
Flexner (S.}, Peabody (F. W.) & Draper (£.)• Epidemic poliomyelitis. Twelfth note:
the visceral lesions of human cases. J. Am. M. Ass., Chicago, 1912,
Iviii, 109-111.
Kohlisch (H.}, Lubarsch (O.) & Smidt (H.). Pathologic der spinalen Kinderldhmung.
In: Ergebn. d. allgem. Pathol. [etc.] (Lubarsch & Ostertag}. Wiesbaden,
1912, xvi, Abth. i, 1-35.
Robertson (H. E.) & Chesley (A. J.}. Pathology and bacteriology of acute anterior polio-
myelitis. Arch. Int. Med., Chicago, 1910, vi, 233-269.
5. Local Reports
Bierring (W. L.). Acute poliomyelitis in Iowa. Interstate M. J., St. Louis, 1912, xix,
35-44.
Francis (E.). Poliomyelitis (infantile paralysis): a report of an outbreak in Texarkana and
vicinity. Pub. Health Rep., Washington, 1913, xxviii, 1693-1698.
Gundrum (F. F.). Acute poliomyelitis in California. J. Am. M. Ass., Chicago, 1912,
Mil, 254-255.
Lovett (R. W.) & Sheppard (P. A. E.). The occurrence of infantile paralysis in Massa-
chusetts in 1910. Boston M. & S. J., 1911, clxiv, 737-742.
6. Diagnosis
Clark (P. F.}, Eraser (F. R.} & Amoss (H. L.}. The relation to the blood of the virus of
epidemic poliomyelitis. J. Exper. M., Lancaster, Pa., 1914, xix, 223-233.
Colliver (J. A.}. Early symptoms of poliomyelitis, with special reference to a new prepara-
lytic symptom. Calif. State J. M., 1913, xi, 443-445.
Fraser (F. /£.)• A study of the cerebrospinal fluid in acute poliomyelitis. J. TZxper. M.,
Lancaster, Pa., 1913, xviii, 242-251.
Clinical observations on ninety cases of acute epidemic poliomyelitis. Am.
J. Med. Sc., Philadelphia, 1914, cxlviii, 1-22.
Gay (F. P.) & Lucas (W. P.}. Anterior poliomyelitis. Methods of diagnosis from spinal
fluid and blood in monkeys and in human beings. Arch. Int. Med.,
Chicago, 1910, vi, 330-338.
Hassin (G. B.}, Lukas (Christine] & Brown (R. O.). RoentgenograpMc bone changes
in a case of poliomyelitis. J. Am. M. Ass., Chicago, 1915, Ixv, 1459-1460.
404 DIAGNOSIS OF INFECTIOUS DISEASES
Kobelew (E.). Contribution a V etude des reactionsmeningees au cours de la poliomyelite
epidemique. [Lyon], Trevoux, 1914, J. Jeannin. 11 4 p. No. 62. 8°.
Martin. (E. G.) & Lovett (R. W.). A method of testing muscular strength in infantile
piralysis. J. Am. M. Ass., Chicago, 1915, Ixv, 1512-1513.
Mills (C. K.). Some recent clinical investigations of poliomyelitis. Internal. Clin., Phila-
delphia, 1911, 21st s., i, 55-39.
Stein (/?.)• Epidemic poliomyelitis: a clinical study of the acute stage. Am. J. M. Sc.,
Philadelphia & New York, 1912, cxliii, 557-571.
Wilbur (R. L.}. Early diagnosis of epidemic poliomyelitis. Calif. State J. M., San Fran-
cisco, 1912, x, 418-426.
7. Special Clinical Forms, etc.
Anderson (J. F.) & Frost (W. H.). Abortive cases of poliomyelitis. An experimental
demonstration of specific immune bodies in their blood-serum. J. Am. M.
Ass., Chicago, 1911, Ivi, 663-667.
Batten (F. E.). Unusual manifestations of poliomyelitis. Brit. J. Child. Dis., London,
1914, xi, 97-105.
Clark (L. P.). A clinical contribution to our knowledge of poliomyelitis irnih cortical in-
volvement. Am. J. M. Sc., Philadelphia & New York, 1912, cxliii,
671-578.
Koplik (H.). The cerebral forms of poliomyelitis and their diagnosis from forms of menin-
gitis. Am. J. M. Sc., Philadelphia & New York, 1911, cxli, 788-803.
Leopold (5.). The polyneuritic form of acute poliomyelitis: a clinical and pathological
. study. Am. J. M. Sc., Philadelphia & New York, 1913, cxlvi, 406-410.
Netter (A.}. The meningeal forms of poliomyelitis. Brit. J. Child. Dis., 1913, x, 531-543.
Un cas de myelite aigue diffuse, guerie par les injections intrarachidiennes
de serum de sujets anterieurement atteints de paralysie infantile. Sero-
therapie de la poliomyelite anterieure. J. d. med. int., Paris, 1914,
xviii, 111-115.
Roussy (G.) & Gauckler (E.). Un cas de poliomyelite subaigue a topographic radiculaire
(type scapulo-humeral) . Rev. neurol., Paris, 1904, xii, 1207-1209.
Sharp (E. A.}. The aborted forms and pre-paralytic stage of ac-ute poliomyelitis as observed
in the Buffalo epidemic. J. Nerv. & Ment. Dis., New York, 1913, xl,
289-299.
Vulpius (O.). The treatment of infantile paralysis. New York, 1913, W. Wood & Co.
93 p. 8°.
E. Other Diseases Due to Filtrable Viruses
1. Foot and Mouth Disease
The filtrable virus of Loeffler-Frosch is the cause of foot and mouth disease
(stomatitis epidemica), which sometimes attacks human beings. Siegel asserts
that he finds extremely minute coccoid bodies in the lesions. The disease is most
often contracted by young children through raw milk. In persons coming into
contact with infected cattle, pigs, sheep or goats, the transmission may be direct.
After certain prodromata (fever, headache, pains in the limb, anorexia, con-
stipation, nausea, and dry mouth), red spots appear on the mucous membrane of
DISEASES DUE TO FILTRABLE VIRUSES 405
the mouth. These soon become vesicular with contents serous at first, later, turbid.
The tongue swells and there is salivation. In a few days, the vesicles rupture,
leaving superficial ulcers behind, which as a rule soon heal. The fingers and toes
may show vesicles also. Most patients recover.
In 1915 one of the students at the Johns Hopkins Medical School developed the
disease in typical form. The case has been carefully described in the paper by
Dr. P. W. Clough.
References
Caspar (M.). Maul- und Klauenseuche (Immunitdt). In: Handb. d. pathogen. Mikroorg.
(Kolle & Wassermann). 2. Aufl. Jena, 1913, vi, 214-223.
Clough (P. W.}. A case of foot-and-mouth disease in man. (Illustrated.) Johns Hopkins
Hosp. Bull, Baltimore, 1915, xxvi, 351-854.
Ebstein (W.). Mittheilungen uber das Maul- und Klauenseuchengift beim Menschen.
Deutsche med. Wchnschr., Leipzig u. Berlin, 1896, xxii, 129-132.
Loeffler (F.) & Frosch (P.). Berichte der Kommission zur Erf orschung der Maul- und
Klauenseuche bei dem Institut fur Infektionskrankheiten in Berlin.
Deutsche med. Wchnschr., Leipzig u. Berlin, 1898, xxiv, 80, 97; also Cen-
tralbl.f. Bakteriol. [etc.], 1. Abt., Jena, 1898, xxiii, 371-391.
Siegel (/.)• Zur Atiologie der Maul- und Klauenseuche. Berl. tierarztl. Wchnschr.,
1912, U, 821-822.
2. Pappataci Fever
The filtrable virus of Doerr and Russ is the cause of the three-day
fever which occurs on the shores of the Adriatic known as pappataci fever;
it is transmitted through the bite of a gnatlike dipterous insect (Phteboto-
mus pappatacii). The disease may be mistaken for abortive typhoid or
for mild undulant fever.
References
Doerr (R.), Franz (K.) & Taussig (5.). Das Pappatacifieber, ein epidemisches Drei-Tage-
Fieber im adriatischen Kiistengebiete Oesterreich- Ungarns. Wien. klin.
Wchnschr., 1909, xxii, 609.
, Das Pappatacifieber (Phlebotomusfieber) . In: Handb. d. pathogen. Mi-
kroorg. (Kolle & Wassermann). 2. Aufl., 1913, viii, 993-1018.
Hale (C. H.}. Pappataci fever at Kamptee, C. P. J. Roy. Army Med. Corps, London, 1912,
xviii, 505-512.
Loughnan (W. F. M.}. Phlebotomus fever and pappataci flies in Aden. J. Roy. Army
Med. Corps, 1913, xxi, 402-408.
Sandwith (F. M.). A lecture on Phlebotomus fever. Clin. J., London, 1911-12, xxxix,
139-143.
3. Transmissible Sarcoma
The filtrable virus of Peyton Eous has been shown to be capable of
reproducing sarcoma in mice ; thus far, we are not sure of the existence of
this virus in sarcomatous human beings.
406
DIAGNOSIS OF INFECTIOUS DISEASES
Fig. 124. — Culture of the Ehrlich Rat Sarcoma. The Central and Completely Opaque Mass Is
the Original Tumor Fragment. The New Cells are Arranged Irregularly Throughout the
Surrounding Medium-IIematoxylin Stain. (After A. Carrel and M. T. Burrows, "Studies
from the Rockefeller Inst. for Med. Res.," Reprinted from J. Exp. Med.)
References
Lange (L. B.). On certain spontaneous chicken tumors as manifestations of a single disease.
II. Simple spindle-celled sarcomata. J. Exper. M., Lancaster, Pa., 1914,
xix, 577-580.
Rons (P.). On certain spontaneous chicken tumors as manifestations of a single
I. Spindle-celled sarcomata rifted with blood sinuses. J. Exper. M.,
Lancaster, Pa., 1914, xix, 570-576.
Rons (P.) & Murphy (/. B.}. On the causation by fillrdble agents of three distinct chicken
tumors. J. Exper. M.} Lanco^ier, Pa., 1914, xix, 52-69.
THE ACUTE EXANTHEMATA 407
IV. DISEASES DUE TO UNKNOWN INFECTIOUS AGENTS
Under this heading will be discussed (1) The Acute Exanthemata,
and (2) Mumps.
A. The Acute Exanthemata
The acute exanthemata include (1) scarlet fever, (2) measles, (3)
rubeola, (4) the fourth disease, (5) chickenpox, (6) smallpox, (7)
sweating sickness, and (8) Kocky Mountain spotted fever.
References
Auche (#.), Surmont (H.) [et al.\. Fievres eruptives. Paris, 1912, J. B. Bailliere &
fils. 258 p. 8°. [Nouv. traite de med. de therap., ii.\
Ochsner (A. J.) & Sturm (M. /.). Isolation rooms in residences for care of patients suffer-
ing with contagious diseases. Internal. Clin., Philadelphia, 1913, 23d s.,
ii, 154-161.
Roily (F.). Akute Exantheme. In: Handb. d. inn. Med. (Mohr & Staeheliri), Berlin,
1911, i, 65-194.
Schamberg (J. F.}. Diseases of the skin and the eruptive fevers. 2d ed. Philadelphia &
London, 1911, W. B, Saunders Co. 573 p. 8°.
1. Scarlet Fever (Scarlatina)
Definition. — A highly contagious disease of unknown etiology, accom-
panied by sore throat, a diffuse red eruption on the skin, and often fol-
lowed by acute glomerulonephritis.
Etiology and Epidemiology. — Scarlet fever has been known since the
epoch-making descriptions of the London epidemics of 1661-1675 by
Sydenham. The disease often occurs in epidemics, which vary greatly in
severity. Some epidemics are so mild that they are not recognized as
scarlet fever at all, though the next year the epidemic may be of a much
more virulent type. They are most common in autumn and winter, rare
in summer. Sporadic cases are common. Susceptibility to the disease
is far less general than in measles.
The most important predisposing factor is age, over 85 per cent of
the cases being in children before the age of puberty.
The source of the infective agent is not positively known, but it is
believed that the disease is spread through the nasal, oral, and bronchial
secretions of infected persons, and probably mainly through desquamated
scales.
The infective agent is unknown. Some believe it to be a streptococcus ;
others assume a protozoon invasion (Cyclosterion scarlatina of Mallory;
Ohrystanzoon scarlatina of Gamalia; leukocytic inclusions of Dohle).
408 DIAGNOSIS OF INFECTIOUS DISEASES
The virus is very resistant to light, to heat, and to drying. It may be
transmitted by contaminated fomites, or through a third person ; but most
often the disease is acquired by direct contact with a patient suffering
from scarlet fever. A child is a menace to others for at least 6 weeks
from the beginning of the disease, in some cases for a much longer period.
The disease is spread largely through the schools, and especially by mild
cases often incorrectly diagnosed as German measles.
Symptoms. — The incubation period varies from 1 day to 1 week, aver-
aging 3-5 days ; it may be as long as 14 days. The onset is sudden, with
fever, vomiting, -and often convulsions ; there is tachycardia, sore throat,
and enlargement of the glands at the angle of the jaw. Within 24 hours,
a red macular eruption appears on the neck, and on the upper part of the
chest; later, this exanthem involves the skin diffusely, the whole body
quickly becoming affected, except for areas around the lips and chin, and
sometimes the extensor surfaces of the extremities. The typical scarlat-
inal eruption is an intense livid hyperemia, often mottled with petechiae.
Often transverse pale lines are seen at the flexor surfaces of the elbows,
knees, etc. A common finding is a red, punctiform mottling of the
mucous membrane of the hard palate and of the skin in the armpits and
groins. Sudaminal vesicles are common.
I would emphasize especially the appearance of the eruption at the
beginning. It appears as small spots, separate from one another, at first
of a light rose color, but soon becoming closely crowded together, and of
a deeper red color. The spots become so numerous that on superficial
examination, the skin may look evenly red ; they do not really become
confluent but remain separate. This is best made out by looking at a
fiery red area and then making it disappear by pressure and watching its
reappearance after the presssure is removed ; the single red spots then
reappear quickly, and soon the almost uniform redness is regained.
If, with the handle of a percussion hammer, a line be drawn over the
red skin, a sharp white line arises, due to vasoconstrictor spasm, and only
slowly disappears ; this is the raie blanche of French writers.
The eruption lasts 3 or 4 days, and then gradually fades. The desqua-
mation, usually beginning on the neck and trunk, is especially marked
on the palms of the hands and the soles of the feet, where the skin may
be shed in lamellae; it occurs from the end of the first, or the middle
of the second, week on. The "strawberry tongue" is characteristic (4th
or 5th day), a furred tongue through which the swollen red papillae are
seen. The throat generally shows evidences of an acute angina; there
may be congestion, congestion with edema and tonsillitis, or a membranous
inflammation, involving pharynx, tonsils and uvula, presenting, with the
cervical adenitis, a picture quite like that of a true diphtheria. The tem-
perature is remittent during its course ; it falls by lysis with the efflorescence
of the rash, becoming normal about the 9th or 10th day. The tachycardia
THE ACUTE EXANTHEMATA
409
(120-180) and tachypnea are generally in proportion to the pyrexia, or
greater. The spleen is frequently enlarged slightly. In severe cases,
r^ ^ delirium and extreme prostration
U. <3cL.^ are aiarmingf jn niild cases the
subjective symptoms are slight.
Hemorrhagic, fulminant and an-
ginose, abortive cases, and even
cases* without eruption, occur.
Polymorphonuclear leulcocytosis
is the rule, high in severe cases,
30,000-60,000; there is usually
some eosinophilia. The urine
shows the ordinary febrile char-
acteristics in uncomplicated
cases, but it should be examined
daily. It is to be remembered
that at the height of the disease,
a trace of albumin and a few
casts need not indicate a serious
nephritis. Epigastric disturb-
ances, except constipation, are
uncommon after the initial vom-
iting, unless uremia due to a
complicating nephritis super-
vene.
The condition long known as sur-
gical scarlatina is not truly a scar-
latina in the medical sense of that
term, but is probably an erythema
due to sepsis following infection of
a wound.
One attack of scarlatina
generally confers immunity; re-
infection occurs in 1 out of 500
cases. Relapse is rare.
Complications and Sequelae. — These include : (1) streptococcus angina ;
(2) streptococcus sepsis; (3) otitis media; (4) scarlatinal polyarthritis;
(5) nephritis (8-22 per cent) ; (6) endocarditis. These are nearly all
complicating infections with streptococci ; nephritis and adenitis are due
to the virus of the disease itself.
In the 3rd or 4th week, or even later, a recurrence in the form of an
acute hemorrhagic glomerulonephritis, and with it fever, angina, and a
postscarlatinal adenitis (Schick) not infrequently develops. These post-
Fig. 125.— Scarlet Fever.
410 DIAGNOSIS OF INFECTIOUS DISEASES
scarlatinal affections have also been carefully studied by Pospischill and
Weiss (1911).
Prognosis. — The mortality varies greatly, 5-30 per cent. In the very
mild epidemics, there may be no deaths; in the severer epidemics, the
mortality may be very high.
Diagnosis. — This is easy in well-marked cases, but is difficult, and some-
times really impossible, in mild and in atypical cases. The disease must
be differentiated (1) from measles (period o'f incubation longer, character-
istic prodromata, rash later and papular with crescentic distribution,
Koplik's spots); (2) from diphtheria (bacteriology of throat; the two
diseases may coexist); (3) from German measles (afebrile; rash; other
cases in epidemic) ; (4) from the initial erythemas in typhoid, pneumonia,
smallpox, and influenza; (5) from drug-rashes (antipyrin, quinin, atro-
pin) ; (6) from serum rash after antitoxin administration; (7) from acute
exfoliative dermatitis ( absence of throat symptoms, no strawberry tongue,
hair and nails affected; the disease is recurrent) ; and (8) from Vincent's
angina (stained smears show spirilla and fusiform bacilli).
References
1. General
Caiger (F. F.) & Dudgeon (L. £.)• Scarlet fever. In: Syst. Med. (Allbutt & Rolleston).
8°. London, 1909, U, pt. 1, 410-475.
McCollom (J. H.) & Place (E. #.). Scarlet fever. Mod. Med. (Osier). 8°. Phila-
delphia & New York, 2d ed., 1914, i, 856-896.
Pospischill CD.) & Weiss (F.). Ueber Scharlach. (der Scharlacherkrankung zweiter
Theil). Berlin, 1911, S. Karger. 147 p. 8°.
Steinhardt (J. D.). The diagnosis and treatment of scarlet fever. Internal. Clin., Phila-
delphia, 1913, i, 23-50.
2. Etiological
Bernhardt (Georg). Die Aetiologie des Scharlachs. II. Teil. Hypothesen, die nicht
Bakterien, sondern Protozoen zum Gegenstand haben. Ergebn. d. inn.
Med. u. Kinderh., Berlin, 1913, x, 358-382.
Kretschmer (M.). Ueber die Aetiologie des Scharlachs. Monatsschr. f. Kinderheilk.,
Leipzig u. Wien, 1913, xii, 11-46.
Schleissner (Felix). Die Aetiologie des Scharlachs. I. Teil. Ergebn. d. inn. Med. u.
Kinderh., Berlin, 1913, x, 343-357.
3. Inclusion Bodies
Doehle (P.). Ueber Blutbefunde bei Syphilis, Masern und Pocken. Med. Klin., Berlin,
1904-05, i, 590-592.
Massini (M.). Ueber die diagnoslische Bedeutung der Dohleschen Leukocyteneinschlusse
fiir die Schartochdiagnose. Med. Klin., Berlin, 1913, ix, 1729-1730,
THE ACUTE EXANTHEMATA 411
Nicoll (M.). Present-day opinions of the value of the so-called inclusion-bodies in scarlet
fever. Arch. Pediatr., New York, 1913, xxx, 346-351.
Pappenheim (A.). Ueber die Natur der Dohleschen Scharlachkorperchen. Fol. haematol.,
Leipzig, Arch., 19U, xv, 379-380.
Ross (E. H.). Cell-inclusions in scarlet fever and measles. A suggestion for the preventive
treatment of these diseases. J. State Med., London, 1914, xxii, 94-98.
Tileston (W.) & Locke (E. A.). The blood in scarlet fever. J. Infect. Dis., Chicago,
1905, ii, 375-411.
4. Complications and Sequelae
Biernacki (J.) & Dykes (A. L.}. Fatal purpura folloiving scarlet fever. Brit. M. J.,
London, 1913, 903-904.
Fishbein (M.). Functional test (phenolsulphonephthalein) of the kidney in scarlet fever.
(Preliminary report.) Arch. Pediat., New York, 1913, xxx, 352-355.
McCrae (/.)• The incidence of nephritis after scarlet fever. Tr. Ass. Am. Physicians,
Philadelphia, 1913, xxviii, 194-197.
Manasse (P.}. Scharlach und Ohr. Monatsschr. f. Kinderheilk., Leipzig u. Wien, 1913,
xii, 59-68.
Schick (/?.)• -^?'e postskarlatinose Lymphadenitis. Jahrb. f. Kinderh., Berlin, 1905 >
Ixii, 660-682.
[ Ueber die Nachkrankheiten des Scharlachs.] Jahrb. f. Kinderh., Berlin,
1907, Ixv, 132-173.
5. Return Oases
Day (John M.). Return cases of scarlatina. Dublin J. M. Sc., 1913, 329-333.
Knopfelmacher (IF.) & Hahn (R.). Hcimkehrfdlle bei Scharlach. Monat,
Kinderh. Leipzig u. Wien, 1913-1914, xii, Orig., 673-686.
Sexton (L. A.). Return cases of scarlet fever. Arch. Pediatr., 1913, xxx, 360-362.
6. Other Articles
Bell (A. /.)• Observations upon scarlet fever, diphtheria and measles at the Cincinnati Con-
tagious Hospital. Am. J. M. Sc., Philadelphia & New York, 1912,
cxliv, 689-681.
Draper (G.) & Hanford (J. M.). Experiments on the transmission of scarlet fever to the
lower monkeys. J. Exper. M., Lancaster, Pa., 1913, xvii, 517-526.
Ker (C. B.}. A note on scarlet fever in the aged. Edinb. M. J., 1913, xi, 492-496.
Kolmer (J. A.). A study of streptococcus antibodies in scarlet fever, with special reference
to complement-fixation reactions. Arch. Int. Med., Chicago, 1912, ix,
Richardson (G.). The Rumpel-Leede phenomenon in the diagnosis of scarlet fever. Edinb.
M. J., 1913, n. s., xi, 496-500.
Weaver (G. H.}. Specific remedies in scarlet fever. Therap. Int. Dis. (Forchheimer). New
York & London, 1914, v, 645-651.
Zinqher (A.). The use of convalescent and normal blood in the treatment of scarlet fever,
J. Am. M. Ass., Chicago, 1915, Ixv, 875-877,
412 DIAGNOSIS OF INFECTIOUS DISEASES
2. Measles
(Morbilli,, Fr. Rougeole, Ger. Masern)
Definition. — An acute, specific, infectious, and extremely contagious
disease, characterized by catarrhal inflammation of the upper respiratory
tract and by a characteristic exanthem.
Etiology. — The infective agent must be a living contagium, but is as yet
wholly unknown. Blood cultures in ascitic fluid are negative after 24
hours in the thermostat, but if a healthy person who has not had measles
be then injected with the mixture of blood and ascitic fluid, he develops
typical measles (L. Hektoen). The unknown virus is present also in the
secretions from the eyes, nose and mouth, in the sputum, and in epidermal
scales. "Droplet infection" is probably an important mode of transmis-
sion. Persons coming down with the disease may communicate it to
others from 3 to 5 days at least before their own eruption appears. The
virus is incapable of long survival outside the human body, in marked
contrast with the virus of scarlet fever. The disease passes directly
from human being to human being, being rarely, if ever, transmitted by
fomites. It is asserted that a room vacated by a measles patient, if it be
simply well-aired for 24 hours, can be occupied next day by susceptible
persons without danger!
Measles, in epidemics, spreads with extreme rapidity. New epidemics
often break out in schools immediately after vacations. Children from
1 to 5 years are most often infected, but the disease may occur at any
age except in sucklings up to the 4th or 6th month. It seems to be a
children's disease, simply because nearly everybody is attacked in child-
hood and has immunity afterward. One attack usually yields permanent
immunity, though undoubted instances of 2 and 3 attacks are on record. .
Natural immunity is extremely rare ; the result is that it is very unusual
for a human being to escape from measles; he is almost sure to contract
the disease at some time or another during his life. The disease is less
common in summer. Sporadic cases may be met with at any time.
Symptoms. — The incubation period is said to be exactly 11 days,
though in rare instances, it varies from the rule, lasting only 7, or as long
as 18 days.
The prodromal stage lasts 3 days; coryza, photophobia, conjunctivitis,
a dry, troublesome, cough, with hoarseness, moderate fever, anorexia, and
malaise, appear. The face and eyelids look swollen; the eyelids stick
together in the morning. The diagnosis at this stage may not be possible,
unless measles is epidemic and one is on the lookout for cases. Shortly
before the appearance of the exanthem, there is a characteristic appearance
of the mucous membrane of the mouth and pharynx (irregular, roundish,
THE ACUTE EXANTHEMATA 413
dark red macules, especially common on the uvula, and soft palate appear).
But in addition, thanks to the New York podiatrist, Koplik, we now have
a sign that often permits the making of a positive diagnosis in the pro-
dromal stage, or even in the last two or three days of the incubation period.
Peculiar white spots, now generally known as "KOPLIK'S SPOTS," appear
on the buccal mucous membrane opposite the molar teeth, or on the inside
of the lips, or at the junction of the gums with the cheeks. They are
slightly elevated, white or bluish white, sharply circumscribed round spots,
the size of the head of a pin, or smaller, surrounded by a slight zone of
redness; they cannot be wiped off; a scraping examined microscopically
shows only epithelium and detritus. It is as though the red mucous mem-
brane had been touched here and there, with a little white paint on the
tip of a fine camel's hair brush. As they grow older, the spots increase in
size, and become more prominent ; they disappear, in from 2 to 5 days,
without residue; 6 to 20 such spots are often visible. They never occur
in scarlet fever, or in other exaiithematous diseases, though some assert
that they are seen occasionally in German measles. They are easily dis-
tinguishable from thrush or from aphtha ; I consider them of great diag-
nostic importance for the early diagnosis of measles ; they are present in
six-sevenths of all cases (Heubner). Occasionally preceded by prodro-
mal erythema, the characteristic skin eruption appears on the 14th day
after infection, that is, 3 days after the prodromata begin. It is a
MACULOPAPULAR, ERUPTION, often grouped, appearing first on the face
(sometimes first on the soft palate), scalp, and in front of and behind
the ears, thence extending to the neck, the upper trunk, and upper arms,
then to the lower trunk, the buttocks and thighs, and finally to the other
portions of the extremities. The full development is reached in 2-2-J days,
but the symptoms do not disappear with the appearance of the eruption.
There is a characteristic variegated mottling of the skin. The color of
the exanthem is at first pink, and the measles are small, rounded or irregu-
lar, though sharply circumscribed ; the color, later, becomes of a darker red,
and is often copper-colored or brownish-red. The outlines grow less dis-
tinct, and become very irregular, adjacent measles often fusing with one
another. If. inside the spots, the sebaceous glands become swollen, the
skin becomes elevated (morbilli elevati) ; sometimes this swelling does
not appear (morbilli laves). Occasionally there are capillary hemor-
rhages (hemorrhagic measles).
The fever during the 3 days of prodromata is remittent and of variable
height ; it then falls, but rises again as the eruption appears and may be
high. The pulse and the respiration are accelerated.
The blood in measles has been carefully studied by Hecker. There
are typical changes, which precede the Koplik spots by from 2-6 days.
A leukopenia (3,000-4,000) appears, with a relative and absolute decrease
of the number of lymphocytes, and relative increase (though slight abso-
414
DIAGNOSIS OF INFECTIOUS DISEASES
CzrlK aet.4
lute decrease) of the polymorphonuclear neutrophils ; the eosinophils are
decreased during the prodromal stage, and vanish entirely during the
eruptive stage. This incuba-
tory leukopenia may be of real
importance for early diag-
nosis. Slight enlargement of
the lymph glands can be made
out. During the exanthem,
the catarrhal symptoms grow
worse; the general condition
changes, the child will not eat,
grows apathetic, and often dull
and delirious. The tongue is
coated; the bowels are consti-
'pated ; the urine is scanty and
High-colored.
The eruption lasts from
3 to 5 days. The temperature
often falls by crisis, after a
precritical rise, and, in a few
hours, the child seems remark-
ably improved; he breaks out
into a sweat, falls into a sleep ;
on waking the psyche is clear,
the cough is looser, and the
appetite begins to return.
Sometimes this critical change
is not seen, the temperature,
instead, falling by lysis dur-
ing 1-2 days of defervescence.
As the eruption fades, bran-
like desquamation sets in dur-
ing the fading, whereas, in
scarlet fever, the lamellar
desquamation does not appear
until a week after the rash has
faded. During the last stage, the patient should be most closely watched
and most carefully nursed, for the danger of complications and of sequelae
is very great. Chilling of the body surface, especially, is to be avoided,
and the presence of any tuberculous person in the proximity of the patient
should be prohibited. During convalescence, there is often a marked
bradycardia, sometimes cardiac arhythmia.
Abortive cases and afebrile cases are known, as well as measles without
an eruption. Sometimes the rash begins in the usual way, then becomes
Fig. 126.— Measles.
THE ACUTE EXANTHEMATA 415
indistinct, and the patient's general symptoms grow more severe. This
form is much feared by the laity, who speak of the measles "striking in!"
In these cases, the skin is usually pale and cyanotic, due to cardiac weak-
ness and to dyspnea due to swelling of the bronchial mucous membrane;
unless the skin can be made hyperemic by a mustard pack, and the circu-
latory conditions improved, the outlook is grave.
The eruption in measles has recently been especially studied by von Pirquet.
During the first day of the eruption, the first signs appear in the form of scat-
tered red papules on the head and trunk, usually first behind the ears and in the
middle of the upper back, then around the mouth and nose, on the cheeks, in front
of the ears, and on the forehead, with possibly a few upon the chest and abdomen.
During the next two to four days, the eruption spreads over the whole body.
At the beginning of the second day, there is an abundant eruption on the head
and back, as far down as the crest of the ilium. The face, in its upper and middle
parts, is intensely inflamed, though the cheeks still show only a scanty eruption.
The eruption is also scanty on the chest, abdomen, shoulders, and medial sides of
upper arms. A few papules can be seen on the arms, thighs, popliteal spaces,
nates, and anterior surface of the legs. The posterior surface of the legs, the
feet, the knees and elbows are still free.
At the beginning of the third day, as a rule, the eruption is intense on the
head, trunk, shoulders, and anterior surface of the upper arm and of the thigh. It
may also be intense, though less constantly so, on the dorsal surface of the upper
arms, the forearms, and the posterior surface of the thighs. A scanty eruption
is seen in the popliteal spaces, on the legs, on the hands and knees, sometimes on
the nates. A beginning eruption is visible on the feet while the elbows still remain
free. By the fourth or the fifth day, the exanthem is, as a rule, fully developed,
except perhaps on the nates, feet and elbows.
As the eruption fades, the rose-red color of the first two days diminishes, and
the rash becomes slightly pigmented. The fading begins, constantly, on the fore-
head, usually at the beginning of the second day. By the beginning of the third
day, the rash on the forehead and the hairy scalp has faded much, and the rash
on the rest of the face, the trunk and the shoulders has begun to fade. By the
beginning of the fourth day, the fading has advanced to the rash on the extremi-
ties. The slight pigmentation on the forehead and hairy scalp has now vanished.
By the beginning of the fifth day the head, with the exception of the cheeks, has
lost all traces of the exanthem, while the pigmentations on the rest of the body
following the rash are still distinct. The elbows and feet often remain entirely
free from rash, more rarely also the knees, nates and hands.
Von Pirquet concludes that the temporal features of the rash stand in definite
relation to the cutaneous arterial supply, the rash appearing earliest on those
parts of the skin in which the arterial distance from the heart is least, and the
circulation liveliest.
He believes that the exanthem depends upon antitoxic reactions to the measles
virus in the cutaneous capillaries, in areas of the skin saturated with antibodies.
He suggests that the freedom from the rash of the elbows, feet and nates can be
explained by assuming that at the time when the most poorly arterialized parts
of the skin become saturated with antibodies, all the measles germs have been
removed from the blood by fixation (agglutination) in other capillaries of the
body. (Cf. von Pirquet, "Das Bild der Masern auf der ausseren Haut,"
Berlin, 1913.)
416 DIAGNOSIS OF INFECTIOUS DISEASES
The course of the disease is usually favorable if there are no compli-
cations. The public does not realize, however, how serious a disease
measles is ; various complications are possible.
Complications of Measles. — These include capillary bronchitis, bron-
cho-pneumonia, necrotizing pneumonia, otitis media, and enteritis with
diarrhea as the more important. Occasionally, severe inflammations of the
eye, of the larynx (measles croup), or of the mouth (noma) are met with.
Nephritis is very rare.
TUBERCULOSIS AFTER MEASLES. — Many children develop rapid tuberculosis after
measles, the infection apparently lowering the resistance against the tubercle
bacillus. If a cutaneous tuberculin reaction is positive before a measles infection,
it becomes negative during the measles (von Pirquet), owing to disappearance
of antibodies (ergins). Many a child, during convalescence from measles, develops
an acute miliary tuberculosis, or a tuberculous meningitis ; a flare-up in tuberculous
mediastinal glands, or of pulmonary tuberculosis, is very common after measles.
CONCURRENT MEASLES. — Measles may occur simultaneously with scarlet fever,
with diphtheria, with whooping-cough, or with chickenpox, in the same patient.
When whooping-cough and measles occur simultaneously, the danger of capillary
bronchitis is very great, especially in young children; the danger of subsequent
tuberculosis is also increased. Varicella, in companionship with measles, is prone
to give rise to deep ulcers and necroses of the skin.
Diagnosis. — In the prodromal stage, the acute catarrhal symptoms with
leukopenia are suggestive, and the Koplik spots are decisive. In the
stage of eruption, the disease must be distinguished (1) from scarlet fever
(not mottled, non-papular, area about mouth free) ; (2) from German
measles (rash not distinctly papular, lighter color, not confluent, often
rudimentary, often afebrile) ; (3) from the initial rash of smallpox
(severe general disturbances, higher fever, absence of Koplik's spots,
nodular eruption later, rapid fall of temperature on appearance of ex-
anthem) ; (4) from typhus fever (absence of Koplik's spots, character of
eruption, higher temperature, course) ; (5) from serum-exanthems
(anamnesis, accompanying phenomena) ; (6) from drug-exanthems ; (7)
from exanthems in sepsis (blood culture).
References
Craster (C. V.}. Analysis of 1,000 cases of epidemic measles. Am. J. Dis. Child., Chicago,
1913, vi, 122-130.
Goldberger (/.) & Anderson (J. F.). An experimental demonstration of the presence of
the virus of measles in the mixed buccal and nasal secretions. J. Am. M. 0.
Ass., Chicago, 1911, Ivii, 476-478.
Hecker (#.)• Cytologische und klinische Beobachtungen wdhrend der Maserninkubation.
Ztschr.f. Kinderh., Berlin, 1911 , Orig., ii, 73-116.
Hektoen (L.). Experimental measles. J. Infect. Dis., Chicago, 1905, ii, 238-255.
Koplik (H.). A new diagnostic sign of measles. Med. Rec., New York, 1898, liii, 505-507.
Leopold (J. S.). The result of recent researches into the etiology of measles. Arch. Pediatr.,
New York, 1913, xxx, 356-359.
Libman (E.). The value of the buccal eruption of measles (Koplik) for early diagnosis.
Med. Rec., New York, 1898, liii, 838-839.
THE ACUTE EXANTHEMATA
417
Lucas (W. /*.)• The value of the blood picture in the early diagnosis of measles, especially
in relation to the question of isolation. Am. J: Dis. Child., Chicago,
1914, vii, 149-159.
v. Pirquet (C. F.). Das Bild der Masern auf der dusseren Haul. Ztschr.f. Kinderh.,
Berlin, 1913, Orig., vi, 1-226.
Plantenga (H. W. G.)« La leucocytose de la rougeole et de la rubeole. Arch, de med.
d. en/., Paris, 1903, vi, 129-152.
Riggs (C. E.). Epidemiology of outbreak of measles at naval training station, Norfolk, Va.
U. S. Naval M.Bull., Washington, 1915, ix.
Ruhr ah (John). Measles, rubella, mumps, the fourth disease, erythema infecliosum. Mod.
Med. (Osier). 8°. Philadelphia & New York, 2d ed., 1914, i, 897-923.
Sieger t (F.). Ein Fall von Masernubertragung durch eine gesunde Mittelsperson auf weite
Entfernung. Munchen. med. Wchnschr., 1906, liii, 1870-1871.
Tileston (W.}. The blood in measles. J. Infect. Dis., Chicago, 1904, i, 551-589.
Williams (/>.)• Measles. In: Syst. Med. (Allbutt & Rolleston). 8°. London, 1909 >,
U, pt. 1, 385-404-
3. Rubeola
(German Measles, Rotelri)
Definition. — A benign, contagious, exanthematous disease, in which the
skin eruption sometimes resembles measles, sometimes scarlet fever, though
the disease is different from both.
Etiology. — The cause is unknown, but it is undoubtedly some infectious
agent. The disease occurs in small epidemics, especially in children (2-10
years), but is common also in adults. Most people are susceptible,, though
20. 22. MK. 21 April 3. May
Fig. 127.— Diagram Showing the Maximal Incubation Period (21 Days) of a Small Epidemic
of German Measles Breaking Out in a Hospital. (After B. Schick, "Ergeb. d. inn. Med. u.
Kinderheilkunde," published by J. Springer, Berlin.)
418 DIAGNOSIS OF INFECTIOUS DISEASES
there is not the universal susceptibility so characteristic of measles. One
attack yields immunity.
Symptoms. — The incubation period varies between 2 and 3 weeks. The
disease may resemble measles closely, but is milder in all ways ; pro-
dromata are often entirely absent. Sometimes there are mild catarrhal
symptoms, as in measles ; also headache, malaise and myalgias. Koplik's
spots are not present. A fine, blotchy, rose-red macular eruption is quite
constantly to be found on the mucous membrane of the throat. The skin
eruption appears first on the face and scalp, and thence extends, in crops,
over the rest of the body within 24-30 hours; it appears usually as small
macules rather than as papules ; these are rose-red and rarely confluent.
When the eruption resembles that of measles very closely, it is called
rubeola macutosa; when it resembles that of scarlet fever closely, it is
called rubeola scarlatinosa. The confusion with scarlatina may be in-
creased by swelling of the cervical, occipital, and retro-auricular lymph
glands, often present. The eruption disappears entirely in from 1-3 days
and is followed by fine desquamation, each crop following this course for
itself.
Prognosis. — The disease is never fatal ; complications are rare.
Diagnosis. — This is easy in epidemics; in sporadic cases, it may 1 o
impossible to tell it from measles on the one hand, or from mild scarlet
fever on the other. When in doubt, it is best to deal with it as though
* O
it were the severer form of disease.
References
Griffith (J. P. C.)« Rubella (Rotheln: German measles'), with a report of 150 cases. Med.
Rec., New York, 1887, xxxii, 11-17, 37-41.
Hess (A. F.). German measles (rubella): an experimental study. Arch. Int. Med., Chi-
cago, 1914, xiii, 913-916.
Koplik (H.). Rotheln. Beitrag zur genaueren Unterscheidung der Rotheln von Maseru
oder Scharlach. Arch. f. Kinderh., Stuttgart, 1900, xxix, 332-344.
Schley (0.). Ueber Ro'teln. Jahrb. f. Kinderh., Berlin, 1910, Ixxi, 571-584.
Schick (#.)• Die Roteln. Ergebn. d. inn. Med. u. Kinderh., Berlin, 1910, v, 280-304.
4. Duke's Fourth Disease
This has been described by Duke as a disease separate from scarlet fever,
measles, and rubeola. I do not think the evidence favors its existence as a separate
entity. The cases so described have been, in my opinion, either rubeola or mild
scarlatina.
References
Dukes (C.). On the confusion of two different diseases under the name of rubella
(rose-rash). Lancet, London, 1900, ii, 89-94.
Filatow (N.). Zur Frage betreifs der Sdbststdndigkeit der Rubeola scarlatinosa. Arch. f.
Kinderh., Stuttgart, 1885-6, vii, 241-247.
DISEASES OF THE PARANASAL SINUSES 563
(2) X-ray examination and transillumination will reveal shadows in
the affected sinuses ; sinuses that are entirely clear on these two methods
of examination rarely need further investigation.
(3) It is often possible to probe, or to irrigate, the maxillary sinus,
either through the sinus maxillaris, or through an accessory opening.
When this is not feasible, an exploratory puncture with a hollow needle
can easily be made, when indicated, through the lateral wall of the inferior
meatus, and the cavity washed out.
(4) If antral disease be excluded, and it is known that pus is being
discharged into the middle meatus, it must come either from a frontal
sinus, or from the anterior ethmoidal cells. To differentiate between these
two sources, the x-ray examination often suffices, but it is sometimes
necessary to remove the anterior portion of the middle concha and any
polypi or hypertrophied mucous membrane in the neighborhood, after
which the openings of the frontal sinus and of the anterior ethmoidal
cells are accessible to rhinoscopic study. It must not be forgotten that
when one paranasal sinus is diseased another may be simultaneously
affected.
(5) In the differentiation between disease of the posterior ethmoidal
cells and disease of the sphenoidal sinus, after the establishment of the
fact that the discharge is into the olfactory fissure or superior meatus, and
not into the middle meatus, we proceed by (a) making an x-ray examina-
tion, and (b) following the suppuration to its source, removing, when
necessary, obstacles to the observation of this source by intranasal oper-
ation.
The general practitioner cannot be expected to command all the special-
istic methods of examination required in the study of disease of the
paranasal sinuses. He should, however, be familiar with the subjective
symptoms and the complaints of patients that suffer from disease of these
sinuses, and should be able to decide when it is necessary to call specialists
to his aid.
Inflammations may extend to (1) the maxillary sinus, or antrum of
Highmore, (2) the frontal sinus, (3) the ethmoid cells, or (4) the sphe-
noid cells.
Causes of Sinusitis. — These include primary infections of the mucous
membrane in influenza, pneumonia, scarlet fever, measles, etc., and second-
ary infections by extension from the teeth (to the antrum), or as complica-
tions in tuberculosis, lues, trauma, etc.
References
Axenfeld (T.). Ein Beitrag zur Pathologic und Therapie der frontalen und der ethmoidalen
Sinusitis und ihrer orbitalen Complikationen. Deutsche med. Wchnschr.,
Leipzig u. Berlin, 1902, xxviii, 713-716.
Ballenger (W. L.). Intranasal frontal sinus operations; conservative surgery. Internal.
Clin., Philadelphia, 1915, 25. s., ii, 260-267. 3 pi.
564 DISEASES OF THE EESPIRATORY APPAEATUS
Berry (H. M.). Radiography in the diagnosis of diseases of the accessory nasal sinuses.
Part I. The posterior-anterior view, anatomical considerations and tech-
nique. Arch. Roentg. Ray, London, 1914-15, xix, 419-436. 8 pi.
Bliss (M. A."). The importance of the paranasal sinuses in the explanation of pain in the
face, head, neck, and shoulders. Am. J. M. Sc., Philadelphia, 1915,
cxlix, 230-235.
Bosworth (F. H.}. Various forms of disease of the ethmoid cells. New York M. «/.,
1891, liv, 505-507.
Brons (C.). Entziindliche Erkrankungen der Orbita und Nebenhohlen. In: Ergebn. d.
allgem. Pathol. [etc.] (Lubarsch & Ostertag). Wiesbaden, 1914, xvi,Erganz.-
Bd., 294-856.
Bryan (J. H.}. Chronic empyema of the frontal, ethmoidal, and both sphenoidal sinuses,
with extensive necrosis of the bones, complicated with adenoma of the pos-
terior ethmoidal and sphenoidal regions. Am. J. M. Sc., Philadelphia &
New York, 1902, n. s., cxxiv, 416-432.
Diseases of the accessory sinuses of the nose. In: Syst. Dis. Ear, Nose and
Throat (Burnett). Philadelphia, 1893, i,. 743-775.
Davis (W. B.). Development and anatomy of the nasal accessory sinuses in man. Phila-
delphia & London, 1914, W. B. Saunders Co. 150 p. 8°.
Delavan (D. B.). The prophylaxis of sinus diseases. J. Am. M. Ass., Chicago, 1903, xl,
602-505.
Finzi (N. S.) & Hett (G. S.). Radiography of the maxillary antrum. Arch. Radiol. &
Electrother., London, 1915, xx, 43-46. 8 pi.
Hajek (M.). Pathologic und Therapie der entzundlichen Erkrankungen der Nebenhohlen
der Nase. 3. ed. Leipzig u. Wien, F. Deuticke, 1909.
Experiences in the endonasal radical operation upon the sphenoid cavity and
the posterior ethmoid labyrinth. Ann. Otol., Rhinol. & Laryngol., St. Louis.
1909, xviii, 64-67.
Holmes (B.). The diagnosis and treatment of infection of the accessory mucous cavities of
the respiratory, digestive and genito-urinary tracts. Lancet-Clin., Cincin-
nati, 1905t n. s., Iv, 621-326.
Howard (W. T.), Jr., & Ingersoll (J. A/.). A contribution to our knowledge of the etiology
of inflammations of the accessory sinuses of the nose. Am. J. M. Sc.,
Philadelphia, 1898, n. s., cxv, 520-543.
Killian (G.)» The accessory sinuses of the nose and their relations to neighboring parts.
Transl. by D. R. Patterson. Jena & Chicago, 1904. roy. 8°.
Lewis (C. J.) & Turner (A. D.}. Suppuration in the accessory sinuses of the nose; a bac-
teriological and clinical research. Edinb. M. J., 1905, n. s., xviii, 893-421.
McLoone (J. /.)• Defects of the singing voice due to nasal and accessory sinus disease.
J. Am. M. Ass., Chicago, 1915, Ixv, 310-312.
Onodi C4.)« The optic nerve and the accessory sinuses of the nose: a contribution to the
study of canalicular neuritis and atrophy of the optic nerve of nasal origin.
London, 1910, Bailliere, Tindall & Cox. 101 p. 8°. Also: W. Wood
& Co., New York.
Ueber die okulo-orbitalen, intrakraniellen und cerebralen Komplika-
tionen nasalen Ursprungs. Med. Klinik, Berlin, 1914, x, 719-721.
Partsch (C.). Die Erkrankungen der Kieferhohle. Handb. d. Zahnheilk., 1892, ii, 2. Abt.,
Pearce (R. M.). The bacteriology of the accessory sinuses of the nose in diphtheria and
scarlet fever. J. Bost. Soc. M. Sc., 1898-99, Hi, 216-223.
Skillern (R. //,). The catarrhal and suppurative diseases of the accessory sinuses of the
nose. Philadelphia & London [1913], J. B. Lippincott Co. 389 p. 8°.
Stark (H. H.). Sudden blindness due to suppuration of the accessory nasal sinuses, with
report of three cases. J. Am. M. Ass., Chicago, 1915, Ixv, 1513-1520.
Stimson (G. W.). Empyema of frontal and ethmoidal sinuse?- J Am. M. Ass., Chicagot
1915, Ixv, 418-41$.
DISEASES OF THE PAKANASAL SINUSES 565
Symposium; disease of the accessory sinuses. Ann. Otol, Rhinol. & Laryngol, St. Louis
1905, xiv, 431-528.
Tilley (#.). Diseases of the accessory sinuses. In: Syst. Med. (Allbutt & Rollestori) 8°
London, 1909, iv, pt. 2, 72-91.
Turner (A. L.). The accessory sinuses of the nose; their surgical anatomy and the diagnosis
and treatment of their inflammatory affections. Edinburgh, 1901. 8°.
Watson- Williams (P.). Cerebro-spinal rhinorrhea with subsequent ethmoiditis and frontal
sinus suppuration. J. Laryngol., London, 1913, xxviii, 623-625.
Intranasal operations for frontal sinus suppuration. J. Larynqol , London
1914, xxix, 225-242. 3 pi.
Note on the technique of the intranasal operation for antral sinus suppura-
tion. J. Laryngol., London, 1914, xxix, 113-116.
Zuckerkandl (E.). Normale und pathdlogische Anatomie der Nasenhohle und ihrer pneu-
matischen Anhdnge. 2. Aufl. Wien & Leipzig, 1893. 8°.
2. Maxillary Sinusitis
(Maxillary Antritis, Antrum Disease)
Definition. — An inflammation (catarrhal or suppurative) of the sinus
maxillaris, due to infection, arising usually by extension from the nose,
or from the root of a tooth, most often from the second bicuspid or the
first molar tooth, the roots of which are nearest to the floor of the antrum.
Symptoms.— The patient may complain of a foul-smelling discharge
from one side of the nose, or of pain, either directly over the antrum or
radiating from it into the side of the face. If the pus has been swallowed
for some time, there may be digestive disturbances or anemia ; metastatic
infections involving the kidneys or the joints are not uncommon complica-
tions. In one of Crowe's cases, the pus from an infected antrum had
passed backward along the !N". maxillaris into the skull cavity and given
rise to an extradural abscess over the temporal lobes and to a meningitis.
When the antritis is secondary to rhinitis, an examination of the nose will
reveal the primary condition; when it is secondary to an infected tooth,
there may be pain in the teeth on the affected side, and a dental rontgeno-
gram may reveal the particular tooth at fault.
Transillumination of the antrum (q. v.) will reveal a shadow if there
be an exudate in the antrum, if its walls be thickened, or if the cavity
be filled by polypoid excrescences. Occasionally, a darkening is due to
thickened bone or to the absence of an antrum on one side. Similarly, a
rontgenogram of the two antra will reveal differences in density on the
two sides. The x-ray photograph should be so taken that the frontal sinuses,
the ethmoidal cells, and the antra of the two sides shall show on the same
plate, as it is necessary to compare the two sides. The x-ray operator
should avoid any superimposition of the foramen magnum and of the
base of the skull over the antra.
Occasionally, after a menthol or a cocain spray, the antrum will bo
seen to drain into the nose (middle meatus) ; but sometimes it is necessary
to open the antral wall, either through the nose, or from the mouth through
566 DISEASES OF THE KESPIKATOKY APPAKATUS
the alveolar process. In passing a trocar into the antrum, great caution
should be observed, since examiners before now have passed it into the
Pig. 164. — Rontgenogram in Influenzal Inflammation of Antrum. E. P., Age 18 — Infection
of Right Antrum of About One Year's Duration Following an Attack of Influenza. Symp-
toms : General Lassitude, Occasional Headaches, Discharge in the Nasopharynx. Con-
firmed by Operation. Pure Culture of B. influenzae. (By courtesy of S. J. Crowe.)
orbit, or into the tissue on the far side of the antrum ! When a chronic
purulent condition has lasted for some time, fistula formation may occur,
with necrosis of bone and the development of polypoid growths. It should
not be forgotten that a purulent discharge originating in a frontal sinus
or in the anterior ethmoidal cells may drain into an antrum, thus giving
rise to a pyosinus.
Differential Diagnosis. — In ACUTE CASES, there may be swelling of the
cheek, lip and eyelicls on the affected side. One may at first suspect (1)
facial erysipelas, but examination and the anamnesis should exclude it,
since in erysipelas the swelling is in the skin itself, not in the deeper
parts; the patient may have had several earlier attacks, and the swelling
will have begun at the nose.
We next rule out (2) furuncle of the upper lip with infection of the
facial veins ; the anamnesis and the site of the original furuncle are usually
decisive.
DISEASES OF THE PAKANASAL SINUSES 567
It is sometimes difficult to differentiate (3) a maxillary periostitis
from an acute flare-up of antral disease; in both there may be swelling of
the face, and tenderness on pressure in the canine fossa. But the anam-
neses differ; in ordinary periostitis, the patient will have had a preced-
ing toothache, and on examination a carious tooth, or a tooth tender on
pressure, will be found, while in acute maxillary sinusitis, a history of a
preceding coryza or influenza will be elicitable ; or if there is an exacerba-
tion of chronic antral disease, there will be a history of periodic discharge
of pus and perhaps of blood from the nose. The soft parts of the face are
less swollen in sinus disease than in maxillary periostitis ; the tenderness
in the former is diffuse over the maxilla, reaching as far as the lower
margin of the orbit, often accompanied by infra-orbital neuralgia, whereas
in periostitis, the tenderness is most marked at the alveolar process of
the upper jaw.
In CHRONIC CASES, rhinoscopy reveals hypertrophy of the mucosa of
the middle concha, and often polypi in the nose. If there be no obstruc-
tion to the orifice of the sinus, the purulent outflow can be observed at
times below the middle concha. When there is retention, transillumina-
tion and rontgenograms will reveal the darkened sinus.
Now and then, there is a possibility of confusing disease of the antrum
with (4) acute dacryocystitis^ in which there is swelling and tenderness
in the naso-orbital angle. But in this case there will be epiphora, due to
blocking of the lacrimal duct, and the patient will probably give a history
of earlier attacks, and, perhaps, of previous treatment of the duct.
Other conditions, occasionally confused with antral disease, especially
in children, are (5) maxillary tuberculosis, and (6) acute parotitis.
3. Frontal Sinusitis
The frontal sinus, on one or on both sides, may be the site of an
acute catarrhal, or an acute purulent inflammation, or, more often still,
of a chronic empyema. Occasionally, cysts, polyps, and hydrops of the
cavities are met with. The sinuses are often the site of anatomical varia-
tion, as x-ray pictures show. The sinuses of the two sides are usually
separated by a septum ; either sinus may be subdivided into several com-
partments.
Symptoms. — On the subjective side, the local symptoms consist of head-
ache and discharge from the nose ; in some patients, there are complaints
of disturbances of the sense of smell, obstruction of the nose, epistaxis, and
eczema of the nostrils. The patients often present neurasthenic symptoms
(incapacity for mental work, irritability, intolerance for alcohol and
tobacco). Neuralgic pains in the domain of the N. ophthalmicus may
occur. On the objective side, in suppurative disease of the frontal sinus,
568 DISEASES OF THE BESPIBATOKY APPAKATUS
the pus appears in the middle meatus, often under the anterior end of
the middle concha. Sometimes polyps or hypertrophied mucosae prevent
inspection of the most anterior part of the middle meatus. When this
is not the case, removal of the pus with a swab will be followed by the
appearance of a streak of pus running down from above and in front.
When the patient sits upright the flow may be continuous, in contrast with
the periodic. flow in antrum disease. In latent stages, however, the flow
need not be continuous; it is then most often visible in the early morning
hours.
The continuous flow is often converted into a periodic flow through the
presence of polypi or of hypertrophied mucous membrane. Such hyper-
Left Right
Side Side
of of
Skull Skull
Fig. 165. — Rontgenogram Showing Clouding of Sinuses in S'nusitis. Ratient, Age 30: Chronic
Infection of the Right Frontal Sinus and the Right Antrum. Symptoms: Headache,
Purulent Discharge, Nasal Obstruction, Indigestion (Hyperacidity). Confirmed by
Operation. (By courtesy of S. J. Crowe.)
trophies usually involve the anterior end of the middle concha, and extend
to the most anterior part of the hiatus and of the infundibulum, whereas
in antral disease the polyps and hypertrophy are limited more to the
posterior part of the hiatus in the immediate neighborhood of the ostium
maxillare.
In disease of the frontal sinus, the most anterior part of the middle
meatus is often narrowed on the diseased side owing to edema of the
mucous membrane on the most anterior part of the concave side of the
middle concha.
DISEASES OF THE PAKANASAL SINUSES 569
There is often tenderness over the anterior wall of the frontal sinus
on percussion with the index finger, or with the percussion hammer. There
may he tenderness on pressure at the root of the nose, on the orbital
surface of the frontal sinus, especially at two spots; namely, (1) the
inner upper angle of the orbit, and (2) the region behind the supra-orbital
notch.
Occasionally, a slight edema of the soft parts of the forehead over the
frontal sinus and of the upper eyelid can be made out ; such an edema is
prone to come and go; it is usually most marked in the morning.
Chronic infection of a frontal sinus occasionally gives rise to extradural
abscess over the frontal lobe of the cerebrum and to meningitis.
Diagnosis. — This depends upon the history, the demonstration of in-
creased discharge in the middle meatus of the nose, the exclusion of antrum
disease, and upon the methods of transillumination and, especially, of
x-ray examination of the sinuses. In some instances, the passage of a
sound into the sinus and washing it out may be necessary ; as a rule, such
sounding should be avoided, since one may easily infect a healthy sinus,
or may perforate the cribriform plate.
4. Ethmoidal Sinusitis
The ethmoid cells are divisible into two groups, an anterior and a
posterior. The number of cells in each group is variable. It is impor-
tant to remember that those of the anterior group chiefly empty into the
middle meatus, and those of the posterior group for the most part
into the superior meatus. Clinically, this division of the ethmoid cells
into those that empty into the middle meatus and those that empty into
the upper meatus is very convenient. The posterior group of cells stands in
close relation to the nasal wall of the orbit, and, occasionally, an infection
of the cells may lead to perforation of the orbital wall and give rise to
unilateral exophthalmos and visual disturbances.
The ethmoid cells are often the site of inflammation, acute or chronic ;
the condition is, unfortunately, frequently overlooked.
Symptoms. — In latent cases, there may be no symptoms except those of
a general run-down condition. In acute cases, and in acute exacerbations
of chronic cases, there is usually headache, dull aching pain in the eyes
and at the root of the nose, purulent discharge from the nose, disturbance
of the sense of smell, nasal obstruction, and often secondary inflammations
of the middle ears, tonsils, cervical glands, pharynx and larynx. The
disease is sometimes the primary focus of infection in chronic arthritis ; in
all cases of chronic arthritis, the paranasal sinuses should be carefully
examined. Various diseases of the eye and disturbances of the eye-
muscles have been observed as sequelae of ethmoidal sinusitis.
Diagnosis. — Chronic empyema of the ethmoid cells includes many of
570 DISEASES OF THE KESPIRATOEY APPARATUS
the cases formerly described as recurring polyp formation, and as fetid
blennorrhea or ozena. Not infrequently the ethmoidal cells are involved
simultaneously with other paranasal sinuses.
It is not uncommon to have one part of the ethmoid cells involved while
the others remain healthy.
Occasionally, mucocele of the ethmoid develops, owing to retention of
serum or mucus in the cells. It may appear as a mass, yielding parch-
mentlike crepitation. It should not be mistaken for a meningocele, a
dermoid, or a neoplasm.
An empyema of the ethmoid cells may be either open or closed. In
the open cases, the pus flows into the nasal cavity and polypi are common.
In- the closed cases, this flow of pus is prevented, owing to obstruction at
the opening into the nose; the patient complains of headache; sometimes
external swellings appear owing to dilatation of the cells ; such swellings
may project into the skull cavity or into the orbit.
In latent cases, the diagnosis can be made only by rhinoscopic study
or by x-ray examination. In manifest cases, it may be suspected even in
the absence of a rhinoscopic examination. Many patients complain of
dryness of the throat, due to atrophy of the secreting glands of the pharynx.
Whenever suspected, a careful rhinoscopic study should be made by a
specialist, and an x-ray examination of the various paranasal sinuses re-
sorted to. The x-ray is more helpful in the diagnosis of disease of the
anterior group of ethmoidal cells than of disease of the posterior group.
The bulla ethmoidalis, situated just beneath the anterior end of the
middle concha, is sometimes large and it may then look like a polyp ;
touched with a probe, however, it is found to be hard (bony), while a polyp
is soft and mobile.
Operative measures on the ethmoid are especially dangerous, owing to
the thinness of the lamina cribrosa, and to the fact that sheaths of dura
surround the filaments of the olfactory nerves; meningitis has occurred
after operation in a number of instances.
5. Sphenoidal Sinusitis
The sphenoidal sinus on either side is less often affected than the
other sinuses, but it is sometimes the site of inflammatory changes,
or of disease of its bony walls. The sinus is related anatomically to the
N. opticus, the sinus cavernosus, the dura mater, and the A. carotis; hence
tl^e occasional complications of blindness from retrobulbar neuritis, of sinus
thrombosis, of meningitis, and of erosion of the A. carotis with fatal
hemorrhage.
Symptoms. — The symptoms are very inconstant, but include headache,
stiffness of the neck, nasopharyngeal catarrh, subjective disturbances of
the sense of smell, vertigo, and general neurasthenic symptoms.
DISEASES OF THE PAKANASAL SINUSES
571
On objective examination, the discharge is found to empty either into
the anterior part of the olfactory fissure, or, much more often, backward
into the nasopharynx at the part of its roof that lies close to the superior
meatus. It is sometimes associated with ozena.
The mucous membrane bounding the olfactory fissure becomes hyper-
trophied, and it is sometimes the site of polypi. Catarrhal inflammations
of the pharynx and larynx are more common in sphenoidal sinusitis than
in inflammations of the other paranasal sinuses. Occasionally, the bony
walls of the sinus become diseased, in which event there is danger of cere-
bral complications (sudden unilateral blindness, due to compression of
the optic nerve in the foramen opticum, or to perineuritis). Sometimes
Fig. 166.— Method of Showing Right and Left Sphenoidal Sinuses. The Upper Arrows Point
to the Foramen magnum and the Odontoid Process; the Four Lower Arrows to the
Sinuses. (By courtesy of Drs. Baetjer and Waters, X-ray Dept., J, .H. H.)
572 DISEASES OF THE KESPIKATOKY APPARATUS
the retrobulbar tissues of the eye become invaded, with resulting exoph-
thalmos. Occasionally, the lateral superior wall of the sinus is perforated,
injuring the sinus cavernosus, and causing thrombosis or fatal hemorrhage.
Diagnosis. — The presence of pus in the olfactory fissure should excite
suspicion ; the nose should be thoroughly cleansed, and then be watched for
the return of pus. The diagnosis may be aided (1) by x-ray examination,
and (2) by the demonstration of the origin of the discharge from the
sphenoidal cells, (a) by direct observation of the outflow from the open-
ing of these cells, or (b) by the passage of a sound, and irrigation of
the cells.
6. Mastoiditis
The mastoid is not a paranasal sinus, but an accessory cavity of
the middle ear. For convenience, however, inflammation of the mas-
toid will be mentioned here. Secondary to otitis media, acute mastoiditis
or mastoid disease frequently develops, and the condition should never
be overlooked. Many cases when neglected go over into a suppurative
process or into a chronic mastoiditis.
A purulent otitis media usually causes rupture of the drum with dis-
charge to the outside. As long as the inflammation is confined strictly
to the tympanic cavity, the main danger is impairment of hearing, but
when it extends beyond this, serious complications often arise. Mas-
toiditis is, as a rule, the connecting link between purulent otitis media
and its graver complications (Reik).
Symptoms. — Following upon the signs of an acute otitis media (local
pain, fever, bulging of the ear drum, perforation^ otorrhea), the pain
may change its location and be assigned by the patient either to the
region just over the mastoid, behind the ear, cr to the depth of the ear
itself. There is localized tenderness on firm pressure over the mastoid,
or higher up over the mastoid antrum at the level of the upper border
of the external auditory meatus. There may be no swelling nor redness ;
when these are observable over the mastoid, they indicate that the abscess
has already broken through the bone and has given rise to a periostitis,
or perhaps to a subperiosteal abscess. Another important sign of mas-
toiditis is swelling of the inner end of the posterior cutaneous wall of
the external auditory canal, so that this portion droops just in front
of the tympanic membrane. The posterior cervical lymph glands under-
go enlargement. In acute mastoiditis there is fever, but in the chronic
cases the temperature may be normal; there is a moderate leukocytosis.
Diagnosis. — Since otitis media is a common complication of scarlet
fever, typhoid fever and influenza, the symptoms due to a developing
mastoiditis are not infrequently attributed to the primary infection, the
important local process being overlooked especially in children. In all
DISEASES OF THE PABANASAL SINUSES 573
acute infections, especially in children, the mastoids should be regularly
examined. Spontaneous pain, in or behind the ear, accompanied by
tenderness over the mastoid is diagnostic, even in the absence of otorrhea
and of local swelling or edema of the soft tissues over the mastoid.
In chronic otorrhea, an involvement of the mastoid by the chronic
suppurative process is very common. Recently, x-ray examinations have
been found helpful in the diagnosis of this condition-
Complications of Mastoiditis. — The intracranial complications are the
Fig. 167.— Rontgenogram of Mastoid Disease. The Large Clear Area (See Arrows) Near
the Tip of the Left Mastoid Indicates the Situation of a Sequestrum and Extradural
Abscess. (It is Necessary in Taking an X-ray of the Mastoid to Have the External and
Internal Auditory Meatus Superimposed — See Arrows, 2 Left Upper Ones.) In this Case
the Right Mastoid Was Normal ; Left Mastoid, Infection of Two Months' Duration
Pure Culture Streptococcus mucosus. Symptoms : Left-sided Headache, Purulent Dis-
charge from the Ear, Local Tenderness Over the Mastoid, Edema of the Walls of the
External Auditory Canal. X-ray Confirmed at Autopsy. . (By courtesy of S. J. Crowe.)
most serious. Any one of the following may occur: (1) pachymenin-
gitis, (2) extradural abscess, (3) leptomeningitis, (4) cerebral or cere-
bellar abscess, (5) thrombosis of the lateral sinus, or (6) purulent laby-
rinthitis.
574 DISEASES OF THE EESPIRATOEY APPARATUS
References
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Bishop (S. S.). Diseases of the masioid process. Internal. Clin., Philadelphia, 1897, 7. s.,
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Caldwell (G. W.). Transillumination of the mastoid cells as a means of diagnosis of mas-
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Also: N. York M. J., 1893, Iviii, 66.
Dench (E. #.)• The diagnosis and treatment of mastoiditis. J. Am. M. Ass., Chicago, 1901,
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C. Diagnosis of Diseases of the Larynx
Four main groups of diseases of the larynx have to be considered:
1. Inflammatory (acute, chronic, specific) ;
2. Circulatory (edema of the glottis) ;
3. Paralytic;
4. Neoplastic (papillary fibro-epithelioma, fibroma, carcinoma) ;
5. Stenotic.
References
Harwell (//.)• Diseases of the larynx. 2. ed. London, 1910, H. Frowde. 266 p. 8°.
Chiari (O.). Die Krankheiten der oberen Luftwege. 3. Teil. Die Krankheiten des Kehl-
kopfes und derLuftrohre. Leipzig u. Wien, 1905, F. Deuticke. 404 P- 8°.
Gottstein (/.)• Die Krankheiten des Kehlkopfes mit Einschluss der Laryngoskopie und der
local-therapeutischen Technic fur praktische Aerzte und Studierende.
4. Aufl. Leipzig & Wien, 1893. 8°.
DISEASES OF THE LAKYNX 575
Grant (D.). Some common errors in diagnosis and treatment of diseases of the pharynx,
larynx and naso-pharynx. Clin. J,, London, 1904, xxiv, 305-310.
Laurens (Georges). Oto-rhino-laryngologie du medecin practicien. Paris, 1912, Masson
& Cie. 418 p. 8°.
Meyer (E.}. Die Erkrankungen des Kehlkopfes. Handb. d. inn. Med. (Mohr & Staehelin).
Berlin, 1914, ii, 107-159.
Semon (F.) & Williams (P. W.). Diseases of the larynx. In: Syst. Med. (Allbutt &
Rolleston). 8°. London, 1909, iv, pt. 2, 179-282.
[For other references, see under (1) Methods of Examination of the Larynx and (2)
Diseases of the Nose.]
1. Inflammatory Diseases of the Larynx
These are met with especially in the members of certain professions :
singers, lawyers, preachers, politicians, auctioneers. The use of alcohol
and especially of tobacco predisposes.
(a) Acute Laryngitis
(Laryngitis acuta)
Two main forms are met with : a catarrhal and a diphtheritic.
i. Acute Catarrhal Laryngitis
(Laryngitis catarrhalis acuta, False Croup)
The attack comes on after "catching cold," with hoarseness, cough,
and sometimes fever. On laryngoscopic examination, redness and swell-
ing of the laryngeal mucous membrane is visible ; occasionally, small ero-
sions or hemorrhages can be seen. The secretion may be only slightly in-
creased ; it is mucous or mucopurulent.
In small children, an acute laryngitis may be associated with paroxysms
of stenosis of the glottis, in the night; these attacks are known as "false
croup." Waking suddenly, they startle their parents with the signs of
an attack of suffocation ; there is barking, crouplike cough, and diffi-
cult, whistling, inspiration, accompanied by retraction of the jugulum and
of the epigastrium ; expiration is also difficult and the voice is hoarse. After
a short time, the respiration usually becomes easier; the acute symptoms
pass off in a few hours, though the child may remain hoarse for several
days. One must make absolutely sure at once that the child has not
diphtheria ; if there be any doubt, antitoxin should be administered. In
false croup, intubation is occasionally, though very rarely, indicated.
Reference
Rice (C, C.). Some of the unusual manifestations of so-called catarrhal laryngitis. N. York
M. /., 1896, Ixiv, 445-449. [Discussion] 467.
576 DISEASES OF THE KESPIEATOEY APPAEATUS
ii. Acute Pseudomembranous Laryngitis
(Laryngitis* pseudomembranacea,, Diphtheritic Laryngitis, True Croup)
The epiglottis is most often affected, but the whole laryngotracheal tube
may he involved. The disease is rarely primary ; it is usually secondary
from the pharynx. A dirty, grayish- white, pseudomemhrane (fihrin,
leukocytes, necrotic epithelium) exists on the surface of the mucosa. The
adjacent mucous memhrane is deeply injected and swollen. Casts of the
larynx and of the trachea are sometimes coughed up.
Etiology. — In most cases true croup is due to the diphtheria bacillus,
though in the form complicating scarlet fever, measles, sepsis, etc., strepto-
cocci may he the cause. When a true false memhrane is present in the
pharynx, or larynx, antitoxin should he promptly administered without
waiting for a bacteriological diagnosis. There is great danger of suffoca-
tion ; intubation or tracheotomy may soon be indicated, and someone
capable of performing them should be present with an outfit at hand.
References
Meltzer (S. /.)• Intubation in cases of foreign bodies in the air-passages; with remarks
concerning feeding after intubation. Med. Rec., New York, 1889, xxxvi,
311-313.
Northrup (W. P.}. Some points concerning intubation of the larynx. Med. Rec., New
York, 1887, xxxi, 26.
O'Dwyer intubation instruments; added small tubes for infants under one
year; exhibition of modern complete set. Arch. Pediat., New York, 1903,
xx, 519-522.
O'Dwyer (/.). Intubation of the larynx. Tr. 9th Internal. M. Cong., Washington, 1887,
Hi, 516-527.
The evolution of intubation. Tr. Am. Pediat. Soc., New York. 1896, viii,
9-19. IpL
(b) Chronic Laryngeal Catarrh
(Laryngitis catarrhalis clironica)
Etiology. — The condition is most often due to chronic irritation from
dust, smoke, etc. It is common in singers, public speakers, cigarette
smokers, millers, stone-cutters, and metal-workers. It is sometimes
secondary to nasopharyngitis or to pulmonary disease.
Symptoms. — The cough is often slight; the voice is feeble or hoarse,
and tires easily, growing weaker on talking. On laryngoscopic examina-
tion, one can make out moderate injection and swelling of the mucous
membrane. Often, visible thickenings of the epithelium of the true
vocal cords can be made out; the horny layer becomes milk-white, or of
a dull blu^ color, is detachable with forceps, and often presents papillary
nodules (pachydermia laryngis) ; this is the condition in the so-called
"singer's nodes" (trachoma of the vocal cords).
DISEASES OF THE LARYNX 577
The secretion from the larynx is tenacious and grayish-white in color ;
or it may be brownish, due to admixture of blood.
Diagnosis. — Before making the diagnosis of simple chronic laryngeal
catarrh, one should exclude tuberculosis and lues, and should examine care-
fully the nose, the pharynx, and the lungs. Use may be made of the
Wassermann reaction, the Calmette test, and, if necessary, of histological
examination of a particle of tissue excised, for the differential diagnosis.
The whole body should be carefully gone over in the search for signs of
lues or of tuberculosis.
References
Chiari (0.). Beitrag zur Kenntniss des Baues der sogennannten Sdngerknotchen. Arch. f.
Laryngol. u. RhinoL, Berlin, 1900-01, xi, 415-422. 2 pi.
Discussion on "the utility or non-utility of local applications in chronic calarrhal laryngitis."
Arch. Laryngol., New York, 1883, iv, 140-144.
Frdnkel (#.). Pachydermia laryngis, ihre Geschichle, pathologische Anatomie und Patho-
logic. Arch. f. Laryngol. u. RhinoL, Berlin, 1894, ii, 106-122.
Giittich (A.}. Die Sdngerknotchen in palhologisch-anatomischerBeziehung. Arch.f.exper.
u. klin. Phonet.,. Berlin, 1913-14, i, 361-371.
Haulier e (E.). Contribution a V etude des nodules vocaux chez les chanteurs; pathogenic et
traitement. Paris, 1901. 8°.
MacDonald (G.). The forms of epithelial hypertrophy in the larynx. Internal. Clin.,
Philadelphia, 1895, 5. s., Hi, 321; 1896, 6. s.,i, 296; 1897 ', 6. s., iv, 306.
M' Bride (P.}. Pachydermia of the larynx. Tr. Med.-Chir. Soc., Edinburgh, 1892-93, n. s.,
xii, 108-121. 1 pi.
Miller (F. E.). Chorditis cantorum; a contribution to the study of the etiology, pathology and
treatment of singers' nodes, or nodules on the vocal cords. Laryngoscope,
St. Louis, 1902, xii, 809-839.
Shurly (E. L.). Chronic laryngitis, simple and traumatic. Syst. Dis. Ear, Nose and
Throat (Burnett}. Philadelphia, 1893, ii, 457-499.
(c) Specific Inflammations of the Larynx
These include the tuberculous, the syphilitic, the typhoidal and other
specific inflammations.
i. Tuberculosis of the Larynx
(Tuberculosis laryngis)
The symptoms and signs are, at first, those of simple catarrh; they
include hoarseness, cough, reddening of the mucous membrane, erosions,
and paresis of the vocal muscles. Later, visible tuberculous infiltration
develops, usually appearing first in the interarytenoid region; this subse-
quently breaks down to give rise to ulcers (flat, sharp margins; granular
base). Sometimes, only a single ulcer develops ; or two symmetrical ulcers
may appear on the vocal cords; sometimes, there are several groups of
confluent, "lenticular," ulcers. The edge of the epiglottis is often involved.
578 DISEASES OF THE EESPIKATOEY APPAKATUS
An infiltrating form, involving especially the adenoid tissue (epi-
glottis, aryepiglottic folds, vocal cords), giving rise to firm swelling, is some-
times seen. Later, caseation and ulceration occur; this form is often
combined with arytenoid perichondritis.
A third form of tuberculous laryngitis is lupus of the larynx; small
gray nodules with a red periphery appear ; they do not undergo ulceration.
In advanced cases of laryngeal tuberculosis, there is pain on swallow-
ing, and occasionally symptoms of stenosis.
The disease is nearly always secondary to pulmonary tuberculosis.
About one-third of the patients suffering from pulmonary tuberculosis
have also tuberculosis of the larynx. Primary tuberculosis of the larynx
is exceedingly rare.
References
Casselberry ( W. E.). The recognition of early changes in the larynx in tuberculosis. J. Am.
M. Ass., Chicago, 1913, Ixi, 1789-1791.
Glas (E.) & Krans (E.). Einfluss der Schwangerschaft auf die Tuberkulose des Kehlkopfest
Med. Klin., Berlin, 1909, v, 963; 1008.
Greene (J. B.). Laryngeal tuberculosis. South. M. J., Nashville, Tenn., 1915, viii, 973—
978.
Hajek (M.}. Tuberkulose Larynxtumoren. Internal, klin. Rundschau, Wien, 1893, vii,
1385; 1428.
Kast (A.} & Rumpel (T.). Tuberkulose des Kehlkopfs. In: Path.-anat. Tafeln, Hamb.
Staatskrankenh., Wandsbek-Hamb., 1896, xiv, pi. R 9, 10, 11 with text.
Killian (G.). Ueber die Behandlung der Kehlkopftuberkulose. Deutsche med. Wchnschr.,
Leipzig u. Berlin, 1912, xxxviii, 585-589.
Kyle (D. B.). Initial forms of tubercular laryngitis. Internal. M. Mag., New York, 1900,
ix, 202-205.
Lake (R.}. Laryngeal phthisis, or consumption of the throat. London, 1901. 8°.
Levy (#.)• Laryngeal tuberculosis. J. Am. M. Ass., Chicago, 1913, Ix, 1518-1523.
Minor (C. L.}. The diagnosis and treatment of the earlier changes in the larynx in pul-
monary tuberculosis. J. Am. M. Ass., Chicago, 1910, Iv, 1806-1808.
Semon (F.). A clinical lecture on laryngeal tuberculosis. Clin. J., London, 1893-94, Hi,
154-167.
Steiner (R.). Zur Kenntniss der primdren Kehlkopftuberkulose. Arch. f. Laryngol. u.
Rhinol, Berlin, 1912, xxvi, 424~435.
Swain (H. L.). Tubercular laryngitis. N. York M. J., 1887, xlvi, 675-682.
Thomson (Sir St. C.). Three years' sanatorium experience of laryngeal tuberculosis.
Brit. M. J., London, 1914, i, 801-803.
Wat son- Williams (P.). Note on the treatment of laryngeal tuberculosis by tuberculin.
Bristol M.-Chir. J., 1914, xxxii, 186-138.
ii. Syphilitic Laryngitis
(Laryngitis syphilitica, Laryngeal Lues)
Symptoms. — The voice is hoarse ; there is sometimes actually aphonia.
Cough and pain are slight, or absent. In secondary syphilis, the laryngeal
picture may be that of subacute catarrh, accompanied by papules and
THE ACUTE EXANTHEMATA 435
Paschen (#.)• Infektion der Hand mil Cowpox-Variola vaccinia. Dermatol. Wchnschr.
Leipzig u. Hamburg, 1914, Iviii, Erganz.-Hefi, 57-60.
Wanklyn (W. McC.). How to diagnose smallpox. New York, 1914, P. B. Hoeber.
102 p.
7. Vaccinia (Cowpox and Vaccination)
The nature of this disease of cattle has heen described above in con-
nection with smallpox.
The lymph from the vaccinia vesicles is used as a vaccine to protect
human beings from smallpox.
Vaccine virus is usually obtained from calves suffering -from cowpox,
though men, monkeys, guinea-pigs, rabbits, rats, camels and many other
animals are susceptible, and lymph from the lesions produced in them
has, also, sometimes been used for vaccination.
Formerly, vaccine virus obtained from human beings was much
employed, but since bovine virus can be purified by glycerin (Copeman),
the use of the latter has become almost universal, and the danger of
syphilitic infection attendant upon the use of human virus is excluded.
Formerly, dry splinters of ivory, coated with vaccine-lymph, were employed
in vaccinating. Now the virus is first treated with glycerin for a time (glycer-
inated lymph) ; this kills ordinary bacteria but preserves the active principle of
the vaccine virus, provided the glycerin has not acted too long upon it (not over
6 weeks in summer, or 3 months in winter). Vaccine virus, even when glycerinated,
always contains bacteria, but when the virus is properly prepared, they are non-
pathogenic for man.
Definition of Vaccination. — By this is meant the transmission of cow-
pox (vaccinia) to man by inoculation, for the purpose of conferring on
him a temporary immunity against smallpox (variola).
Historical. — In May, 1796, Edward Jenner took some of the lymph
from a pustule in a milkmaid who had accidentally inoculated herself
with "original" cowpox, and inoculated an eight year old boy with it.
The boy developed vaccinia and recovered. Jenner then inoculated him
with smallpox virus. The boy did not develop variola inoculata but
remained healthy. During the following two years, Jenner made several
such tests on different persons with the same result, and in 1798 pub-
lished his celebrated article in which he advised the general adoption
of vaccination with cowpox as a prophylactic measure against smallpox.
This was one of the greatest discoveries ever made by a medical man.
Technic. — Vaccination is a slight surgical operation, which should be
aseptically performed. Formerly, vaccination was done by scarification,
or by scratching. This method is now prohibited by law in Germany,
as it invites infection (pyogenic cocci, tetanus bacilli). The best method
436 DIAGNOSIS OF INFECTIOUS DISEASES
of vaccination is by incisions with tlie point of a scalpel, or of a sharp,
flat needle. The incisions should not be deep enough to draw 'blood,
though the line of the cut may be blood-tinged ; if a drop of blood appears,
it does no harm. Three or four incisions, parallel to the long axis of
the arm, 2 cm. apart, each incision being 1 cm. long, are best. The site
usually chosen is the lateral part of the skin on the upper right arm ;
in re-vaccination, the left arm is used. In young women, the front of
the thigh may be selected instead of the arm ; it is unwise to vaccinate
little girls on the thigh. The glycerinated virus is then placed upon the
area incised, and is gently rubbed in with the flat side of the knife, or of
the needle, any unnecessary irritation being avoided.
Simple preparation of the skin (scrubbing with soap and water, fol-
lowed by alcohol and thorough drying) is enough. Antiseptics should not
be used, as they may kill the virus. The skin should be perfectly dry
before incision. The incisions are perhaps best made with a sharp needle,
since it can be easily sterilized by passage through a flame.
After applying the vaccine, the arm should be allowed to dry in the
air for 15 minutes. No dressing is required. An important exception
is made in children, or in adults who are suffering from any skin-lesion
(eczema, prurigo, pemphigus, etc.), for in them, through scratching, the
cutaneous lesions may be infected with vaccine virus, a serious complica-
tion. In such instances, the vaccination site should be covered with a
sterile gauze dressing (free from all disinfectant substances). Shields
are unnecessary and are often harmful. The person vaccinated and the
family should be instructed regarding the possibility of transferring virus
from the inoculation site to the eyes, to small wounds or eruptions, or
to rhagades, on their own bodies, or on the bodies of others, by the fingers
(scratching). Mairinger reports an instance of a child who, bathing in
the same bath-water as that used by a child just vaccinated, was exten-
sively inoculated over the face and trunk.
A 4 per cent alcoholic solution of picric acid is applied to the vac-
cinated area 48 hours after vaccination by Schamberg and Kolmer. It
is said to lessen the local reaction, and to diminish the danger of bacterial
infection. This precaution has not, as yet, been widely applied. During
the scabbing stage, a dusting powder composed of dermatol 10.0, zinc
oxide 10.0, starch 40.0, and talcum 40.0 is recommended by Paul.
Symptoms Following Vaccination. — Except for slight traumatic reac-
tion, nothing is visible for 3 or 4 days (period of incubation). If the vac-
cination "takes," papules begin to appear on the skin at the sites of incision,
usually on the 3d day. They are round, or oval, firm papules, v. Pir-
quet's "papilla/' of a bright red color • they gradually grow more prom-
inent, and are surrounded, up to the 7th day, by a narrow light red
zone, the aula, halo, or inner areola. On the 5th or 6th day, a vesicle
appears at the summit of the papule. This enlarges, becomes distended
THE ACUTE EXANTHEMATA 437
with fluid, looks pearl-gray, is umbilicated, and is, at its base, sur-
rounded by a swollen red areola — THE JENNERIAN VESICLE — resembling
a "pearl upon a rose leaf." The full development is reached by the Yth
or 8th day. The central umbilication is marked; the second red zone,
or outer areola, has formed (outside the aula). Von Pirquet regards the
outer areola as the most striking and characteristic phenomenon of the
vaccinia lesion. A day later, that is, at the beginning of the 2d week,
the STAGE OF SUPPURATION begins. The vesicle turns yellowish, and the
so-called second umbilication appears, the outer areola widens, and its
flaming red color deepens, the perivesicular swelling increasing.
The arm may now be quite painful. By the llth day, the distended
yellow pustules stand out prominently on the bright red, erysipelaslike
areolar plateau ; at the periphery of the plateau, however, the redness
goes over very gradually into the color of the normal skin, in marked
contrast with the sharply circumscribed hyperemia of erysipelas. Palpa-
tion of the axilla reveals enlarged and tender lymph glands. By the llth
day, the redness and swelling begin to go down, and the STAGE OF DESICCA-
TION begins. Two or 3 days later, the vesicle dries up, and by the end
of 1J-2 weeks, a brown, wrinkled SCAB is left, which should be allowed
to drop off from itself, in order that the healing process may go on, undis-
turbed, beneath it. The reddish scar, later, turns white, and remains as
a characteristic "VACCINATION MARK/''
There, are often slight constitutional symptoms, at the beginning of the
suppuration, including fever. The fever is of variable height ; the curve
shows a steplike ascent ; the temperature falls by crisis when desiccation
begins.
Between the Yth and the 14th day, there is sometimes a very transi-
tory universal exanthem, consisting of small roseolar macules, much like
the "morbilliform initial rash" of variola. More often, at the acme, a
few accessory pock-lesions appear near the inoculation site. Rarely, a
generalized vaccinia develops, small pustules breaking out all over the body
at the acme, on the 9th or llth day, soon drying up to small crusts, and
leaving no scars. One of my own children had such a generalized vac-
cinia.
The LEUKOCYTE COUNT, as followed by Sobotka, undergoes strange
changes. On the 3rd or 4th day after vaccination, there is an initial
leukocytosis, which continues until the Yth or 8th day; the count then
falls to normal and lower (leukopenia) , continuing until the 10th or 12th
day, to be followed by a terminal leuJcocytosis, lasting 2-3 days. In the
patients who become more ill, and in whom nasty-looking sores develop,
a complicating pyogenic infection is probable.
Successful vaccination yields IMMUNITY AGAINST SMALLPOX as soon
as the Jennerian vesicle has developed, and also, for a considerable length
of time, against vaccinia itself. The nature of the immunity is unknown.
438
DIAGNOSIS OF INFECTIOUS DISEASES
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THE ACUTE EXANTHEMATA 439
The duration of the immunity against variola from a single vaccination is
temporary, not permanent, the duration varying in different persons.
On the average, the vaccinated person is well protected against accidental
variola infection for about 10 years, though the period of protection against
variola inoculata by vaccination is shorter than this.
Every child should be successfully vaccinated during its first year
(before the second summer), and, again, about the tenth year. If the
first vaccination be not successful, not "taking" at all, or yielding only a
rudimentary result, it should be repeated. Should the second vaccina-
tion with reliable vaccine prove negative, the existence of some natural
immunity may be assumed. On exposure to smallpox, it is well to re-
vaccinate, at once, unless the patient is known to be immune, or has been
successfully vaccinated a very short time before. Vaccination at the be-
ginning of the incubation period of variola will either completely protect,
or protect enough so that only varioloid will develop.
The reactions on RE-VACCINATION have been carefully studied by von
Pirquet and have thrown much light upon 'the phenomena of anaphylaxis
(allergy). Anyone interested in the variable phenomena of re-vaccination
should consult his admirable monograph.
Dangers of Vaccination. — Vaccinia is an acute infectious disease.
Moreover, during vaccination, an open wound is produced, which, if the
work be not done aseptically or the lymph be bad, may become infected
("early infection") ; "late infections," when they occur, are usually due
to improper care of the arm, or to scratching.
When vaccination is performed, with good lymph, and proper instruc-
tions regarding cleanliness and care during the course of the reaction are
followed, the dangers are minimal and the benefit conferred enormous.
In hemophilia, if vaccination be done at all, the greatest caution should
be observed.
In patients with leukemia very severe local reactions have been ob-
served.
The danger of auto-inoculation and hetero-inoculation of the eyes and
of skin lesions has already been referred to.
Complications. — Wound-infection from pyogenic cocci, or from tetanus
bacilli, may occasionally occur. These are best avoided by using pure
glycerinated lymph, and by vaccinating by incision instead of by scarifica-
tion, since glycerin, of itself, may not kill the spores of tetanus. All
vaccine virus is especially tested for tetanus before being placed on sale.
In the days when human lymph was used, the possibility of the trans-
mission of syphilis was much discussed ; the use of animal lymph excludes
this possibility.
Vaccine virus is believed to be a modified form of smallpox virus (see Small-
pox). It is possible that the cause of smallpox is the parasite Cytorrhyctes
variola, described by Councilman, Brinkerhoff and Tyzzer. This parasite appears
440 DIAGNOSIS OF INFECTIOUS DISEASES
to have a sexual and an asexual cycle. According to Calkins, smallpox is caused
by the combined asexual and sexual cycle of the same parasite, the sexual cycle
occurring in a nucleus of the epithelial cell. If the parasite loses its power to
generate by sexual division (as in cowpox), it can never regain it. Thus while
smallpox may be modified into cowpox, cowpox can never be changed back to
smallpox again. Though this view has not yet been generally adopted, it is
suggestive and interesting.
References
Anderson (J. F.). Federal control over the manufacture of serums and vaccines. J. Am. M.
Ass., Chicago, 1913, Ixi, 1838-1840.
Post-vaccination tetanus; studies on its relation to vaccine virus. Pub.
Health Rep., Washington, 1915, xxx, 2111-2117.
Ewing (/.)• The structure of vaccine bodies in isolated cells. J. Med. Research, 1904-05, xiii,
233-251. 6 pi.
Green (A. B.}. The resistance of the vaccine virus to filtration. J. Hyg., Cambridge, 1914,
xiv, 182-185.
Guarnieri (G.}. Studi sulla strutture sullo svihippo dei parassiti della infezione vaccinica.
Clin. mod., Pisa, 1902, viii, 404-406.
H'iickel (A.}. Die Vaccinekorperchen. Beitr. z. path. Anat. u. z. allg. Path., Jena, 1898,
xxiv, 2. Supplhft., 1-148.
van der Kamp (C. J. G.). Uebcr Filtration des Vaccinevirus und Immunisierung mittels
Vaccinefiltrats. Ztschr. f. Infektionskrankh., parasit. Krankh. u. Hyg. d.
. Haustiere, Berlin, 1914, xv, 157; 228.
McFarland (/.)• Tetanus and vaccination; an analytical study of ninety-five cases of fhis
rare complication. Proc. Phila. Co. M. Soc., Philadelphia, 1902-03,
xxiii, 168-178.
Also: J. Med. Research, Boston, 1902, vii, 474~493. 1 pi.
Millar d (C. K.). The vaccination question in the light of modern experience: an appeal
for reconsideration. London, 1914, H. K. Lewis. 261 p. 8°.
Negri (A.). Esperienze sulla filtrazione del virus vaccinico. Gazz. med. ital., Torino, 1905,
Ivi, 123-125.
Paul (G.). Technik und Methodik der Vaccination. In: Kraus & Lcvaditi, Hdb. d. Techn.
u. Meth. d. Immunitdtsf., Jena, 1908, i, 587-681.
von Pirquet (C.). Klinische Studien uber Vakzination und vakzinale Allergie. Leipzig u.
Wien, 1907, F. Deuticke. 198 p. 8°.
Royal Commission. A report on vaccination and its results, based on the evidence taken
by the Royal Commission during the years 1889-1897. New Sydenham
Society, London, 1898, i.
Ruediger (E. H.}. The preservation of vaccine virus. Bull. Manila M. Soc., 1910, ii,
G)G)~t tf)$)G)
&&J. — A?/';//^.
Simon (H.}. Das Prodromal-Exanthem der Pocken. Arch. f. Dermatol., Prag, 1870, ii,
346-392; 1871, Hi, 309-332.
Tyzzer (E. E.}. The etiology and pathology of vaccinia. J. Med. Research, Boston, 1904,
xi, 180-229.
v. Wasielewski (Th.). Beitrdge zur Kenntniss des Vaccine-Erregers. Ztschr. f. Hyg.,
Berlin, 1901, xxxviii, 212-312.
Ueber die Technik des Guarnierischen Impfexperiment.es und seine Ver-
wendung zum Nachweis von Vakzineerregern in den innern Organen von
Impftieren. Munchen. med. Wchnschr., 1905, Hi, 1189-1192.
Williams (A. W.) & Flour noy (T.). Report of studies on the etiology of vaccinia and
variola. New York Univ. Bull. M. Sc., 1902, ii, 145-159. Also: Proc.
New York Path. Soc., 1902-03, n. s., ii, 67-71.
THE ACUTE EXANTHEMATA 441
%
8. Swea t ing-Sickness
(Febris miliaris)
Definition.— Sweating-sickness is a disease formerly prevalent and very fatal
in England, but now largely confined to France and Italy. It occurs in epidemics
in which a large number of persons are attacked witliiri a few days by fever,
profuse sweats, and an eruption of miliary vesicles. In the severe cases, there'
may be delirium, prostration and a .hemorrhagic diathesis.
Etiology.— The cause is unknown. The disease is directly contagious, and the
virus is probably air-borne. The epidemics occur in spring and in summer.
Relapses are common in the first or second week of convalescence.
Diagnosis. — This is difficult to make at the beginning of an epidemic; after-
ward, it is easy. The early cases are often taken to be measles or scarlet fever.
References
Pothet OR.)- Essai critique et historique sur la suette miliaire. 8°. Paris, 1901.
Scholz (W.}. Ueber Miliaria epidemica. Ztschr. f. klin. Med., Berlin, 1906, lix, 542-564.
Webb (F. C.). The sweating-sickness in England. J. Pub. Health, London, 1857, Hi, 105-
124-
Weichselbaum (A.). Ueber Schweissfriesel vom anatomischen, dtiologischen und epidemio-
logischen Standpunkte. Ztschr. f. klin. Med., Berlin, 1907 ', Ixii, 21-50.
9. Rocky Mountain Spotted Fever
Definition. — An acute infection, characterized by chills, fever, pains in the
back and bones, and a macular exanthem, which is sometimes hemorrhagic. It
occurs especially in Montana (Bitter-root Valley), Idaho, Nevada and Wyoming,
in the mountainous districts.
Etiology. — The nature of the virus is unknown, but the disease is undoubtedly
transmitted by a tick (Dermacentor occidentalis) , as shown by King and Ricketts.
Wilson and Chowning believed that the disease is due to a piroplasma, but this
has not been confirmed. Guinea-pigs and monkeys are susceptible. One attack
yields immunity. Immune sera can be produced in guinea-pigs and in horses
(Ricketts; Hanemann and Moore).
Symptoms. — The incubation period is from 3 to 10 days. The onset is then
sudden with chill, fever and pains over the body. A rash appears on the 2d to the
7th day resembling that of typhus exanthematicus, the macules usually becoming
hemorrhagic. Fever of 103°-105° F. develops. Delirium is common. After a
course of 3 weeks, convalescence begins. The mortality is variable; it was small
in Idaho (3 per cent) ; high in Montana (70 per cent). The tick that transmits
the virus lives upon the bodies of horses and of cattle.
Differential Diagnosis. — The disease must be distinguished (1) from measles;
(2) from typhus exanthematicus; (3) from influenza; (4) from dengue; (5) from
epidemic cerebrospinal meningitis; and (6) from typhoid.
References
Anderson (J. F.}. Spotted fever (tick fever) of the Rocky Mountains: a new disease. Am.
Med., Philadelphia,. 1903, vi, 506-508.
On the relation of Rocky Mountain spotted fever to the typhus fever of
Mexico. A preliminary note. Pub. Health Rep., U. S. Mar. Hosp.
Serv., Washington, 1909, xxiv, 1861.
442 DIAGNOSIS OF INFECTIOUS DISEASES
Irons (E. E.). Rocky Mountain spotted fever. In: Therap. Int. Dis. (Forchheimer). New
York & London, 1914, v, 660.
Maxey (E. E.}. Rocky Mountain spotted [tick] fever, with special reference to causal factors,
mortality and geographical distribution in Idaho. Med. Sentinel, Port-
land, Ore., 1908, xvi, 666-678.
Ricketts (H. T.~). Observations on the virus ami means of transmission of Rocky Mountain
spotted fever. J. Infect. Dis., Chicago, 1907, iv, 141-153.
Ricketts (H. T.) & Wilder (R. M.). The relation of typhus fever (tabardillo] to Rocky
Mountain spotted fever. Arch. Int. Med., Chicago, 1910, v, 361-370.
Sambon (L. W.}. Spotted fever of the Rocky Mountains. In: Syst. Med. (Allbutt & Rolle-
ston). 8°. London, 1910, ii, pt. 2, 307-313.
B. Non-Exanthematous Diseases
L Mumps
(Parotitis epidemica, Ger. Ziegenpeter, Fr. Oreillons, Hal. Orecchioni)
Definition. — Mumps is a specific, febrile, infectious disease, most often
met with in the young; it is extremely contagious, and causes an acute in-
flammation of one or more of the larger salivary glands, usually the paro-
tid, on one or both sides. It has been known since the time of Hippoc-
rates, who described it carefully and knew of its contagiousness and of the
occurrence of a complicating orchitis.
Etiology. — The nature of the virus is unknown. It is probably no
ordinary bacillus or coccus, but is more likely a virus like that of the
acute exanthemata or like that of the Heine-Medin disease, lyssa, etc.
Attempts to reproduce the disease in animals have failed, until recently
(1913). Nicolle and Conseil assert that, on intraparotid injection into
monkeys of a punctate from the swelling in human mumps, a mild fever,
lasting several days, is manifested after an incubation period of 16-26
days; in one of the monkeys, the parotid gland became slightly swollen.
Epidemiology. — The disease is directly contagious from person to per-
son, and the danger of contagion lasts for several weeks. The disease
is often met with in epidemics, but sporadic cases also occur. Local
epidemics are common, confined to a single institution (orphan asylum,
jail, ship, barracks), or even to a single house, or to a single room in a
house. The virus can be carried by healthy intermediate persons. It is
remarkable that many persons exposed, and presumably susceptible to
it, do not contract the disease. Spread by fomites has not been estab-
lished. The disease is more common in cold wet weather than at other
seasons, but it occurs at all times of the year. The spread of the disease
seems to correspond more or less closely to that seen in diseases like diph-
theria and epidemic meningitis. One attack usually yields permanent
immunity, but not always ; well-established instances of two, and of even
several, attacks, are. on record,.
NON-EXANTHEMATOUS DISEASES , 443
Symptoms. — The incubation period varies between 14 and 24 days.
After 2 or 3 days of fever, headache, diarrhea, anorexia, insomnia, and
pain in the neck, a triangular swelling rapidly appears in front of. and
beneath, one or both ears, and pain is felt on opening the mouth, on chew-
ing and on swallowing. Sometimes, the swelling of the gland occurs un-
heralded by prodromata.
The fever is intermittent, or remittent, and lasts only 3-4 days, as a
rule, and is not high ; it falls by lysis. Should the disease process extend
to other salivary glands, or should complications, like orchitis, set in, the
fever returns.
The disease is most often bilateral, though one gland swells usually
before the other, the left gland swelling first, as a rule. The inflamma-
tory process involves also the perigiandular tissues, so that the whole cheek
from the ear down to the margin of the mandible, and behind as far as the
mastoid, looks swollen; sometimes the whole face is so markedly swollen
that the person is almost unrecognizable; the face is a huge pyramidal
"lump," covered by white tense skin. The ears stand out from the head
and give the patient a comical facial expression, or one suggestive of
imbecility (hence the German names Ziegenpeter and Bauernwetzel.
Occasionally the other salivary glands are inflamed also, and the lacrimal
glands may be involved. Salivation or suppression of salivary secretion
may occur. When all the salivary glands are swollen, together with the
tissues about them, the head and neck assume the shape of a huge pear !
The neck may be greater in circumference than the head.
The head is held in typical attitudes. In the unilateral affection, the
muscles on the diseased side are relaxed and the head is turned toward
the swollen parotid ; in the bilateral affection, the head is held straight and
rigidly, and the face looks anxious. There is stomatitis and fostor ex ore.
The blood, as a rule, shows no leukocytosis ; in some cases, however, an
outspoken leukocytosis has been met with (16,000; 50,000). There is a
relative increase in the mononuclear elements.
Relapses are not uncommon.
About a week after the glands have begun to swell, the swelling goes
down without suppuration, and no residua are left. In adults, OECHITIS
is not uncommon (oophoritis is less common) ; in rare cases, it may be
the only sign of the disease. The testicle becomes swollen, tender and
hot ; hydrocele often develops. The right testicle is twice as often affected
as the left. The inflammation usually subsides in from 3 to 7 days.
Orchitis is rare in children. In about half the cases of orchitis, atrophy
of the testicle follows, but sexual power remains ; in bilateral orchitis fol-
lowed by atrophy, the patient is sterile. Epididymitis rarely occurs.
Mumps may affect the submaxillary or the sublingual gland alone.
Hegler has described an epidemic of SUBLINGUAL MUMPS (sialoadenitis
sublingualis acuta epidemica) among the Sisters of the Eppendorfer
444 DIAGNOSIS OF INFECTIOUS DISEASES
Hospital in Hamburg. Other occasional complications include (1) pan-
creatitis, (2) meningitis (always benign), (3) mastitis, (4) otitis, (5)
endocarditis, (6) polyarthritis, and (7) iritis.
Diagnosis. — This is easy when an epidemic prevails. Sporadic cases
must be distinguished (1) from toxic parotitis (due to mercury, lead, or
iodin) ; (2) from secondary and infectious parotitis, associated with in-
fections elsewhere in the body, and including "post-operative parotitis" ;
(3) from ascending parotitis (due to oral sepsis) ; (4) from lymphadenitis;
(5) from osteomyelitis; (6) from periostitis; (7) from tonsillitis; (8)
from parutis (subperiosteal abscess of jaw, following abscess at the root
of a tooth) ; (9) from syphilis of the parotid (gumma) ; and (10) from
tumors of the parotid.
References
Acker (G. N.). Parotitis complicated with meningitis. Am. J. Dis. Child., Chicago,
1913, vi, 399-407.
Cheinisse (L.)» La pancreatite ourlienne. Semaine med., Paris, 1912, xxxii, 85-87.
Felling (A.). The blood and the cerebrospinal fluid in mumps. Lancet, London, 1913,
a, 71.
Freund (E.). Beobachtungen uber Parotitis epidemica mil Komplikationen von Seite des
Pankreas. Wiener med. Wchnschr., 1911, Ixi, 3134-3138.
Hegler (C.) Mumps der Sublingualdrusc. Deutsche med. Wchnschr., Leipzig u. Berlin,
1912, xxxiii, 1355.
Sialoadenitis sublingualis acuta. Miinchen. med. Wchnschr., 1912, lix,
Hess (A. F.). A protective therapy for mumps. Am. J. Dis. Child., Chicago, 1915, x, 99-103.
Neurath (R.}. Abdominelle, auf Pancreatitis hinweisende Symptome bei Mumps. Wiener
med. Wchnschr., 1911, Ixi, 1217-1224.
Nicolle (C.) & Conseil (E.). Essai de reproduction experimentale des oreillons chez le
singe. Compt. rend. Soc. deBiol., Paris, 1913, Ixxv, 217-220. .
Smith (E.}. Mumps. In: Syst. Med. (Allbutt & Rollestori). 8°. London, 1909, ii, pt.
1,586-591.
Torpey (J. H.). Primary orchitis with secondary parotitis. J. Am. M. Ass., Chicago,
1911, Ivi, 742.
Zade (/?.)• Ein Beitrag zur Polymorphic der Parotitis epidemica mil besonderer Beriick-
sichtigung secunddrer Meningitiden. Arch. f. Kinderh., Stuttgart, 1912,
Ivii, 261-276.
SECTION III
SPECIAL DIAGNOSIS OF DISEASES DUE TO EXTERNAL
PHYSICAL CAUSES
Among the diseases to be considered under this heading are:
(A) Those due to long exposure to high temperatures (caloric dis-
eases).
(B) Those due to exposure to cold.
(C) Those due to electrical injury.
(D) Those due to injury from x-rays and radium.
(E) Those due to alterations in atmospheric pressure.
(F) Those due to unaccustomed movements, or to alterations of the
direction of movement, of the body (e. g., sea-sickness, car-sickness).
A. Diseases Due to Heat
(The Caloric Diseases)
Occurrence. — Aside from the local effects of heat (burns, scalds),
human beings may show disease symptoms following the long-continued
effect of high temperature. It has been customary to distinguish three
main types of the caloric diseases: (1) sun-stroke, or insolation, resulting
from exposure of the head to the sun's rays ; (2) heat-stroke, or hyperther-
mia, due to a general overheating of the whole body by conducted heat;
and (3) the^ so-called warmth-stroke, or ignisation, the hyperthermia pro-
duced by artificial sources of heat. But there is no real difference be-
tween sun-stroke and heat-stroke, and the effect of radiated heat and con-
ducted heat seem to be the same.
Direct exposure to the sun's rays is, however, the .commonest cause
of the caloric diseases. It has been shown that such direct exposure, even
when the temperature of the air is relatively low, causes a much quicker
rise of body temperature than hotter air without direct exposure to the sun
(Rubner). Heat production through work (as in soldiers on the march),
and hindrance to heat dissipation in still air and when the humidity
is high, are accessory, but not essential causes. Cases described as "heat-
stroke without exposure to the sun" are often, in reality, instances of myo-
cardial insufficiency. The so-called heat prostration occurring in closed
445
446 DIAGNOSIS OF INFECTIOUS DISEASES
rooms in the summer are usually not due to heat alone, but depend upon
exhausted states of the nervous system, alcoholism, or other causes.
In the caloric diseases the hyperthermia may be very marked; temper-
atures of 115°-117° F. have been recorded (Lambert). The temperature
of the body when the heat-stroke suddenly occurs, is usually about 105° F.,
and it goes on rising afterward, reaching 109°-111° F. Heat-stroke
without elevation of temperature is a misnomer.
Human beings can gradually accustom themselves to high tempera-
tures that would be dangerous to the uninitiated; this is well illustrated
by residents in the tropics, and, in temperate zones, by stokers. Clothing
is important, as favoring or hindering heat dissipation. Anything which
enfeebles the body (alcoholism, obesity, chronic disease of the heart or
lungs) favors heat-stroke.
In how far diseases of the nervous system, and of the circulatory
system, may depend upon the chronic eifects of exposure to high tempera-
tures in overheated rooms, or upon exposure to radiating heat from ovens,
or furnaces, among stokers, smelters, cooks, bakers, etc., is not fully known.
Symptoms. — Three stages are distinguishable: (1) the prodromal
stage; (2) the heat-stroke proper; and (3) the stage of recovery.
In the PRODROMAL STAGE, there is palpitation, tachypnea, sweating,
and rase of temperature to 100.5°-101.5° F. The temperature stays at
this level for a time, and then, as a rule, suddenly rises further to around
105° F. at the onset of the stroke.
Before the stroke occurs, various symptoms may appear (headache,
vertigo, weakness, nausea or vomiting, congestion of the head, sudden
profuse perspiration, or epigastric pain). Some patients complain of par-
esthesias, dimness of vision, noises in the ears, difficulty in swallowing,
or of scintillating scotoma. Sudden cessation of perspiration at this stage
is an ominous sign. When such symptoms appear, the heat-stroke can
usually be avoided by prompt cessation of work, or by protection from
the sun.
The HEAT-STROKE PROPER usually occurs suddenly ; the patient becomes
mentally disturbed, fainting, showing delirium, or sinking at once into
deep coma with loss of reflexes. There is marked tachypnea and tachy-
cardia. Vomiting and diarrhea are common. The urine is scanty or sup-
pressed. Twitching of the muscles, or outspoken convulsions, may appear.
The temperature varies now between 105° and 112° F., occasionally reach-
ing 115° or 117° F. If convulsions occur, they may be either general
or Jacksonian in type.
Some patients, instead of becoming comatose, exhibit a peculiar delir-
ium, characterized by convulsions, hallucinations and illusions, flight of
ideas, and pressure of activity, symptoms not unlike those accompanying
the toxic deliria of infectious diseases. Such cases often terminate
DISEASES DUE TO HEAT 447
fatally. -In some instances, the fatal cases show, at autopsy, a focal non-
purulent encephalitis (Steinhausen), the encephalitic lesions correspond-
ing to monoplegias, hemiplegias or aphasias manifest before death.
Sometimes actual twilight states follow exposure to heat. Passing
through the Red Sea on returning from India, in 1899, I saw a delirious
stoker rush up from the boiler-room and commit suicide by jumping into
the sea. The ship's officers told me that this was not a rare occurrence
in those waters.
In the STAGE OF RECOVERY, the patients remain asleep or drowsy for
hours or days, periods of semiconsciousness alternating with paroxysmal
states of unconsciousness. The patients complain of dreadful fatigue,
dizziness, frontal headache, thirst, anorexia, and pains in the muscles.
For some time after the attack, pains in different parts of the body,
dyspnea, and insomnia may persist. Clonic spasms, cramps in the calves
of the legs, neuralgias, and paresthesias are common sequelae. The
tachycardia may give way to an outspoken bradycardia, or to arhythmia.
Anemia or hemoglobinuria may follow the stroke. Vague neurasthenic
symptoms may last a long time, as in the traumatic neuroses.
The principal symptoms in heat-stroke seem to be due to injury to
the brain from overheating (either local overheating of the skull, or from
effects on the brain from the overheated blood).
The majority of cases recover after a few days or weeks, though, in
the severer cases, death may occur, or the recovery be incomplete, owing
to actual encephalitic changes.
Edsall's Disease. — A peculiar form of muscular cramp due to exposure
to heat, has been especially studied in this country by D. L. Edsall.
Diagnosis. — The history of exposure to heat usually makes the diag-
nosis easy. Other causes of coma (alcoholism, hysteria, epilepsy, apoplexy,
cerebral malaria, uremia, etc.) must be considered, in the differential
diagnosis.
References
Edanll (D. L.). Two cases of violent but transitory myokymia and myotonia apparently
due to excessive hot weather. Am. J. M. Sc., Philadelphia & New York,
1904, cxxviii, 1003-1011.
A disorder due to exposure to the intense heat characterized clinically by
violent muscular spasms and excessive irritability of the muscles. J. Am.
M. Ass., Chicago, 1908, li, 1969-1971.
Fayrer (Sir J.}. Sunstrbke. In: Syst. Med. (Allbutt & Rolleston). London, 1910, ii, pt. 2,
771-782. 8°.
Gibbs (H. D.}. A study of the effect of tropical sunlight upon men monkeys and rabbits,
and a discussion of the proper clothing for the tropical climate. Philippine
J. Sc., Manila, 1914, vii, 91-113.
Gordon (A.). Diseases caused by physical agents. In: Mod. Med. (Osier), 2d ed., Phila-
J^&t$eU^Vt air, heat, and cold. Mod. Med. (Osier). PMo-
delphia & New York. 2d ed., 1914, ii, 329-353. 8°.
448 PIAGNOSIS OF INFECTIOUS DISEASES
Lambert (A.). Sunstroke as it occurred in New York city during 1896. Med. News,
New York, 1897, Ixxi, 97-109.
Marchand (F.). Die thermischen Krankheitsursachen. Handb. d. allg. Palh. (v. Krehl
u. Marchand). Leipzig, 1908, i, 49-143. (Literatur.)
Mohr (L.). Die kalorischen Erkrankungen. In: Handb. d. inn. Med. (Mohr & Staehelin).
Berlin, 1912, iv, 743-756.
Pfeiffer (Hermann). Das Problem des Verbruhungstodes. Studie zur Pathologie und
Pathogenese der thermischen Allgemeinschddigung . Wien, 1913, E.
Holzel. 279 p.
Schapals (F.). Das Verhalten der Blutcirculation und des Stoffwcchsels beim gesunden
Menschen unter dem Einfluss verschieden temperirter Bdder. Ztschr. f.
exper. Path. u. Therap., Berlin, 1912, x, 222-240.
Sonnenburg (E.). Verbrennungen und Erfrierungen. Deutsch. Chir., 1879, xiv, 1-16.
B. Diseases Due to Exposure to Cold
The body may suffer from long exposure to cold air, to cold water,
or to snow.
If the air be dry, and there be no wind, temperatures of minus 115°
F. ( — 45° C.) can be borne, without harm, during active exercise. On the
other hand, a much higher temperature may be so cold as to be unbear-
able, if it be accompanied by wind and wet. The danger is greater at
high altitudes; mountain climbers often perish in snowstorms. Among
predisposing factors may be mentioned, (1) emaciation, (2) anemia, (3)
childhood, or senility, (4) non-acclimatization, (5) alcoholism, and (6)
insufficient clothing.
As the body temperature falls, the vital functions become paralyzed.
Animal experiments and human observations indicate that, when the body
temperature falls below 75.2° F. (24° C.), recovery is impossible.
1. Local Effects of Cold
Among the local effects of cold may be mentioned: (1) the anemia
and asphyxiation seen in Raynaud's disease (dead fingers) ; (2) the
itching erythema known as chilblains (perniones), so common in children
and in anemic adults, and affecting especially the acra (fingers, toes,
ears, nose) ; and (3) the local gangrene due to frost-bite, in which the
parts have been actually frozen.
2. Death from Freezing
When a patient "freezes to death," the nervous system, the circulatory
system and the respiratory system are the site of the symptoms. The
excitability of the nervous system gradually decreases, the individual be-
comes benumbed, his capacity for muscular contraction grows less, and
he is overcome by a drowsiness which he cannot resist. The sight grows
DISEASES DUE TO ELECTRICAL INJURIES 449
dim, apathy steals over him, he staggers, and, if left to himself, falls
into his last sleep. An initial tachypnea gives way later to slowed respi-
ration, just as the initial tachycardia is followed, later on, by a slow and
feeble pulse. If the person be discovered before the respiration and the
pulse cease, recovery may still be possible, even though the body be rigid
from the cold, provided care be taken to re-warm the body very gradually.
Unfortunately, death sometimes occurs quite suddenly, even after recov-
ery of consciousness and return to normal temperature.
3. Cold as a Predisposing Factor
That sudden exposure to cold in people not hardened to it predisposes
to certain diseases (pneumonia, influenza, rheumatism) is generally
recognized. This predisposing influence seems to be associated with the
effects of the cold upon the vasomotor nervous system. Much can be
done to harden sensitive persons by systematic vasomotor training through
hydrotherapy.
C. Diseases Due to Electrical Injuries
Formerly, injuries due to lightning were the only ones to be considered
under this heading. With the great industrial and technical development
through electrical energy, a large number of cases of accidental injury
from electrical currents have, in late years, been observed.
About 500 people are killed every year by lightning in the United
States, and the number of electrical injuries associated with electric light-
ing, electric railways, dynamos, etc., is constantly growing. In injury
from lightning, we have to deal with electric currents of very high tension
and of high periodic number.
In order that the body may be injured by an electric current, it must
become a part of an electric circuit, either in a bipolar way, through direct
or indirect contact with two conductors of different potential, or in a uni-
polar way, in that the body conducts directly to the earth.
The tension of the current and the strength of the current are impor-
tant ; the higher the tension, the greater the danger as a rule, though differ-
ences in resistance modify this rule. Thus, one man may, without harm,
let a current of a tension of 500 volts pass through him, while another
may be killed immediately by a current of only 65 volts (Mohr), owing to
differences in resistance at the point of entrance of the current. The
intensity of the current is much more significant, and this, in turn, is
dependent upon the resistance of the body at the site of entrance, and of
exit, of the current, and of the conductor.
Electrical injuries occur both with the alternating current and the
450 DIAGNOSIS OF INFECTIOUS DISEASES
direct current. Currents of a tension below 40-60 volts are not harmful.
In high-tension currents, the period-number is of great importance. Cur-
rents with a period-number of 20 to 70 per second are most dangerous,
and these include most industrial currents. Currents of up to 1,000 volts,
when of high frequency (say 100,000 per second), are devoid of danger
and are used for therapeutic purposes (d'Arsonvalisation; Tesla current).
If the tension exceed 1,000 volts, such currents may become dangerous,
even when of very high frequency, as in lightning. Long contact is much
more fatal than brief contact.
Certain occupations are of course peculiarly exposed to electrical in-
jury ; thus death by lightning is most common among field- workers, death
from currents of industrial electricity, among electrical engine-fitters and
other electro-technical workers. Anyone may, in a town, be accidentally
exposed through unipolar % contact with a broken live wire.
Very serious accidents sometimes occur in private houses through con-
tact with metals near electric light wires.
Recently I was called to see a young lady, who a few moments before
had, on answering a telephone, been thrown violently to the floor, her
muscles becoming rigid so that she could not let go of the telephone until
her father tore away the connection. The accident was due to contact
with an electric lamp wire near by with defectively insulated wiring.
Not long ago a young man from Norfolk consulted me with symptoms
of traumatic neurosis, following an electrical burn of the hand. He had
simply turned on the electric light by a button ; he could not let go of this
button, and the finger and thumb were burned to the bone !
Lightning is more apt to strike high buildings, or buildings up on hills,
than others. Certain trees are more frequently struck than others; thus
oaks are more often struck than beeches.
Local Effects. — The effects of electrical injury may be local, or general.
The local effects consist of burns of variable degree at the site of entrance,
or of exit, of the current. Sometimes the tissues are injured, though the
clothing remains intact.
General Symptoms. — Of the general symptoms, those connected with
the central nervous system and the sense organs are the more important. In
severe electrical injury, the patient cries out and falls unconscious. After
a shorter or longer time, if death does not occur immediately, conscious-
ness returns, though the person may behave as though drunk or delirious.
Retrograde amnesia is common. Paralyses, or convulsive seizures, may
follow, as well as various disturbances of sensibility. Vasomotor disturb-
ances may persist for a long time after the injury.
Respiration is often arrested at first; later, it may be accelerated.
Involuntary passage of urine, feces, or sperm may occur.
Sequelae. — As sequelae, an outspoken traumatic neurosis (q. v.) may
develop. In some cases, symptoms pointing to multiple focal lesions of
DISEASES DUE TO EONTGEN EAYS AND EADIUM 451
the central nervous system, similar to those of multiple sclerosis, have
been observed.
Functional nervous disturbances, following a fright during an elec-
trical storm, are very common among telephone girls in central exchanges.
References
Bernhardt (M.), Die Betriebsunfdlle der Telephonistinnen. Berlin, 1906 (A. Hirschwald).
71 p. 8 .
Dana (C. L.). Electrical injuries. Med. Rec., N. Y., 1889, xxxvi, 477.
Jellinek (/£.). Elektropathologie. Die Erkrankungen durch Blitzschlag und elektrischen
Starkstrom in klinischer und forensischer Darstellung. Stuttgart, 1903,
Knapp (P. C.). Accidents from the electric current. Boston M. & S. J., 1890, cxxii
£65, 392.
Mohr (L.). Erkrankungen durch elektrische Energie. In: Handb. d. inneren Med
Berl., 1912, iv, 763-769.
Oliver (T.). Injuries by electric currents of high pressure. In: Syst. Med. (Allbutt), N.Y.
& Lond., 1898, v, 855-860.
Wcdel. Traumata clectrica. Med. Klin., Berlin, 1909, v, 171-173.
D. Diseases Due to Injuries from Rontgen
Rays and from Radium
Since rontgenologists have learned to protect themselves and their
patients from the injurious effects of the x-ray, burns and injuries due
to this physical agent are becoming less common. The gamma rays, pro-
duced through the electromagnetic impulse waves of the beta rays of
radium, correspond, physically, to x-rays.
Injuries of the body due to such rays depend upon the direct absorption
of the rays by the tissues. A certain intensity of influence and a certain
length of exposure are prerequisites to injury. The soft rays are capable
of injuring the skin ; the hard rays, through their greater penetration,
can reach and injure the internal organs. Certain states of the tissues,
or of the cells, predispose them to radio-injury; thus young tissues — the
lymphadenoid and hematopoietic tissues, and neoplasms — are especially
radio-sensitive, while older tissues — muscle cells, nerve cells, connective
tissue fibers, etc. — are more radio-resistant. Cells undergoing karyokinesis
are particularly sensitive. Histological studies of tissues that have
undergone radio-injury reveal marked changes in the cell nuclei (loss of
capacity to take on the stain, karyolysis), and, later, degenerative changes
in the cytoplasm. Some believe that the rays act primarily by changing
the lecithin of the cells, and that the other changes are secondary to the
lecithin injury. This view is not out of accord with the fact that certain
classes of cells are especially radiosensitive.
452 DIAGNOSIS OF INFECTIOUS DISEASES
1. Rbntjjen-Injury of the Skin
Burns of all degrees may follow radio-injury. It is customary to
divide the effects into four degrees.
Reaction of the First Degree. — At this stage, the signs consist of tem-
porary erythema, followed by loss of hair, desquamation, and slight pig-
mentation. In some cases, erythema does not appear, though, three weeks
after exposure, the loss of hair and the pigmentation occur.
Reaction of the Second Degree. — Outspoken erythema occurs some
twelve days after exposure, with itching, or unpleasant, burning sensation,
red, or reddish blue, discoloration, and loss of hair. The reaction usually
has run its course by the end of the fifth or the sixth week, though perma-
nent changes may follow (atrophy of the skin, telangiectases, scleroderma).
Reaction of the Third Degree. — The skin undergoes a dark, bluish red
discoloration. Small papules appear, which change later into vesicles ;
the latter rupture, and a full-blown moist dermatitis, with formation of
scabs and of crusts, develops. The lesions are accompanied by trouble-
some itching, and by severe pain. On healing, scars, atrophic areas and
telangiectases remain.
Reaction of the Fourth Degree. — Occasionally, an x-ray ulcer de-
velops, as a result of deep necrosis of the skin. Such ulcers present a
peculiar, glistening, yellow appearance. The borders of the ulcer are ir-
regular. Such ulcers may be extremely painful, and are slow to heal ; even
when healing in the center, the ulceration may extend by radial outgrowth
at the periphery. The patient's general Condition may suffer materially
(fever, emaciation, psychoses).
2. Chronic Dermatitis Amonjj Rontgenologists
Specialists in x-ray work, who are exposed over and over again through
long periods to the x-rays, often develop a chronic dermatitis. The skin
becomes rough and dry, and cracks easily. Atrophic patches appear. The
finger-nails become irregular and thickened. The skin about the mouth
becomes dry and wrinkled, with formation of rhagades. Unfortunately, in
many such instances, carcinoma develops later on in the altered skin. The
tumors may be multiple. Sometimes carcim rr.a ar.d sarcoma appear in the
same patient.
Precautions Against Radio-Injury. — In therapeutic applications of
Rontgen rays and of radium, the skin should be carefully protected. The
x-rays should be made to pass through an aluminium filter, 1 mm. thick.
The dosage should be always accurately measured. (See Methods of
Measurement in section on Rontgenology). The intervals between treat-
DISEASES DUE TO RONTGEN EAYS AND EADIUM 453
ments must be cautiously arranged. Rontgenologists now wear protective
gloves and protective aprons, or have their cabinets so arranged that they
themselves are but little exposed to the rays.
3. Rontgen-Injury of the Sex Glands
• If the testes of guinea-pigs or of rabbits be sufficiently exposed to the
x-rays, the animals become sterile from azoospermia, though the capacity
for the sexual act is otherwise uninjured. When the injury is not too.
severe, the power of forming spermatozoa may be regained.
In human beings, sterility may also result from exposure, either of the
testicles or of the ovaries, to the x-rays. Recently, this fact has been
applied therapeutically, in women suffering from prolonged and severe
climacteric changes, and also in the treatment of menorrhagia due to
myoma of the uterus and to chronic endometritis (Kronig). The results
are sometimes remarkable. An especial apparatus is required, with filters
permitting of penetration by deep rays, without injury during long ex-
posures. Some gynecologists believe tnat operations for myoma uteri
will no longer be necessary, thanks to this discovery. Great caution should
be used in employing x-rays for diagnostic or therapeutic purposes during
pregnancy (danger of abortion, or of injury to the child). Drs. Kelly
and Burnam tell me that menorrhagia and metrorrhagia will often yield
to a few local treatments with radium.
4. Rontjjen-Injury of Other Organs
For therapeutic purposes, advantage has been taken of the injurious
effects of x-rays upon young, unripe cells in the various forms of leukemia
(bone-marrow, spleen, lymph glands). Care is to be exercised in begin-
ning the treatment, lest cell-destruction occur too rapidly and severe in-
toxication develop (fever, acute gout from nuclein destruction, with setting
free of purin bodies; disturbances of nutrition). In a few instances,
death has followed such x-ray treatment. Anorexia, albuminuria, diar-
rhea, pains in the bones, are among the symptoms that sometimes
follow injudicious x-ray exposures.
The nervous system seems to be peculiarly resistant to x-ray injury,
though patients sometimes complain of various subjective sensations (head-
ache, vertigo, abdominal pain, nausea, diarrhea) after exposure to x-rays.
These symptoms rarely occur except in neurotic individuals, and are
probably due to suggestive influences. It is asserted that x-ray specialists
are especially prone to cardiac, vasomotor, and gastro-intestinal neuroses,
and that among them arteriosclerosis occurs earlier than in other indi-
viduals.
454 DIAGNOSIS OF INFECTIOUS DISEASES
The thyroid gland appears to be tolerably susceptible to radio-injury.
If overexposed to the x-rays, even when normal, symptoms of thyreoin-
toxication may develop. Cautious exposure of the thyroid to x-rays is
advocated, by some, in the treatment of Graves's disease. Still better
results follow radiation of the thymus in this disorder.
The larger glands of the body (liver, kidney, pancreas) seem to be
highly radio-resistant.
In animals, growth may be arrested by exposure to radium or to x-rays.
Human beings seem to be less susceptible, though until we know more
about the subject, it would be wise to avoid any unnecessary exposure
of young children to either x-rays or radium.
References
Engel (JfiT.). Ueber Rontgenschddigungen mil besonderer Beriicksichtigung der inneren
Medizin. Ergebn. d. inn. Med. u. Kinderh., 1908, Berlin, vii, 115-160.
Mohr (L.). Erkrankungen durch Rontgen- und Radiumstrahlen. In: Handb. d. inn.
Med. (Mohr & Staehelin), 1912, iv, 769-772.
E. Diseases Due to Alterations in
Atmospheric Pressure
Knowledge regarding the pathological states resulting from changes
in atmospheric pressure has grown largely in recent years. The bodily
functions are accustomed to an atmospheric pressure that varies but
little, either above or below T60 millimeters of mercury. A sudden in-
crease of atmospheric pressure causes unpleasant sensations in the ears,
due to increase in the difference between the pressure in the middle ear
and in the external auditory canal. Everyone who has gone through the
tunnel leading under the river into New York, by fast train, is familiar
with this feeling.
Sometimes when the difference in pressure is great, the ear drum
ruptures ; this has occurred in persons near explosions. In the terrible
World War (1914), going on as I write, it is reported that many soldiers
are found dead without any signs of trauma on their bodies, death being
due, presumably, to air-pressure changes near bursting shells.
Diminution of atmospheric pressure varies in its effect according to
whether it occurs suddenly, or slowly. On sudden diminution, changes
occur in the ear and in the paranasal sinuses. A good deal depends upon
whether, before the diminution in the pressure, the body has been exposed
to a higher pressure than normal ; thus, when the animal body is exposed
to a pressure of two atmospheres or more, large amounts of gas become
DUE TO ALTERATIONS IN ATMOSPHERIC PRESSURE 455
dissolved in the body fluids. If, then, the pressure be suddenly lowered,
a large part of this gas goes out of solution. The oxygen and the carbon
dioxid may remain chemically bound, but the nitrogen appears in the form
of bubbles in the blood and lymph, and may mechanically injure the
tissues (caisson disease, diver's disease). Similar changes occur when the
body, exposed to ordinary atmospheric pressure, is suddenly placed in an
environment in which the pressure is less than half an atmosphere (balloon
ascension, aviation). In such instances, symptoms of oxygen-hunger ap-
pear, owing to insufficient arterialization of the blood due to the lessened
pressure of oxygen. Similar oxygen-hunger may arise when the atmos-
pheric pressure is slowly reduced, as in mountain climbing and in resi-
dence at high altitudes (mountain sickness), though in many instances
compensatory processes rapidly set in (polyglobulia), which make the con-
ditions tolerable.
1. Caisson Disease
When the pressure has been very high in a caisson and is then
suddenly lowered, the workmen may become ill. Two forms, one milder,
the other more severe, are distinguished.
In the milder form of caisson disease, the workmen, after a few min-
utes or a few hours, complain of abdominal pain and of pains in the joints
of the extremities ("bends"). The arthralgia is most pronounced in the
knees, though the elbows and hips are also often affected. The Yalleix
points are tender. Epistaxis is common. The patients may be nauseated.
In the severer form, the pains in the extremities become so severe that
the limbs are immobile; there is retention of urine and feces, and all
the signs of spastic paraplegia may develop; this may be partial and
temporary, or more complete. In the latter case, death may follow from
bedsores, or from infection of the urinary passages. Instead of spinal
symptoms, cerebral or cerebellar phenomena may predominate (vertigo,
cerebellar gait, Meniere attacks, delirium, and other psychic disturbances,
partial blindness, aphasia, diplopia, deafness, partial paralysis). In other
instances, the symptoms are those of a traumatic neurosis (q. v.).
Caisson workers should be protected by law from too speedy decom-
pression. For each tenth of an atmosphere of decompression, at least one
minute of time should be allowed. Where the pressure is very high, the
decompression should take place even more slowly, or the method of gradual
decompression suggested by Boykott, Damant and Haldane should be used.
Now that the cause of the disease is known, many patients in whom
symptoms have appeared can be saved by placing them, immediately,
under high pressure again, and then proceeding, extremely cautiously, with
the decompression.
456 DIAGNOSIS OF INFECTIOUS DISEASES
2, Diver's Disease
The conditions are similar to those of caisson disease, except that the
pressure is lower, and the time of exposure to high pressure shorter.
Though there is less danger here, accidents are not uncommon because
fewer precautions are taken than among caisson workers. Professional
divers in the navy, in pearl fisheries, and in sponge fisheries, are subject
to this disorder. Much can be done to prevent the disease by the use
of diving apparatus that prevents too rapid decompression.
3. Air-Pressure Diseases Among Balloonists
and Aviators
When balloonists rise above an altitude of 4,000 to 5,000 meters,
symptoms of air-hunger appear; at an altitude of 8,000 meters, death
may occur, the individual going gradually to sleep (cerebral paralysis).
Life can be maintained at altitudes of 10,000 to 12,000 meters by breath-
ing pure oxygen, but even with this preventive attacks of syncope occur.
Even at relatively low altitudes, tachycardia and tachypnea appear;
the circulation and respiration are so impeded by the shoving up of the
diaphragm, due to expansion of gas in the stomach and intestines.
Aviators suffer at a lower level than balloonists, owing to the con-
centrated attention required of the pilot interfering with deep respiration,
and to the increased amount of oxygen required owing to his muscular
exertion (von Schrb'tter). The speed of ascent is an important factor,
as it gives but little time for readjustment to the lessened oxygen-pressure.
On landing after a flight, aviators suffer from vasomotor disturbances,
with marked rise of blood pressure; they complain of palpitation, con-
gestion of the head, dizziness, and drowsiness. The aviator, Chavez, after
flying over the Alps, died of myocardial insufficiency with severe delirium,
two days later. It is true that, at the end of his flight, he fell and broke
both legs, but his death is attributed to vasomotor disturbances, due to
the diminution of atmospheric pressure during his flight, rather than
to the fractures.
4. Mountain Disease (Acosta's Disease)
Travelers at very high altitudes (Andes, Himalayas) may begin to
suffer from excessive fatigue and drowsiness. There is retching, vomiting
and vertigo. In addition to palpitation and shortness of breath, there may
DUE TO ALTERATIONS IN ATMOSPHERIC PRESSURE 457
be hemorrhages from the mucous membranes and fever. In the severe
cases, the patients pass into coma and die. The disease was first described
by a Jesuit Father, Acosta, who observed it during his travels at a high
altitude in Peru (1590).
Most patients recover, even at the high altitude, if they remain quiet.
The symptoms are usually over in a week or two, though with many patients
it may be months before they feel well again. The disease most often
attacks patients with weak hearts, and those who are under-nourished or
over-fatigued.
Various theories have been advanced to account for the disease. The
true explanation seems to lie in the diminution of the oxygen-tension in
the pulmonary alveoli, and the resulting incomplete saturation of the
hemoglobin with this gas (Paul Bert). Some individuals are more sus-
ceptible than others, probably owing to variations in the regulatory mech-
anisms controlling the oxygen supply to the various organs.
The true mountain disease is, of course, not to be confused with
myocardial insufficiency, or with cerebral apoplexy, occurring at high
altitudes.
Physicians should always be careful, in giving permission to patients
to visit high altitudes, to instruct them how to travel. In increasing
the altitude as much as 1,000 meters, a day or two should be spent at some
half-way place, on the way up, if there be any doubt as to the strength
of the heart. If any symptoms, either of circulatory disease or of true
mountain disease, appear, they will usually pass off if the patient remain
at absolute rest in bed for a few days at the level at which he finds him-
self inconvenienced, or he may be quickly and cautiously transported
to. a lower level. It is surprising to what altitudes human beings can
accustom themselves, if they go about it cautiously.
References
Aschoff (L.). Der Luftdruck als Krankheitsursache. In: Handb. d. allg. Path. (Mar-
chand-Krehl), Leipzig, 1908, i, 190-197.
Bassoe (/>.)• The late manifestations of compressed-air disease. Am. J. M. Sc., Phila-
delphia, 1913, cxlv, 526-542.
Bert (P.). La pression barometrique ; recherches de physiologie experimentale. Paris,
1878, G. Masson. 1168 p. 8°.
Bornstein (A.). Versuche uber die Prophylaxe der PressluftkranKneit. Berl. klin.
Wchnschr., 1910, xlvii, 1272-1276.
Hill (L.). Caisson disease. In: Syst. Med. (Allbutt & Rolleston). London, 1910, vii, 686-
698. 8°.
von Schrotter (H.). Hygiene der Aeronautik und Aviatik. Wien & Leipzig, 1912, W.
Braumuller. 208 p., 1 pl,fol.
Staehelin (R.}. Die Luftdruckerkrankungen. In: Handb. d. inn. Med. (Mohr & Slaeho-
lin), 1912, iv, 777-785.
458 DIAGNOSIS OF INFECTIOUS DISEASES
F. Diseases Due to Unaccustomed Move-
ments, or to Alterations of the Direction
of the Movements of the Body (Sea-Sick-
ness, Car-Sickness, Kinetoses)
When the human body is subjected to movements, or to alterations of
the direction of movements, to which it is unaccustomed, it often reacts
with a peculiar set of symptoms of a functional nervous nature (mental,
gastric, circulatory). Among the conditions that give rise to these
unpleasant sensations may be mentioned (1) the movements of boats,
or of ships, at sea (sea-sickness), and (2) the movement of trains along
sharp curves (car-sickness). Slight sensations, allied to the more severe
disturbances, are often experienced in swings, in elevators, on merry-,
go-rounds, or during earthquakes. Undoubtedly, psychic influences may
play a part in the production of the symptoms, but in the majority of cases
true somatic disturbances are concerned also.
Sea-Sickness
Occurrence. — The movements of the ship most likely to cause symp-
toms are (1) "pitching" and (2) "cork-screw-like motion," while "rolling"
is less likely to cause them. During pitching, it is the moment just aftef
the ship has risen and begins to sink again that is associated with that
unpleasant feeling in the epigastrium which immediately nauseates many
people, and is followed by vomiting and retching. The larger the ship,
as a rule, the more steady it is ; the nearer the center of the ship, the less
the motion. Individual susceptibility varies greatly, though nearly every-
one will be attacked when the movements are extreme. Women are more
susceptible than men. Infants and very young children rarely suffer.
Disturbances of digestion and alcoholic excess predispose.
Symptoms. — The mental state is characteristic (ill-humor, apathy,
depression, disinclination for conversation). Among the somatic symp-
toms, headache, dizziness and nausea appear early. The patient turns
pale, and breaks out into a cold sweat ; the eyes become fixed ; and, finally,
vomiting occurs, sometimes giving relief to the symptoms. Some patients
are not relieved by vomiting, but are nauseated continuously, and, with
every movement of the ship, suffer from violent retching; this, when the
stomach is empty, is often harder to bear than vomiting. Constipation
and leucorrhea are common. The skin is cold and clammy, despite the
sweating.
DUE TO UNACCUSTOMED MOVEMENTS 459
People rarely die of sea-sickness, though many long to die of it. As
the sea becomes smoother, the symptoms let up; even when it continues
rough, persons usually grow accustomed to the movement ; they "get their
sea-legs on."
Deaf-mutes, made so from labyrinthine disease, are said to be insus-
ceptible to sea-sickness. The essence of the disease appears to consist
in disturbances of equilibrium, and in disorientation in space, due (1)
to rapid changes in optic impressions, (2) to abnormal stimulations of the
vestibular apparatus, and (3) to irritation of the abdominal sympathetic,
following the movements of the ship.
Ocean travel is less to be feared than formerly by those subject
to sea-sickness, owing to the many mechanical devices which now limit
motion, and to the increased size and comfort of the trans-oceanic liners.
Travelers have also learned the importance (1) of staying on deck, in the
fresh air, (2) of the assumption of the recumbent position, on deck, in
the middle of the ship, and (3) of the wearing of an abdominal band.
Courage, a certain tension of the will, the avoidance of all excess in food
and drink, and guarding against constipation, go far toward preventing the
disorder.
References
Barany (/?.). Die Seekrankheit. In: Handb. d. N enrol. (Lewandowsky), Berlin, 1912 1
Hi, 864-873.
Schepelmann (E.). Die Seekrankheit. Berlin u. Leipzig, 1912, W. Rothschild. 115 p. 8°.
Stacker (J. R.). Sea-sickness. In: Syst. Med. (Allbutt & Rollestori). 8°. London,
1910, Hi, 230-243.
Part V.
Diagnosis of Diseases of the
Respiratory Apparatus
SECTION I
METHODS OF EXAMINATION
The methods of examination of the organs belonging to the respiratory
system will first he taken up, after which the diagnosis of the special dis-
eases of this system will follow.
Under the respiratory apparatus we include, (1) the nasal cavity (cavum nasi),
(2) the larynx, (3) the trachea and bronchi, (4) the lung (pulmo), and (5) the
pleural cavity (cavum pleurae), that on the right being separated from that on the
left by the mediastinal septum (septum mediastinale) .
The nasal cavity opens in front through the nares, or anterior apertures, and
behind it communicates with the pharynx through the choanae, or posterior aper-
tures. The septum nasi, or- nasal septum, divides the cavity into two halves. Part
of this septum is bony, part cartilaginous, and part membranous. The wall of the
nasal cavity is lined by mucous membrane (membrana mucosa nasi). On the lat-
eral wall of the nasal cavity are the three turbinated bones, or conchae. These
include the superior, the middle, and the inferior nasal conchae. Below each
concha, and lateral from it, is a meatus (meatus nasi superior, medius, and infe-
rior).
Connected with the nasal cavity are certain accessory cavities known as the
paranasal sinuses (sinus paranasales) . Their openings into the nasal cavity are de-
scribed further on. These sinuses include the maxillary sinus, or antrum of High-
more (sinus maxillaris [Highmori'] ), the sphenoidal sinus (sinus sphenoidalis) , and
the frontal sinus (sinus frontalis) on each side. In addition, the ethmoid cells
(cellulae ethmoidales) , and the ethmoidal bulla (bulla ethmoidalis) belong here.
The portion of the nar,al cavity connected with the sense of smell is a small area
on the upper part of the superior concha and on the adjacent septum (regio
olfactoria). The rest of the mucous membrane is thinner (regio respiratoria) .
The larynx possesses a cartilaginous framework, including the thyroid cartilage,
the cricoid cartilage, the arytenoid cartilage, the cartilage of the epiglottis, and the
minute corniculate cartilages of Santorini and the cuneiform cartilages of Wris-
berg. These cartilages are held together by means of ligaments and joints. The
intrinsic muscles of the larynx include the M. cricothyroideus, the M. crico-ary-
tenoideus posterior, the M. crico-arytenoideus lateralis, the M. thyro-arytenoideus,
460
METHODS OF EXAMINATION 461
the M. epiglotticus, the M arytenoideus obliquus, the M. vocalis, the M. ventricu-
laris, and the M. arytenoideus transversus.
The cavity of the larynx is covered by mucous membrane (tunica mucosa laryn-
gis). The ventricle of the larynx is a deep groove, bounded by two folds: — (1) the
plica vocalis, or true vocal cord, and (2) the plica ventr'.cularis, or false vocal cord.
Between the two plicae vocales lies the slit of the glottis (rima glottidis), consisting
of a longer anterior portion (pars intermembranacea) , and a shorter posterior por-
tion (pars intercartilaginea) .
The trachea begins opposite the seventh cervical vertebra and undergoes bifur-
cation opposite the fourth or fifth thoracic vertebral body into the two bronchi.
In the trachea there are 16-20 horseshoelike strips of cartilage (cartilagines
tracheales).
There are two bronchi, one on the right side (bronchus dexter}, and one on the
left side (bronchus sinister). The finer subdivisions of the bronchi are known as
bronchioles (bronchioli) . Each bronchiole opens through an alveolar duct and
atria into the air sacs, and the whole surface of each of these sacs is studded with
minute cavities known as pulmonary alveoli (alveoli pulmonis). The lobule of the
lung (lobulus pulmonis) is made up of one alveolar duct with all the sacs and alve-
oli given off from it.
Each lung possesses a blunt tip (apex pulmonis), and a broad base (basis pul-
monis). Each lung presents three surfaces, one in contact with the diaphragm below
(fades diaphragmatica) 1 one in contact with the ribs (fades costalis), and one
directed toward the pericardium and the mediastinum (fades mediast'nalis) . The
inferior margin of the lung (mar go inferior) lies at the junction of the costal sur-
face with the diaphragmatic surface, while the anterior margin of the lung (margo
anterior) lies at the junction of the costal surface with the mediastinal surface.
The bronchi, blood vessels and nerves enter into relation with the lungs at a fossa
on the mediastinal surface known as the Jiilus pulmonis. The structures here, in-
cluding the pulmonary lymph glands, are known as the root of the lung (radix
pulmonis).
The upper lobe (lobus superior) of each lung is separated from the lower lobe
(lobus inferior) by a deep fissure (indsura interlobaris) . On the right side a
second fissure goes off from the main incisure in a horizontal direction at the level
of the fourth intercostal space; the portion of lung between this and the main
incisure is known as the middle lobe (lobus medius).
In the anterior margin of the left lung there is a deep notch (indsura cardiaca)
opposite the heart. The narrow portion of the upper lobe that projects forward
below this notch is called the lingula pulmonis.
Each pleural cavity (cavum pleurae) is a slitlike space lined by a smooth serous
membrane (pleura). This pleura is divisible into a part that covers the lung
(pleura pulmon's) and a part that lines the walls of the thoracic cavity (pleura
parietalis). The latter is divisible into (1) the costal pleura (pleura costalis),
which covers the inner surface of the ribs, vertebrae, sternum, thoracic muscles, etc. ;
(2) the diaphragmatic pleura (pleura diaphragmat'.ca) , which covers the upper
surface of the diaphragm, and (3) the mediastinal pleura (pleura mediastinalis),
which covers the mediastinal septum; a part of the latter, fused with the pericar-
dium, is often called the pericardiac pleura (pleura pericardiaca) , whereas the rest
of it is known as the mediastinal layer (lamina mediastinalis). The pleural cavity
ends, above, in a blind saclike prolongation known as the cupula pleurae. At the
lower part of the pleural cavity the diaphragmatic pleura lies in contact with the
costal pleura, thus bounding the sinus phrenicocostalis ; on inspiration, the lung
passes into this sinus pleurae, but never as far as the line of reflection.
The mediastinal septum (septum mediastinale) is divisible into a smaller, ante-
462 DISEASES OF THE KESPIRATOKY APPARATUS
rior portion (spatium mediastinale anterius), and a larger, posterior portion
(spatium mediastinale posterius). In the former lie the internal mammary arteries
and veins, the phrenic nerves, the thymus, and certain lymph glands; while in the
latter are situated the. thoracic aorta, the intercostal arteries, the azygos and hemi-
azygos veins, the thoracic duct, the pneumogastric and the splanchnic nerves, the
esophagus, and certain lymph glands. The functions of this mediastinal septum
and its weak spots are described further on.
A. Examination of the Nose and the
Paranasal Sinuses
The interior of the nose may be examined from the front (anterior
rhinoscopy) , or from behind through the choanae (posterior rhinoscopy).
1. Anterior Rhinoscopy
The nasal orifice is held as wide open as possible by means of a
bivalve nasal speculum, care being taken to avoid causing pain. It is
essential to have a satisfactory illumination of the parts under examina-
tion. The examiner wears the ordinary reflecting head mirror, looking
through the hole in its middle. A good lamp, gas-flame, or electric light
serves as a source of light behind and at one side of the patient, on a level
with his head ; the light-rays and the rays of the image should go nearly
parallel to one another. In the physician's office, a Coakley-McKenzie
electric light stand with large
McKenzie condenser is conven-
ient. Still better is the use of
an electric light (dry-cell battery)
on a metal head-band; then no
reflecting mirror is required. The
patient and the examiner sit op-
posite each other on chairs, and
so close to each other that the legs
'of the patient are between the
knees of the observer. The mir-
ror, or the head-light, is arranged
so as to give the best illumination
possible. The patient's head is
held and directed by the exam-
Fig. 132. — Electric Light on Metal Head-bands.
(After H. O. Reik.)
iner's one hand while he manipu-
lates the nasal speculum with the
other. The blades of the speculum
are inserted, closed, into one nostril, and then opened gently; no pain
should be caused. A regular routine should be followed. One examines :
EXAMINATION" OF THE NOSE 463
(1) On the medial side, the surface o'f the nasal septum, noticing
curves, spurs, crests, or deflections, as
well as ulcerations or perforations, if
present.
(2) On the lateral side, separated
from the septum by a broader, or nar- ^ ,00
J > . . Fig. 133.— Bivalve Nasal Speculum.
rower, interspace: (a) the inferior (After H. o. Reik.)
concha, or turbinated bone, the ante-
rior end of which is easily visible; (b) the anterior extremity of the
middle concha, or turbinated bone, better seen when the patient's head is
inclined slightly backward ; (c) the middle meatus, or nasal passage, situ-
ated between these two conchae, in which lie the important openings (1)
into the sinus maxillaris (antrum of Highmore) and (2) into the sinus
frontalis; (d) the inferior meatus, below the inferior conchae, and (e) the
narrow slit (rima olfactoria) lying between the middle concha and the
septum.
In case the nostril is occluded, or is very narrow from swollen conchae,
the examination is facilitated if the swelling is reduced by the application
of a wad of cotton soaked in cocain solution (4-10 per cent) to which a
few drops of 1/10 of 1-per-cent solution of adrenalin chlorid have been
added. As adrenalin is very irritating to the nasal mucous membrane, it
is often better to avoid its use, and to depend upon cocain or menthol as
shrinking agents.
One should look carefully for an abnormal outflow of secretion below
the middle concha (hiatus semilunaris) ; by bending the patient's head
forward and toward the opposite side, the outflow will be favored in
some instances, interfered with in others, or one may compress the bulb
of a Pollitzer air bag, introduce the nozzle into the nostril, and by suction
try to make pus or abnormal secretion exude from the openings. When
secretion is present on first inspection, it is well to wipe it off and then see
if more appears.
When the conchae are enlarged, it is necessary to determine whether
the swelling is due simply to hyperemia, or to so-called "hypertrophy" ;
hyperemic swellings disappear under cocain and adrenalin, and are soft
when palpated with the nasal sound. One notes, further, the presence or
absence of polypi and of tumors, the character of the mucous membrane,
and the size of the nasal Cavity. Foreign bodies, if present, will be visible.
References
Goodale (J. L.). An experimental study of the respiratory functions of the nose. Boston
M. & S. J., 1896, cxxxv, 457; 487.
Lommel (F.). Diagnostik der Krankheiten der obersten Luftwege. In: Lehrb. d. klin.
Diagnostik (P. Krause), 2d ed., Jena, 1913, G. Fischer, 90-107.
464 DISEASES OF THE EESPIEATOEY APPARATUS
MacDonald (£.)• Rhinoscopy. 'In: Syst. Med. (Allbutt & Rolleston). 8°. London,
1909, iv, pt. 2, 8-6.
Reik (H. O.}. Methods of examination of the nose and throat. In: Diseases of the Ear, Nose
and Throat. New York, 1911, 211-224.
Walsham (W. J.)» Nasal obstruction; the diagnosis of the various conditions causing it
and their treatment. London, 1898. 8°.
Yeardsley (M.). The respiratory functions of the nose and their bearing on disease of the
upper air passages. Med. Times & Hosp. Gaz., London, 1902, xxx, 129;
161.
[For other references, see Special Diagnosis of Diseases of the Nose.]
2. Posterior Rhinoscopy and Pharyngoscopy
Using the same head mirror, or an electric head-light, one places a
small, plain, long-handled mirror, previously warmed (tested against over-
heating on the back of the hand), behind the soft palate, so that its surface
looks forward and upward. The patient is told to breathe through his
nose, as this relaxes the soft palate ; meanwhile, the tongue is held down by
a spatula or a depressor. Care should be taken not to touch either the soft
palate or the posterior pharyngeal wall with the mirror, otherwise gagging
occurs. The mirror should be almost at right angles to the handle, the
latter being held towards the angle of the mouth, to get it out of the line
of vision. If desired, a mirror, the inclination of which may be altered
by pressure on the handle, may be used. If necessary, the soft palate a ml
the wall of the pharynx may be cocainized, or the uvula and soft palate
may be drawn forward with a hooked spatula. Sometimes a better view is
obtained if the patient be asked to say ''hah," in a nasal tone. Here again,
the examination of the parts should be systematic, while the rhinoscopic
mirror is tilted into different positions, as follows:
(1) The choanae, or posterior orifices of the nasal cavities, separated
from one another by the light-colored, perpendicular, posterior border of
the septum (vomer).
(2) The posterior ends of the inferior conchae or turbinated bones,
projecting from the sides into the choanae.
(3) Above them, less distinctly visible, the middle conchae, and some-
times the superior conchae.
(4) Turn the mirror sidewise so as to examine the lateral walls of the
nasopharynx and look for a reddish-yellow bulging, presenting a pale,
funnel-shaped indentation at its middle; this is the orifice of the eusta-
chian tube (tuba auditiva). Above and lateral from the tube-projection
is a dark depression, known as Rosenmullcr' s fossa. The structures should
be examined first on the right side, and then on the left.
(5) If the surface of the mirror be now turned still further upward,
the roof of the pharynx will become visible, including the origin of the
pharyngeal tonsil. Hypertrophy of this (adenoid vegetations) will be
EXAMINATION OF THE NOSE 465
visible as ridges or as stalactite growths. In children, they often interfere
seriously with nasal breathing.
(6) Note especially the presence or absence of pathological secretion,
of ulcers, of hypertrophied conchae, and of tumors. Sometimes, a tumor
originating in the hypophysis cerebri (sella turcica) projects into the
nasopharynx. The nasopharynx can be still more easily inspected with
the aid of Hay's electric pharyngoscope. (See Examination of the
Larynx).
3. Sinusoscopy
In rare instances, it may be desirable to examine the maxillary sinus
(antrum of Highmore) by means of a small instrument, a sinusoscope, built
on the principle of the cystoscope ; an instrument of 4 mm. in size can be
introduced into the antrum, through a hole bored through the alveolus of a
tooth. The same instrument can be used for examination of special partc
of the nasal cavity and of the nasopharyngeal space.
4. Palpation oi the Nose and Nasopharynx
Through the nasal speculum, the consistence of abnormal structures
can be felt by means of a sound, the end of which is protected by a little
cotton soaked in borax solution ; one can thus easily distinguish between
the soft nature of hyperemic conchae and the tough hypertrophy and hyper-
plastic conditions of these structures. There is often tenderness on pres-
sure in the fossa canina when the antrum is diseased, and at the root of
the nose and the adjoining portions of the frontal bone when the frontal
sinus is affected. Tenderness over tlie frontal sinus in sinusitis can most
often be elicited by pressure on the floor of the sinus ; we ask the patient
to look down, so as to get the upper lid out of the way ; the finger is then
pressed upward between the eyeball and the orbital roof as deeply as pos-
sible, avoiding pressure on the N. supra-orbitalis.
Palpation of the nasopharynx is especially valuable in young children,
where posterior rhinoscopy may be difficult or impossible. Making sure
that the nail on the fore-finger of the right hand is cut short, one disinfects
the finger carefully, or covers it with a sterile finger-cot, and, placing the
child on a stool, holds its head firmly with the left hand ; the examining
finger is then introduced between the soft palate and the posterior wall of
the pharynx and passed upward into the nasopharynx. It is easy to feel
the roof of the pharynx, and the tubal projections; and one can detenu im
at once whether or not the pharyngeal tonsil is hypertrophied, or whether
all is smooth. One can easily avoid being bitten, by placing, with the
examining hand, the lower lip of the patient over the lower front teeth.
466 DISEASES OF THE RESPIRATORY APPARATUS
5. Transillumination of the Paranasal Sinuses
This is especially valuable for the examination (1) of the sinus maxil-
laris, or antrum of Highmore, and (2) of the frontal sinuses. The method
requires a small electric light, on a suitable holder, and the examination
must be made in a dark room, or under a canopy that shuts out daylight.
To transilluminate the maxillary sinuses, the electric light is placed
inside the patient's mouth and the patient is instructed to close his lips
on the holder. If one antrum contain pus, or if its mucous membrane
be greatly thickened, more light will be absorbed by the diseased side
than by the healthy side, and the former will look much darker than
the other.
A similar method may be employed for examining the frontal sinuses.
An electric lamp, provided with a lens and screened by a rubber cap, is
pressed close against the skin at the medial upper margin of the orbit. If
one frontal sinus be diseased, the illumination will be less widespread on
that, side than on the healthy side.
References
Heryng (T.). Die elektrische Durchleuchtung der Highmorshohle bei Empyem. Berl. klin,
Wchnschr., 1889, xxvi, 774; 798.
Robertson (W.). The electric light in antral disease, etc. J. LaryngoL, London, 1892, viy
64; 109; 154.
Tilley (#.). Transillumination. In: Syst. Med. (Allbutt & Rolleston). 8°. London,
1909, iv, pt. 2, 6-7.
Vohsen (/£.)• Die Durchleuchtung der Oberkiefer- und Slirnhohle und der en Erkrankungen.
Berl. klin. Wchnschr., 1890, xxvii, 1060-1063.
6. Rontgenography of the Paranasal Sinuses
By observation of a careful technic, it is often possible to recognize the
existence of disease of one or more of the paranasal sinuses (maxillary,
frontal, ethmoidal, sphenoidal) by the appearance of dark shadows, in
corresponding situations, in the x-ray plate. The etiology of certain
cephalalgias and trigeminal neuralgias, and of many cases of metastatic
infection (arthritis, nephritis) is, occasionally, made clear by the dis-
covery of previously unsuspected sinus disease.
Kontgenography of the Frontal Sinuses. — The patient lies on his face
with his arms and hands along the edge of the table. In order to avoid
the strong shadows thrown by the temporal bone, a photograph is taken by
throwing the pyramid of Rontgen rays in a direction from above the
occipital protuberance behind, toward the orbit in front. The sagittal
middle plane of the head should be perpendicular to the photographic
EXAMINATION OF THE NOSE
467
plate; this is difficult, but very
shadows. The forehead and
nose should rest upon the plate.
Or, the photograph may be
taken in the sitting posture, if
the head be firmly held in posi-
tion either by a clamp, or by
sandbags in a box standing on
a table in front of the sitting
patient; in the sitting position,
the head contains less blood than
in the recumbent posture, and a
clearer negative is obtained.
important, in order to avoid deceptive
Fig. 134. — Patient in Position for Rontgenography
of the Paranasal Sinuses. (After C. A.
Waters and C. W. Waldron, Am. J. Ront-
genol.)
Rontgenography of the Maxillary Si
nuses. — The negative may be made either
in the recumbent or in the sitting posture,
as above described. But the pyramid of
rays is now directed from behind so that
the center of the bundle of rays passes
through the middle line, where it cuts a
line passing through the middle of the pos-
terior margins of the ascending rami of the
mandible; passing forward, the center of
the bundle of rays will then emerge in front
at the middle of the dorsum nasi. Since
disease of the antra sometimes depends on
lesions at the roots of the teeth, special ront-
genograms of these may also be desirable.
(See Digestive System.)
"CT £? RSntgenography of the Ethmoidal and
photographic Plate in the An- Sphenoidal Sinuses. — By especially care-
SZTaTC T^r^aS; fuUy arranged postures,' these sinuses can
sinuses. (After c. A. Waters also be photographed. The sphenoidal
R5ntgenol.T' Waldr°n' *"' *' sinUS SnOWS Wel1 in kteral Vi6WS °f th°
468 DISEASES OF THE RESPIKATOKY APPARATUS
Fig. 136. — Rontgenogram of Normal Paranasal Sinuses in the Adult. The Frontal Sinuses are
Large and Show Orbital Extensions ; the Anterior and Posterior Ethmoidal Cells are
Well Defined ; the Maxillary Sinuses are Well Developed ; there is an Air Cell in the
Crista galli. See Fig. 137. (After C. A. Walters and C. W. Waldron, Am. J. Rontgenol.)
skull, such as are made to reveal the sella turcica (q. v.). Here the rays
enter in the region of the external auditory canal.
Waters and Waldron (1915) have published an important paper on rontgenog-
raphy of the paranasal sinuses, describing a new teehnic which affords greater effi-
ciency in diagnosis. The occipitofrontal position, first used by Caldwell in America,
and by Killian in Germany, has been slightly modified by them so that a single
rontgenogram reveals clearly the frontal and maxillary sinuses and the anterior
and posterior ethmoid cells on the same plate without obscuring the outlines of the
antra by shadows of the petrous portions of the temporal bones. The patient lies
on a horizontal table with his face downward and the chin resting on a cassette,
which holds the plate and an intensifying screen. Upon the occiput, a compression
EXAMINATION OF THE NOSE
469
diaphragm 18 cm. deep is screwed down tightly, a felt pad 2 cm. in thickness being
interposed. Three rules are emphasized, (1) the chin must rest upon the plate, (2)
the long axis of the tube must be
parallel to the plate, and (3) the
nose of the patient should be from
1 to 1.5 cm. from the plate, under
no condition touching it. Two dis-
tinct types of face (the concave
and the convex) are distinguished,
requiring a variation of an angle
of about 2° in the vertical axis of
the skull. With a concave face, the
course of the base of the skull is
high, necessitating an increase of
£ cm. in the distance of the nose
from the plate. The authors rec-
ommend keeping the nose of the
concave face 1.5 cm. distant from
the plate, while with the convex
face the nose is placed only 1
cm. distant, with the long axis
of the tube still parallel to the
plate. A moderate milliamperage -jD^Qrornrncch'^ Key lo 7V o 3.
is employed as well as a soft
tube with intensifying screen, since
these conditions yield the great-
est amount of detail. They have
employed the method in 1,000
cases and are firmly convinced of its superiority from the diagnostic stand-
point.
Fig. 137. — Diagrammatic Key to Preceding Fig-
ure, Illustrating a Rontgenogram of Nor-
mal Paranasal Sinuses in Adult. (After
C. A. Waters and C. W. Waldron, Am. J.
Rontgenol.)
References
Albrecht (W.). Die Bedeutung der Rontgenographie fur die Diagnose der Nebenhohlen-
erkrankung. Arch. f. Laryngol. und Rhinol., Berlin, 1907, xx, 175-196.
2pL
Coakley (C. G.). Skiagraphy as an aid in the diagnosis and treatment of diseases of the
accessory sinuses of the nose. Ann. OtoL, Rhinol. & Laryngol., St. Louis,
1905, xiv, 16-20.
Turner (A. L.) & Porter (W. 6r.). The skiagraphy of the accessory nasal sinuses. New
York, 1914, P. B. Hoeber. 45 p.
Waters (C. A.) & Waldron (C. W.}. Roentgenology of the accessory nasal sinuses, de-
scribing a modification of the occipito-frontal position. Am. J. RoentgenoL,
Detroit, 1915, ii, 633-639.
7. Sounding the Maxillary Sinus
The passage of sounds into openings of the several paranasal sinuses,
and the exploratory puncture of the maxillary sinus, or antrum, from the
inferior meatus nasi, are methods sometimes employed for diagnosis ; for
a description of these special text-books and monographs may be consulted.
470 DISEASES OF THE RESPIRATORY APPARATUS
B. Examination of the Larynx, Trachea
and Larger Bronchi
The larynx and trachea are visible, especially in thin people, in the
front of the neck (external examination). With the aid of specially
devised instruments, it is possible also to inspect the interior of the larynx
(laryngoscopy) and the trachea and larger bronchi (bronchoscopy) .
1. External Examination of the Larynx and Trachea
(a) Inspection of the Larynx and Trachea Externally
The larynx lies normally between the upper margin of the third and
the lower margin of the sixth cervical vertebra ; during respiration, phona-
tion and deglutition, it rises to higher, and descends to lower, levels. On .
external examination, one pays attention to the size, form, and position of
the larynx (and trachea), especially to lateral displacements, and to rota-
tions of the larynx as a whole. Marked swelling may be visible in peri-
chondrial inflammations.
The respiratory movements of the larynx are diminished in stenosis of
the trachea or of the large bronchi, the head tending to be bent forward,
while in stenosis in the larynx itself, the head is inclined backward and
the respiratory movements of the larynx are markedly increased. In
inflammatory and edematous conditions of the larynx (diphtheria, edema
of the glottis, tumors, paralysis of» the openers of the glottis, spasm of the
closers of the glottis), respiration is difficult, the breathing being slower
than normal, inspiration, especially, being long-drawn-out and accom-
panied by a rough noise (stridor).
Reference
Killian (G.)» Schwebelaryngoskopie. Arch. f. Laryngol. u. RhinoL, Berlin, 1912, xxvii,
277-317. 1 pi.
Webb (G. B.), Forster (A. M.) & Gilbert (G. B.}. Trachea position. Nat'l Ass. Study
& Prev. Tuberc., Baltimore, 1915, 69-71.
(b) Palpation of the Larynx and Trachea
On palpation, the consistence of swellings of the thyroid and cricoid
cartilages may be examined, and tenderness on pressure sought for. Espe-
cially important, here, is the examination for the presence or absence
of a tracheal tug (Oliver-Cardarelli sign). In aortic aneurism, pulsating
shocks are transmitted to the trachea ; sometimes these are visible, but they
are most easily recognized by placing the thumb and the fore-finger
EXAMINATION OF THE LARYNX AND TRACHEA 471
beneath the cricoid cartilage while the patient inclines his head somewhat
backward, in order to make the structures in front of the neck a little
tense. If a tracheal tug is present, the fingers will detect a cardiosystolic
tug upon the larynx.
(c) Percussion of the Larynx
On percussion, the larynx yields a tympanitic sound, the pitch of which
is higher when the mouth is open, lower when the mouth is closed.
(d) Auscultation of the Larynx and Trachea
On auscultation with the stethoscope over the larynx and the trachea,
very loud tubular breathing is normally audible (laryngeal and tracheal
breathing).
With the naked ear, one should pay attention to the sounds produced
by the larynx on phonation, as they are of some value in diagnosis.
Difficulty in speech, due to disturbance of the respiratory passages, is
known as dysphonia; inability to speak above a whisper as aphonia, or loss
of voice.
Dysphonia may be due to inability to expel a forcible current of air
through the larynx (feeble voice) ; this is often seen in diseases of the air
passages, as well as in some paralyses of the vocal cords. When high and
low tones cannot be produced, the voice becomes monotonous, and when
abnormal accessory sounds accompany the voice it becomes hoarse.
Aphonia, or loss of voice, is very common in hysteria, but may appear
temporarily in inflammatory conditions of the larynx. In certain laryn-
geal diseases, either a falsetto (unnaturally high and piping), or a deep
bass voice, may appear. The peculiar phenomenon known as double voice
(diplophonia) is met with in polyp of the larynx; during phonation, the
polypus becomes engaged between the free margins of the vocal cords, and
gives rise to different vibrations in the two portions of the cords. A
peculiar nasal twang in the voice, especially in pronouncing m, n and ng
(ask the patient to say "Good-morning"), is due to obstruction in the
nose or nasopharynx (hypertrophies, tumors, adenoids'). An opposite
condition is met with in paralysis of the velum palatinum; the nasal
cavities cannot be closed off from the mouth cavity on speaking, and one
then hears the so-called "open nasal voice," the nasal twang being promi-
nent and causing difficulty, especially in the pronunciation of the explosive
letters, &, p, k and t.
Reference
Iglauer (Samuel). Value of rcentgenography in diagnosis of diseases of larynx and trachea.
J. Am. M. Ass., Chicago, 1914, Ixiii, 1827-1831.
472 DISEASES OF THE RESPIRATORY APPARATUS
2. Internal Examination of the Larynx (Laryngoscopy)
The most important method of examining the larynx is by inspection
of the interior; this may be done directly (direct laryngoscopy or auto-
scopy), or indirectly through a mirror (ordinary or indirect laryngoscopy).
The latter method is by far the more important.
(a) Direct Laryngoscopy
This may be carried out, either (1) by the autoscopy of Kirstein, or,
better, (2) by the use of Hay's electrical pharyngoscope.
i. Autoscopy of Kirstein
The patient, seated in a chair, bends his head well backward, so as to
make as direct a line as possible from the mouth-opening to the larynx.
The examiner presses the base of the tongue forward and backward with a
strong spatula, until the posterior half of the larynx becomes visible
(electric illumination with Kirstein's lamp). The method is uncomfort-
able for the patient, but often affords a very satisfactory view, especially
of the back of the larynx. In children, it is sometimes the only method
of getting a view of the larynx. The procedure is occasionally resorted to
when operations are performed upon the larynx under anesthesia.
Fig. 138.— Hay's Pharyngoscope. Easy to Use, and Affords a Good View, under Bright
Illumination, of the Nasopharynx, Tubal Orifices and the Larynx. (After H. O. Reik.)
EXAMINATION OF THE LARYNX AND TRACHEA 473
ii. Direct Laryngoscopy with Hay's Pharyngoscope
Direct inspection of the interior of the larynx has been made compara-
tively easy by the invention of this ingenious instrument. The apparatus
(Fig. 138) is a modified form of telescope. The tube of the instrument
depresses the tongue. At the. inner end of the tube is a small electric lamp
and a very small reflecting mirror, which can be rotated by moving a knob
on the handle. At the outer end of the tube is the eye-piece through which
the examiner peers. Bright illumination is obtained by attaching the
instrument to a wall-socket controller.
Instead of Hay's pharyngoscope, the instrument of Holmes or that
of Schmuckert may be
used if preferred.
Technic. — The tube
is passed over the tongue
into the pharynx, and
the patient closes his
mouth. By turning the
mirror in different direc-
tions, one can, at his
leisure, view (1) the in-
terior of the larynx, (2)
the vault of the pharynx,
and (3) the lateral re-
gions of the pharynx,
including the orifices of
the eustachian tubes.
After a little practice,
excellent views are ob-
tainable. Along with a
small portable dry bat-
tery, this instrument can
be carried in the consultation bag, and used in house visits where no
other electric current is available.
Fig.
139. — Schmuckert's Electric Pharyngoscope.
(By courtesy of the Kny-Scheerer Co.)
References
Brunings (W.). Die direkte Laryngoskopie, Bronchoskopie und Oesophagoskopie. Ein
Handbuch fur die Technik der direkten okularen Methoden. Wiesbaden,
1910, J. F. Bergmann. 419 p. roy. 8°.
Kirstein (A.). Autoskopie des Larynx und der Trachea (Laryngoscopia directa, Euthy-
skopie, Besichtigung ohne Spiegel}. Arch. f. Laryngol. u. Rhinol., Berlin,
1895, Hi, 156-164. Also: Berl. klin. Wchnschr., 1895, xxxii, 476-478.
Waagett (#.). Direct laryngoscopy, tracheoscopy, bronchoscopy, ocsophagoscopy and gas-
troscopy. In: Syst. Med. (Allbutt & Rolleston). 8°. London, 1909, iv,
pt. 2, 299-322.,
474 DISEASES OF THE EESPIEATORY APPARATUS
(b) Indirect Laryngoscopy
The patient, seated, protrudes bis tongue and holds it firmly in a
towel, or a small napkin, between his thumb and fore- finger, opening the
mouth as wide as possible. By pulling the base of the tongue forward in
this way, the epiglottis is lifted. The head is held upright (inclined
neither backward nor forward), and the examiner sits close to his patient,
the legs of the patient between the knees of the examiner. By means of
the head mirror, or, better, a head-light, as broad a light as possible is
thrown into the throat. The round laryngeal mirror, somewiiat larger than
that used in posterior rhinoscopy, is warmed over the lamp, so that
moisture will not be precipitated upon it, tested on the back of the hand
against over-heating, and then its back is pressed lightly against the uvula
so as to hide the latter entirely, it and the soft palate being displaced gently
backward and upward in order to supply the necessary space. The handle
of the mirror, held in the examiner's hand like a pen, should be kept out
of the way by displacing it sidewise to the angle of the mouth. The
position of the mirror can be sufficiently varied by rotation of the handle
on its long axis, the patient being asked to vocalize, repeating ah-ah, in
order that the movements of the vocal cords may be studied.
Some patients are so sensitive that the gagging reflex interferes with
the examination. Skill, a little patience and reassurance will often over-
come this, but it may sometimes be necessary to swab the base of the
tongue, the uvula, the soft palate and the posterior pharyngeal wall with a
5-per-cent solution of cocain, the patient being warned to spit out any
excess of the solution in order to avoid cocain poisoning.
When satisfactory views of the larynx begin to be obtained, the exami-
nation should proceed in an orderly way.
i. General View, and View of the Anterior Parts of the Larynx
It is to be remembered that the anterior part of the larynx (i. e., the
epiglottis) will appear above in the mirror, while the posterior part of the
larynx (the arytenoid cartilages) will appear at the lower margin of the
mirror. The right side of the larynx will appear in the side of the mirror
turned toward the patient's right, and the left side in that toward his left.
Usually, one sees first the curved margin of the epiglottis, which at the
sides goes over into the aryepiglottic folds. The region of the arytenoid
cartilages will be recognized by the projecting nodules (cartilages of
Santorini) beneath the mucous membrane, lateral from which are the
nodules formed by the cartilages of Wrisberg. On good illumination, one
can next make out, lower down, the white vocal cords, especially their
posterior parts. They become wider apart during inspiration, and closer
together during expiration. To get the overhanging epiglottis out of the
way, so as to see the cords in their whole extent, as far forward as the
EXAMINATION OF THE LAKYNX AND TKACHEA 475
anterior commissure, one asks the patient to say aAh-h-h" or a long-drawn-
out, high pitched "Hay." During phonation, the vocal cords come close to-
gether, in the middle line, and become visible throughout their whole
length and surface. In this position, one notes the general appearance of
the structures, the respiratory mobility of the vocal cords and of the aryte-
noid cartilages, the prompt and equal approximation of the cords in the
Plica
glosso-epiglot-
Tuberculum epiglotticum tica mediana Epiglottis
Labium vocale _ .~^fil £-- Ventriculus laryngis
(Morgagnil)
Plica aryepiglottica
Tuberculum corniculatum (Santorini)
Tuberculum cuneiforme
(Wrisbergi)
Pig. 140. — Indirect Laryngoscopic View of the Larynx from Above with the Epiglottis Raised
and the Glottis Open. (After P. Krause, "Lehrb. d. klin. Diagnostik," published by G.
Fischer, Jena.)
middle line on vocalizing, the color and blood supply of the vocal cords and
of other visible parts, and the presence or absence of scars, ulcers, tumors,
etc.
ii. View of the Posterior Wall of the Larynx
In order to examine the posterior wall of the larynx, and the trachea
as far as its bifurcation, the patient sits higher, or stands up, and bends his
head well forward, until the chin touches the manubrium sterni. The
examiner sits, or kneels, in front of the patient, and looks almost vertically
upward at the mirror held horizontally in the patient's throat. The
illumination must be good. One sees the tracheal rings (perspectively
shortened), and sometimes, in the depth, a whitish sagittal ridge, the
bifurcation spur, and, on each side, the opening into a bronchus.
On examining the posterior wall of the larynx, in the interarytenoid
region, the mirror is held a little further forward in the throat than
ordinarily (method of Killian).
iii. Lateral View of the Interior of the Larynx
This is best obtained by the method of Avellis. Thus if one wish to
examine the left side of the larynx, the patient bends his head to the right,
and the back of the mirror is placed against the right side of the soft
palate ; one can get a good view of the edges of the left false cord and the
476 DISEASES OF THE EESPIKATOKY APPARATUS
left vocal lip, and, on phonation, can sometimes see the floor of the
ventricle of Morgagni.
For the pathological findings on laryngoscopic examination, see Special
Diagnosis of Diseases of the Larynx.
References
Avellis (G.). Cursus der laryngoscopischen und rhinoscopischen Technik. Berlin, 1891. 8°.
Ballenger (W. L.}. The teaching of rhinology and laryngology, College of Physicians and
Surgeons, Department of Medicine of the University of Illinois. Laryngo-
scope, St. Louis, 1906, xvi, 910-914.
Bedos (J.). De V ictus larynge essentiel. Paris, 1895. 4°-
Bergengriin (P.) & von Bergmann (E.) [et al.]. Handbuch der Laryngologie und Rhin-
ologie. Wien, 1896-1900. 3 v. in 5. 8°.
Coakley (C. G.}. The teaching of laryngology and rhinology in the New York University,
University and Bellevue Medical College. Laryngoscope, St. Louis, 1906 ,
xvi, 903-905.
Cohen (J. S.}. Laryngology and its relation to general medicine. J. Am. M. Ass., Chicago,
1900, xxxv, 138.
Grabower (H.). Die Forderung der Medicin durch die Laryngologie. Berl. klin. Wchnschr.,
1901, xxxvi, 721-725.
Hunt (J. M.}. Laryngeal vertigo. Liverpool M.-Chir. J., 1898, xviii, 310-313.
Ingals (E. F.). Laryngology in America. J. Am. M. Ass., Chicago, 1899, xxxii, 1234-1236.
Killian (G.). Die Demonstration laryngoscopischer Bihler vermittelst der directen Projection.
Munchen. med. Wchnschr., 1893, xl, 103-107.
Kir stein (A.). Autoscopy of the larynx and the trachea (direct examination without mirror}.
Authorized translation (altered, enlarged and revised by the author) by Max
T homer. Philadelphia, 1897. 12°.
Mackenzie (J. N.). The study of laryngology in the university and in the higher medical
schools. J. Am. M. Ass., Chicago, 1901, xxxvii, 158-161.
Makuen (G. //.)• Some notes on two cases of voluntary laryngeal whistling. J. Am. M.
Ass., Chicago, 1901, xxxvi, 1097.
Roe (J. O.). Laryngeal whistling. Arch. Laryngol., New York, 1882, Hi, 30-32.
Schrdtter (L.). Vorlesungen uber die Krankheiten des Kehlkopfes, der Luftrohre, der Nase
und des Rachens. Wien, 1887-1896. 2 v. 8°.
Seifert (O.). Was leistet die heutige Laryngologie? Internal. Centralbl. f. Laryngol., Rhinol.
[etc.], Berlin, 1903, xix, 387-397.
Seifert (O.) & Kahn (M.). Atlas der Histopat hologie der Nase, der Mundrachenhohle und
des Kehlkopfes. Wien, 1895. 8°.
Semon (Sir F.). An address on the relations of laryngology and rhinology to general practice.
Lancet, London, 1907, i, 859-862.
Swain (H. L.). Laryngology and its place in medical education. Tr. Am. Laryngol. Ass.,
New York, 1901, xxiii, 1-17.
3. Bronchoscopy
The technic of the direct examination of the larger bronchi (bron-
choscopy), as worked out by Killian and by Chevalier Jackson, consists in
the introduction of straight, metal, fenestrated tubes, through the mouth,
EXAMINATION OF THE LARYNX AND TRACHEA 477
into the larynx, and through it into the trachea, after thorough cocainiza-
tion of the parts; in children, or in neurotic persons, general anesthesia
may he necessary. The tubes have a diameter of 7-10 mm. for adults, or
of 5-6 mm. for children. The outer wall of the tuhe carries a centimeter
scale. The tuhes for adults measure 30-45 cm. in length; for children,
15-25 cm. The illumination can be made with a panelectroscope.
Technic. — The fasting patient sits (or lies) with his head thrown far
back. The base of the tongue is drawn forward and downward, and the
warmed and lubricated tube is introduced into the larynx. During an
inspiration, it is passed gently through the glottis. It is then passed cau-
tiously deeper down, the head of the patient now being brought a little
more forward. If one of the wider, shorter tubes is passed in first,
narrower and longer ones, for examination of the deeper parts, can be
shoved in through it. With some practice, it is possible to view the bifur-
cation of the trachea, the entrance into the two chief bronchi, and, aleo,
by passing the tube into the right or left bronchus, the subdivision of a
main bronchus into bronchi of the second order may be brought into view.
The same apparatus can be used for esophagoscopy, and for gastroscopy.
Hooks, forceps, and cutting instruments can be passed through the tubes
for the removal of foreign bodies, the dilatation of a stricture, the removal
of a polyp, the excision of a particle of tissue for diagnosis, etc. Only
experts can be expected to use the apparatus, but the general practitioner,
knowing of the method, can call in such an expert, in case of need.
References
Bowen (C. F.). The vse of the fluoroscope as a guide for the bronchoscope and esophago-
scope in the removal of foreign bodies. Tr. Am. Rontgen Ray Soc., 1911,
xii.
French (T. R.) . Laryngeal and postnasal photography with the aid of the arc light. Tr. Am.
Laryngol. Ass., New York, 1897, 271-279
Ingals (E. F.) & Friedenberg (S. A.}. Fluoroscopic bronchoscopy. Ann. Otol, Rhinol.
& Laryngol., St. Louis, 1914, xxiii, 519-522.
Jackson (C.). Per oral endoscopy and laryngeal surgery. St. Louis, 1915, The Laryngo-
scope Co.
Killian (£.)• Ueber directe Bronchoskopie. Munchen. med. Wchnschr., 1898, xlv, 844-
847.
Zur Bronchoskopie bei kleinen Kindern. Deutsche med. Wchnschr.,
Leipzig u. Berlin, 1911, xxxvii, 1204-1209.
Mann (AT.). Lehrbuch der Tracheobronchoskopie. Wurzburg, 1914, C. Kabitzsch. 208 p.
8°.
Ridpath (R. F.). Routine use of the bronchoscope in the out-patient department. Laryngo-
scope, St. Louis, 1914, xxiv, 942—947.
Schoonmaker (P.)- The use of the bronchoscope in direct examination of the larynx,
trachea, bronchi and esophagus. Laryngoscope, St. Louis, 1914, xxw,
667-372.
478 DISEASES OF THE RESPIRATORY APPARATUS
C. Examination of the Lungs and the
Pleurae
In studying, clinically, the condition of the lungs and of the pleurae, \ve
use the methods of inspection, thoracography, spirometry, palpation,
.. Midclavicular line
... Parasternal line
._ Sternal line
-- Anterior median line
Fig. 141. — Diagram of Anterior Surface of the Chest, Showing Bony Landmarks and Lines
Referred to in Descriptions of Topography.
mensuration, percussion, auscultation, x-ray examination, examination of
the sputum, and exploratory puncture.
References
Earth (H.}. Semiologie de VAppareil respiratoire. Paris, 1908, J. B. Bailliere & fits.
164 P- 8°. [ Nouv. Traite de Med. et de Therap., xxviii.]
Flint (Austin), Sr. A practical treatise on the physical exploration of the chest and the
diagnosis of diseases affecting the respiratory organs. 2d ed. Philadelphia ,
1866, H. C. Lea. 595 pp. 8°.
A manual of auscultation and percussion, embracing the physical diagnosis
of diseases of the lungs and heart and of thoracic aneurysm. 5th ed. Re-
rised by J. C. Wilson. Philadelphia, 1890, Lea Bros. & Co. xii, 13-268.
8°.
Gee (Samuel). Auscultation and percussion, together with the other methods of physical
examination of the chest. 5th ed. London. 1907, H. Froude [etc.]. 325 p.
8°.
Gerhardt (/>.)• Diagnostik der Krankheiten des Respirationsapparates. In: Lehrb. d. klin.
Diagnostik (P. Krause), 2d ed., Jena, 1913, G. Fischer, 108-158.
EXAMINATION OF THE LUNGS AND PLEURAE 479
•
Mackenzie (H.). Physical signs of the lungs and heart. In: Syst. Med. (Allbutt & Rolles-
ton}. 8°. London, 1909, v, 3-26.
Matthes (M.). Die Erkrankungen der Atmungs- und Kreislauforgane. In: Handb. d.
PathoL d. Stoffwechsels (v. Noordcn), Berlin, 1906, i, 828-880.
Minkowski (/.) & Bittorf (A.). Pathologic der Atmung. In: Handb. d. allgem. Pathol.
(Krehl & Marchand), Leipzig, 1912, ii., 456-620.
Steell (Graham). The physical signs of pulmonary disease for the use of clinical students.
2d ed. Philadelphia, 1900, P. Blakiston's Son & Co. 98 p. 12°.
West (5.). How to examine the chest. A practical guide for the use of students. 2d ed.
London, 1890. 12°.
1. Inspection of the Thorax in Relation to Diseases
oi the Lungs and Pleurae
(a) Forms of Thorax
The two forms of thorax of especial importance in this connection are:
(1) the extreme expiratory type of thorax, or thorax paralyticus ; and (2)
the extreme inspiratory, or emphysematous type.
Scapular line
Posterior median line
Fig. 142.— Diagram of Posterior Surface of the Chest, Showing Bony Landmarks.
i. Thorax paralyticus or Flat Chesi
The extreme expiratory type of thorax is easily recognized by (a) its
flatness ; (b) the absence of the normal projection forward of the sternum
and anterior wall of the chest; (c) the short anteroposterior diameter; (d)
480 DISEASES OF THE KESPIRATOKY APPARATUS
the wide intercostal spaces ; (e) the low position of the arches of the ribs,
separated from the crest of the ilium by only one or two fingers' breadth ;
(f) the prominent clavicles, with deep supra- and infraclavicular fossae;
and (g) the prominent angles of
the ribs behind, with lateral
displacement of the winglike
scapulae. In some instances
there is a deep cuplike or fun-
nel-shaped depression known as
"funnel chest,"
This form of bilateral con-
traction of the thorax, usually
present from birth, or acquired
in early childhood, strongly
predisposes its owner to pul-
monary tuberculosis.
ii. Barrel-shaped or Emphysema-
IOILS Thorax
The extreme inspiraiory
type of thorax is just the op-
posite of the preceding, being
characterized by (a) its gen-
eral fullness; (b) the marked
projection forward of the ster-
num, and of the anterior parts
of the chest; (c) the long an-
teroposterior diameter; (d) the
narrow intercostal spaces; (e)
the high position of the arches
of the ribs, and the great dis-
tance between the rib-margins and the iliac crests; (f) the high position
of the clavicles and the shortness of the neck; and (g) the bulgings in
the supra- and infraclavicular fossae.
This type of thorax appears to be acquired in persons that have
for one reason or another (bodily over-exertion, bronchitis, etc.) been
compelled to inspire excessively; it is most marked in pulmonary
emphysema.
Other deviations from the normal in addition to the two main types above
described include: (1) the alar or pteri/goid chest (small capacity; angles of scapu-
lae projecting like wings) ; (2) the transversely constricted chest (sulcus at level
of xiphoid known as "Harrison's groove") ; (3) the pigeon breast or pectus cari-
natum (thorax triangular in cross-section; sternum projects forward; true ribs
straightened in front of their angles) ; and (4) the rickety chest (shallow vertical
Fig. 143. — Funnel Chest in a Man with Expira-
tory Type of Thorax — Thorax paralyticus.
(Med. Service J. H. H., Photograph by Dr.
John Hewetson.)
EXAMINATION OF THE LUNGS AND PLEUKAE 481
groove on each side, nearly parallel with the sternum; "rickety rosary" at junctions
of ribs and costal cartilages).
iii. The Normal Thorax
The two sides are symmetrical ; the respiratory movements are equal
and contemporaneous on the two sides.
(6) Asymmetry of the Thorax in Relation to Diseases of the
Lungs and Pleurae
While the normal thorax is symmetrical and the two halves participate
equally in the respiratory movements, an asymmetrical form of movement
is not uncommon in pulmonary or pleural disease. One side may be
either pathologically expanded or pathologically contracted.
i. Pathological Expansion of One Half of the Thorax
This may be due to the presence of air, or of fluid, in one pleural
cavity (pneumothorax, pleuritic effusions).
A similar expansion may, in rare cases, be due to tumors within the
thorax or in the upper abdomen (e. g., in the liver). In pneumothorax,
where the pleural cavity is dilated with air under pressure, there is an
accompanying obliteration of the intercostal spaces, and marked displace-
ment of the heart.
When one side of the thorax is pathologically expanded, the respira-
tory excursions on that side are diminished.
ii. Unilateral Contraction of the Thorax
This is more common than one-sided expansion, and is most often due
to retraction of the lung (in cirrhosis pulmonum, in pulmonary tubercu-
losis, or after pneumonia), or to pleural disease (incomplete expansion of
lung after absorption of pleuritic exudate, pleural adhesions).
In unilateral contraction of the thorax, the anterior chest wall on the
contracted side looks flattened, and its movements lag behind those of the
other side on inspiration ; the intercostal spaces are deeper than normal.
The unilateral contractions, due to chronic pulmonary tuberculosis,
most often affect the upper parts of the lung, beginning with apical retrac-
tion ; they are characterized by deepening of the supra- and infraclavicular
fossae, by flattening of the upper thorax on one side, and by an increase of
the area of the heart in contact with the chest wall with more diffuse pulsa-
tion and with an apex beat displaced upward and lateralward. Ketraction
of the lower part of the thorax, on one side, with corresponding displace-
ment of the apex beat, is most often due either to interstitial pneumonia
or to chronic pleuritis.
482 DISEASES OF THE EESPIRATOEY APPARATUS
References
Bien (G.). Zur Anatomic und Aetiologie der Trichterbrust. Beitr. z. pathol. Anat. u. z. allg.
PathoL, Jena, 1912, Hi, 567-576.
Ebstein (W.). Ueber die angeborene und crworbene Trichterbrust. Volkmann's Samml.
klin. Vortr., Leipzig, 1909, Nos. 541-542.
Freund (W. A.}. Ueber primdre Thoraxanomalien, speziell iiber die starre Dilatation des
Thorax als Ursache eines Lungenemphysems. Berlin, 1906, S. Karger.
28 p. 8°.
Henderson (M. S.}. Cervical rib; a report of thirty-ons cases. Am. J. Orthop., Surg.,
Philadelphia, 1914, xii, 408-430.
Hofbauer (L.). Die Jdinische Bedeutung der Thoraxsenkung. Wien. klin. Wchnschr.,
1913, xxvi, 2127-2128.
Jones (F. W.). The anatomy of cervical ribs. Proc. Roy. Soc. Med., London, 1913, vi,
Clin. Sect., 95-113.
Keen (W. W.). The symptomatology, diagnosis and surgical treatment of cervical ribs. Am.
J. M. Sc., Philadelphia & New York, 1907, n. s., cxxxiii, 173-218.
Mendel (K.). Ueber Halsrippen. N enrol. Zenlralbl., Leipzig, 1913, xxxii, 556-559.
Murphy (J. B.). A case of cervical rib with symptoms resembling subclavian aneurism.
Ann. Surg., Philadelphia, 1905, xli, 399-406. 4 pi.
Sawyer (Sir /.)• A clinical lecture introductory to the use of inspection in diseases of the
lungs and pleurae. Brit. M. J., London, 1901, ii, 7.
2. Inspection of the Respiratory Movements
The lungs, during respiration, make no active movements of their
own, but simply follow, passively, the movements of the wall of the thorax
and of the diaphragm. Two main types of inspiratory expansion of the
thorax are seen. In the costo-abdominal type, the expansion is due chiefly
to the descent of the diaphragm, and less to the elevation of the ribs by the
Mm. scaleni, Mm. levatores costarum and Mm. intercostales (masculine
type of breathing). In the costal type, the opposite is the case, the ex-
pansion being due chiefly to elevation of the ribs (feminine type of breath-
ing.)
The diminution in size of the thorax during expiration depends
normally upon the elasticity of the lungs and ribs, not upon muscular
contraction.
The times occupied by inspiration and expiration, respectively, are
approximately equal, and there is no pause between the two.
References
Beriel (L.) & Durand (P.). Sur les paralysies respiratoires. Lyon med., 1913, cxxi,
786; 846; 885.
Hoover (C. F.). Disturbances of respiration due to nuclear and infranuclear disease. J.
Am. M. Ass., Chicago, 1911f Mi, 1733-1736.
Sutherland (G. A.). Graphic records of respiratory paralysis. Lancet, London, 1913,
dxxxv, 7k.
EXAMINATION OF THE LUNGS AND PLEUKAE 483
(a) The Diaphragm Phenomenon (Litten's Sign)
In emaciated adults, the respiratory movements of the lower margin
of the lung can sometimes be observed as a furrow, descending during
inspiration over the intercostal spaces, especially in the lower right thorax
(Litten's sign). This is due to the separation of the diaphragm from the
thoracic wall when it contracts; before the lung can follow it, the atmos-
pheric pressure causes a depression of the soft parts. In children,
Harrisons groove arises from the same cause, and corresponds to the
middle position of the diaphragm.
To observe Litten's sign, the patient is best examined in a room that
receives light from only one window, the other windows being darkened.
The patient lies with his feet toward the window, the examiner standing
three or four steps to one side, at an angle of about forty-five degrees, his
back toward the window; the lower part of the thorax, between the
axillary and the mammillary lines, is then closely watched. When the
movement is visible,- linear shadows, interrupted by the ribs, travel down
and up during inspiration and expiration respectively ; they are easily
visible at the level of the sixth or of the seventh rib. These shadows travel
over two or three intercostal spaces.
Litten's sign disappears in inflammatory diseases of the lung and
pleura, to reappear in convalescence ; it may also be absent when the descent
of the lung is prevented by pleural adhesions.
References
Bartius (F.). Das Zwerchfellphdnomen. Wien. med. Wchnschr., 1895, xlv, 417-419.
Dexter (/£.)• Certain physical signs referable to the diaphragm and their importance in
diagnosis. Am. J. M. Sc., Philadelphia, 1915, cl, 200-209.
Eppinger (#.)• Allgemeine und spezielle Pathologic des Zwerchfells. Wien u. Leipzig,
1911 , A. Holder. 276 p., roy. 8°.
Gwyn (N. B.). The diaphragm phenomenon — the so-called Litten's sign. Johns Hopkins
Hosp. Bull, Baltimore, 1898, ix, 35-38.
Hoover (C. F.). The functions of the diaphragm and their diagnostic significance. Trans.
Ass. Am. Physicians, Philadelphia, 1913, xxviii, 16-29.
Kure (K.)f Hiramatsu (T.) & Naito (#.). Zwerchfelltonus und Nervi splanchnici.
Ztschr. f. exper. Path. u. Therap., Berlin, 1914, xvi, 395-425. 2 pi.
Litten (M.). Ueber die Normaliter bei jeder Respiration am Thorax sichtbaren Zwerchfells-
bewegungen. Deutsche med. Wchnschr., Leipzig & Berlin, 1892, xviii,
273-275.
Also, transL: Province med., Lyon, 1895, ix, 278-281.
Das Zwerchfellphdnomen und seine Bedeutung fur die klinische Medicin.
Wien. klin. Wchnschr., 1895, viii, 79-81.
Also, transl: Med. Rec., New York, 1895, xlviii, 901.
(6) Frequency and Rhythm of the Respirations
The number of breaths taken by healthy adults varies between 16 and
¥5 per minute ; in the new-born, it averages 44 per minute. The normal
relation between respiration rate and pulse rate is as 1 :3 J, or as 1 :4.
484 DISEASES OF THE KESPIKATOKY APPARATUS
The rate in disease may be increased or decreased.
Increase of the frequency of respiration (tachypnea) is met with (1) in
most diseases of the respiratory system (pneumonia, pleurisy, pulmonary
tuberculosis, emphysema, pneumothorax) ; (2) in many diseases of the
heart; and (3) in those diseases of the abdomen that hinder the move-
ments of the diaphragm (ascites, abdominal tumors, peritonitis). In
tachypnea, the number of respirations may reach 40, 60, or more, per
minute, and the relation between respiration rate and pulse frequency
changes from 1 : 4 to 1 : 2. In certain diseases of the nervous system
(vagal attacks, hysteria), excessive tachypnea (60 to 80 respirations per
minute) may occur in paroxysms.
Slowing of the respiration (bradypnea) may be met with (1) in affec-
tions of the brain or of its membranes (increased intracranial pressure);
(2) in irritations of the respiratory center in the medulla; (3) in severe
infections; (4) in uremia; and (5) in the death agony. A special form of
pathological bradypnea is met with in diabetic coma, where the respirations
though slow are loud and deep (large breathing, or air hunger of Kuss-
maul).
References
Douglas (C. G.). Die Regulation der Atmung beim Menschen. In: Ergebn. d. Physiol.
(Asher & Spiro), Wiesbaden, 1914, xiv, 838-430.
Schenck (F.). Innervation der Atmung. In: Ergebn. d. Physiol. (Asher & Spiro), Wies-
baden, 1908, vii, 65-98.
i. Cheyne-Stokes Breathing
In this form of respiration, periods of complete cessation of the re-
spiratory movements (apnea) alternate with periods in which the respira-
tions slowly increase in frequency and volume to a maximum, and then
again decrease until they cease. During the apneic phase, the patients
are sleepy, and the pupils are contracted and non-reactive ; as the respir-
atory movements return, the psyche awakens, and the pupils dilate and
again become responsive. The phenomenon is met with, most often, (1)
in cardiorenal cases (uremia, decompensation) ; (2) in extensive arterio-
sclerosis, especially wrhen the cerebral vessels are involved; and (3) in
severe lesions of the brain (apoplexy, embolism, brain tumor, cerebral
abscess).
The behavior of the blood pressure in Cheyne-Stokes breathing is
interesting. (See Harvey Gushing' s article.)
A slight periodicity to the breathing, somewhat resembling Cheyne-
Stokes rhythm, may be met with in health during sleep ; in feeble children
and in old age, the resemblance may be very close.
In meningitis the so-called meningitic breathing, or Biot's breathing,
is sometimes observable and is of grave omen. The respiratory pauses
EXAMINATION OF THE LUNGS AND PLEUEAE 485
are very long (5-30 seconds or more), in periods which may recur more
or less regularly or wholly irregularly.
References
Barbour (H. G.). Two types of periodic respiration due to morphin. J. PharmacoL &
Exper. Therap., Baltimore, 1914, v, 393-424.
Eyster (J. A. E.). Clinical and experimental observations upon Cheyne-Stokes respiration.
J. Exper. Med., Lancaster, Pa., 1906, viii, 565-613.
Blood-pressure changes in Cheyne-Stokes respiration. Johns Hopkins
Hosp. Bull., Baltimore, 1906, xvii, 296-299.
Gibson (G. A.). An examination of the phenomena in Cheyne-Stokes respiration. Edin.
M. J., 1888-89, xxxiv, 585; 681; 801; 887; 1020; 1105; 1890-91, xxxvi,
910-922; 1891-92, xxxvii, 635; 928; 1116.
Githens (T. S.) & Meltzer (S. /.). Apnea as an after-effect of pulmonary distension and
its dependence upon the vagus nerves. Am. J. Physiol., Baltimore, 1914-
15, xxxvi, 363.
Goodhart (J. F.). A clinical lecture on the Cheyne-Stokes respiration. Clin. J., London,
1892-93, i, 285-289.
Milroy (T. H.). The apnatic pause. Quart. J. Exper. Physiol., Lond., 1913, vi, 373-391.
Sherrington (C. S.}. Note on Cheyne-Stokes breathing in the frog. J. Physiol., Cambridge,
1891, xii, 292-298. 1 pi.
Traube (L.). Zur Theorie des Cheyne-Stokesschen Atmungsphdnomens. Berl. klin.
Wchnschr., 1874, xi, 185; 209.
White (W. H.), Ryffel (J. H.), Poulton (E. P.), Johnson (W.) & Chisholm (R. A.).
Study of a case of very prolonged Cheyne-Stokes breathing. Quart. J. M .,
Oxford, 1914, vii, 389-402. 2 pi.
ii. Dyspnea
Healthy persons, while at rest, breathe quietly and easily. Any
condition, however, that increases the carbon dioxid content of the
blood leads to acceleration and deepening of the respirations. This is
seen normally on exercise, and in disease either of the lungs or of the
circulatory apparatus it may become very marked, causing shortness of
breath (dyspnea). According to the phase of the respiratory process in
which the difficulty of breathing appears, we distinguish an inspiratory
type, an expiratory type, and a mixed type of dyspnea.
In the inspiratory type, the ordinary muscles of inspiration (dia-
phragm, external intercostals, scaleni) undergo exaggerated contraction,
and, in addition, three other auxiliary groups of inspiratory muscles are
called into play : ( 1 ) those expanding the thorax by lifting the ribs ( M. ser-
ratus posterior superior and M. sternocleidomastoideus) ; (2) those reliev-
ing the thorax of the weight of the upper extremities (M. trapezius, M. leva-
tor anguli scapulae, M. rhomboideus major and minor) ; and (3) those that
help to expand the thorax when the shoulder girdle is fixed by the activity
of the preceding groups (M. serratus anterior major, M. pectoralis major,
M. pectoralis minor). When all three groups are active, the patient sits
up in bed, with his head, arms and thorax held rigid, panting for breath ;
486 DISEASES OF THE KESPIRATOKY APPARATUS
the condition is known as orthopnea. In marked dyspnea, the extensors of
the spine, the muscles that dilate the nostrils, and those that open the
mouth and larynx are also active. In the highest grades of inspiratory
dyspnea, one can observe an inspiratory retraction over the xiphoid carti-
lage and over the lower ribs, especially when the dyspnea is due (1) to
stenosis of the larynx, trachea or bronchi, (2) to a diffuse capillary
bronchitis, or (3) to an extensive pneumonia.
In the expiratory type of dyspnea, it is the contraction of the thorax
that is faulty, and the duration of expiration becomes longer than that
of inspiration. Instead of the normal contraction, due to elasticity, certain
expiratory muscles become active, especially the abdominal muscles and
the M. quadratus lumborum. Bronchospasm is often an important fac-
tor in the origin of an expiratory dyspnea.
Expiratory dyspnea is met with especially in pulmonary emphysema,
where it is permanent, and in bronchial asthma, where it is paroxysmal.
The term asthma is used to designate paroxysmal dyspnea. One dis-
tinguishes nervous or bronchial asthma (asthma bronchiale) from the
paroxysms of dyspnea that occur in cardiac disease (asthma cardiale),
usually due to temporary paralysis of the left heart, and those in renal
disease (asthma uremicum), which are toxic in origin, not to be confused
with the cardiac asthma due to myocardial insufficiency that may ac-
company the nephropathy.
Mixed dyspnea, in which both inspiration and expiration are more dif-
ficult than normal, is met with in most affections of the lungs and pleurae
that diminish the respiratory surface or limit the respiratory movements.
Mixed dyspnea is also met with in circulatory diseases. Here, the di-
minished velocity of the blood in the pulmonary vessels leads to disturb-
ance of gas exchange; and this is further complicated by the structural
and functional changes in the alveolar epithelium in chronic passive con-
gestion.
Recent studies on dyspnea show a close relation of the stimulation of the respir-
atory center to acidosis. One of the best methods of determining the degree of
an acidosis is to measure the carbon dioxid tension in alveolar air (Forges, Leim-
dorfer and Markovci). A decreased alkalinity of the blood such as is met with in
acidosis is accompanied by a corresponding decrease of the carbon dioxid tension
in the blood, and this is associated with a decreased carbon dioxid tension in the
alveolar air.
The alveolar air can be obtained for examination by the method of Haldane and
Priestley, or by the simplified methods of Boothby and Peabody, of Plesch and
Higgins, or of Roth, the air collected being analyzed in the laboratory by means
of Haldane's small type of air analysis apparatus.
Less exact analyses, but probably sufficient for clinical purposes, can be made
by the very simple method described by Fridericia.
Since Hasselbach showed that an increase in the irritability of the respiratory
centers will induce a lowering of the carbon dioxid tension, such studies have be-
come of still greater clinical interest.
EXAMINATION OF THE LUNGS AND PLEUEAE 487
References
Beckmann (K.~). Alveolargasanalyses. II. Ueber Aenderungen in der Atmungsregulation
durch psychische und pharmakologische Einfliisse. Deutsches Arch. f. klin.
Med., Leipzig, 1915, cxvii, 419-437.
du Bois-Reymond (#.). Mechanik der Atmung. Ergebn. d. PhysioL, Wiesbaden, 1902.
i, Abt. ii, 377-402.
Bohr (C.). Die funktionellen Aenderungen in der Mittellage und Vitalkapazitat derLungen.
Deutsches Arch. f. klin. Med., Leipzig, 1906-07, Ixxxviii, 385-434.
Boothby (W. M.} & Peabody (F. W.). A comparison of methods of obtaining alveolar
air. Arch. Int. Med., Chicago, 1914, xiii, 497-506.
Campbell (J. M. H.}, Douglas (C. G.), Haldane (J. 5.) & Hobson (F. G.). The re-
sponse of the respiratory centre to carbonic acid, oxygen and hydrogen ion
concentration. J. PhysioL, Cambridge, 1913, xlvi, 301-318.
Dixon (W. E.) & Ransom (F.). The effect on the respiration of altered vascular conditions
in the lungs. J. Pharmacol. & Exper. Therap., Baltimore. 1913-14, v.
539-547.
Evans (C. L.) & Starling (E. H.). The part played by the lungs in the oxidative processes
of the body. J. PhysioL, Cambridge, 1913, xlvi, 413-434.
Fitzgerald (M. P.). The alveolar carbonic acid pressure in diseases of the blood and in
diseases of the respiratory and circulatory systems. J. Path. & Bacteriol.,
Cambridge, 1910, xiv, 328-343.
Fridericia (L. S.}. Eine klinische Methode zur Bestimmung der Kohlensdurespannung in
der Lungenluft. Berl. klin. Wchnschr., 1914, li, 1268-1271.
Grey (E. G.) & Hirschfelder (A. /).)• A clinical investigation of the carbonic acid in the
alveolar air. Arch. Int. Med., Chicago, 1913, xi, 551-563.
Hahn (M.) & Heim (R.). Die Bestimmung der Kohlensdurespannung in der Alveolarluft
mittelst des Interferometers. Berl. klin. Wchnschr., 1913, I, 197-200.
Haldane (J. S.) & Priestley (J. G*). The regulation of the lung-ventilation. J. PhysioL,
London, 1905, xxxii, 224-266.
Hasselbach (K. A.}. Neutralitdtsregulation und Reizbarkeit des Atemzentrums in ihren
Wirkungen auf die Kohlensdurespannung des Blutes. Biochem. Ztschr.,
Berlin, 1912, 403-439.
Hasselbach (K. A.) & Lindhard (/.)• Bur experimentellen Physiologic des Hohenklimas.
III. Biochem. Ztschr., Berlin, 1915, Ixviii, 295-310.
Henderson (L. J.)» The theory of neutrality regulation in the animal organism. Am. J.
PhysioL, Boston, 1908, xxi, 427.
Henderson (F.)» The time that the breath can be held as an index for acidosis. J. Am. M.
Ass., Chicago, 1914, Ixiii, 318.
Henderson (Y.} & Russell (Z>. G.)« A simple method for determining the carbon dioxide
content of the alveolar air by means of baryta. Am. J. Physiol., Boston,
1911-12, xxix, 436-440.
Higgins (H. L.). The influence of food, posture and other factors on the alveolar carbon
dioxide tension in man. Am. J. PhysioL, Boston, 1914, xxxiv, 114-126.
Higgins (H. L.) & Means (J. H.}. The effect of certain drugs on the respiration and gaseous
metabolism in normal human subjects. J. Pharmacol. & Exper. Therap.,
Baltimore, 1915-16, vii, 1-30.
Higley (G. O.)« Some notes on the form of the curve of carbon-dioxide excretion resulting
from muscular work following forced breathing. Biochem. Bull., New
York, 1913, ii, 390-392.
Hofbauer (L.). Semiologie und Differentialdiagnostik der verschiedenen Kurzatmigkeit auf
Grund der Atemkurve. Jena, 1904, G. Fischer. 156 p. 8°.
Hoover (C. F.) & Gammon (J. E.). The dead space in moderate and large respiratory
ventilation. Arch. Int. Med., Chicago, 1915, xv, 501-513.
488 DISEASES OF THE RESPIRATORY APPARATUS
Krogh (Marie). The diffusion of gases through the lungs of man. J. PhysioL, London,
1915, xlix, 271-300.
Lewis (T.) & Barcroft (/.)• Notes of further observations upon dyspnea and its relation
to blood reaction. Quart. J. Med., Oxford, 1915, viii, 97-118.
Loewy (A.). DieGase des Korpers und der Gaswechsel. In: Handb. d.Biochemie (Oppen-
heimer), Jena, 1908, iv, 1.
Milroy (T. H.). Changes in the hydrogen ion concentration of the blood produced by pul-
monary ventilation. Quart. J. Exper. PhysioL, London, 1914, viii. 141-
153.
Minkowski (O.) & Bittorf (A.}. Die Pathologic der Atmung. In: Krehl (L.) u. Mar-
chand (F.}, Handbuch der allgemeinen Pathologie, Leipzig, 1912, S.
Hirzel, ii, L Abt., i, 446-622.
Peabody (F. W.). Clinical studies on the respiration, No. 1. The effect of carbon dioxid
in the inspired air on patients with cardiac disease. Arch. Int. M., Chi-
cago, 1915, xvi, 846-864
Plesch (/.). Die pathologische Physiologic des Lungenvolumens und seine Beziehung zum
Kreislauf. Ztschr. J. exper. Pathol. u. Therap., Berlin, 1913, xiii, 165-245.
Porges ((>.)• Ueber die Beziehungen der Kohlensaurespannung des Blutes zur Lungenven-
tilation. Nach Versuchen von A. L. Sample (Baltimore) mitgeteilt. Bio-
chem. Ztschr., Berlin, 1913, liv, 182-188.
Porges (O.)> Leimdorfer (A.) & Markovici (E.). Ueber die Kohlensaurespannung des
Blutes in pathologischen Zustdnden. Mitteilg. 2: Ueber die Kohlen-
saurespannung des Blutes in der kardialen und pulmonalen Dyspnde.
Ztschr. f. klin. Med., 1913, Ixxvii, 446-463.
Ueber die Kohlensaurespannung des Blutes in pathologischen Zustdnden.
Ztschr. f. klin. Med., Berlin, 1911, Ixxiii, 389-427.
Roth (P.). The estimation of carbon dioxid tension in alveolar air. J. Am. M. Ass.,
Chicago, 1915, Ixv, 413-418.
Rover. Ueber Atmung des gesunden und saurevergiftelen Menschen. Ztschr. f klin. Med.,
Berlin, 1913, Ixxvii, 228-267.
Scott & Wilson (H.). A method for estimating acetone in animal liquids. J. PhysioL,
London, 1911, xlii, 444-470.
Siebeck (/?.)• Ueber die Beeinflussung der Atmenmcchanik durch krankhafte Zustdnde des
Respirations- und Kreislaufapparat s. Deutsch. Arch. f. klin. Med.,
Leipzig, 1910, c, 204-220.
Sjoblom (J. Ch.). Experimentelle Untersuchungen uber den Einfluss einiger zentripetaler
N erven auf die Atmung. Leipzig, 1914, Veil & Co. 114 p. 8°.
Straub (//.)• Alveolargasanalysen. I. Ueber Schwankungen in der Tdtigkeit des Atem-
zentrums, speziell im Schlafe. Deutsches Arch. f. klin. Med., Leipzig,
1915, cxvii, 397-418.
Venza (A.). Respiratorische Neurosen traumatischen Ursprungs und deren Simulation.
Ztschr. f. d. ges. Neurol. u. Psychiat., Berlin u. Leipzig, 1914, xxiv, Orig.,
692-616.
Vernon (H. M.). The biochemistry of respiration. Science Progr. 20th Cent., London,
1914-15, ix, 251-269.
3. Determination of the Volume of the Inspired and
of the Expired Air (Spirometry)
The measurement of the air entering and leaving the lungs in each
phase of respiration can be made by means of a spirometer.
The apparatus originally used was that of Hutchinson (1846) ; a better instru-
ment is that devised by Tissot (1904). More recently, Pleseh's modification of
EXAMINATION OF THE LUNGS AND PLEUKAE 489
the apparatus of Bohr has come into use. For the determination of the residual
air, either pneumotometric methods (Hartesz, Gad, Pflliger) or gas-mixture meth-
ods (Davy, Allen and Pepys, Durig, Plesch) can be used. As these methods are
applied only in research work, it does not seem desirable to give the details of
the technic in this treatise.
Certain terms in connection with spirometry should be understood. By
vital capacity is meant the amount of air that, after the deepest possible
inspiration, can be expelled on full expiration; it averages in healthy
men 3,600 c.c., varying from 3,000-4,000 c.c. ; in women it averages
2,500 c.c., varying between 2,000-3,000 c.c. The value depends upon the
height of the body, each centimeter of height in the adult corresponding
to 22 c.c. of expiratory air. This vital capacity is smaller in childhood
and in old age, as well as in all diseases of the respiratory system. The
stomach should be empty when the test is made.
By complementary air is meant the amount that, after a quiet in-
spiration of normal depth, can be taken in by the most forcible inspiration.
It amounts to about 1,500 c.c. By reserve air is meant the amount
that, after the normal quiet expiration, can still be expelled by extremely
forcible expiration (1,500 c.c.). By respiratory breathing air is meant
the amount that is taken in, and given out, on quiet respiration (500
c.c,). By residual air is meant the amount that remains in the lung,
after the deepest possible expiration (800 to 1,600 c.c.).
The sum of the complementary air, the reserve air and the breathing
air, therefore, corresponds to the vital capacity, which is measured by
the spirometer ; the total lung capacity is this sum plus the residual air ;
the mean capacity is the sum of the residual and the reserve air. The
amount of air taken in during a minute on quiet respiration varies from
5-7 liters.
The vital capacity of the lungs enlarges on bodily exercise and in
pathological states accompanied by dyspnea ; the latter is a compensatory
process, the temporary pulmonary emphysema (a sort of physiological
reflex [Bohr] ) favoring an easier and quicker circulation of the blood
through the pulmonary blood vessels.
It looks now as though studies of vital capacity may turn out to be
of distinct value in clinical diagnosis (F. W. Peabody).
References
Bohr (C.) . Die funktionellen Aenderungen in der Mittellage und Vitalkapazitat dcr Lungen.
Deutsches Arch. f. klin. Med., Leipzig, 1906-07 , Ixxxviii, 880-484.
Campbell (J. M. #.), Douglas (C. G.) & Hobson (F. G.). The sensitiveness of the re-
spiratory center to carbonic acid and the dead space during hyperpncea.
J. Physiol., London, 1914, xlviii, 302-316.
Haldane (J. S.). The variations in the effective dead space in breathing. Am. J. Physiol.,
Baltimore, 1915, xxxviii, 20-%8.
490 DISEASES OF THE EESPIEATOKY APPARATUS
Henderson (T.). A quantitative respirometer. J. PhysioL, London, 1915, xlix, p. xxiv.
Henderson ( Y.), Chillingworth (F. P.) & Whitney (J. L.). The respiratory dead space.
Am. J. PhysioL, Baltimore, 1915, xxxviii, 1-19.
Rubow (V.). Untersuchungen liber die Atmung bei Herzkrankheiten. Ein Beitrag zum
Studium der Pathologie des kleinen Kreislaufes. Deutsches Arch. f. klin.
Med., Leipzig, 1908, xcii, 255-281.
Twort (J. F.) & Hill (L.). The effect of the depth of pulmonary ventilation on the oxygen
in the venous blood of man. Proc. Roy. Soc., London, 1915, s. B, lxxxviiit
548-553.
4. Thoracography or Pneumojjraphy
The alterations in the circumference of the whole thorax or of one half of it
can be registered in the form of respiratory curves, so that changes in the fre-
quency, rhythm, extent and course of the respiration can be more exactly studied.
A very good instrument for clinical work is that of Marey. Various modifications
(Brondgeest, Ochnike, Knoll) are in use.
Still more exact instruments are used in research work (Stethometer of Gibson,
Recording Stethometer of Burdon-Sanderson, Thorakographs of Pick, Levy-Dohrn,
and P. Bert). Such instruments and the technic of using them are described in
F. Schenck's article in Tigerstedt's Hdb. d. physiol. Technik, Leipzig, 1911, II.
A normal pneumogram is shown in Fig. 144. Expiration is perhaps
a trifle longer than inspiration and there is a very brief pause between.
r\ \
A A
UkMVJi
Fig. 144. — Normal Pneumographic Tracing or Pneumogram. The Curve Shows Transmitted
Vascular Pulsations. Inspiration 0.8 Sec. ; Inspiratory Pause 0.3 Sec. ; Expiration 0.9
Sec. ; Expiratory Pause 1.3 Sec. (Med. Service, J. H. H.)
In normal breathing, inspiration proceeds quickly and evenly as a result of
contraction of the muscles of inspiration. The ascending limb of the pneumographic
curve therefore shows an even inspiratory course. When expiration begins, the
curve descends quickly at first, but a little more slowly toward the end before the
expiratory pause is reached. The form, extent and frequency of the respirations
of the normal man while awake are tolerably constant, but in pathological state*
EXAMINATION OF THE LUNGS AND PLEUBAE 491
any one of these features may be altered. Thus, in orthopnea, the conditions are
such that the inspiration may still be easy, though expiration is difficult, owing to
depression of the normal elastic forces of respiration. On sitting up, the dia-
phragm is displaced some distance caudalward; this separation of the diaphragm
from the center of the thorax causes a stronger tension of the lungs and thus
facilitates expiration. Furthermore, the muscles of the abdominal wall can aid
more in expiration when the patient is sitting up.
The general disturbances of the form of respiration have been carefully de-
scribed by L. Hofbauer. These nmy involve changes in inspiration, in expiration,
or in the expiratory pause.
Inspiration may be prolonged in diseases of the air passages (tracheal stenosis,
croup, edema glottidis, whooping-cough, bronchostenosis) . Prolongation is also
Fig. 145. — Pneumogram in Pneumonia. Inspiration 0.4 Sec. ; Expiration 0.6 Sec. ; Pause 0.4
Sec. (Med. Service, J. H. H.)
met with in diseases of the lungs (croupous pneumonia, lung abscess, lung gan-
grene, pulmonary tuberculosis), in the cardiac asthma of heart disease, in uremia
and in diabetic coma.
Inspiration may be shortened in the air hunger of uremia, though it is length-
ened in the air hunger of diabetic coma.
Flattening of inspiration is always associated with prolongation of inspiration,
and deepening of the inspiration is met with in all cases of air hunger (both
uremic and diabetic).
Expiration is prolonged in tracheal obstruction from foreign bodies, in polypi
beneath the glottis, in bronchial asthma, in cardiac asthma, in mediastinal tumor,
in pericarditis, and in many cases of chronic circulatory insufficiency. The same is
true in pleuritis and in most diseases of the lung.
Expiration is shortened in uremia during the stage of air hunger; a shortening
of expiration has also been observed in cardiac decompensation and in the asthma
of Graves' disease.
The so-called "active expiration" due to muscular contraction (in addition to the
normal expiration due to elastic forces) is accompanied by prolonged expiration;
it is met with in bronchial asthma, in pleurisy, in pneumonia, in pneumothorax,
and in tumors of the mediastinum and of the pleura. A similar active expiration
492 DISEASES OF THE BESPIEATOEY APPAKATUS
* >
Fig. 146. — Pneumogram In Emphysema with Bronchiectasis. Inspiration 0.6 Sec. ; Inspira-
tory Tause 0.3 Sec. ; Expiration 1.1 Sec. ; Expiratory Pause 0.8 Sec. (Mod. Service,
J. H. H.)
has been observed in cerebral diseases and in nephritis. One can sometimes recog-
nize active expiration in the pneumographic curve by the disappearance of the
terminal flattening of the curve ; in other cases, it is manifested by the intercalation
of a steep portion in the expiratory curve (normally parabolic).
The expiratory pause is prolonged in the air hunger of uremia, in the asthma
of Graves' disease, and in certain focal diseases of the brain (especially in tumor
or abscess of the cerebellum, and in cerebral hemorrhage).
The expiratory pause is shortened in all cases of tachypnea, as in the ordinary
asthma of Graves' disease and in hysterical tachypnea; it is also shortened in all
•vTAT-NTV
Fig. 147. — Pneumogram in Chronic Circulatory Insufficiency (Cardiac Asthma). Inspira-
tion 0.8 Sec. ; Inspiratory Pause 0.2 Sec. ; Expiration 1.4 Sec. ; Expiratory Pause 0,8
Sec, (Med. Service, J. H, H.)
EXAMINATION OF THE LUNGS AND PLEURAE 493
Fig. 148. — Pneumogram from Patient with Ascites. Inspiration 0.8 Sec. ; Inspiratory Pause
0.4 Sec.; Expiration 0.4 Sec.; Expiratory Pause 0.8 Sec. (Med. Service, J. H. H.)
cases in which the individual respirations are prolonged (pneumonia, pleurisy, pneu-
mothorax ) .
For full descriptions of other disturbances of the pneumographic curve and for
the changes met with in individual diseases, the excellent article by Hofbauer may
be consulted.
Fig. 149. — Pneumogram Illustrating Paradoxical Breathing In a Patient Suffering from
Severe Renal Disease. Compare the Abdominal with the Thoracic Curve. Inspiration
0.8 Sec. ; Expiration 0.6 Sec. ; Expiratory Pause 0.8 Sec. There was "Active Expira-
tion." (Med. Service, J. H. H.)
References
Conner (L. A.) & Stillman (R. G.}. A pneumographic study of respiratory irregularities
in meningitis. Arch. Int. Med., Chicago, 1912, ix, 208-219.
Hofbauer (L.). Storungen der dusseren Atmung. Ergebn. d. inn. Med. u. Kinderk., Berlin,
1909, iv, 1-4*.
494 DISEASES OF THE RESPIRATOKY APPAEATUS
Kellogg (J. H.). Graphic methods of recording diseased conditions of the lungs and a new
form of pneumograph. Sanitarian, New York, 1890, xxv, 505—519.
Knauer (A.) & Maloney (W. J. M. A.). The pneumograph; a new instrument for record-
ing respiratory movements graphically. J. Nerv. & Menl. Dis., New
York, 1914, xli, 567-574.
Ransome (A.}. Stethometry in the prognosis of chest disease. Med.-Chir. Trans., London,
1881, Ixiv, 185-216. 5 pi.
5. Palpation of the Thorax Over the Lungs and
the Pleurae
A most important part of the palpation of the thorax is the testing of
the vocal fremitus, the tremor of the voice propagated to the thoracic wall
through the bronchi and pulmonary tissue. The test is made by placing
the two hands on symmetrical portions of the thoracic wall and asking the
patient to repeat in a loud, deep voice ("1, 2, 3," "99"). In health, the
vocal fremitus may be a trifle more marked on the right than on the left
side, owing to the greater diameter of the right bronchus. It is feebler
when the voice is weak and of high pitch (especially in women). If a
patient be asked to sing the scale, the fremitus will be found most marked
at one of the lower notes, a level corresponding to the resonance of the
lung. In women, the tone-level of the voice is usually higher than the
resonance of the lung, so that the latter is not aroused to sympathetic
vibration (F. Miiller).
As a clinical method, palpation of the vocal fremitus has approxi-
mately the same value as auscultation of the respiratory murmur; some-
times it is a more delicate test, especially in deciding whether a dullness
over the lower thorax is due tp* infiltration of the lung or to pleural
effusion ; an increased vocal fremitus indicates better conduction from the
larynx to the lung surface (infiltration), while an enfeeblement or an
abolition of the fremitus suggests pleural effusion or pneumothorax. Cer-
tain exceptions to this rule should, however, be noted. In massive pneu-
monia, with plugging of the bronchus, the propagation of the voice may be
temporarily interfered with ; again, in pleural effusion, there may be less
diminution of the vocal fremitus than might be expected because pleural
adhesions, uniting the lung to the wall of the thorax, may favor the
conduction of the voice-tremor, or an atelectasis, due to the pressure of the
exudate, may increase the vocal fremitus more than the effusion weakens
it CD. Gerhardt).
Reference
Hochhaus (H.). Ueber den Pektoralfremitus. Deutsch. Arch.f. klin. Med., Leipzig, 1911,
ci, 571-585.
EXAMINATION OF THE LUNGS AND PLEUKAE 495
6. Mensuration of the Thorax
By passing a tape around the chest, just above the nipples, the arms
being held out from the sides, we measure the circumference of the chest.
On physical examinations for entrance to the army, navy, etc., this value
is used as a measure of the development of the thorax, and serves as a clew
to the general constitution of the person. In healthy young men, the
circumference should exceed 80 cm.
More important as regards the state of the lungs themselves is the
difference in circumference on deep inspiration and on deep expiration.
Normally, this difference amounts to about 7 cm. (extremes 5-7 cm.).
The sternovertebral diameter, measured by calipers from the manu-
brium to the back, in a horizontal plane, amounts to 16 cm. ; from the
lower end of the corpus sterni to the back, it amounts to 19 cm. The
transverse diameter (diameter costalis), at the level of the nipples,
measures about 26 cm.
The comparison of the circumference of each of the two halves of the
chest shows normally a difference of J-2^ cm., in favor of the right side.
In an asymmetrical thorax, due to unilateral expansion or retraction, exact
measurement is important for the record, though, for the actual recogni-
tion of the asymmetry, experience teaches that slight differences in
circumference of the two halves of the chest can be more easily recognized
by careful judgment with the eye than by mensuration.
Exact records of the form of the thorax can be made with a cyr-
tometer.
7. Percussion Over the Lungs and Pleurae
Percussion. — By percussion, we produce sounds that permit us to
draw conclusions regarding the structure of the organs beneath the part
percussed. The shock given by the percussion stroke gives rise to sounds
that vary with the elasticity (capacity for vibration) of the parts struck;
the greater the elasticity, the more marked is the sound production.
Historical. — The method of percussion was first devised by L. Au-
enbrugger (1761). It became generally known and applied to the study of
the heart through Corvisart (1808). It reached its flower when it was
applied in a most thorough way to the diagnosis of diseases of the lungs by
Laennec (1810). These clinicians all used DIRECT PERCUSSION, produc-
ing sounds by simply tapping the surface of the thorax with the finger tips
of one hand. INDIRECT PERCUSSION was devised by Piorry (1826), a
plessimeter being intercalated between the chest wall and the percussing
fingers; and, later, Wintrich (1841) substituted a percussion hammer for
the percussing fingers.
496 DISEASES OF THE RESPIRATORY APPARATUS
Principles of Percussion. — Airless bodies enter into sound-producing
vibration only when they are rigid, or in a certain state of tension. In
the human body, bones alone correspond to such a state, but even they are
surrounded by soft parts, so that they are not reached by the percussion
V. cava
superior
Aorta
Right
Atrium
Right
Ventricle
Heart
Lung Borders
- Pleural Boundaries ; Incisurae interlobares
... Diaphragm
Liver
Fig. 150. — Topography of the Thoracic and Upper Abdominal Viscera from in Front, a-b —
Boundary of Right Pleural Cavity ; c-d — Boundary of Left Pleural Cavity ; e-x — Edge of
Right Lung; 9-h — Edge of Left Lung; i — Upper Incisura lobularis (Right Lung);
Lower Incisura lobularis (Right Lung) ; 1 — Left Incisura lobularis; m-n — Right; n-o —
Lower ; p-o — Left Border of Heart ; q — Mediastinal Sinus Situated Between the Pleural
Boundaries and the Incisura cardiaca of the Anterior Edge of the Left Lung; r — Highest
Point of the Liver, Overlapped by Lung ; s — Lower Edge of Liver ; t — Pars cardiaca ;
u — Pars pylorica ; v — Lesser Curvature ; w — Greater Curvature of the Stomach.
stroke, or, if reached, transfer their vibrations to adjacent vibrating (be-
cause air-containing) soft parts, and so are less responsible than the latter
for any sounds produced.
The sounds yielded by soft parts when percussed depend upon their
air (or gas) content (Skoda). If the air or gas be contained in large
cavities, it is set into vibration, and along with it the wall of the cavity is
started vibrating to a greater or less degree ; if the air be distributed in
the form of small alveoli throughout the whole tissue, as in the lungs, the
EXAMINATION OF THE LUNGS AND PLEURAE 497
air and the tissue vibrate together on percussion. Obviously, then, per-
cussion ^permits us (1) to find the limits of juxtaposed airless and air-
containing structures, and (2) to form judgments regarding (a) the air
content, and (b) the degree of tension of air-containing organs.
Direct Percussion. — This is but little used nowadays, perhaps less than
it should be. It is valuable for quick orientation (1) regarding the
' Lung Borders
— — Pleural Boundaries ; Incisurae interlobares
_ Liver and Spleen
Kidneys
Fig. 151. — Topography of the Viscera, Viewed from Behind.
comparative state of the two sides of the lower thorax behind, and (2)
regarding the position of large areas of infiltration (pneumonia, tubercu-
losis), or of large pleural effusions.
One arranges the finger tips of the right hand in a plane and, to pro-
duce the sounds, delivers the stroke directly upon the surface of the thorax,
without any intermediary plessimeter.
Indirect Percussion. — In this method, the blow, instead of being
struck directly upon the body surface, is delivered upon some intermediate
body placed upon the part under study. This intermediate body is called
a PLESSIMETER or pleximeter. As a plessimeter, we may use the index, or
the middle finger, called a "plessimeter-finger," or, instead, a platelet
made of rubber, gutta-percha, ivory, glass or metal. To ascertain the'
condition of the structures behind the clavicle, we often use the clavicle
itself as a plessimeter.
498 DISEASES OF THE KESPIEATOKY APPAKATUS
The advantages of a plessimeter lie in the facts that by means of it
(1) the percussion stroke can be made to reach to a greater depth on the one
hand, and (2) it can be applied to a smaller surface area on the other.
Lack of compressibility and the greatest possible elasticity are desiderata
in a plessimeter, since, when an elastic plessimeter is struck, the hammer
or the percussing finger rebounds from it before the underlying parts are
pressed in, and there is less of the actual energy of the percussion stroke
lost, so that the effect of the percussion extends farther into the depth.
Plessimeters of ivory, metal, and glass conform most closely to ideal re-
quirements ; soft rubber is just as elastic, but is more compressible, so that
the effect of the percussion does not extend so deep and the percussion
sound is not so. loud.
The plessimeter finger is most often used, partly because it is always
available, and partly because it permits
us to judge of the FEELING OF RESIST-
ANCE, thus yielding most valuable in-
formation accessory to the percussion
sounds. Moreover, it is possible easily
to approximate it to the surface in re-
gions difficult of access to a rigid ples-
simeter (e. g., intercostal spaces in
front, supraclavicular fossae. On the
other hand, as regards elasticity and
compressibility, the finger is far inferior
to an ivory plessimeter.
As a PERCUSSOR, or PLESSOR, it is
customary in America to use the middle
finger of the right hand, flexed to an
obtuse, or almost a right, angle at the
terminal joint, and slightly flexed at
the proximal joint of the finger. The
stroke is delivered entirely from the
wrist, the forearm remaining in posi-
tion. With practice one soon learns
how best to deliver the stroke, gently
= ?$S!Sr&£S5?; lnc,s«rae .nter.obare, f°r "superficial percussion »
stomach and Kidney more forcibly for "deep per-
Liver and Spleen . * JT JT
cussion." As a rule, the
Fig. 152. — Topography of the Thoracic . ,-> 1111 -n i ,
and upper Abdominal viscera, Viewed percussing finger should be allowed to
from the Left Side. rebound immediately from the plessim-
eter after it has struck, in order that the
plessimeter may freely vibrate with the part beneath. In some instances,
it may be desirable more or less to dampen the vibration by the fingers on
each side of the plessimeter finger, or, again, one may use three fingers
EXAMINATION OF THE LUNGS AND PLEURAE 499
Fig. 153. — Gold-
scheider's Ortho-
percussion. (After
A. D. Hirschfeld-
er, "Diseases of
the Heart and
Aorta," published
by J. B. Lippin-
cott Co., Phila.)
in succession as plessimeter fingers, passing quickly from one to another.
In gentle percussion, the plessimeter finger should lie merely in smooth
contact with the part under study ; for deep percussion,
it may be firmly pressed against this part. Many clini-
cians, especially in Europe, make use of a percussion
hammer, the head of which is covered with hard rubber,
leather, or felt (to avoid the production of a tone de-
pendent upon the hammer and the plessimeter them-
selves, and masking the sound produced by vibration of
the underlying organ).
In ortliopercussion, the force of the blow is directed
exactly perpendicular to the surface. (Figs. 153 and 154.)
The STRENGTH OF THE PERCUSSION STROKE should
vary greatly according to the conditions of the exam-
ination. When the soft parts over the organ under
examination are thick, the stroke must, of course,
be harder to set that organ in vibration; otherwise,
delicate differences in the intensity of the sound
produced are more easily perceived when the sound is not loud. Thus,
in determining the so-called SUPERFICIAL, OR ABSOLUTE DULLNESS of
the heart, or of the junction of an air-containing organ with an air-
less part (lung limits), feeble percussion should be employed. For
this purpose, the NO-SOUND STROKE,
as described by Henry Lee Smith, is
very helpful; the strength of the
stroke is such that no sound at all is
produced (just disappears) over an
airless area. Passing from this to
an air-containing or gas-containing
area with the same strength of stroke,
a percussion sound is immediately
produced as the boundary is passed
(lung limits, edge of liver, etc.).
In the determination of so-called
DEEP OR RELATIVE DULLNESS, however
(as, for example, the lateral margin
of the heart or the upper surface of
the liver covered by lung), it is
necessary to use a somewhat stronger
stroke, though even here one does
best to use percussion of medium force rather than the very strong per-
cussion so often employed. Goldscheider has shown that the no-sound
stroke can also be used for determining the location of the boundaries
of deep dullness (so-called threshold-value percussion).
Fig. 154. — Percussion with the Ortho-
plessimeter. (A) J. O. Hirsch-
felder's Orthoplessimeter and Its
Mode of Application. (B) Supposed
Line of Transmission of the Percus-
sion Impulse from the Orthoples-
simeter. Res, Resonant Percussion
Note. (After A. D. Hirschfelder,
"Diseases of Heart and Aorta," pub-
lished by J. B. Lippincott Co., Phila.)
500 DISEASES OF THE RESPIRATORY APPARATUS
References
Cabot (Richard Clarke}. Physical diagnosis. 5th ed. New York, 1912, W. Wood &
Co. 540 p. 5 pi, roy. 8°.
Essentials and non-essentials in physical diagnosis. Wisconsin M. J.t
Milwaukee, 1911-12, x, 183-201.
Flint (A.). Prize essay. On variations of pitch in percussion and respiratory sounds, and
their application to physical diagnosis. Buffalo, 1852, Jewett, Thomas &
Co. 47pp. 8°.
Futcher (Thomas Barnes). Outlines of physical diagnosis of the circulatory and respira-
tory systems. Prepared from his lectures by J. G. Murray, Jr., Baltimore,
1915, The Students' Book Store. 175 p.
Gee (Samuel /.)• Auscultation and percussion, together with the other methods of physical
examination of the chest. 5th ed. London, 1907, H. Frowde. 325 p.
12°.
Geigel (R.). Die Sldrke des Perkussionsschlages. Munchen. med. Wchnschr., 1907, liv,
459-460.
Goldscheider (A.}. Untersuchungen liber Perkussion. Deutsches Arch. f. klin. Med.,
Leipzig, 1908, xciv, 480-528.
Huntress (L.), Jr. The pitch of the percussion sound. Med. Communicat. Mass. M. Soc.,
Boston, 1882-86, xiii, 805-317.
May (R.) & Lindemann (L.). Graphische Darstellung des Perkussionsschalles. Munchen.
med. Wchnschr., 1906, liii, 810.
Muller (F.). Principles of percussion and auscultation. Lancet, London, 1913, 61J+-675.
Piorry (P. A.). De la percussion mediate el des signes obtenus a I' aide de ce nouveau moyen
d" exploration, dans les maladies des organes thoraciques et abdominaux.
Paris, 1828. 33 p. 8°.
Traite de plessimetrisme et d'organographisme. Paris, 1866. 8°.
Plesch (/.)• Ueber ein verbesserles Verfahren der Perkussion. Munchen. med. Wchnschr.,
1902, xlix, 620-621.
Selling (T.) & Edelmann (M.). Experimented Untersuchungen des Perkussionsschalles.
Verhandl. d. Kong.f. innere Med., Wiesbaden, 1906, xxiii, 668-671.
Sewall (H.). Bimanual palpatory percussion, apparently a new method in physical ex-
amination. Arch. Diag., New York, 1912, v, 13-15.
Sieur (C.). De la percussion metallique combinee d V auscultation dans le diagnoslique des
epanchements liquides de la plevre. Bordeaux, 1883. S. 5. 41 P- 4°-
Skoda (./.)• A treatise on auscultation and percussion. Transl. from the 4th ed. by W. O.
Markham. Philadelphia, 1854, Lindsay & Blakiston. xxxiv, 35-380. 8°.
Smith (H. L.). The use of a no-sound stroke in percussing out the boundaries of super-
ficial dulness of airless bodies. J. Am. M. Ass., Chicago, 1914, Ixiii,
320-321.
(a) The Intensity and the Quality of the Sounds Produced
on Percussion
In the percussion of the thorax, as elsewhere, one pays attention to
the following points, regarding the sounds produced :
1. Their loudness (loud or feeble, clear or dull).
2. Their fullness (full or empty, long or short).
3. Their pitch (high pitch or low pitch).
4. Their clang or timbre (tympanitic or non-tympanitic ; clang-rich
or not clang-rich; metallic or non-metallic).
i. The Loudness of the Percussion Sounds
This depends, essentially, upon the amount of air or gas in the organ
examined. Airless parts yield only a feeble sound (dull, or flat, sound;
EXAMINATION OF THE LUNGS AND PLEUKAE 501
"thigh sound"). In general, the sound is louder and "clearer," the
greater the air content of the organ percussed, though the tension of the
walls has some influence upon this (see Tympanitic Sound).
In other words, the terms "clear" and "dull" refer to the intensity of the
sound. Measurements by means of microphone and galvanometer, as well as by
means of the phonograph, have shown that the clear sound, or resonance, of the
normal lung corresponds to waves of decidedly greater amplitude than the dull
sound (F. Miiller). It should be especially noted that the expressions "clear"
and "dull" are used, clinically, in a different sense from that of ordinary speech.
In the latter, by a "clear note," is usually meant a high clang, and by a "dull
sound," a low clang. Clinically, on the contrary, one refers to the loudness of
the sound, that is, to the amplitude of the sound waves that strike the ear drum.
This intensity depends on (1) the capacity for vibration, especially upon the
amount of air in the organ percussed; and (2) the strength of the percussion blow.
In comparative percussion, therefore, one should always use exactly the same
force, and should especially avoid confirming a preconceived opinion by unequal
force of the percussion blows, for unequal force will produce unequal sounds and
dullness may thus be simulated.
ii. The Fullness of the Percussion Sounds
The terms "fullness" and "emptiness" have to do mainly, as experi-
ments with the microphone and the phonograph prove, with the duration
of the sounds, the full sound lasting long, the empty sound being hrief .
Healthy, air-containing lung yields a full sound (0.42 seconds in length) ;
the solid, infiltrated lung yields an empty sound (0.28 seconds) (F.
Miiller). The difference in duration is not great, hut is distinctly per-
ceptible by the ear.
A percussion sound is full (of long duration) when it is rich in low
tones, because these tend to die away more slowly (pulmonary emphysema,
pneumothorax). The term "empty sound" is not precisely equivalent to
"dull (feeble)," though, as a rule, the loud sounds are also full and the
dull sounds are also empty (F. Miiller).
iii. The Pitch of Percussion Sounds
In the physics of sound, as is well known, the pitch of a tone depends
upon the number of vibrations per second. The greater the number of
vibrations, the higher the tone. From the standpoint of pure physics,
percussion sounds are always noises, composed of a large number of indi-
vidual tones. In th»i percussion sounds elicited over the lungs, experi-
ments with large resonators (F. Miiller) have shown that the tone series
present extends from C down as far as F. The upper limit of this series
is unimportant, since it depends, mainly, on the plessor and the plexim-
eter, but the lower limit is of great significance. The percussion sound
over the healthy lung contains lower tones in the adult than in the child ;
the lowest tones are met with over the distended lungs in pulmonary
502 DISEASES OF THE KESPIEATOEY APPAKATUS
emphysema and especially in pneumothorax (even as low as E). When the
apex of the lung is infiltrated (e. g., in tuberculosis), low tones are absent
over it, though they are still present over the other healthy apex, and the
percussion sound is, therefore, said to be of "higher pitch" (better, of
"less low" pitch) on the diseased side.
Of all the tones in a series contained in the sounds elicited on percus-
sion of the lungs, the lowest ones tend to be the loudest, and to die away
most slowly (being also of longer duration). A percussion sound, there-
fore, that contains (1) very low tones is usually also (2) loud ( — clear)
and (3) full ( — long-lasting).
The ear should be carefully exercised in the appreciation of the
lower tones, especially on percussion. When one tone is dominant, as in
tympanitic sounds, the height of its pitch is easily recognizable to one
that has a good tone-pitch sense. The recognition of differences in the
pitch of the dominant tone in tympanitic sounds lies at the basis of the
recognition of the so-called "alterations in pitch," on change of conditions,
of Wintrich, Gerhard t, etc. (vide infra).
Tympanitic sounds are fuller (i. e.] of longer duration) than non-
tympanitic sounds, a fact that sometimes helps us to recognize them.
iv. The Clang-content, or Timbre, of Percussion Sounds
The tympanitic sound resembles a clang and usually permits of the
recognition of the definite pitch of the fundamental, dominant tone in the
clang. A tympanitic percussion sound is met with over large cavities,
containing air or gas (e. g., over the larynx, the trachea, the stomach, and
the intestine). The healthy lung yields a non-tympanitic sound on per-
cussion; in this there is no definite, fundamental, dominant tone. A
single exception must be made ; over the lower part of the left lung, where
we, in reality, percuss over a thin lung-margin, and over the diaphragm,
we may elicit the tympany of the underlying stomach.
A typical tympanitic sound can be experimentally produced by percussion over
a hollow membranous sphere; thus, if one cut out a stomach and blow it up, it
will be found that tympany, on percussion, is most distinct when the walls are under
a certain optimal degree of tension. The tympany will become less distinct when
the tension is of lower, or of higher, grade. If, after the degree of distention cor-
responding to the maximal tympany has been reached, the stomach be gradually
blown up further, and be tested from time to time, one can convince himself, as the
tension of its walls increases, not only that the richness in clang changes, but that
there is also a change in the pitch of the sound; as it becomes poorer, or "harder,"
in clang, the pitch becomes higher; in other words, the percussion sound becomes
(1) higher and (2) emptier. Physicists assert that this change in the character
of the clang, through the tension of the walls, is due to the fact that both .the gas
content and the walls are concerned in the production of the sound. The more
capable of vibration both are, the easier it is for each to adapt its vibration to
that of the other; thus, when the wall is adaptable, the rhythm of the vibrations
depends essentially on the size of the cavity; here the "gas dominates the sound
EXAMINATION OF THE LUNGS AND PLEURAE 503
and hence the tone is of low pitch." But if the wall, through its tension, is made
incapable of performing slow vibrations, it will then hinder the origin of low tones,
even in the gas space; the vibrations of the gas must then adapt themselves to
those of the wall; the "wall becomes the dominator of the sound" (D. Gerhardt).
The explanation of tympanitic and non-tympanitic sounds over the lungs is
somewhat more complicated than for the simple gas of a large hollow space,
such as has just been described. As a matter of fact, the normal lung, in situ,
yields a non-tympanitic sound on percussion, but the lung removed from the body
and percussed yields a tympanitic sound, though it loses the tympanitic clang again
if it be artificially blown up. It has been suggested that the collapsed lung is
comparable, in its vibratory capacity, to a layer of foam. In both cases there
arises, on percussion, a note of such low pitch that it cannot possibly belong to the
proper tone of the small alveoli ; it seems certain that the many small air-containing
alveoli, and the fine fluid- or tissue-membranes separating them from one another,
vibrate as a whole, for the low pitch of the sound increases with the size of the
piece of lung, or of the foam mass, percussed, the sound being lower in pitch than
would correspond to that of a cavity of the same size. The elastic partitions act,
therefore, on the vibrating air mass like ballast, slowing the periodic number.
If now the conditions be changed so that the elastic partitions no longer vibrate
freely like the fine fluid-membranes of a foam-layer, 'an'd are unable to adapt
themselves to the vibrations of the air space, but have become rigid through the
distention of the lung, the capacity of the lung for vibration diminishes. The
tympanitic, low-pitched, fundamental tone then gradually disappears, and there
remain only tones of higher pitch (as in the over-distended stomach) ; the sound
becomes emptier, and is no longer tympanitic.
A tympaniiic sound over the lung, except in Traube's space, points to
an abnormal condition within the thorax: (1) to smooth-walled cavities
(lung cavities, bronchiectatic cavities, abdominal viscera dislocated into
the thorax) ; (2) to a change in the structure of the lung that leads to
loss of Hie tension of the alveolar walls; (a) in atelectasis of the lung,
from bronchial occlusion, or from compression due to high position of the
diaphragm, large pericardia! effusions, or pleural effusions ; (b) in edema
of the lung; (c) in certain stages, of pneumonia when the alveolar septa
have changed in texture from the inflammation, though the air content is
not yet essentially diminished; (3) to bronchi (running in airless tissue)
having a sufficient air content to give rise to a tympanitic note; and (4)
to the trachea behind solid lung tissue (as, sometimes, in the child's
thorax).
Metallic Sounds, or Metallic Clangs. — A metallic ring (or amphoric
sound) on percussion depends upon the presence of high over-tones ac-
companying and obscuring a low fundamental tone. It arises in large
gas-containing cavities with smooth walls, but the walls must be tense.
It will appear in the blown-up stomach (see above), if the distention be
sufficiently increased. To grow familiar with this sound, it may be
elicited by percussing over the cheek after the mouth has been so strongly
distended by air that the tympanitic sound, present on less distention,
disappears. It is best brought out, when elicitable over the thorax, by
504 DISEASES OF THE RESPIRATORY APPARATUS
percussing with the handle of a percussion hammer or with a lead pencil
upon the pleximeter (Heubner's method), and listening, with the stetho-
scope, over an adjacent area, for the metallic ring or bell-like sound. (See
also Coin Sound in Pneumothorax.)
A cracked-pot sound (or metallic chink) arises, on strong percussion,
if air or gas be thereby driven out of a cavity through a narrow opening.
The sound may be imitated by clasping the hands loosely together, and
striking the back of one of them upon the knee. It can also be elicited by
strong percussion of the chest of a healthy, crying baby. Or, if one hold
his own mouth slightly open and the cheek much relaxed, sharp percussion
(indirect or direct) of the cheek will give rise to the characteristic sound.
Reference
Astrowski (S.~). Diaqnostische Bedeutung des Klanges einer Kupfermunze (signe du sou)
bei Lunqenentzundung und Pleuritis bei Kindern. Jahrb. f. Kinder-
heilk., 1913, Ixxviii, 341-346.
(b) The Feeling of Resistance on Percussion
A person percussing is able to draw more conclusions from his percus-
sion than is the listening bystander, since, in addition to hearing better,
he experiences certain tactile sensations, not accessible to the bystander,
which may be of great value in diagnosis. The sense of resistance, felt by
the fingers, on percussion varies with the compressibility of the part per-
cussed. The resistance over solids and liquids is great; that over air-con-
taining parts is much less.
Gerhardt illustrates this point by the sensations received by the finger
when it percusses a glass filled with a foaming fluid ; as long as the fluid
is covered by a thick layer of foam, there is a tympanitic sound; when
the foam has disappeared, the sound becomes feebler and shorter, and the
percussing finger striking the bottom of the glass feels distinctly that the
glass has become less vibratory — it feels harder. In other words, the more
vibratory a body is on percussion, the softer it feels.
It will be seen that the conditions that give rise to feeble and to
empty sounds are those in which the sense of resistance also is great, and,
vice versa, the conditions that give rise to loud (clear) and to long-
lasting (full) sounds are those in which the sense of resistance is less.
Upon these facts, also, the so-called tactile percussion (Ebstein) is based.
(See Delimitation of Deep Cardiac Dullness in the Section on Diagnosis
of Diseases of the Circulatory Apparatus.)
(c) Topographical Percussion of the Lungs
Before comparing the percussion note over symmetrical areas of the
two lungs, it is best to mark out, by percussion, the borders of both lungs
(topographical percussion). In delimiting the lung margins, we use
EXAMINATION OF THE LUNGS AND PLEUEAE 505
very gentle percussion (finger-finger, or hammer pleximeter) ; here the
"no-sound" stroke (H. L. Smith) and the "threshold-value" percussion
of Goldscheider are very helpful. Since the percussion sounds over the
healthy lungs are non-tympanitic, are loud (clear), and die away slowly
(of long duration, or full), it is easy to mark off their borders, (1) from
adjacent solid organs (heart, liver, spleen, muscles, etc.), which yield a
feeble (dull) and short (empty) sound, and (2) from gas-containing
abdominal organs, since they yield a tympanitic sound. In outlining the
lung limits by percussion, the pleximeter should be moved along lines
parallel to the long axis of the body. In very exact work, we may resort
to (1) the linear percussion of Wintrich, in which the pleximeter is held
obliquely, on its edge, while we percuss on its surface; (2) to the finger
position of Plesch (q.. v.) ; but these are refinements of technic, upon
which I do not lay. much stress.
By the determination of the limit of the pulmonary resonance adjacent
to a solid organ is meant the finding and marking of the line at which
the loud, full, sound of the lung disappears, on feeble percussion, to
give place to the completely dull and empty sound of the solid organ.
The Upper Limits of the Pulmonary Resonance on Percussion. — This
is, normally, in the same position on the two sides. To determine it the left
fore-finger is placed in the supraclavicular fossa, parallel to the clavicle;
we then percuss, passing upward and from the side into the neck. The
line of the lung margin passes obliquely, from above, downward and for-
ward, to go over into the medial margin of the lung alongside of the
sternocleidomastoid muscle and behind the manubrium. It extends for a
distance of from 3-4 cm. above the clavicle at the level of the spine of the
6th or 7th cervical vertebra, and, behind, goes over the edge of the M.
trapezius obliquely downward and medialward into the posterior medial
lung limit at the level of the spine of the second thoracic vertebra.
Kronig's Fields of Pulmonary Resonance at the Apices. — In addition
to this medial upper limit of the resonance of the lung, Kronig determines,
by percussion, the lateral limit of the lung resonance. The patient
sits on a stool, with his head bent forward and his arms hanging
loosely by his sides. The examiner, while delimiting the medial and
lateral boundaries, alternately stands to the right and to the left side
of the middle line of the patient. The lateral upper limit of resonance
crosses the margin of the M. trapezius about 5 cm. medialward from the
acromion, and thence runs (both in front, and on the back) downward
(and slightly lateralward) towards the axilla. The widths of the zone of
resonance at the margin of the M. trapezius amounts normally to from
6-7 cm.
These areas of Kronig do not, of course, correspond to the anatomical
projection of the lung apices, but represent only the "areas of resonance,"
to the apices. Goldscheider's method, on the other hand (threshold-
506 DISEASES OF THE EESPIEATOKY APPAKATUS
value percussion, with sagittally directed percussion stroke) gives, he
asserts, almost exactly the anatomical projection of the lung apices on the
front of the chest. Normally, the upper margin of the lung reaches a
point, ahove the clavicle, corresponding to the position of the tubercle on
the first rib, which can be felt, on palpation, between the heads of the
sternocleidomastoid muscle. Goldscheider, accordingly, determines first
the position of the upper margin between the two heads of the muscle,
then maps out the medial boundary, and subsequently by percussion of
the first rib itself delimits the subapical parts. Though his method seems
to yield accurate results in his hands, it is difficult to apply in practice.
Considerable skill is required, and the room must be absolutely quiet.
Moreover, the older methods, though they yield percussion areas that
do not correspond to anatomical projections, permit one to recognize
pathological changes in a satisfactory way, and, as Gerhardt emphasizes,
through them, we are able to percuss the apical region from three sides, so
that anomalies are less likely to be overlooked.
Lung-liver
Limit
Absolute Liver
Dullness
Border of
Lung
~~ Superficial
Cardiac
1 Dullness
- Traube's Space
Lower Border of
Liver Dullness
Fig. 155. — Normal Percussion Boundaries of the Lungs, the Liver, the Spleen, and Traube's
Space on the Anterior Surface of the Body.
The Lower Limits of the Pulmonary Resonance on Percussion. — These
can be easily determined by gentle percussion according to the methods de-
scribed above, except at the junction of the left-lung resonance and the
stomach tympany (lateral from the left mammillary line).
The limits should be determined during quiet breathing. The normal
limits are as follows ;
EXAMINATION OF THE LUNGS AND PLEUEAE . 507
EIGHT SIDE. — (1) In the lateral sternal line, the lower margin of the
5th-6th rib ;
(2) In the mammillary line, between the lower margin of the 6th and
the upper margin of the 7th rib ;
(3) In the axillary line, the lower margin of the 7th or the upper
margin of the 8th rib ;
(4) In the scapular line, the 9th or 10th rib;
(5) Near the vertebral column, behind, the level of the 'spine of the
llth thoracic vertebra.
->—-/• Border of Lung
—• /- Spleen
Fig. 156. — Percussion Boundaries of the Lung, the Liver, the Spleen, and Traube's Space on
the Left Side.
LEFT SIDE. — The lower margin of the lung, beginning at the sternum,
extends lateral ward, behind the 4th rib, as far as the parasternal line (the
lingula being too thin to yield resonance), and then behind the 6th rib;
curving along the left margin of the superficial cardiac dullness, it turns,
at the 6th rib, horizontally backward ; in the mammillary line, it is at the
lower margin of the 6th rib ; in the axillary line, it reaches the level of the
7th-8th rib ; in the scapular line, that of the 9th-10th rib ; near the verte-
bral column, it is opposite the spine of the llth thoracic vertebra.
This lower limit of the pulmonary resonance varies ( 1 ) with the phases
of respiration, and (2) with the position of the patient. On forced inspi-
ration, the boundaries may descend 2-3 cm, below the level found in quiet
508 DISEASES OF THE EESPIEATOEY APPARATUS
breathing. In the dorsal decubitus, the lower margin is 1-2 cm. below its
position in the sitting posture ; in the lateral decubitus, that of the upper
lung may descend 3-4 cm. lower.
The medial margins of the lung, in front, are outlined when the super-
ficial cardiac dullness is determined (q. v.).
Abnormal Position of the Boundaries of the Lungs. — The determina-
tion of the lung limits may, in pathological states, show (1) a general
expansion, (2) a displacement only of the lower boundaries, (3) a general
contraction, or (4) a displacement either of the lower, or of the upper
limit.
General expansion of the lung limits is met with in chronic emphysema
and in the temporary inflation of the lungs due to tracheal or laryngeal
stenosis, diffuse bronchitis and bronchiolitis, or asthma. The lower limit
may be lower than normal from compensatory emphysema of the lower
part of the lung (a) when the upper part is diseased (e. g.f in apical
tuberculosis), or (b) when the lung is diseased on the opposite side of the
body.
General contraction of the lung limits is met with when the total
amount of air-containing tissue in the lungs is diminished from any cause
(cirrhosis of the lung, prevention of entrance of air into the lung, com-
pression of the lung).
The lower limit of a lung may be higher than normal (a) when the
diaphragm is high (abdominal distention), (b) in retraction of a lung
(from cirrhosis, or from tuberculosis), or (c) when parts of .the lung are
deprived of air (bronchostenosis, etc.). A very common cause for dis-
placement of the lower limit of pulmonary resonance upward is the
accumulation of fluid in the pleural cavities. When the pleura is non-
adherent, the fluid tends to accumulate chiefly in the lateral parts; the
line of the dullness does not, as a rule, run horizontally, but in a curve,
the highest point of which lies approximately in the posterior axillary
line, descending rather abruptly in front, and more gradually behind
(Ellis7 curve, S-shaped line of Gardner, parabolic dullness-curve of
Damoiseau).
Retraction of the upper limit is most often due to pulmonary tubercu-
losis. The retraction of the apex is usually first demonstrable at the upper
medial margin in front, and by Kronig's method can be demonstrated
also at the upper nae.dial margin behind,
References
1. General
Kronig (G.)» Zur Topographic der Lungenspitzen und ihrer Percussion. Berl. klm.
Wchnschr., 1889, xxvi, 809-812.
Sahli (H,), Die topographische Percussion im Kindesalter. Bern, 1882, 8°.
EXAMINATION OF THE LUNGS AND PLEUKAE 509
2. The Curved Line of Dullness in Pleural Effusions
Damoiseau (H.). Recherches diniques sur plusieurs points du diagnostic des epanchements
pleuretiques. Arch. gen. de med., Paris, 1834, Hi, 129, 408.
Ellis (C.)« The curved line of pleuritic effusion. Boston M. & S.J., 1876, xcv, 689-697.
Garland (G. M.). Some experiments on the curved line of dullness with pleuritic effusion.
Boston M. & S. J., 1874, xci, 269-272.
The letter S curve. N. York M. J., 1879, xxx, 494-502.
Mouisset (F.). <Semeiologie de I'espace de Traube. Progres med., Paris, 1914, 3. s., xxx,
230-236.
Wood (N. JK".). Percussion of the lungs. I. An effort to standardize the degrees of dullness.
II. The advantages over the opposite method of percussion from base to apex.
Med. Press & Circ., London, 1914, n. s., xcviii, 644-646.
(d) Comparative Percussion of the Lungs
It should be kept in mind that, even in health, the pulmonary resonance
on percussion varies somewhat over different areas of the thorax corre-
sponding (1) to the variable thickness of the soft parts, and (2) to the
variable volume of lung beneath. In some places, the sound is louder
(clearer), and fuller (longer), than in others. By repeated percussion of
the healthy chests of different persons, one gradually fixes in his mind
memories of the normal sounds heard, and of the normal resistance felt,
on percussion over the lungs, and one learns gradually to estimate how
much muffling, or dulling, of the sound may be due to varying degrees of
obesity and to different degrees of muscular, and of mammary, develop-
ment. The sound produced by percussion over the bones of the thorax
(ribs, sternum, clavicles, scapular spines) is somewhat duller, shorter, and
higher pitched than in the intercostal spaces. The percussion sound is
nearly always somewhat clearer in front and at the sides than behind. In
fat people, especially, the resonance on percussion over the back suffers
markedly.
It is always well to compare the percussion sounds yielded by sym-
metrical parts on the two sides of the chest (comparative percussion),
beginning with percussion of the supraclavicular fossae above and passing
downward on the two sides over the several intercostal spaces, making
sure to percuss always with the same force and to direct the stroke in
the same way.
The breathing should be shallow during the examination, since, on
feeble percussion, the sound produced is duller, shorter, and higher in pitch
during inspiration, while, on strong percussion, it is lower in pitch during
inspiration.
The loudest sounds are normally met with between the third and the
fifth rib in front. The sound is a little feebler and shorter between the
second and the fourth ribs on the left side than on the right; from the
fourth rib downward on the right, the sound begins to be shorter, owing
to the relative liver dullness.
In comparative percussion, too, the influence of (a) the cardiac dull-
I
510 DISEASES OF THE EESPIKATOKY APPAKATUS
ness, (b) the tympanitic space of Traube (4th-6th rib on) due to the stom-
ach in the lower part of the left front, and (c) the slight asymmetry of the
two apices of the lung, on the pulmonary resonance, must be kept in mind.
Further, slight asymmetries of the two sides of the thoracic wall are im-
portant in comparative percussion; even a slight grade of scoliosis may
affect the sounds.
Behind, the percussion sounds are less loud, and of shorter duration,
over the shoulder blades; beneath the angle of the scapula, they become
louder and fuller, rather more so on the left than on the right on account
of the relative liver dullness.
In pathological conditions, changes in the normal intensity, duration,
and pitch are recognizable. (See below.)
References
Da Costa (J. C., Jr.}. Dorsal percussion in enlargements of the tracheobronchial glands.
Am. J. M. Sc., Philadelphia & New York, 1913, cxlvi, 660-671.
Fetterolf (G.) & Norris (G. W.). The anatomical explanation of the relatively less resonant,
higher pitched, vesiculotympanitic psrcussion note normally found at the
right pulmonary apex. Am. J. M. Sc., Philadelphia & New York, 1912,
cxliii, 637-649.
Norris (G. W.}. The anatomic causes of the differences in the physical signs over the upper
lobes of the lungs. Tr. Am. Climat. Ass., Philadelphia, 1913, xxix, 26-33.
Squire (J. E.). The physiological difference between tJie two sides of the chest in the physical
signs obtained over the upper part-of the lung. Brit. M. J., London, 1903,
i, 1198-1200.
Thayer (W. S.} & Fabyan (M.). The paravertebral triangle of dulness in pleural effusion
(Grocco's sign). Am. J. M. Sc., Philadelphia & New York, 1907, cxxxiii.
14-28.
Wolff (A.). Erfahrungen mil der Perkussion der Lungenspitzen nach Kronig. Deutsche
med. Wchnschr., Leipzig u. Berlin, 1903, xxix, 93-95.
i. Dullness and Flatness on Percussion
The percussion sound may bo dull, where it is normally loud, in all
conditions in which the air content of the portion of the lung percussed
is less than normal.
This may be due (1) to infiltration of the lung; (2) to collapse, or
atelectasis, either from external pressure, or from absorption of the air
after bronchial occlusion; or (3) to the presence of fluid, or of abnormal
tissue, between the lung and the thoracic wall.
In order that airless lung shall be recognizable on percussion, the area
deprived of air must be at least as large as the pleximeter used, and must
extend 2 cm. deep.
Infiltration of the lung occurs in pneumonia (croupous and catarrhal),
tuberculosis, hemorrhagic infarction, abscess, and neoplasm ; atelectasis of
the lung may be due to compression (pleuritic or pericardial exudates, or
neoplasms), or to absorption of the air from the alveoli after the bronchi
have been plugged (bronchial stenosis).
EXAMINATION OF THE LUNGS AND PLEUKAE 511
When the lung is separated from the chest wall by fluid (pleur^l
effusions, empyema, hydrothorax), there must be at least 400 c.c. (in the
adult) to yield dullness on percussion. Pleuritic thickening, and neoplasms
separating the lung from the chest wall, can also cause dullness.
The boundaries of the dullness, due to the fluid in exudative pleuritis,
change as a rule but little, if at all, with change of position of the patient
(encapsulation by adhesions) ; in hydrothorax, which is usually bilateral
though it may be unequal on the two sides, the level of the fluid changes
with change of position, but only slowly after 15-30 minutes. An im-
mediate change of the dullness (in the case of fluid in the pleural cavity)
with change of position, indicates the simultaneous presence of air and
fluid (pyo- and seropneumothorax) ; in such cases, the patient/ on sitting
or on standing, may present dullness in both lower fronts, while, when
lying on his back, the fluid sinks backward at once and the percussion
sound becomes loud in front where it was previously dull.
Pathological Fullness or Emptiness of the Sound. — In pulmonary
emphysema, and in pneuinothorax, the percussion sound is abnormally full
(rich in tones of low pitch). A pathologically empty sound is met with in
most cases where the note is abnormally dull, though emptiness (shortness)
and dullness, as has already been pointed out, are not synonymous terms.
ii. Pathological Tympanitic Sounds on Percussion Over the Lungs
Aside from the tympany in Traube's space (lower left front), due to
gas in the stomach, any tympanitic sound elicited on percussion over an
area corresponding to any portion of either of the two lungs is abnormal.
Thus, tympany on percussion may be met with (1) in infiltrations of the
lung; (2) in relaxation of the lung tissue; (3) in conditions in which air
and fluid are present, at the same time, in the alveoli; (4) over large,
smooth-walled, air-containing cavities in the lung tissue; and (5) some-
times in pneumothorax.
Tympany Over Infiltrated Lung. — The tympanitic sound heard over
infiltrated areas of the lung tissue is due to the better conduction between
the thoracic wall and the normal air-containing cavities of the chest
(bronchi). The note is simultaneously dull and tympanitic (e. g., in
pneumonias, and in compressions of the lung and other atelectases). This
tympanitic bronchial sound is more often elicitable over the upper lobes
(owing to the thinner chest wall there) than over the lower; the pitch is,
in such cases, slightly altered when the patient opens and closes his mouth,
but not on change of position of his body.
Tympany Over Ralaxed Lung. — Eel axed lung tissue yielding a tympa-
nitic note may exist (1) in the neighborhood of extensive infiltrations, or of
pleuritic and pericardial exudates (Skodaic resonance), (2) owing to com-
pression of the lung from enlargement of the heart or liver, or from tumor
growths, or (3) when the bronchi are occluded. The tympanitic note
512 DISEASES OF THE KESPIKATOKY APPAKATUS
elicited in such circumstances does not change in pitch on opening and
closing the mouth. A tympanitic note over one upper lobe may arouse
suspicion, early in the physical examination, of the existence of a pneu-
monia, or of other cause of relaxation of lung tissue, in the lower lobe on the
same side. If, at autopsy, a relaxed lung be percussed on removal from
the body, it will yield a tympanitic sound ; if it be subsequently blown up,
the tympany will diminish.
Tympany Over Lung Containing Air and Fluid in the Alveoli. — Air
and fluid in the pulmonary alveoli yielding a tympanitic note are met with
in the first and third stages of croupous pneumonia, in catarrhal pneu-
monia, in pulmonary edema, and, occasionally, in hemorrhagic infarcts.
Tympany Over Certain Cavities. — A tympanitic percussion sound can
be brought out over cavities (tuberculous, gangrenous, bronchiectatic),
when they are as large as a walnut, or larger, when their walls are smooth
and not too tense, and when they are close to the surface of the lung, or are
situated in the interior of infiltrated tissue. (For the change of pitch
over such cavities, see below. )
Tympany Over a Valvular Pneumothorax. — Over a pneumothorax,
especially of the valvular variety in which the air may be under great
tension, a tympanitic percussion sound may sometimes be elicited. In
most cases of pneumothorax, however, the percussion sound is not tym-
panitis, but is abnormally loud, and of low pitch.
iii. Variations in the Pitch of Tympanitic Percussion Sounds
In listening to tympanitic sounds elicited on percussion, we pay
attention, especially, to the dominant tone. The pitch of this dominant
tone has been found to be variable under certain conditions immediately
to be described.
1. Wintrich's Change in Pitch. — In this type, the tympanitic percus-
sion sound becomes higher in pitch on opening the mouth, and lower on
closing it. It can be imitated by percussing on the cheek while the mouth
is opened and shut. This variation in pitch is met with (1) over those
cavities in the lungs that communicate freely with a bronchus ; it is also
sometimes observed (2) in the form of pneumothorax in which there is
open communication with a bronchus, and (3) over a pneumonia, or above
a large pleuritic exudate (owing to percussion vibration of the air in the
bronchi through the infiltrated or relaxed tissue). If Wintrich's variation
in pitch be present in one position and absent in another, it is probable
that, in the position in which it is absent, the conducting bronchus has been
occluded by fluid ("interrupted Wintrich's change of pitch").
2. Friedreich's Change in Pitch. — This is less important; by it is
meant the change in pitch of a tympanitic sound over a cavity during
respiration; the sound becomes higher in pitch on inspiration, and lower
in pitch on expiration.
EXAMINATION OF THE LUNGS AND PLEUEAE 513
3. Gerhardt's Change in Pitch. — This is met with over oval cavities
partially filled with fluid. If the long axis of the cavity be in the sagittal
direction, the pitch of the tympanitic percussion sound is higher on sitting
than on lying; if the long axis of the cavity be in the anteroposterior
direction, the pitch is lower on sitting than on lying; in other words, a
shortening of the long diameter of the cavity heightens the pitch. This is
interesting, but practically unimportant.
4. Biermer's Change in Pitch. — By this is meant the change in pitch
that is met with sometimes over seropneumothorax ; the pitch of the
percussion sound is lower on sitting than on lying owing to the fact that,
in the sitting position, the pressure of the fluid causes descent of the dia-
phragm and increases the area of the resounding space.
References
Friedreich (N.). Ueber die respiratorischen Aenderungen des Percussionsschalles am
Thorax unter normalen und pathologischen Verhdltnissen. Deutsches Arch.
f. klin. Med., Leipzig, 1880, xxvi, 24-82.
Gerhardt (C.). Ueber Differenzen des Percussionsschalles der Lunge beimSitzen undLiegen.
Deutsche Klinik, Berlin, 1859, xi, 108.
von Smolenski (S.). Bemerkungen iiber das Wintrich'sche Perkussionssymplom. Wien.
med. Wchnschr., 1889, xxxix, 1041-1043.
Wintrich (M. A.). Beschreibung einer neuen Percussions-Methode. Berl. med. Cenlr.-Ztg.,
1841, x, 1-4.
iv. Metallic Sounds Over the Lungs
The characters of these metallic sounds have been described above.
A metallic ring is heard on percussion over the thorax: (1) in pneu-
mothorax; and (2) over large, smooth-walled cavities (diameter of 4 cm.
and more). The acoin sound" is a metallic ring.
The cracked-pot sound may be heard on percussion (1) over superficial
cavities that communicate, through a narrow opening, with the bronchi,
and (2) sometimes over relaxed and infiltrated lung tissue. The cracked-
pot sound is best elicited when the patient holds his mouth open; the
examiner's ear or the bell of the stethoscope should be held close to the
open mouth.
8. Auscultation of the Lungs
In health, and in disease, various sounds arise within the body; hy
listening to these (auscultation), we can draw certain inferences regarding
the structure, or the conditions, of the organs in which they arise.
On auscultation of the lungs we listen to (1) the voice sounds audible
over the thorax; and (2) the sounds that accompany inspiration and
expiration.
We listen either (1) with the naked ear separated from the chest wall
by a thin towel (immediate ascultation) , or (2) with the aid of a stetho-
scope (mediate auscultation).
514 DISEASES OF THE RESPIRATORY APPARATUS
The voice sounds are better heard with the naked ear than with the aid
of a stethoscope, but the breath sounds, and, especially, some of the modi-
fications that these undergo in disease, as well as some of the sounds
that accompany them, are better recognized and localized by the use of
the stethoscope.
On examining the front of the chest, the stethoscope is better than the naked
ear, for obvious reasons. On the other hand, the ear applied directly to the chest
is often most useful in examining the back.
In patients that are very ill, lying on their backs in bed, and especially when
they are very heavy, a Bowles stethoscope may be found convenient, since it per-
mits of a more extensive examination with less change of position than other
forms in use. For ordinary work, the Ford stethoscope is a good model. In
some countries, the monaural wooden stethoscope is still highly prized; in North
America, the binaural stethoscope is everywhere in use and a monaural instru-
ment is rarely employed.
(a) Auscultation of the Voice Sounds Over the Thorax
In practice, one begins the auscultation of the chest by listening to the
breath sounds, and then afterwards listens to the voice sounds; but in a
systematic consideration of thoracic auscultation it is better to approach
the subject by way of the voice sounds, since their origin is much better
understood.
In studying the voice sounds we have to consider, first, their origin,
and next the changes that they undergo on conduction through the air
passages and the lungs to the chest wall.
i. Origin of the Voice Sounds
Here two processes play important parts : (1) the production of funda-
mental tones in the larynx, where the vocal cords of the glottis act like a
reed instrument; and (2) the process of articulation, in which the different
tones produced in the larynx are modified by changes in shape of the mouth
cavity, and adjacent cavities, the larynx itself being wholly unable to
articulate. The mouth cavity, in association with the laryngeal and nasal
cavities, constitutes a resonating chamber. As such, it intensifies that
particular tone or overtone of the sound produced in the larynx the wave-
length of which corresponds in resonance to the dimensions of the cavity.
Variations in the shape of the cavity will modify its function as a
resonating chamber in that it will vibrate in unison with notes of different
wave-length or pitch. Thus, through changes in the resonating chamber,
different overtones may be intensified or weakened and corresponding
changes in the voice sounds produced. In whispering, there is articulation
of the breath sounds only, the glottis being passive and giving rise to no
loud tones.
EXAMINATION OF THE LUNGS AND PLEURAE 515
ii. Changes in the Voice Sounds After Their Formation
These sound waves of the glottis, articulated by the mouth, pass back-
ward through the narrow glottis into the trachea, and thence, through the
bronchi, to the deeper portions of the lung. Owing to the fact that the
current of air is in the opposite direction and that the articulated tones are
compelled to pass through the narrow opening of the glottis, the sound
waves that pass down the trachea are, on the way, somewhat altered.
Beyond the bifurcation of the trachea, the sound waves spread through the
diverging ramifications of the bronchi; the sounds become weak and
muffled, probably owing to the diminution in the rigidity of the tubes and
to the increased conduction of the vibrations away from the air columns
by the tissues, owing to the increased surface exposed to the sound waves.
The lung tissue in its natural distended state is such, a bad conductor that
the sounds in the large bronchial tubes are not audible over the thoracic
wall.
iii. Voice Sounds Audible Over the Thorax in Healthy Persons
Now when one listens to the voice sounds over the healthy lung of a
person pronouncing the number "99" in a voice of low pitch, the sounds
audible are nearly everywhere weak and muffled (normal voice sounds),
instead of being loud and clear like those audible over the larynx. In
women and children, indeed, voice sounds may not be audible at all over a
large part of the chest. In many healthy persons, however, quite loud
and relatively clear voice sounds are audible in the back over the spinous
processes of the upper thoracic vertebrae (opposite "the trachea and the
bifurcation of the bronchi). When loud, clear voice sounds are audible
directly over the bronchi of the healthy cbest, the condition is known as
bronchophony, the term bronchophony including such sounds audible in
health, and all degrees of clearness greater than this in disease when the
voice sounds audible over the thorax may become almost as loud and clear
as those audible over the larynx (pathological bronchophony). It has been
the practice of many clinicians to use the term vocal resonance when de-
scribing the voice sounds audible over the thorax ; this is unfortunate, for
resonance has very little to do with the origin of the sounds, either in
health or in disease, and the term vocal resonance should, therefore, in my
opinion, be discarded.
iv. Coughing Sounds and Crying Sounds
What applies to the voice applies also to the cough and the cry. One
has to depend upon these sounds rather than upon the voice sounds on
making the physical examination of the chest in young children.
516 DISEASES OF THE RESPIRATORY APPARATUS
v. Abnormalities of the Voice Sounds Audible Over the Thorax
The voice sounds audible over the chest may be either feebler and less
distinct, or louder and more distinct, than normal. We pay attention,
however, to clearness or distinctness rather than to loudness of the sounds,
since distinctness and loudness are often opposed to one another, and it is
the former that is important for diagnosis rather than the latter.
Diminished clearness or distinctness of the voice sounds is of little
value for clinical diagnosis. Since, normally, the sounds are muffled and,
in some persons, wholly inaudible, unless one note that the sounds have
become less clear where formerly they were more distinctly heard, but little
attention need be paid to the sign. Occlusion of the bronchi is the most
common cause of such diminution of distinctness; other causes include (1)
pleural effusion, (2) thickened pleura, and (3) large masses of fat or
muscle between the skin and the lungs.
Increased clearness or distinctness of the voice sounds (pathological
bronchophony) is the term applied when sounds as clear as, or clearer than,
those heard over the upper thoracic spine in health are met with in any
other part of the chest, since nowhere else are they normally present. The
phenomenon is due either to increased conducting, or to increased reflecting
power, of the lung tissue. The conducting power of the spongy structure
of the lung is increased by any change that makes the lung structure
more homogeneous. Thus the lung becomes more homogeneous (1) when
it becomes more solid (infiltration, collapse, neoplasm, compression), or
(2) when it contains more air (cavities from bronchiectasis, tuberculosis,
or gangrene; marked emphysema). When cavities exist, there is increased
reflection of the sound waves in addition to the improved conduction. In
normal alveolar tissue, reflection of sound practically ceases, but, in
cavities, reflection of the waves may be as great as in normal bronchi. In
large smooth-walled cavities, the reflection may be so great as to yield a
highly reverberating character to the voice sounds (cavernous voice
sounds) .
Whispered bronchophony is sometimes clearer than that of the voice.
The terms pecioriloquy , and whispered pecioriloquy, are sometimes ap-
plied when the sounds are very clear, apparently close to the ear, and
exactly circumscribed. It is maintained by Baccelli that clear pleural
exudates conduct the whispered voice (voce afona) better than exudates
rich in cells (e. g., in empyema). Too much stress should not, however, be
laid upon "Baccelli's sign."
A special kind of bronchophony known as egophony is sometimes heard
above the level of the fluid in large pleural effusions that cause partial
compression and narrowing of the bronchi. The voice sounds have a
more nasal quality than is usual ; there is an echoing quality to the sound
and it is rhythmically intensified and interrupted. The term egophony
EXAMINATION OF THE LUNGS AND PLEUEAE 517
was applied by Laennec to indicate the similarity of the sound to that of
the bleating of a goat ; he also compared the sound to the voice of Punch.
Over large cavities containing air, and especially over a pneumothorax,
the voice sounds may have an amphoric, metallic, ringing quality
(amphorophony) .
Auscultation of the voice sounds yields information comparable in
large part to that afforded by palpation of the vocal f remitus ; when the
voice is not strong enough or deep enough to yield a palpable fremitus,
auscultation of the sounds may give information not otherwise obtainable.
(6) Auscultation of the Breath Sounds Over the Thorax
During respiration, the breath sounds (inspiratory and expiratory) are
audible over the lungs. When one listens over the larger air tubes, a
certain quality is present that is absent when one listens over the alveolar
masses of the lung. The former type is called bronchial breathing, and
the latter vesicular breathing.
In diseased states, owing to the secretion of mucus, to swelling of the
bronchial mucous membrane, or to fibrinous exudation upon the surfaces
of the pleurae, certain accessory or adventitious sounds arise (rales, crepita-
tion, friction sounds), distinguishable from the actual breath sounds.
i. Vesicular Breathing
On inspiration, a soft blowing murmur is audible over the healthy
lung and, on expiration, either no sound at all, or a feeble blowing or
aspirating sound can be heard ; these sounds are those of normal vesicular
breathing. The inspiratory sound can be imitated by placing the mouth
and lips in the position of articulating the letter / and drawing in air ; the
expiratory sound can be simulated by driving out air with the lips in the
same position.
Origin of Vesicular Breathing1. — There has been much dispute as to the
origin of the normal inspiratory and expiratory breath sounds. Many have been
attracted by the view that the glottis is the only source of the breath sounds. The
passage of the inspired and of the expired air, through the narrow glottis, into
wider spaces above and below it gives rise to "fluid veins" ; the sounds thus arising,
modified by resonance in the pharynx above and in the trachea below, are con-
ducted down the air tubes, just as the voice sounds are carried- (vide supra).
Owing to the bad conducting qualities of alveolar tissue, the glottidean sound is
converted into the inspiratory and the expiratory, vesicular breathing, while, over
the larger bronchi, the glottidean sound approaches its primary intensity and
quality (bronchial breathing). More recent study and criticism indicate, however,
that, though the above explanation probably holds for the expiratory part of
vesicular breathing, it is inadequate fully to explain the origin of the inspiratory
sound. The tendency at present is to accept the view of Gerhardt, who assumes
that, during inspiration, there are actual vibrations of the alveolar lung tissue,
which is made tense by the entrance of the air. Gerhardt grants that the very
518 DISEASES OF THE RESPIRATORY APPARATUS
feeble, scarcely audible, sound of expiration is a bronchial sound weakened by the
alveolar tissue.
Variations in the Breath Sounds in the Normal Chest. — The inspira-
tory and expiratory breath sounds just described are audible over the
whole chest, though the intensity varies (1) with the depth of the respira-
tions, and (2) with the condition of the lung over which one listens.
The breath sounds are, normally, loudest just beneath the clavicles,
where the thoracic walls are thin and where the pulmonary tissue is best
ventilated ; over the apices, the sounds are feebler. When, on auscultation
over a definite area of the chest wall, one hears pure vesicular breathing,
it is fair to conclude that air-containing tissue lies beneath this area and
participates in respiration.
Modifications of Vesicular Breathing in Disease. — Clinically, one has
to observe whether the vesicular breathing is of normal intensity, is abnor-
mally loud (accentuated), or is abnormally weak (enfeebled).
Loud, or accentuated, vesicular breathing, or roughened breathing, is
met with normally in children, and is hence often spoken of as PUERILE
BREATHING, the air on inspiration entering the very elastic child's lung
with greater force ; this puerile breathing is often audible during adoles-
cence, for a longer period in girls than in boys.
When such roughened breathing is heard over a part of the lung in the
adult, it may indicate obstruction to the entrance of air into some part of
the lung other than that where the roughened breathing is heard ; thus it is
often audible in the neighborhood of infiltrated areas, especially at the
apex, in incipient pulmonary tuberculosis, and in healthy lung close to a
consolidating area, at the beginning of pneumonia.
Sometimes there is PROLONGATION" OF THE EXPIRATORY SOUND of
vesicular breathing so that this becomes as long as, or even longer than,
the inspiratory sound. This change is met with sometimes, normally, in
the supraspinous fossae. The expiratory sound may also, normally, be a
little longer over the right apex than over the left. Elsewhere, a pro-
longation of the expiratory part of the vesicular breath sounds usually
indicates an expiratory dyspnea (emphysema, asthma, bronchitis), if the
distribution be general ; or a beginning infiltration, if it be local.
If the inspiratory sound, instead of being continuous, be interrupted so
as to consist of two or more parts, the inspiration assumes a jerking, or
saccadate character (COG-WHEEL BREATHING). Assuming that the mus-
cular contractions are smoothly and evenly made during inspiration, such
jerking breathing occurs when local, quickly yielding, obstructions to the
entrance of the air current into the alveoli are temporarily overcome. The
sign has been looked upon as uf importance for the diagnosis of beginning
apical tuberculosis. Too much stress should not, however, be laid upon it,
since it is often met with in persons of feeble musculature, in nervous
EXAMINATION OF THE LUNGS AND PLEURAE 519
people, and in children after crying. This sign has also heen observed in
insufficiency of the pulmonary valves of the heart ; here it seems to be due
to the fact that the sudden regurgitation of blood into the right ventricle
during diastole gives rise to a phenomenon in the pulmonary capillaries
comparable with the capillary pulse that appears in the general circulation
in aortic insufficiency.
Enfeeblement, or SUPPRESSION OF VESICULAR BREATHING, occurs when-
ever the inspiratory expansion of the lungs is interfered with. When
bilateral, it may be due to tracheal or laryngeal obstruction, or to emphy-
sema. More often, it is unilateral, in which case it may be due to: (1)
obstruction of a large bronchus (fibrinous bronchitis, aortic aneurism,
fibrosis) ; (2) to separation 'of the lung from the chest wall in pleurisy,
hydrothorax or pneumothorax ; the vesicular breath sounds may be entirely
absent over large pleuritic effusions; or (3) to the prevention of deep
inspiration from pain, especially from the pain due to pleuritic involve-
ment over the affected lobe at the beginning of an infiltration in lobar
pneumonia.
ii. Bronchial Breathing
The peculiar character of bronchial breathing is best learned by listen-
ing to it. It is difficult adequately to describe it. It has an aspirate
character and may be artificially imitated by making the lips and mouth
assume the attitude used in pronouncing h or ch and then forcibly
breathing in and out.
Bronchial Breathing" Audible Over the Normal Thorax. — Such bron-
chial breathing is audible even in healthy persons over the spinous proc-
ess of the 7th cervical vertebra, corresponding to the position of the bifur-
cation of the trachea ; it can also be heard, close to the spine, in the inter-
costal spaces down as far as the spinous process of the 5th thoracic vertebra,
since, here, the larger bronchi lie near the surface. Still louder and more
intense sounds are audible, normally, over the trachea (tracheal breathing),
and over the larynx (laryngeal breathing).
The sounds arise, chiefly, in the glottis; they are due to liquid veins,
which arise, below and above this narrow slit, on inspiration and on
expiration. The air in the trachea and bronchi is set into vibration so
that a clanglike sound is produced by the air tubes, which, like organ
pipes, are attuned to a certain fundamental tone.
Thus, the inspiratory sound arises when air passes from the choanae
into the nasopharynx and from the glottis into the larger laryngeal cavity
and into the trachea ; and the expiratory sound arises when the air passes
through the glottis into the supraglottidean portion of the larynx. The
loudness of bronchial breathing is not important. It is the special quality
of the sound — the aspirating, hollow or reverberating character — that is
520 DISEASES OF THE EESPIEATOEY APPAEATUS
peculiar, and this is often as well marked when the sounds are weak as
when they are loud. Especial attention should be paid to the expiratory
portion of the sound; in tubular breathing this approaches the inspira-
tory sound in intensity; its duration is abnormally great; .and it often
manifests the special quality better than inspiration. But this is not
always so, for the expiration, though usually prolonged, is sometimes
wholly inaudible.
Pathological (or Accidental) Bronchial Breathing. — In disease, bron-
chial breathing appears in places where, normally, it is not audible ; it is
then due, as a rule, (1) to obliteration of the normal damping by the
alveolar structure of the lung (from solidification due to collapse or to
infiltration), or (2) to destruction of alveoli with cavity formation. In
both cases, it is the sounds in the larger air passages that become au-
dible ; thus, in cavity formation, these sounds will, obviously, be conducted
better from the bronchial tubes to the chest wall, and in consolidation of
the lung, the solid tissue gives a better support to the bronchial walls
than under normal conditions and the sounds are then better maintained
and more easily conducted to the surface than they are through air-con-
taining tissue. Solid tissue acts also as a resonator so that, in consoli-
dation, the bronchial sounds undergo an actual intensification. Over
hepatized lung, the bronchial breathing is sometimes characterized by a
well-marked whiffing quality (TUBULAR BREATHING), but how this special
quality is acquired is not known.
The solidifications of the lung over which pathological bronchial breathing
becomes audible include: (1) infiltrations (due to pneumonia, tuberculosis, or
hemorrhagic infarction) ; (2) compression (behind pleural exudates, tumors, etc.) ;
and (3) atelectasis. The solid areas, in order to yield pathological bronchial
breathing, must have a diameter of at least 1.5 cm. and must then either be near
the surface, or be connected with it by means of a good sound-conducting medium;
moreover, the communicating bronchi must be open.
The cavities arising from the destruction of air sacs, over which pathological
bronchial breathing may become audible, include: (1) bronchiectatic cavities;
(2) tuberculous cavities; and (3) larger emphysematous cavities. The communi-
cating bronchi must be open, and the cavities must be near the surface, or must
communicate with it by sound-conducting media.
Thus, the two principal causes of pathological bronchial breathing,
namely, (1) solidifications and (2) cavities, are also the two main causes
of pathological bronchophony (vide supra).
Bronchial breathing of metallic character, or with amphoric echo, may
be audible over cavities when the conditions are those in which, on percus-
sion, metallic sounds arise (vide supra). METALLIC BRONCHIAL BREATH-
ING is characterized by the addition of high pitched overtones of long dura-
tion, while in the AMPHORIC ECHO one hears a metallic clang with very deep
fundamental tone. The latter can be imitated by blowing over an empty
EXAMINATION OF THE LUNGS AND PLEUEAE 521
wide-mouthed bottle or jar. Metallic breathing, and amphoric echo or
hum, when heard, indicate the presence either of a large cavity, or of a
pneumothorax, being observable in the latter especially when there is a
wide fistula connecting the pneumothorax with a large bronchus.
iii. Mixed Breathing, Bronchovesicular Breathing, and Indefinite Respiration
In certain areas one sometimes hears bronchial breathing and vesicular
breathing simultaneously, sometimes one component, sometimes the other,
being dominant. This is often referred to as mixed breathing, or broncho-
vesicular breathing. It arises where the conditions for the occurrence of
bronchial breathing and of vesicular breathing exist alongside one another
and where, accordingly, neither of these types of breathing is audible in a
pure state. Thus it may be met with in beginning, or in incomplete,
infiltration of the lung tissue, especially where small foci of solidification
alternate with areas of air-containing tissue (e. g., in tuberculosis, in
diffuse infiltration, and in bronchopneumonic foci).
The so-called indefinite breathing (unbestimmtes Atmen of the Ger-
mans) is usually such mixed breathing, though, in some instances, it is
enfeebled vesicular breathing, or weak bronchial breathing. Thus, over
pleuritic exudates or when loud rales are present, the respiratory murmur
may be so feeble that one cannot distinctly recognize its character. In
slowly-developing infiltrations of the lung, the first change noticeable in
the breath sounds is, often, a lengthening and roughening (or sharpening)
of the expiration following normal vesicular inspiration. Later, the in-
spirium becomes indefinite while the expirium assumes a bronchial char-
acter; finally, when the area is wholly deprived of air, the inspiratory
sound also becomes bronchial.
In both bronchial breathing and mixed breathing one should note
whether the sound is loud or feeble. Feeble bronchial breathing is often
heard behind a pleuritic exudate and may be due either to pneumonic
infiltration, or to simple collapse from compression by the exudate.
By metamorphosing breathing is meant the form in which the breath
sound audible during inspiration suddenly changes in character. Usu-
ally, it begins with a sharp hissing sound and then changes to a softer
bronchial breathing. It was described by Skoda as a "veiled puff" and is
probably identical with the souffle voile of Laennec. It is believed that it
is due to the. sudden removal, at a certain stage of inspiration, of some
obstruction to the passage of air through a bronchus that communicates
with a cavity.
iv. Accessory or Adventitious Respiratory Sounds Audible in Disease
In addition to the natural breath sounds (vesicular and bronchial
breathing) and the changes these undergo in disease, certain sounds arising
522 DISEASES OF THE RESPIRATORY APPARATUS
inside and out-idc the lung, wholly additional to those described ai,
i, now be con-idercd. Of such ad vent i t .ions respiratory sounds, we
(I) tinguish two great groups, (1) rales, or crackles; and (2) friction
sounds.
Rales; Crackles; Rhonchi
These are sounds that arise during respiration from movements of
abnormal contents of the air passages by the air breathed. They may arise
( 1 ; from the presence of fluid (mucus, .scrum, Mood, etc.) in bronchi and
in cavities, leading to the formation of air bubble-, that break; (2) from
the movement, of different masses of mucus or secrclion; ('.'») from the
sudden -epjirafion of sticky miieous membrane-; ;md (4) from 'li1 ; .'""
of air through ahnormal loc.al narrowings.
These sounds may, in intently, he loud or feeble, in frequency, nu-
merous or few; I hey are most oflen in-piratory in time, thoiiLdi tliey may
orr-;,sioM}illy U: jiudihK; din iralion frhonr-hi part ieularly ). On
I'- \\\\<fri for the pre-.em-e of r;'i!«' . OB6 li I'-n while the pati'-nt, is a-l:ed to
take a deep hrealh or to eoii^li. It is important, to not ice whether flu:
rales disappear or arc modified on ron-.diint.'1. \V(i divide rules into two
•ups: (\) dry rale-:, and (-2) moi t rah- .
Dry Rales, or Rhonchi. — The 6 Rfe rather Ion-/, v.hi-tlinL'; or snoring
:ounds that <li(; away slowly. They are due to the vihration of tou-jh
mncn jitlached to tlin walls of the hronchi, or to the p;i--aL'-e of the ;iir
through Inmina. narroucd hy spa.-m of the hronchioles or hy swelling
of their mucous mendjranc. 'I h< . arc often aceom panicd hy palpahh;
vihration of the r|M- I. wall. The sounds, vvlicn low pilch<-d, have a snoring
charaeler ( ::nnnmnx rlionrlii, ) ; when |iip|, pitched, they are more whistling
or pi|iin^ in character ( ••Hiilmif rlmi^'lii). 'l\ic sonorous rhonchi [iroh-
ahly ari e in the lar-'cr tuhe , t IH- sihilant, in the smaller tubes.
Moist Rales.- These sounds arise when fluid i- present in the air
passives. They an; er;ic|.liii«»; or bubbling sounds that, resenihh; the, nois(;s
prodiie.e*! in bubhlin«.'; fluids, and they may be very well imitated by blow-
ing into a glass of water lliron^b straws of different sixes. In contra I.
with the more continuous, chiefly expiratory, sounds described above, as
llbilant and WnOrOUH rhonchi, the (! nioi I rales a TO i ntcrrnpt(-d, bubbling
or crackling BOUndf, heard chiefly during inspiration.
The moi.:!. rales are sometimes ela;-.silied according to the apparent size
of the bubbles or crad.lcH, the birger bubbles bein:-1 known as f/nrt/finf/
I'llr:-, i ho . M, .1 in si/c as medium sized bubblin;/ n//''\ or crackles, and
lho:.e of iM;i||er :,i/.e, a,: /////• rmr/.Vr.v. or a xiilirrr />i ln.nl and crc/iil-unli
<«/> . I be ound of the so-called crepitant rale can be very well imitated
by rubbing a lock of the hair between the fingers close- to the ear, or by
'•cparaliii" the moi h-m-d , iirfaccs of the, thumb and forefinger when in
EXAMINATION OF THE LUNGS ANP PLEURAE 523
contact beside tho oar. Thoso sounds aro not unliko tho sounds of salt
crackling in a tiro, or of tho si/./ling ot' soola \vator. Such crepitation con-
sists of numorous small crackling souiuls of ovon si/.c, hoard ehioily, and
usually exclusively, during inspiration. It is mot with in pnoumonia in
tho staire of endorsement (crcpiUitio inJiU'} and also in tho staiiv of resolu-
tion {crcfntutio m/u.r). It may also bo hoard in pulmonary edema, and
in atolootasis where somo of tho oollapsod alvoolar walls or walls of minuto
bronchioles aro torn apart by entering air ourrouts. In fooblo pationts,
and during oonvalosoonoo from sovoro disoaso, ono ofton hoars, on oxamina-
tion, siioh oropitalion in tho lowor and postorior parts of tho hni£ during
tho tirst doop inspirations takon.
Tho oropitant ralo, no manor in what condition it is mot with, is
boliovod to bo duo to tho. opening up of oollapsod air saos or minuto
bronchioles; occasionally, it may bo a vory lino mucous ralo. It is olis
tinguishable from othor moist rales ^H chiefly, by tho short duration,
or small si o, of oaoh of tho successive oropitat ions ; and ^_M by tho lar^v
numbor of crepitations attending oaoh inspiration.
Small mucous ralos approaolmur tho oropitant ralo in duration and
iu si/.o aro somotimos oallod ^nbcrc^ilanf rnlt's.
Ringing (or Consonating) and Non-ringing (or Non-consonating)
Rales.- Ralos that soom to lu^ oloso to tho oar and to bo attoudod by a oor
tain olaii£ (not, howovor, an outspokon motallio soumH that doos not ao-
oompaiiy ordinary ralos aro said to bo "riuji-iiiix" or "oonsonatiui;" ralos.
Thoso aro usually raihor lar«:o, bubbling sounds, arising in a oavity ^r in
a larii'or bronohus, and Wi>ll propagated to tho surfaoi' tlinuiii'h infiltrated
lun<>' tissuo; tlu> hiii'lior tonos aro strengthened through rosouauoo iu tho
brouohi. \Vho,i air ooutaiuiiij;- tissuo lios bolwoon tho oavilios or brom-hi
in which tho ralos ariso ami tlu^ wall of tlu^ tlu>rax, tho ralos aro not
riutniiir or oonsonatiiiir. This rin^inu1 oharaotiM- of a ralo is tliorol'oro of
oousidoral-.lo diaii'iiostio importanoo in intiltralious of tho lun^. Couso
iialiiiix ralos ooour uiulor tluv samo ooiulitions in general as iloos bronchial
breathing; ihoy somoiimos IK"!)) us out iu diagnosis whon I ho breath sounds
aro iudotinito v«'. «/., ovor small bnniohojnuMimouio foci).
(icrhardt sH^osts that tlu> dilVoronco in sound bolwocn cousoua! iui;-
and uon o«»n^Miatiuii- ralos can bo well imitated by bloxvinii; throuivh a
^lass tubo inlo \\ator, coutaim>d, in tho ono ca>o in a hi^li i^lass or bottle,
in the other in a Hat saucer or soup plalc.
Metallic Ringing Rales.- Those occur under oondit ions similar to thoso
in which a metallic olauix on poroussi»>n and motallio bronchial breathing
(</. r.) ooour. They have, accordingly, tin* samo si^uilicancc, imlioatiui;
oitlu'r i-a\itios in tho luiiix or a piUMimothorax.
A ^pooial sound to bo considered hero U the so oallod nn'lallif tinkling.
nnd of ///<• f nil in(i <//•()/). tirst nlludod to by Thomas Willis, li
compared bv l.aouuoo to the sound produced iu a metal or a porcelain cup.
524 DISEASES OF THE RESPIRATORY APPARATUS
when it is struck gently by a pin. It is a single sound, tolerably constant
on coughing, a little less constant on speaking; with the breath sounds,
it is usually heard intermittently, not accompanying each respiratory
movement. The patient may sometimes hear it himself. It occurs most
often in pyopneumothorax, or in large tuberculous cavities ; and it appears
to be due to a large drop falling upon the wall of the cavity or upon the
surface of its fluid content, though, sometimes, it may be due to the
bursting of a bubble. The relatively low pitched sound heard at first is
followed by a high, harmonic or "metallic" echo; smooth walls and a
resonating cavity are prerequisites to such a sound.
Cardiopneumatic murmurs, or cardiac rales, are referred to in the
section dealing with Diseases of the Heart.
Pleural Friction Sounds
These arise during respiration from the rubbing together of the pleural
surfaces, roughened by fibrinous, inflammatory exudates.
They arise most often between the costal pleura and the pulmonary
pleura, but they may arise between the pulmonary pleura and the medi-
astinal pleura, or between the pulmonary and the diaphragmatic pleura.
The sounds may be fine (soft, aspirative), or coarse (scratching, creak- -
ing) ; and they may be loud (intense), or feeble.
The softer, gentler friction sounds may sometimes be confused with
vesicular breathing; the coarser, crackling friction sounds may occasion-
ally be mistaken for rales. The pleural friction sounds can, however,
generally be recognized as such, if one bear the following facts in mind :
(1) they seem close to the ear; (2) they are intensified by pressure of
the stethoscope; (3) they are often accompanied by a palpable friction
fremitus; (4) they do not disappear, nor are they, as a rule, much modi-
fied, on coughing; and (5) they are usually accompanied by pain, whereas
intrapulmonary sounds are not. Pleural friction sounds indicate the
presence of a "dry" pleurisy in the region in which they are audible.
In milary tuberculosis involving the pleura, soft friction sounds may be
heard over large areas of one or of both lungs. Friction sounds sometimes
become audible in tumors of the pleura, or when the pleura is merely
abnormally dry (cholera).
Near the heart, pleural friction may be heard" not only with the
respiratory movements, but also synchronously with the heart's action
owing to the rubbing of the pericardial pleura against the adjacent pul-
monary pleura (pleuropericardial friction). The differential diagnosis
between this extrapericardial friction and true pericardial friction is
described under pericardial friction (q. v.).
EXAMINATION OF THE LUNGS AND PLEUKAE 525
Oilier Pleural Sounds
Besides (1) friction sounds, (2) the amphoric hum or metallic reso-
nance (q. v.), and (3) metallic tinkling (q. v.), two other abnormal aus-
cultatory phenomena referable to the pleura can sometimes be elicited by
the physician on examination; namely, (4) the succussion splash, and
(5) the coin sound.
Succussion Splash. — When the pleural cavity contains both liquid and
air, and the patient is given a vigorous shaking while the physician listens
to the chest, a splashing sound is heard (Hippocratic succussion). The
patient may be able to hear it and to produce it at will himself. It is a
metallic splash. Care should be taken not to confuse it with the splash
produced in the stomach when the latter contains both fluid and gas.
Though this succussion splash is usually due to sero- or pyopneumo-
thorax, it is occasionally heard in the absence of pneumothorax, when large
cavities exist in the lung.
Coin Sound. — If one listens with the naked ear or with a stethoscope in
front to the wall of the chest of a patient, while an assistant percusses at
about the same level on the same side of the chest behind, using two coins
as plexor and pleximeter, a clear ringing sound may be heard if a large
cavity containing air exists in the lung, or if pneumothorax be present.
This sound contrasts markedly with the sound audible under similar con-
ditions over the healthy chest or on the opposite, relatively normal, side
of the patient's chest. This coin sound, sometimes spoken of as the "bell
sound" or "metallic ring," is in reality identical with the metallic ring of
percussion (q. v.) as heard by the ear close to the chest or through the
stethoscope.
References
Beau (J. H. S.). Recherches sur la cause des bruits respiratoires pergus an moyen de I' aus-
cultation. Arch. gen. de med., Paris, 1834, 2e s., v, 567-571.
Cabot (R. C.). Normal auscultatory differences between the sides of the chest. Am. J.
M. Sc., Philadelphia & New York, 1909, cxxxviii, 813-814.
Flint (A.). Physical exploration of the lungs by means of auscultation and percussion. A
course of three lectures delivered by invitation before the Philadelphia County
Medical Society. Philadelphia, 1882, H. C. Lea's Sons & Co. 83 pp. 12°.
Gee (Samuel). Auscultation and percussion [etc.]. 5. ed. London, 1907, H. Frowde.
825 p.
Gerhardt (C.). Lehrbuch der Auskultation und Perkussion [etc.]. 6. Aufl. besorgtvonD.
Gerhardt. Tubingen, 1900, H. Laupp. 381 p.
Hippocrates. Succussion splash. In: De Morbis, i, 6; 15; ii, 47; Hi, 16.
Laennec (R. T. H.}. Traite de V auscultation mediate, et des maladies des poumons et du
cceur. Paris, 1879, Asselin & Cie, xxix. 986 pp. 1 pi. 8°.
A treatise on the diseases of the chest [etc.]. Transl. from the S. French ed.
by John Forbes. New York, 1838, S. S. & W. Wood, xlviii. 784 PP-
2 pi. 8°.
Montgomery (C. M.) & Eckhardt (E. A.). Pulmonary acoustic phenomena. Phila-
delphia, 1915, Phipps Inst. 117 p. 8°.
526 DISEASES OF THE RESPIRATORY APPARATUS
Sewall (H.). The auscultatory determination of early pathologic changes in the lungs. J.
Am. M. Ass., Chicago, 1913, Ix, 2027-r'
Shaw (H. B.). A lecture on some unusual auscultatory phenomena met with in the examina-
tion of the lungs. Clin. J., London, 1903, xxii, 825-329.
Tuffier (T.)« De la difficulte de localiser les lesions pulmonaires par les signes stetho-
scopiques. Bull, et mem. Soc. d. hop. de Par., 1899, 3. s., xvi, 114-122.
[For other references, see under Percussion.]
9. The Relation of Physical Signs to Conditions in
the Lungs and Pleurae
On examining the chest by the physical methods above described, one
should try, at first, merely to draw inferences regarding the air content
of the underlying lungs and the physical state of the pleural cavities,
and only subsequently to seek the pathogenetic explanation of these
physical conditions of the lungs and pleurae. In the table on page 527 a
general view of the relations between physical signs and underlying con-
ditions is presented.
10. Examination of Sputum
(a) Sources of Sputum
The sputum expectorated on hawking or coughing consists of a mix-
ture of secretions from the mucous. membranes with pus, blood or other
materials given off from the respiratory apparatus. The secretions come
from the mucous membranes of the larynx, trachea and bronchi, pharynx
and back of the nose (choanae). In addition to the above, the sputum
contains saliva, secretions from the mucous membranes of the mouth, and
sometimes food particles.
It is obviously important to distinguish, when possible, the sputum
that comes from the lungs and deeper air passages from that originating
in the mouth or nasopharynx. Pulmonary sputum should be collected,
whenever practicable, by methods that guarantee its relative freedom from
admixture with constituents from the mouth, nose and nasopharynx (See
Sputum Cultures). It may be received in a sterile Petri dish, or in a
wide-mouthed bottle, previously cleaned, boiled in water, and dried.
Mouth sputum usually consists chiefly of saliva and is recognizable as
an opaque, sticky fluid in which, on microscopic examination, swollen,
flat, epithelial cells and leukocytes, singly or in groups, are visible.
Nasopliaryngeal sputum consists chiefly of mucus more gelatinous than
that in the saliva and met with usually in the form of roundish balls or
lumps the size of a pea or bean, which do not run together, or mix well
EXAMINATION OF THE LUNGS AND PLEUKAE 527
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528 DISEASES OF THE KESPIRATOKY APPAKATL^
with the rest of the sputum. This mucus from the nasopharynx may be
transparent or purulent; it may be gray or black from admixture with
coal dust, or it may contain tough, dry, wrinkled scabs, yellowish, brown-
ish or greenish in color.
When the sputum is purulent it is often difficult to decide whether
the pus has had its origin in the mouth and pharynx or whether it has
come from lower down. An admixture with saliva, or a very putrid odor,
is suggestive of a buccal or a pharyngeal origin, though very fetid sputum
is expectorated also in putrid bronchitis, in bronchiectasis and in pul-
monary gangrene.
Sputum of pulmonary origin, when scanty, may sometimes be in-
creased by the administration of a few doses of potassium iodid or
ammonium chlorid. In early pulmonary tuberculosis, especially in chil-
dren, the tubercle bacilli may sometimes be found in sputum swallowed
during the early morning hours ; the sputum is obtained by washing out
the stomach before breakfast (T. Hausmann).
In handling- sputum precautions should be taken to avoid personal infection.
The sputum should be kept in well-covered receptacles until disposed of. In hos-
pitals the sputa and sputum cups should be sterilized after examination in an
autoclave. If chemical sterilization is relied upon a 5-per-cent solution of carbolic
acid will suffice if the quantity of sputum be small.
References
Jones (Edith P.). The disposal of sputa. Am. J. Nursing, Philadelphia, 1906-07, vii,
106-108.
Manning (W. J.). Disposal of sputum. J. Am. M. Ass., Chicago, 1909, liii, 829-832.
Thorn (W.). NeueBeitrdge zur Frage der Sputum-Beseitigung und chemisch-physikalischen
Sputumdesinfektion. Ztschr. f. Tuberk. u. Heilstatt., Leipzig, 1902-03,
iv, 143-153.
Walsh (/.). Preventing infection by the proper disposal of sputum. Outdoor Life, Trudeau,
N. Y., 1905, ii, 191-194-
(b) Varieties of Sputum
According to the principal constituent, four main varieties of sputum
may be described : (1) mucous; (2) purulent; (3) serous; and (4) bloody.
Other forms of sputum are admixtures of these (e. g., mucopurulent,
mucohemorrhagic, etc.). One should always notice whether the different
constituents of sputum are intimately mixed with one another to form
a homogeneous fluid, or remain separated from one another as recognizably
different parts.
Mucous Sputum. — When the sputum consists of pure mucus it is usually
either from the choanae or from a beginning bronchitis. Sputum from the
choanae (nasopharyngeal) is usually hawked up; bronchitic sputum is
coughed up. .
EXAMINATION OF THE LUNGS AND PLEUKAE 529
Purulent Sputum. — When not from the mouth or the pharynx, pure
purulent sputum (free from mucus) is due to the rupture of an abscess
of the lung, or of a neighboring organ (empyema, liver abscess), into the
bronchi.
Mucopurulent Sputum. — Mucus and pus may be intimately mixed with
each other in the sputum in diffuse bronchitis. In bronchoblenorrhea, the
thin mucopurulent sputum often separates on standing into three layers.
Similarly, three layers are met with in bronchiectatic sputum, in lung
gangrene, and in fetid bronchitis. The upper layer is frothy and consists
of lumps and balls; the middle layer consists of thin mucus and serum
with a few shreds hanging down from the upper layer; while the lower
layer contains a sediment of confluent pus and whitish particles.
In pulmonary tuberculosis, the sputum contains pus and mucus,
usually not well mixed, the pus appearing as ball-shaped or coin-shaped
masses surrounded by mucus (nummular sputum). If large cavities exist
in a tuberculous lung, nearly homogeneous sputum may be expectorated.
Serous Sputum. — In pulmonary edema, an abundant thin but very
frothy sputum, resembling beaten egg-white, is expectorated, or may run
out of the mouth. It may be colorless, but it is sometimes tinged with pink
(blood). This form of sputum is highly characteristic and of great im-
portance for diagnosis.
Bloody Sputum. — Sometimes pure blood is expectorated (HEMOPTYSIS)
in bronchiectasis, in pulmonary tuberculosis, in leaking aneurism, and,
occasionally, in lung abscess or in lung tumor. In hemoptysis, the blood
is coughed up ; it can be distinguished from the blood that is vomited up
from the stomach (hematemesis) (1) by its bright red color, (2) by the
froth in it, and (3) by the fact that it is not mixed with food.
When blood is intimately mixed with mucus in the sputum, the color
varies according to the relative quantities of these two constituents and
the length of time the blood has remained in the air passages before it
is expectorated. Thus, in pneumonia, the sputum may have a brick dust
tint (rusty sputum), or, especially in alcoholic cases, it may be outspokenly
hemorrhagic. Mucohemorrhagic sputum is also met with in hemorrhagic
infarction of the lung and in neoplasm.
The so-called prune-juice sputum is a serohemorrhagic sputum. It is
met with when a croupous pneumonia is complicated by edema of the
lung. A peculiar mucohemorrhagic sputum of sticky consistency, re-
sembling currant jelly, is seen in neoplasm and sometimes in lung syphilis.
Small streaks of bright blood in sputa otherwise of mucous character
usually originate in the upper air passages (nose, pharynx, larynx) or in
the mouth.
Blood-stained saliva is often brought to the physician by the hysterical
and by simulants ; it is usually a thin fluid, of stale odor and of brownish-
red color.
530 DISEASES OF THE RESPIRATORY APPARATUS
References
Hawes (J. B.). Hemoptysis. Its significance and treatment at out-patient departments,
dispensaries and in private practice. (A study of 114 cases from the Out-
patient Department of the Massachusetts General Hospital, Boston.) Bos-
ton M. & S. J., 1912, clxvi, 735-737.
M utter (F.). Beitrdge zur Kenntnis des Mucins und einiger damit verwandter Eiweiss-
stoffe. Ztschr. f. Biol., Munchen u. Berlin, 1901, xlii, 468-664.
Ward (S. M.). Hysterical blood spitting. Med. & Surg. Reporter, Philadelphia, 1887, Ivii,
139-141.
Widal (F.). Hemoptysie. Diet, encycl. d. sc. med., Paris, 1888, 4. s., xiii, 304-335.
(c) Color of Sputum
Aside from the above-mentioned purulent sputa (yellow or yellowish-
green) and hemorrhagic sputa (red, brown, or yellowish-red), sputum
may assume different tints from the admixture of various coloring matters.
Black sputum is seen in coal- and iron-workers; blue sputum is occa-
sionally seen in workers in dye-works ; green sputum is met with in pneu-
monia with jaundice, sometimes in caseous pneumonia, and occasionally
in pyocyaneus infections ; yellow sputum may be due to hematoidin in
lung abscesses, or to bile when liver abscesses break into the lung. In
chronic passive congestion of the lung in cardiac disease, a yellowish-red
tint may appear, owing to the large number of pigment-containing cells
— "heart-failure cells" — in the sputum. White sputum resembling starch
is sometimes seen in bakers and in millers; the starch granules can be
demonstrated microscopically.
(d) Odor of the Sputum
Usually stale, the odor of sputum may become putrid from decomposi-
tion in the mouth or in the air passages (fetid bronchitis, bronchiectasis,
lung gangrene). To people that come in contact with patients, there is
no odor more trying than that of fetid sputum, unless it be that of
bromidrosis !
(e) Consistence of the Sputum
This depends mainly upon the relative amount of mucus the sputum
contains; in asthma, and sometimes in pneumonia, the sputum is so
tenacious that it will not flow out of the sputum cup held upside down.
(/) Protein Content of Sputum
Sputum arising chiefly from increased secretion of the bronchial
mucous membrane, as in asthma and in bronchitis, is poor in protein,
whereas sputum arising in inflammations of the lung substance itself
(pneumonia) or in transudations (pulmonary edema, chronic passive con-
gestion) is more close to blood serum in its chemical composition and thus
EXAMINATION OF THE LUNGS AND PLEURAE 531
is rich in protein. The amount of protein present in the sputum may
therefore be helpful in differential diagnosis. One makes the test as
follows (F. Miiller) :
Thirty to fifty cubic centimeters of sputum are placed in an Erlen-
meyer flask, double the quantity of 1-per-cent aqueous solution of
acetic acid is added, and the mixture well shaken. The acetic acid
precipitates the mucin and leaves the proteins proper in solution. The
mucin is filtered out, and a 10-per-cent solution of ferrocyanid of potas-
sium added to the filtrate. An abundant precipitate indicates much
protein and points to an inflammation of, or a transudate into, the lung.
References
Bezanqon (F.) & de Jong (S. /.)• L'exsudat sero-albumineux, le mucus, et les aspects
reticules muqueux des crachats. Bull, et mem. Soc. med. d. hop. de Paris,
1907, 3. s., xxiv, 805-811.
Falk (F.}. Zur Chemie des Sputums. In: Ergebn. d. Physiol. (Asher & Spiro). Wies-
baden, 1910, ix, 406-432.
Gee (5.). Albuminous expectoration. St.Barth. Hosp. Rep., London, 1886, xxii, 99-101.
Goodman (E. H.). The diagnostic importance of albumin and albumose in the sputum
and their relation to occult blood. Arch. Int. Med., Chicago, 1911, viii,
163-168.
Hartley (P. //. S.}. Albuminous expectoration following paracentesis of the chest. St.
Earth. Hosp. Rep., 1905, London, 1906, xli, 77-110.
Lesieur (C.)« Sur I'albumoptysie, I'albumino-reaction des crachats de H. Rogers; 190
observations personnelles. Butt. Soc. med. d. hop. d. Lyons, 1910, ix, 312-
321.
Ldwenbein (L.). Ueber die Eiweissreaktion des Sputums bei Lungenluberkulosc. Zlschr.
f. Tuberk., Leipzig, 1914, xxiii, 122-126.
Plesch (J.)« Chemie des Sputums. In: Handb. d. Biochem. (Oppenhcimcr) . Jena, 1910,
Hi, 1. Hlfte., 7-19.
Ridge (P. B.} & Treadgold (H. A.}. The albumin reaction in sputum: its significance
and causation. Lancet, London, 1913, ii,
(g) Amount of Sputum
This is extremely variable. The largest amounts are met with (1) in
certain bronchial affections (bronchoblenorrhea) ; (2) in large bronchi-
ectatic or phthisical cavities (as much as one to two litres daily) ; (3) in
pulmonary edema, or when abscesses or empyemas break into the bronchi.
In such cases the sputum may be brought up in mouthfuls. In bronchi-
ectasis the patients usually empty their cavities on changing their position
after waking in the morning.
(h) Larger Particles or Masses in the Sputum Recognizable
by the Naked Eye
(1) Fragments. — Occasionally, pieces of lung tissue (sequestra) are
coughed up, in gangrene or in lung abscess. Pieces of tumor may appear
in the sputum; the histological examination is important for diagnosis.
532 DISEASES OF THE RESPIRATORY APPARATUS
One of my patients coughed up both arytenoid cartilages from his larynx
in the course of a laryngeal perichondritic complication of typhoid fever.
(2) Bronchial Casts. — Sometimes branched fibrinous casts of the bron-
chi are coughed up in fibrinous bronchitis, in croupous pneumonia or in
Fig. 157. — Fibrin Cast. (Photographed from Emerson's Clin. Diag.)
diphtheria. When they are small, one can isolate them by shaking the
sputum with water. They stain red in Ehrlich's triple stain, while masses
of mucous origin (Curschmann's spirals) stain green.
(3) Curschmann's Spirals. — These consist of a central mucous thread,
either straight and surrounded by a twisted mantle of mucus, or twisted
or coiled like a rope and then usually ensheathed in clear mucus. The
central thread measures 0.5-2 cm. in length and 0.5-1 mm. in thickness.
In the mucus, one can usually make out eosinophils, 'epithelial cells, pus
cells, and, sometimes, Charcot-Leyden crystals. Such spirals are met with
jpost often in cases of recurring bronchiolitis combined with asthmatic
EXAMINATION OF THE LUNGS AND PLEUEAE 533
attacks, but Curschmann's spirals may occur also in patients that are not
asthmatic, and, moreover, not all paroxysms of asthma are associated with
Fig. 158. — Curschmann's Spirals, (a) x 80, (b) Part of (a) x 300. (After T. Brugsch and
A. Sohittenhelm, "Lehrb. d. klin. Unter.," published by Urban & Schwarzenbei»g, Berlin.)
the expectoration of spirals. They can usually be found with the naked
eye if one look for sagolike lumps of mucus, but one can scarcely be
certain of them with the naked eye and the. macroscopic examination
should lie controlled with the microscope.
(4) Tuberculous Lenses. — In the sputum from phthisical cavities, little
particles, occurring singly or in small groups, each the size of the head
of a pin, of a grayish-white or grayish-yellow color, of rather firm con-
sistency, and resembling crumbs of bread in their appearance, are often
met with. These "lenses" contain large numbers of tubercle bacilli, and
sometimes also networks of elastic fibers. They have their origin in the
caseous walls of a cavity.
(5) Dittrich's Plugs. — In the decomposing sputum of putrid bronchi-
tis, of bronchiectasis, and of lung gangrene, small yellowish-white masses,
closely resembling the tuberculous lenses described above, are sometimes
seen. They have a very penetrating, foul odor. They consist of .tissue
534 DISEASES OF THE EESPIKATOKY APPARATUS
particles, or of small pus masses, which have undergone decomposition
in the lungs, or in the bronchi. Microscopically, they contain numerous
fatty-acid crystals and bacteria (cocci and long bacilli).
(6) Fungus Colonies. — These appear as small yellowish-white particles
about the size of tuberculous lenses or of Dittrich's plugs, but of softer
consistency. They are common (-1) in pulmonary tuberculosis and in
chronic bronchitis, where they are found microscopically to consist of
masses of fungi; (2) in actinomycosis, then usually as the so-called
"sulphur bodies,77 in which the microscope reveals the typical ray-fungus ;
and (3) in pneumonic aspergillosis, and in other mycoses of the lung (q. v.).
(7) Echinococcus Cysts. — Echinococcus cysts, or pieces of them, may,
occasionally, be met with in sputum.
(8) Lung Stones. — Occasionally, a small si one is found in sputum;
most often, it is a portion of a calcified bronchial aland.
References
Curschmann (//.)• /•,'///./>• ttcnn-rknugcn iiber die im Bronchialsecrct vorkommenden Spira-
l< n.. I)rtitNcln's Arch./, klin. Med., Leipzig, 1884-85, xxxvi, 578-585.
Dittrich. C7mw/.sr //<•/• Bronchialcatdrrh, mil sackigen Erweiterungen der Luftrohre.
r/Y//.sr//r./. d. prakt. Heilk., Prag, 1846, ii, 116.
Malcolm. Calcareous Imdfi-N, which were expectorated. Tr. Belfast Clin. & Path. Soc.t
1854, 78-80.
Pel (P. K.}. Zur Deutung <l< r .sm/rw/ //.//./<•//. »S'/>m//- nn.d CentraJfdden im Sputum. Ztschr. f.
klin. Med., Berlin, 1885, ix, 29-39.
(i) Microscopic Study of the Sputum
Microscopically, sputum is studied for: (1) cells; (2) ela'stic fibers;
(3) crystals; and (4) bacteria and parasites.
To make preparations of sputum for microscopic examination, m:n
spreads out a larger mass on a glass plate on a dark background, picks
out suspicious particles from several areas, and, with a needle, places
these on a glass slide and applies a cover slip, avoiding too great pressmv
in order not to destroy the characteristic constituents (spirals, crystals,
etc.). If necessary to dilute the sputum, one may add a drop of physio-
logical salt solution. The following examinations (i-iv) are made with
fresh, unstained sputum.
i. Cells in (he Sputum
Among the mucous threads, one finds, normally, some epithelial cells
and a few white blood corpuscles.
Squamous epithelium arises from the mouth, the pharynx, or the
outer portion of the larynx.
Cylindrical epithelium may come from the nose, the upper pharynx
or from the larynx and bronchi ; the cilia are usually invisible. Cylin-
EXAMINATION OF THE LUNGS AND PLEURAE 535
drical cells are abundant in catarrh of the mucous membranes and in
bronchial asthma.
Alveolar epithelial cells are round cells with a vesicular nucleus; the
cells are a little larger than white blood corpuscles. Fat granules, coal
particles, and myelin droplets may be seen within the protoplasm ; the fat
granules stain orange red on the addition of a drop of alcoholic solution
of Sudan III; myelin does not stain. In chronic passive congestion of
the lung (cardiac disease), such cells are numerous in the sputum, and
they contain then also yellowish-brown granules of hemosiderin or hema-
toidin (so-called "heart-failure cells") ; such cells are also present in the
sputum after any form of bronchial or pulmonary hemorrhage, and do
not necessarily, therefore, depend upon myocardial insufficiency.
Wlrite blood corpuscles of the polymorphonuclear neutrophil type are
abundant in purulent sputum ; their nuclei are easily made visible by the
addition of a drop of a 1-per-cent solution of acetic acid. Eosinophilic
leukocytes are abundant in the sputum of asthmatic patients, where they
may make up 60 per cent of all the leukocytes present (F. Miiller). They
may also be abundant in certain forms of chronic bronchitis, and during
periods of improvement in some cases of pulmonary tuberculosis. In
searching for eosinophil cells in the sputum, one makes a smear, dries it
in the air and then stains with Jenner's stain (eosinate of methylene blue),
just as one stains a blood smear. The cells are also easily recognizable
in fresh unstained sputum through the presence of large highly re-
fractive granules in the protoplasm.
Lymphocytes may also be present in sputum, sometimes in large
numbers. They are easily recognizable as small mononuclear elements,
the nucleus being surrounded by a narrow rim of non-granular protoplasm.
Red blood corpuscles are present in the hemorrhagic sputa met with
in bronchiectasis, pulmonary tuberculosis, lung tumor, etc.
Tumor cells are sometimes recognizable in the fresh sputum. In carci-
nomata and in sarcomata of the air passages and lungs, cells from the tumor
are sometimes broken off and expectorated. It is rarely safe, however,
to make a diagnosis of tumor from the sputum unless the tumor particles
are large enough to harden, section, and stain f6r histological examination.
References
Bezancon (F.}. Etude histo-chimique et cytologique des crachats. Folia din. chim. et
micros., Salsomaggiore, 1909, ii, 39-66.
Bezancon (F.) & de Jong (S.-I.). ' Les methodes nouvelles d'examcn des cracfiats en
dehors de la bacteriologie. Gaz. d. hop., Paris, 1910, Ixxxiii, 913-951.
Frank (/.). The sputa. Med. Monog., Topeka, Kansas, 1899, i, 305-319.
de Jong (S.-I.). Etude histo-chimique et cytologique des crachats. Paris, 1907. 8°.
Lenhartz (H.). Examination of the sputum. Dominion M. Month., Toronto, 1902, xix,
98-116.
536 DISEASES OF THE KESPIKATOKY APPAKATUS
Ley den (£'.)• Ueber eosinophile Zellen aus dem Sputum von Bronchialasthma. Deutsche
med. Wchnschr., Leipzig, 1891, xvii, 1085.
Schmidt (A.). Neuere Arbeiten iiber das Sputum. Fortsch. d. Med., Berlin, 18$5, xiii,
56-64.
Teichmiiller (W.). Das Vorkommen und die Bedeutung der eosinophilen Zellen in Sputum.
Deutsches Arch. f. klin. Med., Leipzig, 1898, Ix, 576-606.
ii. Elastic Fibers in Sputum
These are found in the sputum in all destructive diseases of the lungs,
especially in pulmonary tuberculosis and in lung abscess; occasionally,
they occur in the sputum in gangrene, though in the latter disease they
are usually absent, since a ferment that dissolves them is present.
In searching for elastic fibers one chooses a suspicious particle of
sputum (e. g.j a tuberculous lens), places it on a slide, and adds a drop of
10-per-cent 3£OH solution. Or one may mix 30 to 50 c.c. of sputum with
an equal amount of the alkali and warm on the water bath until clear.
The mixture is then allowed to sediment in a conical glass or is centrif ugal-
ized, and the sediment is examined microscopically. The elastic fiber*
are easily recognizable; they occur either singly or in networks corre-
sponding to the alveoli; occasionally, sheets of elastic tissue, possibly arte-
rial in origin, are seen. The fibers are uniform in diameter, present sharp
outlines, are highly refractive, tend to curl up at the ends ; they are often
branched; pressure on the cover slip does not give rise to varicosities or to
changes in caliber. They are thus easily distinguishable from fatty-acid
crystals (q. v.). They may be stained differentially, if desired, either
fresh by magenta, or, after fixation, by Weigert's elastic-fiber method, or
by the orcin method used in histology.
iii. Crystals in Sputum
Several varieties of crystals are met with in different sputa. They
include hematoidin crystals, fatty-acid crystals, amino-acid crystals, cho-
lesterin crystals, and the so-called Charcot-Leyden crystals.
(1) Hematoidin Crystals. — These occur in the form of brownish-red
nodules, rhombic plates, and sometimes as amorphous yellowish-brown
granules, usually lying in bundles; they are most common after old
hemorrhages in the lung, or after rupture of lung abscesses or of liver
abscesses into the lung.
(2) Fatty-acid Crystals. — These appear as fine, curved, colorless
nodules, which melt to form fat droplets on warming the slide. They
are soluble in ether and in KOH : on pressing on the cover slip, varicosities
appear in the crystals. They are most abundant in Dittrich's plugs
(q. v.) of putrid bronchitis, of bronchiectasis, of lung abscess, and of
gangrene.
PLATE IX
Fig. 1. — Actinomyces with Spores. (After
Lenhartz, in L. Mohr u. R. Staehelin,
"Handb, d. inner. Med.," published by
J. Springer, Berlin.)
Fig. 2. — Actinomyces from the Sputum — •
Unstained. (After W. Kolle u. II.
Hetsch, "Die experimentelle Bakteriolo-
gie, etc.," published by Urban &
Schwarzenberg, Berlin.)
ff
& vQi
Fig. 3. — Cells in the Sputum — a, Alveolar Epithelial Cells Containing Coal Dust ;
6, Squamous Epithelial Cell ; c, White Blood Cells ; d, Cylindrical Epithelial
Cell ; e and f, Heart-failure Cells ; g, Cells Showing a Peculiar Degeneration ;
h, Those with Myelin Droplets ; i, One Full of Fat Droplets ; /, Free Myelin ; 7c,
Red Blood Cells ; I, Bacteria ; in, Free Blood Pigment X 400. (After C. P.
Emerson, "Clinical Diagnosis," published by J. B. Lippincott Co., Philadelphia.)
EXAMINATION OF THE LUNGS AND PLEURAE 537
' (3) Amino-acid Crystals. — In the sputum from pulmonary abscess,
arid in that from putrid bronchitis and from gangrene, one sometimes sees
characteristic crystals of leucin and of tyrosin. Such crystals arise as the
result of the action of proteolytic ferments.
(4) Cholesterin Crystals. — The characteristic large rhomboid plates of
this secondary alcohol are occasionally seen in sputum along with ammo-
acid crystals.
(5) Charcot-Leyden Crystals. — These are sharply-pointed, octahedral
crystals, greatly variable in size, sometimes seen lying singly, or in
groups, among the cellular elements
of the sputum. They are soluble in
hot water, in mineral acids, and in
alkalies. The crystals show an affin-
ity for eosin. They are very fragile,
being easily broken in making the
preparation. They are most often
met with in asthmatic sputum where
they occur along with Curschmann's
spirals and eosinophils. It has been
suggested that the eosinophils sup-
ply the material that gives rise to
the crystals; indeed, it seems very
probable that they owe their origin
to the disintegration of eosinophil
cells. In searching for them, one
picks out yellow specks or strips in
the sputum. Besides in asthma, they
have been observed in fibrinous bronchitis, in hay fever, and in distomiasis
pulmonalis.
References
Cohn (T.). Beitragzur Kenntniss der Charcot' schen undBottcher'schen Krystalle. Deutsches
Arch. f. klin. Med., Leipzig, 1894-95, liv, 515-524.
Riesman (/>.). Cfiarcot-Leyden crystals. Phila. Polyclin., 1896, v, 361-363.
Fig. 159.— Charcot-Leyden Crystals— 100/1.
(After T. Brugsch and A. Schittenhelm,
"Lehrb. d. klin. Unter.," published by
Urban & Schwarzenberg, Berlin.)
iv. Parasites as Seen in Fresh Sputum
Amebae, eggs of the lung fluke, and echinococcus hooklets, when pres-
ent, are easily visible in unstained specimens; these are described below,
, under stained preparations.
v. Bacteria and Parasites as Seen in Stained Specimens of Sputum
Bacteria are always present in sputum. They are few in number in
the pure mucous sputa of chronic bronchitis, of asthma, and of chronic
538 DISEASES OF THE RESPIRATOKY APPAEATUS
passive congestion, but they are present in large numbers in purulent
sputa and in the various putrid sputa. In the former, staphylococci, strep-
tococci, pneumococci and influenza bacilli are most often met with, while
in the latter large anaerobic bacilli are also found.
The predominant organisms in the sputum may often be identified
simply by examining a stained smear, but it is preferable to make also
a culture from fresh sputum especially collected and washed with sterile
salt solution for the purpose.
In making bacteriological cultures from the sputum, the following
method is used: The patient is instructed how to expectorate from the
lung into a sterile Petri dish. With a heavy sterile platinum needle,
the examiner immediately picks out a ball of spiftuni and washes it in
several successive Petri dishes containing sterile water or salt solution,
in order to remove, as far as possible, bacterial contaminations from the
mouth. Stained smears made before and after washing the sputum show
the importance of this washing process (J. A. Luetscher). With sterile
needles, the sputum mass is then broken up in a tube of bouillon, and a
little bit, taken preferably from the center, is used for the making of
cultures and of smear preparations. (For the media most suitable for
the different bacteria suspected, see section on Diagnosis of the Infec-
tious Diseases.)
The three bacterial forms in the sputum that are most important
for clinical diagnosis are: (1) the tubercle bacillus; (2) the pneurno-
coccus; and (3) the influenza bacillus. Other forms of vegetable micro-
organisms sometimes of importance here, include (4) the pyogenic cocci
in lung abscesses and in bronchiectasis, (5) diphtheria bacilli, (6) strepto-
thrix actinomyces and other forms of streptothrix, (7) aspergillus, (8)
blastomyces, and (9) the thrush fungi.
Examination of Sputum for Tubercle Bacilli. — One chooses the more
purulent part of the sputum, or looks for the tuberculous lenses. The
bacilli are most abundant in the sputum that comes from the walls of
cavities in the lung. (For the preparation of cover slips, an'1 for methods
of staining, see section on the Diagnosis of the Infectious Diseases.)
Examination of Sputum for Pneumococci. — These may be present in
small numbers in Gram-stained specimens of almost any sputum examined.
They are very numerous and are usually present in pure culture in the
carefully collected rusty sputum of croupous pneumonia. They appear
as lanceolate diplococci, often encapsulated. They may be isolated
by cultural methods (q. v.) and their pathogenicity tested by inocu-
lation of mice (at the root of the tail), or of rabbits (injection into ear-
vein).
Examination of Sputum for Influenza Bacilli. — These extremely
minute, polar-staining, bacilli occur usually in large masses when they are
present in the sputum. Though in cover-slip preparations, stained by car-
PLATE X
Fig. 1. — Smear from Pneumonic Sputum,
Stained with Dilute Carbolfuchsin.
(After W. Kolle u. H. Hetsch, "Die ex-
pcrimentelle Bakteriologie, etc.," pub-
lished by Urban & Schwarzenberg, Ber-
lin.)
Fig. 2. — Bacillus influenzae from Nasal Se-
cretion. Fuchsin Stain. (After W.
Kolle u. H. Hetsch, "Die experimentelle
Bakteriologie, etc.," published by Urban
& Schwarzenberg, Berlin.)
Fig. 3. — Micrococcus catarrhalis — Gram-
fuchsin Stain. (After N. v. Jagic u. IT.
K. Barrenschen. "Atlas u. Grund. d.
Klin. d. Mikroskopie," published by M.
Terles. Wien.)
Fig. 4.— Tubercle bacilli. Stained with
Fuchsin and Mcthyloiif Hluo. tAft.M- N.
v. Jagic u. IT. K. Barreusc'lu'ii, "Alias u.
Grund. d. Klin. d. Mikroskopie." pub-
lisbed by M. IVrles, Wien.)
EXAMINATION OF THE LUNGS AND PLEUEAE 539
bolfuchsin diluted with 10 parts of distilled water and allowed to act for
10 minutes, their nature may be suspected; the proof of their identity
should be brought by means of cultures made upon blood-agar.
Examination of Sputum for Fungi. — Of the fungi met with in sputum,
three varieties are of especial importance, (1) actinomyces, (2) asper-
gillus, and (3) blastomyces.
STREPTOTIIRIX ACTINOMYCES. — In actinomycosis of the lungs, the
sputum is sometimes glairy and mucilaginous, more often purulent, and
contains yellow granules about the size of a small pin-head or of a sand-
grain — the so-called "sulphur granules." The yellow color may not be
visible except under the low power of the microscope; to the naked eye
the particles may look grayish white. If one of these' particles bo placed
on a glass slide,' under a cover glass, and pressure be applied, one can see
under the high power a central area consisting of fine, closely aggregated
fungous threads, and a peripheral area, made up of branched, flask-shaped
and clublike processes. Staining is unnecessary for recognition, but the
fungus is brought out very beautifully if a little Lugol's solution be run
under the cover slip. In dried-and-fixed smears, one may use methylene
blue or Gram's stain for the mycelium, using safranin or carmin as a
counterstain for the clubs.
OTHER FORMS OF STREPTOTHRIX. — Recently streptothrix infections
of the lung resembling pulmonary tuberculosis have been reported, and
forms of streptothrix have been found in the sputum during life and in
the lesions in the lung at autopsy (See Part IV).
ASPERGILLUS. — In aspergillus infections (pneumonomycosis aspergil-
lina) the characteristic doubly-contoured threads (usually unbranched)
containing numerous brownish pigmented spores are found. They are
best seen on treatment of the sputum with 10-per-cent KOH. The fungus
occasionally occurs in bronchiectatic, and in tuberculous, cavities.
BLASTOMYCES. — This parasite is occasionally met with in the sputum
in cases of systemic blastomycosis or oidiomycosis (q. v.). It is best
brought out by treating fresh sputum with dilute KOH, when the doubly-
contoured refractive yeastlike bodies become visible. If budding forms
are seen, the fungus is probably a true Blastomyces; if endosporulation
be visible, it is probably the fungus of coccidioidal granuloma (See
Part IV).
Animal Parasites in Sputum. — The three animal parasites most likely
to be met with in sputum are: (1) echinococcus booklets and scolices; (2)
ova of the lung fluke ; and (3) Entameba histolytica.
ECHINOCOCCUS SCOLICES AND HOOKLETS IN SPUTUM. — Rarely pri-
mary in the air passages, echinococcus material occasionally reaches them
by rupture of a cyst of the liver into the lung, and then portions of
the membranes, degenerated scolices, or hooklets may be found in the
sputum.
540 DISEASES OF THE RESPIRATORY APPARATUS
OVA OF PARAGONIMUS WESTEKMANI. — The lung fluke that causes
parasitic hemoptysis is, in America, a rare parasite, though it is not at
^^^ all uncommon in Japan. When in Tokyo, in 1899, I
/^2pr\ was shown a typical case by Dr. K. Miura. In that
country, when hemoptysis occurs, they always look for
?'f /^vMt\ tne presence of the eggs of this parasite. The eggs are
• v . ^ brown and are about 0.1 mm. long and 0.05 mm. broad;
there is a cover, or operculum, on the blunt end.
. I ENTAMEBA HISTOLYTICA. — When amebic abscess of
\; '' $!/ the liver breaks through into the lung, amebae may be
*5fev/ found in the sputum. In a case, personally observed,
the hepatic condition was not suspected until the ac-
x^ tively motile parasites appeared in the sputum. Tb?
should be obtained fresh, and should be exam-
Fi<r ico— E of
Faragonimus west- ined-on a warm stage; the amebae present the same
tumani ooo/i Aft- Pearance as wlien theJ occur in the feces- (See
er Katsurada, in Dysentery.) It should not be forgotten that amebae
Dl.e mav be present in the sputum in pyorrhea alveolar is.
thienschen Parasi- " . .
ten des Menschen," and that microscopically it may be impossible to dis-
Sonf&'Danfeis^on! tinguish between the entameba histolytica and the
London.) entameba buccalis.
References
Allen (R. W.). The bacterial diseases of respiration and vaccines in their treatment. Lon-
don, 1913, H. K. Lews. 246 p. pi. 8°.
Boardman ( W. W.}. The use of antiformin in the examination of the sputum for the tubercle
bacillus. Johns Hopkins Hosp. Bull, Baltimore, 1911, xxii, 269-272.
Castellani (A.). A note on broncho-oidiosis. J. Trop. M. & Hyg., 1913, xvi, 102-104-
Cecil (R. />.)« Streptococcus viridans in its relation to infections of the upper respiratory
tract. Arch. Int. Med., Chicago, 1915, xv, 150-168.
Chalmers (A. J.} & O'Farrell (W. R.}. Bronchial spirochcetosis. J. Trop. M. & Hyg.,
1913, xvi, 329-334.
Hastings (T. W.) & Niles (W. L.). The bacteriology of sputum in common non-tuberculous
infections of the upper and lower respiratory tracts, with special reference
to lobar and broncho-pneumonia. J. Exper. Med., Lancaster, Pa., 1911,
xiii, 638-651.
Holt (L. E.). The bacteriology of acute respiratory infections in children as determined by
cultures from the bronchial secretion. J. Am. M. Ass., Chicago, 1910, Iv,
1241-1246. Also: Tr. Ass. Am. Physicians, Philadelphia^ 1910, xxv,
223-237.
Leared. Expectoration df portions of hydatid cysts; apparently the result of an accident to the
patient. Tr. Path. Soc., London, 1856-57, viii, 92-98.
Loffler (F.). Ein neues Anreicherungsverfahren zum fdrberischen Nachweise spdrlicher
Tuberkelbazillen. Deutsche med. Wchnschr., Leipzig u. Berlin, 1910,
xxxvi, 1987.
Lord (F. T.). A method of staining sputum for bacteriological examination. Bost. M. &
S. J., 1902, cxlvii, 659.
Luetscher (J. A.). A bacteriological and clinical study of the non-tuberculous infections of
the respiratory tract, with special reference to sputum cultures as a means
of diagnosis. Arch. Int. M., Chicago, 1915, xvi, 657-780.
EXAMINATION OF THE LUNGS AND PLEUKAE 541
Macintyre (/.). Demonstration on the pathogenic organisms of the upper respiratory tract.
Lancet, London, 1893, ii, 479-482.
Manson (P.). Endemic haemoptysis. Tr. Hongkong M. Soc., 1899, i, 80-86.
Mautner (H.). Eine bisher nicht beobachtete Moniliaart bei chronischer Bronchitis. Wien.
med. 'Wchnschr., 1914, Ixiv, 1065-1067.
Odell (Anna). Bacteriology and bacterial therapy of the upper air passages. J. Mich. M.
Soc., Grand Rapids, 1915, xiv, 24-28.
Roe (J. O.)« Phlegmons of the upper respiratory tract. N. York M. J. [etc.], 1914, c,
1049-1052.
Rowlette (R. J.). A note on vaccines in the treatment of respiratory diseases. Dublin J.
M. Sc., 1915, cxl, 103-111.
Sachs-Muke. Die Sedimentierung der gesamten Tagesmenge des Auswurfs durch die
gleichzeitige Anwendung von Wasserstoffsuperoxyd und Sublimat. Ztschr.
/. drztl. Fortbild., Berlin, 1907, iv, 556-562.
Smith (7\). A comparative study of bovine tubercle bacilli and of human bacilli from sputum.
J.Exper. M., New York, 1898, Hi, 451-511.
Smith (W. H.}. A method of staining sputum for bacteriological examination. Bost. M.
& S. J., 1902, cxlvii, 659-662.
Stiles (C. W.) & Hassell (A.}. Parasitic hcemoptyses present in the United States. Pub
Health Rep. U. S. Mar. Hosp. Serv., Washington, 1900, xv, 3017-3027.
Theisen (C. F.}. Pneumococcus infections of the nose and throat. Ann. Otol., Rhinol. &
Laryngol., 1913, xxii, 175-179.
Tunnicliff (Ruth). An anaerobic vibrio isolated from a case of acute bronchitis. J. Infect.
Dis., Chicago, 1914, xv, 350.
Vhlenhuth (/*.)• Neuere Methoden der Sputumuniersuchung. Med. Klin., Berlin, 1909,
v, 1296-1300.
Uhlenhuth (P.) & Xylander. Antiformin, ein bacterienauflosendes Desinfektionsmittel.
Berl. klin. Wchnschr., 1908, xlv, 1346-1349. *
Wellmann (C.). Comments on tropical medicine: endemic hemoptysis. Calif. State J.
M., San Francisco, 1910, viii, 23; 66; 102; 312; 346.
Williamson (C. S.). The value of the Loffler method of sputum examination. J. Am. M.
Ass., Chicago, 1912, Iviii, 1005.
Wittich (F. W.}. Vaccines in the treatment of bacterial diseases of the lungs complicating
pulmonary tuberculosis and their preparation. Canad. M. Ass. J.,
Toronto, 1915, v, 289-297.
Wollstein (M.}. The influenza bacillus in inflammations of the respiratory tract in in-
fants. J.Exper. M., New York, 1906, viii, 681-691.
11. Cough
This is an important symptom in various nervous and inflammatory
diseases of the respiratory passages. Cough consists of a forcible, explosive
expiration, during which the glottis is first closed and then quickly opened.
The air current passing between the vocal cords gives rise to a noise that
is at first of high pitch, becoming lower as the glottis opens.
Cough is a defensive mechanism, helping to cleanse the larynx, the
trachea, and the larger bronchi. It is a reflex act, the sensory limb of
the arc running in the N. vagus. The center in the medulla oblongata lies
close to the respiratory center.
542 DISEASES OF THE EESPIKATOKY APPARATUS
Violent coughing can injure the elasticity of the lung, especially in its
upper parts. It also exerts an. important influence upon the circula-
tion. Thus, on coughing, the intrathoracic pressure is increased, the
inflow of venous blood is hindered, and the outflow of arterial blood is
favored, so that the arterial pressure may momentarily be markedly in-
creased. This sudden heightening of the blood pressure may lead to
arterial rupture in atherosclerosis or in aortic aneurism ; it accounts also
for the conjunctival hemorrhages in whooping-cough.
According to the sputum brought up, a cough is said to be dry or
moist. When nothing is expectorated, it is called an empty cough (e. r/., in
cutaneous or in pleuraL irritation). The cough may have a very metallic
ring when cavities within the thorax are set into sympathetic vibration.
When the glottis is not completely closed, or when the expiratory force is
feeble, the cough may be devoid of clang (laryngeal paralysis, emphysema).
A hacking or frequently-recurring feeble cough indicates continuous
slight irritation ; it is met with in chronic catarrh of the upper air passages,
especially in incipient pulmonary tuberculosis. Violent paroxysms of
coughing, difficult to allay, are common in convalescence from influenza.
The so-called goose cough of aortic aneurism is characteristic, and should
always arouse suspicion. The whoop of pertussis (q. v.) has only to be
heard once to be, afterward, easily recognizable.
References
Boruttau (//.)• Die Atembewegungen und ihre Innervation. Handb. d. Physiol. des
Menschen (W. Nagel). Braunschweig, 1909, i, 1-53.
Minkowski (O.). Die besonderen Schutzvorrichtungen der Atmungsorgane. In: Handb.
d. allgem. Pathol (Krehl & Marchand). Leipzig, 1912, ii, Abt. 1, 546-
554'
New (C. F.}.- Post-operative hysterical hiccough. St. Paul M. J., Minneapolis, 1913, xv,
465.
Newman (D.). Clinical lecture upon cough and disturbance of respiration, as indications of
disease of the upper air passages, with a few illustrative cases. Glasgow
M. J., 1890, xxxiii, 321-339.
Oppenheim (77.). Respirationskrampfe. In his: Lehrb. d. Nervenkrankh. 6. Aufl.
Berlin, 1913, ii, 1668-1669.
12. Examinations of the Lungs, Pleurae and Diaphragm
by Means of Rontgen Rays
Much progress has been made recently in the diagnosis of diseases of
the respiratory organs by means of Rontgen rays. Rontgenoscopy (or
fluoroscopy) and rontgenography are both employed. Stereoscopic rb'nt-
genography of the thorax as worked out by* Dunham, Wenckebach, and
others is especially helpful.
(a) Rontgenoscopy of the Lungs
In studying the lungs by means of Rontgen rays, it is best to begin
with a general rontgenoscopic view, preferably by dorsoventral transillu-
EXAMINATION OF THE LUNGS AND PLEUKAE 543
mination, the tube being placed at the back of the patient and the fluorescent
screen over the front of his thorax. One can 'then decide, whether to use
rontgenography for the whole thorax, or for certain regions only (e. g.y
Lilus, medial portions of apex, etc.)., In special cases, however, ventrodor-
sal transillmnination as well as frontal and oblique transilluminations for
rontgenoscopy may be helpful.
(6) Rontgenography of the Lungs
General View. — During the exposure of the plate, the patient may either
sit or stand. A soft tube (say 3 Benoist-units, or 6 to 7 Wehnelt-units)
is used, at a focal distance of 50-60 cm., the anticathode being placed
opposite the spinous process of the 6th thoracic vertebra. In adults of
average size, the time of exposition required is from 5 to 10 seconds.
Excellent pictures can also be obtained by brief exposures, provided an
intensifying screen be used.
In dor so ventral (sagittal) illumination, the arms may be folded over
the plate-holder in front so as to displace the scapulae as far as possible to
the sides. The exposure is made while the breath is held at the end of a
deep inspiration ; in this way, there is a maximal amount of air in the lung
at the time of exposure, the intercostal spaces are widened, the diaphragm
stands at a low level, and the best view possible of the lower parts of both
lungs is obtained. The patient should practice taking and holding a few
deep breaths before the exposure is made, and the operator should make
sure that the instructions to be followed at the time of exposure are fully
understood.
In women, the breasts should be displaced lateralward, and held there
by pressure of the plate-holder; otherwise, they give rise to disturbing
shadows over the lung areas. When the breasts are huge, it may be advan-
tageous to use ventrodorsal, rather than dorsoventral, illumination.
Local Views. — To obtain sharp pictures with maximal differentiation
of the structures in local areas in the lung, it is best to use small cones or
tubes to cut off the peripheral rays. This method is especially useful in
making exposures of the apex, or of a hilus, of one lung. Here the anti-
cathode should stand over the first intercostal space, in order to avoid the
covering of the latter in the negative by the. shadow of the second rib. The
center of the bundle of rays is directed toward the jugulum, the head being
bent back as far as possible.
Recently, a special method of making rontgenograms of the upper
aperture of the thorax has been devised (Hart and Harras). The patient
lies prone, the head raised by a high sand-bag, and the chest supported by
a flat cushion. Between this cushion and the neck and upper chest is
placed an 18 x 24 plate, no plate-holder being used. The spine must be
straight, the shoulder blades of the two sides equidistant from the plate,
the head not laterally flexed nor rotated. The x-rays pass, from behind,
544 DISEASES OF THE KESPIKATOEY APPARATUS
through a tube or cone, so directed that the lower aperture of the tube forms
a plane parallel to that formed by the upper aperture of the thorax.
Stereoscopic Views of the Lungs. — For studying and precisely localiz-
ing cavities, calcifications, infiltrations and foreign bodies in the lungs,
as well as for examining pleural effusions, empyemas, and the air sacs of
pneumothorax, stereoscopic rontgenographic views are exceedingly helpful,
and should be made use of much more often than is at present the custom.
In no other way can such exact information be arrived at regarding the
spatial relations of intrathoracic lesions; the situation of a cavity, for
example, can be precisely determined not only in the lateral but also in
the anteroposterior direction. The technic of stereoscopic work has al-
ready been described in the section dealing with Examinations with
Rontgen Rays.
(c) Appearances of the Thorax, Lungs, Pleurae, Diaphragm,
etc., on X-Ray Examination
The student should early familiarize himself with the appearances
presented by the lungs and other organs in the thorax on rontgenoscopy and
on rontgenography.
One view only can be
described here; namely,
that on dorsoventral
transillumination. The
two large clear areas
(lung areas) are sepa-
rated from one another
by the median shadow
(cardiovascular stripe) ;
they are bounded above
and at the sides by the
shadows of the soft parts
and the bones, and be-
low by the two convex
shadows that correspond
to the two halves of the
diaphragm.
The median shadow
(cardiovascular stripe)
is due to the sternum, the
heart and the great vessels, the mediastina, and the spine. In the upper
third of this median shadow, a lighter stripe may be seen corresponding
to the air-containing trachea. The cardiovascular stripe will be described
in detail under the Circulatory System.
Fig. 161.— Diagram Illustrating the Mode of Making a
Ronlgenogram of the Apices of the Lungs and the
Superior Aperture of the Thorax. (After C. Hart and
P. Harrass, "Der Thorax phtisicus, etc.," published by
F. Enkc, Stuttgart.)
EXAMINATION OF THE LUNGS AND PLEURAE 545
The shadow of the right half of the diaphragm is ordinarily on a little
higher level, is more intense, and moves less on respiration than that of the
left half. The pulsating part of the cardiovascular stripe (apex of the
heart) goes over into the shadow of the left half of the diaphragm ; some-
times, in the latter, one can make out a clear area due to gas in the stomach
(so-called "stomach bubble").
The ribs are seen as dark bands crossing the clear lung areas ; the pos-
terior portions of the ribs, concave below, are more distinct ; the anterior
portions, with convexity downward, are less distinct.
The scapula is visible on each side as a light triangular shadow. The
clavicles yield a deeper shadow extending lateralward and slightly down-
ward from the median shadow. Lateralward and below, the edge of the
M. latissimus dorsi is usually easily visible.
In the upright position, the apices of the lungs may be obscured by the
shadows of the first rib and of the clavicle, in which event it is necessary
to change the position slightly or to move the clavicles, so as to make the
apices accessible to observation.
Normal Appearance of the Lung Area. — Even normally, certain shad-
ows, due to the variable concentration of the tissues (lymph glands, bron-
chi, blood vessels) within the lung, appear in the otherwise clear lung area,
giving it a mottled, or networklike, appearance. These are normally most
abundant near the hilus. They radiate out from it, and decrease in
intensity, and in number, as the periphery of the lung is approached.
The hilus, itself, yields a crescentic shadow on each side with processes
of varying intensity running out radially from it. The whole of this
hilus-crescent is visible on the right side, but only a part of it can be seen
on the left.
Beneath the hilus-crescent on each side is a shadow passing downward
to the diaphragm known as the "companion-shadow of the heart" (v.
Scriegen). That on the right side is usually separated from the heart-
shadow proper by a narrow clear zone.
The clearness of the lung area depends, on the one hand, on the hard-
ness of the tube used and the intensity of its rays, and, on the other hand,
on the air content of the lung, the phase of respiration, the obesity, and
the muscularity of the patient.
Situation, Form and Motility of the Diaphragm. — The form and posi-
tion of the diaphragm depend upon the state of the thorax and of the
thoracic and the abdominal viscera; the rib-level of the diaphragm is of
relatively little significance.
The motility can easily be observed through the fluoroscope. On quiet
breathing, there is a movement of 1-3 cm. on each side, while on deep
breathing it may amount to 5-7 cm., the right side, however, usually
descending somewhat less than the left.
Bilateral elevation of the shadow of the diaphragm occurs when the
546 DISEASES OF THE BESPIKATORY APPAKATUS
abdomen is distended (ascites, tympanites, pregnancy, tumors, obesity).
That faulty notions may be yielded by percussion is well demonstrated
by x-ray examination.
Unilateral elevation of the diaphragmatic shadow is found: (1) in
unilateral retraction of the lung (mobility also lessened) ; (2) in unilateral
paralysis of the diaphragm; (3) in congenital atrophy of the diaphragm
(on the left side) ; (4) in subphrenic abscess (lessened, or abolished,
mobility) ; and (5) sometimes in hemiplegia.
Bilateral depression of the diaphragmatic shadow is met with (1) in
emphysema and in rigid thorax (with lessened mobility) ; (2) in some
asthmatic paroxysms; (3) in bilateral pleural effusion; (4) and in laryn-
geal stenosis.
Unilateral depression of the diaphragmatic shadow is met with (1)
in unilateral pleural effusions (with lessened mobility) ; (2) in unilateral
pneumothorax (extremely low position, shadow flat and immobile) ; and
(3) in some acute asthmatic attacks, with loss of mobility.
Abnormal respiratory mobility of the diaphragm is met with in various
states. In incipient apical tuberculosis, the movement of the half of the
diaphragm corresponding to the diseased side sometimes lags behind the
other half on respiration (F. H. Will inn is). In serothorax, in hemo-
thorax, and on pyopneumothorax, if the fluid ho not thick, its surface may
be seen to rise on inspiration and to fall on expiration (paradoxical dia-
phragmatic movement of Kienboeck). Opinions differ as to the reasons
for this.
Abnormal forms of diaphragmatic shadow may be seen, on deep inspi-
ration, when pleuritic or pleuropericardial adhesions exist (angular notch-
ings, wavelike curves).
Appearances in the Lung Areas in Pathological States. — Pathological
changes in the lungs are recognizable in x-ray pictures as an increase or a
decrease in the clearness in the lung areas, either diffusely over the whole
lung, or involving larger or smaller circumscribed areas.
In emphysema, for example, the whole lung area on each side is abnor-
mally clear, while in chronic passive congestion (cardiac decompensation),
owing to the increased consistence of the lung, the areas are everywhere
less clear than normal.
Circumscribed lung shadows indicate the presence, of solidifications, or
of exudations, in the lungs, or of fluid or of thickenings in the pleurae.
Nodules in the lung must be of a certain size in order to cast visible
x-ray shadows. The exact position of a nodule is best shown by stereo-
scopic pictures. Fluoroscopic examination of lung shadows is useful only
for the more extensive lesions; for finer changes, x-ray photographs (rb'nt-
genograms), taken while the breath is held, are necessary.
The changes in the x-ray picture characteristic of various pathological
states will be described under the several diseases.
EXAMINATION OF THE LUNGS AND PLEUEAE 547
References
Abrams (A.). Roentgen rays in pulmonary disease. J. Am. M. Ass., Chicago, 1902,
xxxviii,
Assmann (H.). Erfahrungen uber die Rontgenuntersuchung der Lungen unter besonderer
Berucksichtigung anatomischer Kontrollen. Mit einem Vorwort v. A. v.
Strumpell. (Arb. a. d. med. Klin, zu Leipzig, H. 2.) Jena, 1914. 167 p.
Beclere (A.), Oudin (P.) & Barthelemy. Applications de la methode Rcsntgen au
diagnostic des affections thoraciques, et en particulier au diagnostic des
lesions de I'appareil respiratoire. Bull, et mem. d. hop. de Paris, 1897,
3. s., xiv, 910-919.
Bibb (L. /?.) & Gilliland (C. E.). Skiagraphic study of thorax, thoracic wall and thoracic
viscera. . Arch. Int. Med., Chicago, 1915, xv, 558-573.
Crombie (R. H.). Roentgen rays in the diagnosis of lung disease. Lancet, London, 1903,
a, 212-214. i pi.
Decloux (L.) & Dumas (L. R.}. Diagnostic radiologique de la granulie pulmonaire.
Bull, et mem. Soc. med. d. hdp., Paris, 1913, xxix, 581-587.
Dunham (H. K.), Boardman (W. W.) & Wolman (5.). The stereoscopic X-ray ex-
amination of the chest, with special reference to the diagnosis of pulmonary
tuberculosis. Johns Hopkins Hosp. Bull., Baltimore, 1911, xxii, 229-
288.
Engel (#.)• -^'e ana.tomisch.en und rontgenologischen Grundlagen fur die Diagnostik der
Bronchialdriisentuberkidose beim Kinde. Ergebn. d. inn. Med. u. Kinderh.,
Berlin, 1913, xi, 219-275.
Fraenkel (E.). Anatomisch-rdntgenologische Untersuchungen uber die Luftrohre. Fortschr.
a. d. Geb. d. Rdntgenstrahl, Hamburg, 1913, xxi, 267-284.
Groedel (F. M.). Das Thoraxbild bei zentrischer (sagittaler, frontaler, schrager) und ex-
zentrischer Rontgenprojektion. Fortschr. a. d. Geb. d. Rdntgenstrahl. ,
Hamburg., 1913, xx, 541-554.
Hoesslin (H. p.). Klinisch-rontgenologischo Untersuchungen ilber Lungenkavernen mit
Flussigkeitsspiegel. Deutsches Arch. f. klin. Med., 1913, cxii, 580—592.
Kraus (F.). Rontgenuntersuchung von Pleura und Zwerchfell. In: Rieder (H.) & Rosen-
thai (J.} Lehrbuch der Rontgenkunde, Leipzig, 1913, J. A.Barth, i. 612 p.
Krause (P.) & Friedrich (O.)» Beitrdge zur Rontgendiagnostik von Lungenkranken.
Ztschr. f. med. Elektrol. u. Rontgenk., Leipzig, 1908, x, 16; 65.
Levy-Dorn (Af .) & Zadek. Zur Untersuchung mit Rontgenstrahlen bei Lungenechinococ-
cus. Berl. klin. Wchnschr., 1899, xxxvi, 431.
Rach (E.}. Radiologisch erkennbare anatomische Typen der kindlichen Lungentuberkulose.
Milnchen. med. Wchnschr., 1914, Ixi, 642-645.
Rieder (H.}. Rontgenuntersuchung der Lungen. In: Rieder (H.) u. Rosenthal (J.) Lehr-
buch der Rontgenkunde, Leipzig, 1913, J. A. Earth, i. 612 p.
Schut (H.). Die Lungentuberkulose im Rontgenbilde. Beitr. z. Klin. d. Tuberk., Wurz-
burg, 1912, xxiv, 144-191.
Skinner (E. H.). Stereoscopic radiography. J. Missouri M. Ass., St. Louis, 1913-14, x,
103-106.
Stubbert (J. E.). Roentgen ray diagnosis of pulmonary tuberculosis and other diseases of
the lungs and heart. Yale M. J., New Haven, 1897-98, iv, 205-220.
Walsham (Hugh) & Orton (G. Harrison). The Rontgen ray in the diagnosis of diseases
of the chest. London, 1906, H. K. Lewis. 80 p. 16 p. 8°.
Wenckebach (K. F.). The radiology of the chest. Arch. Roentgen Ray, London, 1913,
xviii, 169-182.
Weil (A.). Drei Falle von Lungentumoren mit ungewohnlichem rontgenologischen Befund.
Fortschr. a. d. Geb. d. Rontgenstrahlen, Hamburg, 1912, xix, 142-148.
Williams (F. H.}. Roentgen ray examinations in incipient pulmonary tuberculosis. Am.
Climat. Ass., 1899, xv, 68-86; Med. News, N. Y., 1899, Ixxv, 353-368.
SECTION II
SPECIAL DIAGNOSIS OF THE MOKE IMPOKTANT
DISEASES OF THE KESPIRATOKY SYSTEM
A. Diagnosis of the Principal Diseases of
the Nose
We can refer here only to (1) certain inflammations (acute, chronic
and specific), (2) epistaxis, (3) foreign bodies and parasites, and (4)
the most common tumors (including polypi). Mention will also be made
of (5) deflections of the nasal septum, and (6) nasal hydrorrhea.
References
1. Larger Texts
Ballenger (W. L.)« The diseases rf the nose, throat and ear, medical and surgical. 4. ed.
Philadelphia & New York, 1914, Lea & Febiger. 10SO p. 8°.
Bosworth (F. H.). A treatise on diseases of the nose and throat. Vol. 1. Diseases of the
nose and naso-pharynx. 3. ed. New York, 1898. 2 v. 8°.
Burnett (Charles H.}. A system of diseases of the ear, nose and throat. Philadelphia,
1893, 2 v. 8°.
Cartaz (A.}, Castex (A.) & Barbier (H.}. Maladies du nez et du larynx. Par.,
1912, J. B. Bailliere & fils. 277 p. 8°. [Nouv. Traite de Med. de
Therap., xxvii.]
Chiari (O.)* Die Krankheiten der Nase. Leipzig & Wien, 1902. 8°.
Coakley (C. G.). A manual of diseases of the nose and throat. 5. ed. Philadelphia &
New York, Lea & Febiger. 615 p. 12°.
Forrest (/.)• Eye, nose, throat and ear. London, 1914, H. Kimpton. 411 p. 8°.
Goppert (F.). Die Nasen-, Rachen- und Ohrerkrankungen des Kindes in der tdglichen
Praxis. Enzykl. d. klin. Med., Berlin, 1914, J. Springer. 182 p. 8°.
Hall (F. De II.) & Tilley (H.). Diseases of the nose and throat. 2. ed. London, 1901.
12°.
Jones (J. H. M.) & Stewart (W. R. H.) [et a\.]. The practitioner's handbook of diseases
of the ear and naso-pharynx. 6. ed. London, 1902. 8°.
Kassel (Karl). Geschichte der Nasenheilkunde. Bd. i. Wiirzburq, 1914 , C. Kdbitzsch
476 p. 8°.
Kyle (D. B.). A text-book of diseases of the nose and throat. 4. ed. Philadelphia &
London, 1907, W. B. Saunders Co. 797 p. 8°.
McBride (P.). Diseases of the throat, nose and ear; a clinical manual for students and prac-
titioners. 3. ed. Edinburgh & London, 1900. 8°.
548
DISEASES OF THE NOSE 549
Meyer (E.}. Erkrankungen der oberen Luftwege. In: Handb. d. inn. Med. (Mohr &
Staehelin), Berlin, 1914, ii, 1-162.
Packard (F. R.). Text-book of diseases of the nose, throat and ear. 2. ed. Philadelphia
& London [1913], J. B. Lippincott Co. 377 p. 8°.
Reik (H. O.) & Reik (A. J. N.}. Diseases of the ear, nose and throat. New York & Lon-
don, 1911, D. Appleton & Co. 374 P- 8°.
Schmidt (M.). Die Krankheiten der oberen Luftwege. Aus der Praxis fur die Praxis.
4. Aufl. von Edmund Meyer. Berlin, 1909, J. Springer. 766 p. 8°.
Thomson (St. C.). Diseases of the nose and throat, comprising affections of the trachea
and esophagus. London, 1911, Cassell & Co. 807 p. 8°. Also: D.
Appleton & Co., New York & London.
Waggett (E. B.). Diseases of the nose. London, 1907, H. Frowde. 282 p. 12°.
2. Briefer General Articles
Brown (G. V. /.)• The application of orthodontia principles to the prevention of nasal dis-
ease. Dental Cosmos, Philadelphia, 1903, xlv, 765-775.
Cohen (S. S.). Look beyond the nose. Tr. Am. Laryngol. Ass., 1890, New York, 1891,
xii, 28-32.
Endriss (G.). Die bisherigen Beobachtungen von physiologischen und pathologischen Bezie-
hungen der oberen Luftwege zu den Sexualorganen. Wiirzburg, 1892,
Becker. 88 p. 8°.
Fliess (W.). Die Beziehungen zwischen Nase und weiblichen Geschlechtsorganen in ihrer
biologischen Bedeutung dargestellt. Leipzig u. Wien, 1897, F. Deuticke.
245 p. 8°.
Hajek (M.)» Der Kopfschmerz bei Erkrankungen der Nase und deren Nebenhohle. Aerztl.
Rundschau, Munchen, 1899, ix, 209-212.
Korner (Otto). Untersuchungen uber Wachstumsstorungen und Missgestaltung des Ober-
kiefers und des Nasengeriistes infolge von Behinderung der Nasenatmung.
Leipzig, 1891, S. C. W. Vogel. 20 p. 1 pi. 8°.
Kuttner (A.). Die nasalen Reflexneurosen und die normalen Nasenreflexe. Berlin, 1904,
Kohler, 260 p. 8°.
Mackenzie (J. N.). The physiological and pathological relations between the nose and the
sexual apparatus of man. Johns Hopkins Hosp. Bull., Baltimore, 1898,
ix, 10-17.
Watson- Williams (P.)- Specialism and the medical curriculum, mainly in reference to
otology, rhinology and laryngology. Bristol M.-Chir. J., 1913, xxxi, 291-
803. 2 pi.
White (J. A.). Neuroses of the nose and nasopharynx. In: Syst. Dis. Ear, Nose and
Throat (Burnett). Philadelphia, 1893, ii, 90-148.
3. Bacteriology of the Nose
Dunham (E. K.). A few observations on the meningococcus and allied organisms from the
nasopharynx. Proc. N. York Path. Soc., 1905-06, n. s., v, 134-139.
Hallock (W.} & Wright (/.)• Nasal bacteria in health. J. Laryngol., London, 1898, xiii,
124-130.
Kuster (E.). Die Bakterien in der gesunden Nase. In: Handb. d. pathogen Mikroorg.
(Kolle & Wassermann). 2. Aufl. Jena, 1913, vi, 450-457.
Kyle (D. B.}. Nasal bacteria; the relation they bear to disease. J. Am. M. Ass., Chicago,
1899, xxxii, 1298.
Meyer (E.}. Erkrankungen der oberen Luftwege. Handb. d. inn. Med. (Mohr & Staehelin).
Berlin, 1914, ii, 1-162.
Minchan (E. A.} & Fantham (H. B.}. Rhinosporidium kinealyi, n. g., n. sp., a new
sporozoon from the mucous membrane of the septum nasi of man. Quart.
J. Micr. Sc., London, 1905-06, xlix, 521-532. 2 pi. on 3 I,
550 DISEASES OF THE EESPIKATOKY APPAEATUS
Onodi (A.). Pathologic und Therapie der Nasenkrankheiten. Wien & Leipzig, 1910,
A. Holder. 165 p. roy. 8°.
Park (W. #.) & Wright (/.)• Nasal bacteria in health. Tr. Am. Laryngol. Ass., 1897,
New York, 1898, 168-178.
Schiff (A.). Ueber die Beziehungen zwischen Nase und weiblichen Sexualorganen. Wien.
klin. Wchnschr., 1901, xiv, 57-64-
Thomson (St. C.). The bacteriology of the normal nose. J. Laryngol, London, 1900, xv,
405-409.
1. Inflammatory Diseases of the Nose (Rhinitis)
(a) Acute Rhinitis
Under this heading may be considered: (1) the acute catarrhal form
of acute rhinitis, (2) the purulent form of acute rhinitis, (3) the pseudo-
membranous form of acute rhinitis, and (4) hay fever.
i. Acute Catarrhal Rhinitis
(Rhinitis catarrhalis acuta, Common Cold in the Head, Coryza)
There is hyperemia and swelling of the nasal mucous membrane,
together with the secretion of a thin, clear, strongly alkaline fluid con-
taining swollen epithelial cells, leukocytes, and bacteria (few at first, abun-
dant later). Usually we see redness, and, sometimes, erosion and scabbing
of the anterior nares. Sometimes the inflammation extends to the para-
nasal sinuses or to the conjunctivae.
An acute catarrhal rhinitis may be primary (due to bacteria in the
nose, exposure to cold predisposing to infection), or secondary, as a part
of some general disease (influenza, measles, scarlet fever, etc.).* A me-
chanical or chemical rhinitis is sometimes seen (dust, irritating vapors,
iodism).
Symptoms. — In the premonitory stage, the patient feels chilly, ill at
ease, and "stuffy in the head" ; he begins to sneeze, to have itching or
prickling sensations in the nasal passages and in the eyes, and, perhaps,
complains of headache, backache, and slight pains in the extremities.
Anterior rhinoscopy reveals hyperemia of the nasal mucosa, and, a little
later, a profuse serous discharge. The temperature undergoes slight eleva-
tion. The patient is soon forced to breathe through the mouth, which
dries the throat and parches the tongue. On the second or third day the
discharge thickens, becoming mucoid, then purulent; the general consti-
tutional symptoms abate; by the end of a week or ten days, in uncom-
plicated cases, the attack is over.
Complications and Sequelae. — Paranasal sinusitis, laryngitis, otitis
media, chronic nasal catarrh.
* Typhoid fever is almost never ushered in by an acute rhinitis.
DISEASES OF THE JSTOSE 551
ii. Acute Purulent Rhinitis
(Rhinitis purulenta acuta, Blennorrhea)
In this condition, there is reddening, and swelling, of the nasal mucous
membrane. The secretion is mucopurulent, or may consist of pure pus;
it is often fetid. Erosions and scab formations at the anterior nares and
on the upper lip are common. The secretion is often abundant, sometimes
accumulating in the paranasal sinuses (empyema of sinus) and then often
maintaining the inflammation for some time. (See Sinusitis.)
Etiology. — The origin is always bacterial (streptococci, pneumococci,
staphylococci, meningococci, influenza bacilli, etc.). Certain predisposing
factors should be kept in mind (foreign bodies, tumors, infectious granu-
lomata).
Complications. — There may be an extension (1) to the pharynx and to
the larynx (pharyngitis, laryngitis) ; (2) through the eustachian tube to
the middle ear (otitis media) ; or (3) through the lymph sheaths of the
Nervi olfactorii to the cranial cavity (meningitis). The disease may go
on to a chronic purulent or to an atrophic stage. (See Ozena.)
References
Bosworth (F. #.). Acute rhinitis. Syst. Dis. Ear, Nose and Throat (Burnett). Phila-
delphia, 1893, i, 611-623.
Gerber (P. H.). Rhinitis acuta. Handb. d. Laryngol. u. Rhinol. Wien, 1896, Hi, 327-
376.
Howell (Katherine). Complement fixation in acute rhinitis. J. Infect. Dis., Chicago,
1915, xvi, 456-460.
Tunnicliff (Ruth). Further observations on the bacteriology of rhinitis, with special refer-
ence to an anerobic organism (Bacillus rhinitis). J. Infect. Dis., Chicago,
1915, xvi, 493-495.
iii. Acute Pseudomembranous Rhinitis
(Rhinitis pseudomembranacea)
Here, a yellowish-white or greenish deposit, more or less adherent,
can be seen upon the swollen, reddened mucous membrane ; it can be pulled
off in shreds, or as a definite false membrane. It may be due to infection
with streptococci, pneumococci or diphtheria bacilli (bacteriological exami-
nation).
References
Abbott (A. C.). The etiology of membranous rhinitis (rhinitis fibrinosa) . Tr. Coll. Phys.,
Philadelphia, 1893, 8. s., xv, 122-132.
Casselberry (W. E.}. Membranous rhinitis, diphtheritic and non-diphtheritic. Medicine,
Detroit, 1897, iii, 567-571.
Gerber (P. H.) & Podack (A/.). Ueber die Beziehungen der sogenannten primdren Rhini-
tis fibrinosa und des sogenannten Pseudodiphtheriebacillus zum Klebs-
Loffler'schen Diphtheriebacillus. Deutsches Arch. f. klin. Med., Leipzig,
1894-95, liv, 262-304.
Wishart (D. J. G.). Fibrinous rhinitis. Canad. J. M. & Surp., Toronto, 1899, vi, 262-268.
552 DISEASES OF THE KESPIKATOKY APPARATUS
iv. Hay Fever
Definition. — A more or less severe inflammation of the mucous mem-
branes of the nose, throat, and bronchi, occurring in susceptible persons
in the spring or in the autumn, and caused by the inhalation of pollens
of certain plants.
Historical. — ^The disease was formerly believed to be a neurosis. In
1873, Blackley pointed to the periodic occurrence of the affection, and
established a relationship to the prevalence of certain pollens in the air at
these periods. A most careful scientific study of the relations of pollens
to the disease has been made by Dunbar.
Etiology. — The albumins of certain pollens act as intense irritants to
the respiratory mucosa of certain susceptible people. Quantities of
the isolated albumin of the pollen as small as one forty-thousandth of a
milligram can yield a reaction in sensitive persons. The condition is
almost certainly one of anaphylaxis, at least in part.
There are two periods in which hay fever is prevalent, the spring
(early June) and the early autumn (middle or late August) ; the hay fever
occurring in the spring is known as Vernal Hay Fever, June Cold, Rose
Fever, or European Hay Fever, that occurring in the late summer and
autumn as Autumnal Catarrh, or North American Hay Fever.
In the spring, the pollens of the Graminae and of the Cyperaceae are
toxic, as are also those of privet, lily of the valley, thistle, swamp-pink,
hairy Solomon's Seal, rape, green cabbage, and spinach.
In the autumn, the pollens of the Ambrosiaceae (rag- weed) and of the
Solidago (golden-rod family) are most important; in addition, those of
asters, chrysanthemums, daisies, and blue-bottles appear to be active.
Why some persons are susceptible to pollens and others not is still a
mystery. Among hay fever sufferers, there are marked differences in
susceptibility to the several pollens; some are sensitive to one kind of
pollen only, others to a variety of pollens. Those that suffer in the spring
are often immune in the autumn and vice versa; a few are susceptible to
both the vernal and the estivo-autumnal pollens.
The disease often causes marked depression and other nervous symp-
toms, but it is no more prevalent among persons generally psychoneurotic
than among others. Nor has the disease any relation to local abnormalities
of the nose, such as enlarged turbinates.
Symptoms. — In affected persons, the disease comes on about the same
time every year, corresponding to the period when the pollen concerned is
present in the inspired air. After a day or two of slight nasal and con-
junctival irritation with sneezing, a severe coryza develops ; there is itching
and burning of the nose, eyes, and larynx with profuse serous nasal dis-
charge requiring the constant use of handkerchiefs in relays. The nose
soon becomes obstructed, preventing nasal breathing; inspection through
DISEASES OF THE NOSE 553
a speculum reveals swollen, intensely hyperemic conchae, which can tem-
porarily be shrunken with an epinephrin spray, after which by palpation
with a blunt probe hypersensitive areas on the anterior extremities of the
conchae and on the septum, may, if desired, be marked out. The conjunc-
tival and laryngeal symptoms are often marked ; not a few patients suffer
from distressing attacks of bronchial asthma at the height of their hay
fever. The constitutional symptoms (headache, malaise, general weakness,
palpitation, insomnia, mental depression) vary considerably in different
cases. Autumnal attacks end after a hard frost.
The sneezing reflex is often set free by exposure to bright sun-light.
Patients that spend the hay fever season in regions free from the
causative pollens remain free from attacks. Thus those that suffer from
the autumnal type are free from the disease while on the ocean (far enough
from shore), or while in Europe where there is practically no rag-weed
or golden-rod. In the United States, many patients are free from attacks
in the White Mountains, especially at Bethlehem, N. H. The Hay Fever
Association publishes a list of places suitable for sufferers.
A favorite resort for hay fever sufferers of both the United States and
Canada is the Georgian Bay (among its 30,000 islands) ; other places, rela-
tively immune, include Chester (Nova Scotia), Murray Bay (Quebec),
Muskoka (Ontario), and Mackinac Island (Michigan). In the pine-woods
on the divide in Northern Wisconsin (Trout Lake), many patients are
entirely free from hay fever. In all places, the irritation is less when the
wind blows off the water, than when there is a land-breeze, laden with
pollen. Flowers in a living room or in a sleeping room may be provoca-
tive of an attack.
Patients compelled to live in pollenous districts during the hay fever
periods should stay in-doors and avoid dust as much as possible. Experi-
ments are being made with antitoxins (pollantiri) , and with prophylactic
pollen-inoculations, but, thus far, with results not wholly satisfactory.
Oppenheimer, Clowes and others advise testing the sensitiveness of the
skin and mucous membranes to dilute solutions of proteins derived from
various pollens in order to determine which pollen is responsible, and if
possible to bring about anti-anaphylaxis by desensitizing methods. The
physician should protect the hay fever patient from the useless nasal
operations of overzealous surgical enthusiasts !
References
Alexander (D. A/.). The specific treatment of hay fever. Liverpool M.-Chir. J., 1914,
xxxiv, 260-266.
Cooke (R. A.). The treatment of hay fever by active immunization. Laryngoscope, St. Louis,
1915, xxv, 108-112.
Dunbar (W. P.). Zur Ursache und specifischen Heilung des Heufiebers. Miinchen &
Berlin, 1903, R. Oldenbourg. 66 p. 3 pi. 8°.
Aetiologie und specifische Behandlung des Herbstkatarrhes. Berl. klin.
Wchnschr., 1903, xl, 635-637.,
554 DISEASES OF THE KESPIKATOKY APPAKATUS
Dunbar (W. P.)- Hay fever. Mod. Mcd. (Osier & McCrae). 2.ed. Philadelphia & New
York, 1914, ii, 855-866.
Emrys-Roberts (E.). Alterations in the blood occurring in hay fever. Brit. M.J., London,
1914, i, 1176-1178.
Freeman (/.). Vaccination against hay fever: report of results during the last three years.
Lancet, London, 1914, i, 1178-1180.
Gottlieb (M. J.) & Oppenheimer (£.)• Active immunization to hay fever. Biochem.
Bull., New York, 1915, iv, 127-135.
Iskowitz (#.)• Multipollen vaccines in the treatment of hay fever. Med. Rec., New York,
1915, Ixxxviii, 270-272.
Koessler (K. K.). The specific treatment of hay fever by active immunization. Illinois
M. J., Chicago, 1914, xxvi, 120-127.
The specific treatment of hay fever (Pollen disease}. In: Therapeusis of
internal diseases (Forchheimer}. New York & London, 1914, v, 671-706.
Manning (E. T.). Hay fever, its treatment by injection of a solution of ragweed pollen.
J. Am. M. Ass., Chicago, 1915, Ixiv, 655-657.
Oppenheimer (S.) & Gottlieb (M. /.). Pollinosis (hay fever). A consideration of its
treatment by active immunization. Maryland M. J., Baltimore & Wash-
ington, 1915, Iviii, 220-228.
Prausnitz (C.). Heufiebergift und Heufieberserum. In: Handb. d. pathogen. Mikroorg.
(Kolle & Wassermann). 2. Aufl. Jena, 1913, ii, 2, 1469-1498.
Wolff-Eisner (A.}. Das Heufieber, sein Wesen und seine Behandlung. Kor.-Bl. d. allg.
arztl. Ver. v. Thuringen. Jena, 1906, xxxv, 209-211.
Wood (F. M.). Hay fever and asthma. Chicago M. Recorder, 1915, xxxvii, 453-459.
(b) Chronic Rhinitis
Three forms may be distinguished: (1) chronic nasal catarrh; (2)
chronic purulent rhinitis, and (3) chronic atrophic rhinitis.
i. Chronic Nasal Catarrh
(Rhinitis catarrhalis clironica)
There may be only slight redness and swelling of the nasal mucous
membrane, often visible only in patches ; the secretion is mucopurulent, and
tenacious. This type of nasal catarrh is often an occupation disease, due
to dust (city-dwellers, millers, stokers, stone-workers, screw-makers, etc.).
It is predisposed to by anything that narrows the nasal passages, e. g., a
deflected septum.
ii. Chronic Purulent Rhinitis
(Rhinitis purulenta chronica)
This state often follows the acute purulent form of rhinitis. The
mucous membrane is red and swollen ; there is a long-continuing purulent
secretion. The turbinated bones, and the mucosa over them, undergo
hyperplasia (protective or hyperplastic rhinitis). The mucous membrane
of the lower concha may be diffusely thickened, or may present cauliflower-
like excrescences; occasionally, the periosteum is thickened, Similar pro-
DISEASES OF THE NOSE 555
liferations may occur in the paranasal sinuses. Closure of their openings
leads to chronic empyemas of the sinuses, which may cause atrophy of the
hony wall and extension of the suppuration into the nose, the orbit, the
cranial cavity or the subcutaneous tissue. There is danger of meningitis,
of sinus thrombosis and of cerebral abscess (see Sinus Disease).
iii. Chronic Atrophic Rhinitis
(Rhinitis cJironica atrophica; Ozena)
This condition is usually the sequel of a hyperplastic rhinitis; the
mucous membranes and the conchae waste away; the ciliated epithelium
is replaced by flat epithelium ; there is atrophy of the glands and widening
of the nasal cavities ; the scanty purulent secretion tends to accumulate in
the form of greenish, dry scabs and crusts ; decomposition of the secretions
yields the foul odor characteristic of the disease (ozena).
References
Abel (-R.). Die Aetiologie der Ozaena. Ztschr. f. Hyg. u. Infektionskrankh., Leipzig, 1895,
xxi, 89-155.
Baker (C. H.}. The diseased middle turbinate. J. Am. M. Ass., Chicago, 1903, xl, 708-714.
Barth (E.). Der gegenwdrtige Stand der Pathologie und Therapie der Ozaena. Fortschr. d.
Med., Berlin, 1901, xix, 981-990.
Freer (O. T.}. Chromic rhinitis; its varieties and treatment. Phys. & Surg., Detroit & Ann
Arbor, 1904, xxvi, 49-69. 1 pi.
Goodale (/.). An etiologic study of atrophic disease of the upper air passages based upon an
examination of two hundred cases. J. Am. M. Ass., Chicago, 1898, xxx,
471-474.
Grosskopff (W.). Die Ozaena; eine Monographic und Studie. Klin. Vortr. a. d. Geb. d.
Otol. u. Pharyngo-Rhinol., Jena, 1901-02, v, 295-338.
Grunwald (L.). Altes und Neues uber die Stinknase. Munch, med. Wchnschr., 1894, xli,
284-286.
Der heutige Stand der Ozaena-Frage. Arch. f. Laryngol. u. Rhinol.,
Berlin, 1902, xiii, 250-272.
Also: Transl. [Abstr.], Ann. d. mal. de Voreille, du larynx [etc.], Paris, 1902,
xxviii, 246-250.
Holmes (C. R.). Hypertrophy of the turbinated bodies and their relations to inflammation
of the middle ear, with report of fifteen-hundred operations. N. York M. J.,
1900, Ixii, 529; 617.
Horn (//.)• The etiology and treatment of ozena. A preliminary report. J. Am. M. Ass.,
Chicago, 1915, Ixv, 788-793.
Hutinel. Les rhinites chroniques; les polypes muqueux des fosses nasales; Vozene. J. de
med. int., Paris, 1905, ix, 14-17.
Kyle (J. /.). Atrophic rhinitis. Indiana M. J., Indianapolis, 1902-03, xxi, 153-155.
Lautmann (5.). Vozene atrophiant; clinique, pathogenic, serotherapie. Paris, 1897. 8°.
Also, In: Ann. d. mal. de Voreille, du larynx [etc.], Paris, 1897, xxiii,
Richardson (C. W.). Atrophic rhinitis. Wash. M. Ann., 1903, u, 81-95.
Schonemann (A.). Die Ozana; Sammelreferat nach der Literatur der letzten vier Jahre.
Internal, Centralbl. f. Ohrenh., Leipzig, 1903, i, 283-%90f
556 DISEASES OF THE RESPIRATORY APPARATUS
Senac-Lagrange. Rhinites et surdites. Ann. d. mal. de I'oreille, du larynx [etc.], Paris,
1890, xvi, 331; 338; 463; 616.
Shurly (E. L.)» Remarks on the etiology of hypertrophic rhinitis. Trans. Am. Acad. Ophth.
[etc.], Oto-Laryngol. Sect., St. Louis, 1903, 25-33.
Stucky (J. A.}. Atrophic rhinitis. Internal. M. Mag., New York, 1903, xii, 92-94.
Wingrave. Preliminary notes of an investigation concerning the morbid anatomy of hyper-
trophic and atrophic turbinal disease. Tr. Brit. Laryngol. & Rhinol. Ass.,
1891, London, 1894, Hi, 16-23.
(c) Specific Inflammations of the Nose
The two more important ones are: (1) tuberculosis and (2) lues;
the three less commonly met with are: (1) glanders, (2) leprosy, and
(3) rhinoscleroma.
i. Nasal Tuberculosis
Three forms are met with :
(1) Tuberculous ulcers, in phthisical patients, usually in the naso-
pharynx; (2) tuberculous granulomata, broad-based tumors, most often
occurring on the cartilaginous septum, occasionally presenting grayish-red
ulcerating or fungous surfaces; these are not as a rule associated with
pulmonary phthisis; and (3) lupus, usually occurring at the vestibule
of the nose, or in the nasopharynx.
References
Chiari (O.)« Ueber Tuberculome der Nasenschleimhaut. Arch. f. Laryngol. u. Rhinol.,
Berlin, 1893, i, 121-134.
Hajek (M.). Ueber Tuberkulose der Nasenschleimhaut. Internal, klin. Rundschau, Wien,
1889, Hi, 13; 118; 174; 214.
Tuberkulose der Nasenschleimhaut. Internal, klin. Rundschau, Wien,
1892, vi, 1617-1620.
Knight (C. #.)• Tuberculosis of the nares. Laryngoscope, St. Louis, 1904, xiv, 417-422.
Neumann (/?.)• Ueber Tuberkulose der Nasenschleimhaut. Breslau, 1902. 8°.
Thomas (C.). Contribution d V etude des tumeurs tuberculeuses primitives des fosses nasales.
Paris, 1902. 8°.
ii. Nasal Syphilis
This may be congenital or acquired. Coryza, leading to a stubborn,
chronic nasal catarrh, is often the first sign of hereditary lues; occasion-
ally, ulceration of the septum occurs.
In acquired nasal syphilis, the lesions may be primary (external
chancre), secondary (macules and papules on the mucous membrane), or
tertiary (periosteal or perichondrial gummata, which quickly break down
and give rise to syphilitic ozena ; perforation of the septum). Later,
saddle nose and internal deformations are common. The Treponema pal-
lidum can often be demonstrated in the lesions, and the Wassermann re-
DISEASES OF THE KOSE 557
action is positive. Entirely similar pathological changes occur in the
nose in tertiary yaws (gangosa, q. v.).
References
Gerber (P. H.). Die Syphilis der Nase, des Halses und des Ohres. Berlin, 1910, S. Karger.
144 P* 4pL 8°.
Goodale (J. L.). Syphilis of the cartilaginous septum. Ann. OtoL, Rhinol. & LaryngoL,
St. Louis, 1904, xiii, 8-18.
Knight (C. H.}. The sequelae of syphilis and their treatment; nasal sequelae. Tr. Am.
LaryngoL Ass., New York, 1897, 150-161.
Martin (H. H.}. Syphilis of the nose and throat. South. M. /., Nashville, 1913, vi, 19.
Strandberg (O.). Bemerkungen uber die Differentialdiagnose zwischen Tuberkulose und
Syphilis der Schleimhdute der oberen Luftwege. Ztschr. f. LaryngoL,
Rhinol. [etc.], Wurzburg, 1914, vii, 1-7.
Thomson (St. C.). The rhinitis of inherited syphilis. J. LaryngoL, London, 1899, xiv,
395-398.
2. Epistaxis
Hemorrhage from the nose (epistaxis) may result from hyperemia
(active or passive), trauma, severe infection (especially typhoid), arterial
hypertension (nephritis, atherosclerosis), or hemorrhagic diathesis
(anemia, chlorosis, leukemia, scurvy, multiple telangiectasis, etc.) ; occa-
sionally, it is due to vicarious menstruation. In severe cases, life may he
endangered unless the bleeding vessel be obliterated by the application of
the thermocautery or the nose be plugged both in front and behind. In
every case the bleeding point should be sought for ; it will be found most
often on the anterior third of the cartilaginous part of the septum.
References
Dock (G.). A case of fatal epistaxis (from endothelioma of the nose), with a study of the
blood. Tr. Ass. Am. Phys., Philadelphia, 1899, xiv, 125-136.
Fink (E.}. Ueber neuropathische Epistaxis. Heilkunde, Wien, 1897-98, ii, 402-407.
Forgue & Boine. Epistaxis. Diet, encycl. d. sc. med., Paris, 1887, xxxv, 250-259.
Fullerton (/?.). Notes and observations on certain forms of epistaxis. Glasgow M. J., 1894,
xli, 349-356.
Osier (W.). On multiple hereditary telangiectases with recurring hemorrhages. Quart. J.
Med., Oxford, 1907-08, i, 53-58. 2 pi. [col.].
Rendu (/J.). Epistaxis repetees chez un sujet porteur de petits angiomes cutanes et muqueux.
Bull, et mem. Soc. med. d. hop. de Paris, 1896, 3. s., xiii, 731-733. Alsi:
Gaz. d. hop., Paris, 1896, Ixix, 1322.
Rice (C. C.). Epistaxis, its causes and treatment. Internal. Clin., Philadelphia, 1891, Hi,
345-347.
Roth (W.). Die habituellen Nasenblutungen. Wien. med. Presse, 1893, xxxiv, 881; 930.
3. Foreign Bodies and Parasites in the Nose
In children, buttons, beads, pins, coins, beans, peas, screws, etc., may
be found lodged in the nasal passages above or below the inferior concha.
558 DISEASES OF THE EESPIKATOKY APPAEATUS
Khiiioliths are uncommon. Ascaris and oxyuris are occasionally present
in the nose. In vagrants, fly larvae may fill the nostrils.
When the presence of a foreign body is suspected, the open nostril
should be closed and the patient told to blow through. If this does not
reveal the object, one may try blowing air into the free nostril with a
Pollitzer bag. If the foreign body be tightly wedged in, one should locate
it with the speculum under bright illumination, after which it may be
possible to pass a delicate, blunt, hook-shaped sound around it. In look-
ing for a foreign body, it is, in general, wise to avoid the use of forceps
and to take care not to dislocate the foreign body backwards on account
of the danger of its falling into the larynx. If blood clots are present
and make inspection difficult, the passages may first be cleansed by an
alkaline spray; when the soft parts are swollen, a spray of cocain (4 per
cent) and epinephrin (0.1 per cent) may be used to shrink them.
References
Burrows (H. A.). The symptoms, treatment and report of three cases of invasion of the nasal
cavity by Texas screw-worm. Texas Cour.-Rec. Med., Fort Worth, 1901-
02, xix, 152-154.
David (V.). Des corps etrangers des fosses nasales. Paris, 1900. 8°.
Foster (H.). Report of a case of two hundred and seven screw-worms taken from the nose.
Kansas City M. Index, 1897, xviii, 421.
Herisset (A.). Contribution a I' etude des rhinolithes. Paris, 1904. 8°.
Neumann (J.). Ueber eine mil Cholestearin vollstandig ausgefiillte Nasenhohle. Arch. f.
Path. Anat. [etc.], Berlin, 1893, cxxxii, 377-380.
Poole (W. H.}. Rhinolith or nasal calculus; report of a case and exhibition of pathological
specimen. N. York M. J., 1898, Ixviii, 45.
Powell (A. M.). Myasis narium. St. Louis M. & S. J., 1888 , lv, 206-207.
4. Tumors of the Nose; Nasal Polypi
The most common tumor of the nose is a fibroma, which occurs as a
gelatinous, polypoid mass of variable size on the lateral wall. Polypi are
often a sign of underlying disease of the paranasal sinuses. Hard fibro-
mata (nasopharynx, paranasal sinuses), fibro-adenomata, and carcinomata
are much rarer.
References
Alexander (A.}. Die Nasenpolypen in ihren Beziehungen zu den Empyemen der Nasen-
nebenhohlen. Arch. f. Laryngol. und RhinoL, Berlin, 1896, v, 324-381.
2 pi.
Cobb (F. C.). Malignant growths of the nose and nasal phraynx. Laryngoscope, St. Louis,
1904, xiv, 577-581.
Delamarre (A.}. Contribution a V etude des sarcomes des fosses nasales. Paris, 1902. 8°.
Ingals (E. F.}. Nasal mucous polypi. Internal. Clin., Philadelphia, 1897,6. s., Hi, 332-
837.
Minor (C. L.). Malignant disease in the nose, with report of cases. Laryngoscope, St.
Louis, 1905, xv, 917-934.
DISEASES OF THE NOSE 559
Packard (F. R.}. The etiology of nasal polypi, with especial reference to their association
with other pathological conditions. Tr. Am. Laryngol. Ass., New York,
1903, xxv, 157-166.
Thudichum (J. L. W.}. On polypus in the nose and other affections of the nasal cavity;
their successful treatment by the electro-caustic and other new methods. A
monograph based entirely upon original experience. 7. ed. enl. & rev.
London, 1892. 8°.
5. Deflections and Distortions of the Nasal Septum
Occurrence. — Normally the septum should be vertical, dividing the nasal cavity
into two equal parts. Slight deviations from the normal are of no importance,
but in many persons there is a marked curving or bending to one side (deflection
of the septum). The deflection may be (1) a gentle curve of the entire septum,
(2) a wavy line of curvature involving most of the septum, or, (3) a sharp curve
or a bend of a circumscribed area of the septum. Small projections from the
surface of the septum are known as nasal spurs; a single spur or several spurs
may be present.
The majority of septal deviations are developmental, depending either upon
delayed dentition and irregular eruption of the incisor teeth, or upon failure of the
hard palate to develop properly.
Symptoms. — Spurs or deflections that do not interfere with nasal function
need no especial consideration, but if the lesion obstruct breathing, hinder the free
flow of secretions from the paranasal sinuses into the nose, or cause irritation by
coming into contact with the mucosa of the conchae, symptoms develop. These
may consist of (1) a feeling of stuffiness in the nose due to obstruction, (2) ma-
tutinal frontal headache, (3) asthmatic attacks through reflex irritation, or (4)
chronic nasal catarrh.
Diagnosis. — Any of the symptoms above mentioned should lead to a careful
examination of the nose. On rhinoscopy, the abnormality of the septum will be
easily visible, and in many cases secondary changes in the nasal mucosa or in the
paranasal sinuses can be made out.
One of the definite advances of modern rhinology has been the introduction of
the simple operation of submucous resection of the septum in these cases.
References
Bergeat (H.). Die Aetiologie der Verbiegungen und Auswuchse am Geriiste des Nasen-
septums. Monalsschr. f. Ohrenh., Berlin, 1896, xxx, 486-496.
Bert (G. M. J.). Traitement des deviations de la cloison nasale. Bordeaux, 1901. 8°.
Blanc (F.). Varietes cliniques et traitement chirurgical des deviations de la cloison des fosses
nasales. Lyon, 1905. 8°.
Casselberry (W. E.). Deformities of the septum narium; their classification with a view to
treatment. J. Am. M. Ass., Chicago, 1899 , xxxii, 469-471.
Fisher (L.). One thousand submucous resections of the nasal septum; what I have learned
in performing them. New York M. J. [etc.], 1915, ci, 1058-1062.
Freer (O. T.). Deflections of the nasal septum; a critical review of the methods of their cor-
rection by the window resection, with a report of 116 operations. Ann.
Otol, Rhinol. & Laryngol., St. Louis, 1905, xiv, 213-266.
Goldmann (E. E.) & Killian (G.). Ueber die Verwendung der X-Strahlen fur dieBestim-
mung der nasalen Nebenhohlen und ihrer Erkrankung. Beitr. z. klin.
Chir., Tubingen, 1907, liv, 1-22.
Jackson (C.). Failures in attempted correction of septal deviation. Tr. Am. Laryngol.,
Rhinol. & Otol Soc., 1902, New York, 1903, viii, 332-343.
560 DISEASES OF THE EESPIEATOEY APPAKATUS
Katz (Leo). Die Krankheiten der Nasenscheidewand und ihre Behandlung. Wurzburg,
1908, C. Kabilzsch. 179 p. 8 pi. 8°.
Killian (€?.)• Die submucose Fensterresektion der Nasenscheidewand. Arch. f. Laryngol.
& Rhinol., Berlin, 1904, xvi, 362-387.
Kyle (D. /?.)• Appropriate treatment for certain varieties of nasal deflections and redundancy.
Tr. Am. Laryngol., Rhinol. & Otol. Soc., 1S99, New York, 1900, v, 66-77.
6. Nasal Hydrorrhea; Rhinorrhea
In neurotic persons, attacks of watery discharge from the nose (hydrorrhea)
are not uncommon. They are probably of vasomotor origin, and are sometimes
described as attacks of coryza vasomotoria.
In some instances, known as cerebrospinal rhinorrhea, an actual flow of cerebro-
spinal fluid from the nose has been observed (L. Hektoen).
References
Hektoen (L.)- Spontaneous escape of cerebro-spinal fluid from the nose. Indiana M. J.,
Indianapolis, 1899-1900, xviii, 336.
Kahn (//.)• A short study on the etiology of nasal hydrorrhoea, with case reports. J. Ophth.
& Oto. -Laryngol., Chicago, 1914, viii, 412-414-
Kassel (/£.)• Fall von Rhinitis vasomotoria verursacht durch Spulwurm. Ztschr. f. Laryngol.,
Rhinol. [etc.], Wurzburg, 1914-15, vii, 559.
Marland (L.). Du diagnostic differentiel des hydrorrhees nasales. Lyon, 1900. 8°.
Philip (J. //.) & Brown (P. K.). One case of cerebro-spinal rhinorrhea and two cases of
nasal hydrorrhea. Tr. M. Soc. Calif., San Francisco, 1900, xxx, 4?4~479.
Schwab (S. /.) & Green (/.)» Jr* A case of cerebrospinal rhinorrhea, with retinal changes.
Am. J. M. Sc., Philadelphia & New York, 1905, n. s., cxxix, 774-781.
B. Diagnoses of Diseases of the Paranasal
Sinuses
1. General Remarks on the Diagnosis and Differential
Diagnosis of Inflammatory Diseases of the Paranasal
Sinuses
Before the application of the methods of transilhimination and of ront-
genography to the study of sinus disease, physicians had to depend for
the diagnosis of these affections upon (1) the subjective symptoms, and
(2) rhinoscopic examination. While these older methods are still of
very great value and should be employed in every case, the introduction
of the two newer methods above mentioned has revolutionized the clinical
study of diseases of the'paranasal sinuses and permits us to make diagnoses
much more easily and certainly than formerly ; very often, too, with their
aid it is possible to avoid some of the intranasal diagnostic operations
which were formerly necessary.
DISEASES OF THE PAKANASAL SINUSES
561
562 DISEASES OF THE KESPIRATOKY APPARATUS
For clinical purposes it is convenient to divide the paranasal sinuses
into two series : ( 1 ) the paranasal sinuses of the first series, or those that
empty into the middle meatus ; this series includes the maxillary sinus or
antrum, the frontal sinus, and the anterior ethmoid labyrinth; (2) the
paranasal sinuses of the second series, namely, those whose cavities open
into the olfactory fissure or
superior meatus ; to this
series belong the posterior
ethmoid cells and the sphe-
noidal sinus.
If on rhinoscopic exam-
ination pus quickly reappear
after the nose has been me-
chanically cleaned, the first
question we ask ourselves is:
Is the suppuration in a para-
nasal sinus belonging to the
first series or to the second
series? If the pus reappear
in the middle meatus, either
in front, below the anterior
half of the middle concha,
or, owing to obstruction to
forward flow, behind, above
Fig. ins.— Diagram Showing the Relations of the the inferior concha, then we
Paranasal Sinuses to the Hiatus semilunaris. knOW that W6 must be deal-
s.m. — Maxillary Sinus; s.f. — Frontal Sinus; s.e. . . , ,. . ,
— Ethmoidai sinus ; s.sph.— Sphenoidai Sinus ; mg with a disease ot the an-
o.m. — Maxillary Ostium ; o.f. — Frontal Ostium. trum, of the frontal sinUS, Or
(After M. Ilajok, "Nebenhohlen der Nase," pub- /. . ,-, . j -,
Hshed by F. Deutiche, Leipzig.) of the anterior ethmoidal
labyrinth, or, possibly, with
simultaneous involvement of two or three of the paranasal sinuses of
the first series. If, on the contrary, the pus appear in front in the ol-
factory fissure, or in the superior meatus above the middle concha, we know
it must come from one or both of the paranasal sinuses of the second series,
that is, from the posterior ethmoidal cells or from the sphenoidal sinus.
The next step in the investigation is to decide upon the particular
sinus in a series whence the pus is derived. In this connection, a few
points may be emphasized:
(1) Disease of the maxillary sinus is by far the most common of the
sinus diseases. With the patient in the upright position, the flow of pus
from a maxillary sinus is usually intermittent, but the flow can be in-
creased by inclination of the head forward ; while the flow of pus from
a frontal sinus is often continuous, and the outflow is diminished when
the head is bent forward.
DISEASES OF THE PAKANASAL SINUSES 563
(2) X-ray examination and transillumination will reveal shadows in
the affected sinuses ;" sinuses that are entirely clear on these two methods
of examination rarely need further investigation.
(3) It is often possible to probe, or to irrigate, the maxillary sinus,
either through the sinus maxillaris, or through an accessory opening.
When this is not feasible, an exploratory puncture with a hollow needle
can easily be made, when indicated, through the lateral wall of the inferior
meatus, and the cavity washed out.
(4) If antral disease be excluded, and it is known that pus is being
discharged into the middle meatus, it must come either from a frontal
sinus, or from the anterior ethmoidal cells. To differentiate between these
two sources, the x-ray examination often suffices, but it is sometimes
necessary to remove the anterior portion of the middle concha and any
polypi or hypertrophied mucous membrane in the neighborhood, after
which the openings of the frontal sinus and of the anterior ethmoidal
cells are accessible to rhinoscopic study. It must not be forgotten that
when one paranasal sinus is diseased another may be simultaneously
affected.
(5) In the differentiation between disease of the posterior ethmoidal
cells and disease of the sphenoidal sinus, after the establishment of the
fact that the discharge is into the olfactory fissure or superior meatus, and
not into the middle meatus, we proceed by (a) making an x-ray examina-
tion, and (b) following the suppuration to its source, removing, when
necessary, obstacles to the observation of this source by intranasal oper-
ation.
The general practitioner cannot be expected to command all the special-
istic methods of examination required in the study of disease of the
paranasal sinuses. He should, however, be familiar with the subjective
symptoms and the complaints of patients that suffer from disease of these
sinuses, and should be able to decide when it is necessary to call specialists
to his aid.
Inflammations may extend to (1) the maxillary sinus, or antrum of
Highmore, (2) the frontal sinus, (3) the ethmoid cells, or (4) the sphe-
noid cells.
Causes of Sinusitis. — These include primary infections of the mucous
membrane in influenza, pneumonia, scarlet fever, measles, etc., and second-
ary infections by extension from the teeth (to the antrum), or as complica-
tions in tuberculosis, lues, trauma, etc.
References
Axenfeld (T.). Ein Beitrag zur Pathologic und Therapie der frontalen und der ethmoidalen
Sinusitis und ihrer orbitalen Complikationen. Deutsche med. Wchnschr.,
Leipzig u. Berlin, 1902, xxviii, 713-716.
Ballenger (W. L.). Intranasal frontal sinus operations; conservative surgery. Internal.
Clin., Philadelphia, 1915, 25. s., ii, 260-267. 3 pi.
564 DISEASES OF THE RESPIRATORY APPAEATUS
Berry (H. M.). Radiography in the diagnosis of diseases of the accessory nasal sinuses.
Part I. The posterior-anterior view, anatomical considerations and tech-
nique. Arch. Roentg. Ray, London, 1914-15, xix, 419-436. 8 pi.
Bliss (M. A.). The importance of the paranasal sinuses in the explanation of pain in the
face, head, neck, and shoulders. Am. J. M. Sc., Philadelphia, 1915,
cxlix, 230-235.
Bosworth (F. H.}. Varizus forms of disease of the ethmoid cells. New York M. J.,
1891, liv, 505-507.
Brons (C.). Entziindliche Erkrankungen der Orbita und Nebenhohlen. In: Ergebn. d.
allgem. Pathol. [etc.] (Lubarsch & Ostertag). Wiesbaden, 1914, xvi,Ergdnz.-
Bd., 294-356.
Bryan (J. H.). Chronic empyema of the frontal, ethmoidal, and both sphenoidal sinuses,
with extensive necrosis of the bones, complicated with adenoma of the pos-
terior ethmoidal and sphenoidal regions. Am. J. M. Sc., Philadelphia &
New York, 1902, n. s., cxxiv, 416-432.
Diseases of the accessory sinuses of the nose. In: Syst. Dis. Ear, Nose and
Throat (Burnett}. Philadelphia, 1893, i, 743-775.
Davis (W. B.). Development and anatomy of the nasal accessory sinuses in man. Phila-
delphia & London, 1914, W. B. Saunders Co. 150 p. 8°.
Delavan (D. B.). The prophylaxis of sinus diseases. J. Am. M. Ass., Chicago, 1903, xl,
502-505.
Finzi (N. S.} & Hett (G. S.). Radiography of the maxillary antrum. Arch. Radiol. &
Electrother., London, 1915, xx, 43-46. 8 pi.
Hajek (M.). Pathologic und Therapie der entzundlichen Erkrankungen der Nebenhohlen
der Nase. 8. ed. Leipzig u. Wien, F. Deuticke, 1909.
Experiences in the endonasal radical operation upon the sphenoid cavity and
the posterior ethmoid labyrinth. Ann. OtoL, Rhinol. & LaryngoL, St. Louis.
1909, xviii, 64-67.
Holmes (B.). The diagnosis and treatment of infection of the accessory mucous cavities of
the respiratory, digestive and genito-urinary tracts. Lancet-Clin., Cincin-
nati, 1905, n. s., Iv, 621-626.
Howard (W. T.)> Jr., & Ingersoll (J. M.}. A contribution to our knowledge of the etiology
of inflammations of the accessory sinuses of the nose. Am. J. M. Sc.}
Philadelphia, 1898, n. s., cxv, 520-543.
Killian (G.)- The accessory sinuses of the nose and their relations to neighboring parts.
Transl. by D. R. Patterson. Jena & Chicago, 1904. roy. 8°.
Lewis (C. /.) & Turner (A. D.}. Suppuration in the accessory sinuses of the nose; a bac-
teriological and clinical research. Edinb. M. J., 1905, n. s., xviii, 393-421.
McLoone (J. /.)• Defects of the singing voice due to nasal and accessory sinus disease.
J. Am. M. Ass., Chicago, 1915, Ixv, 310-312.
Onodi (A.). The optic nerve and the accessory sinuses of the nose: a contribution to the
study of canalicular neuritis and atrophy of the optic nerve of nasal origin.
London, 1910, Bailliere, Tindall & Cox. 101 p. 8°. Also: W. Wood
& Co., New York.
Ueber die okulo-orbitalen, intrakraniellen und cerebralen Komplika-
tionen nasalen Ursprungs. Med. Klinik, Berlin, 1914, x, 719-721.
Partsch (C.). Die Erkrankungen der Kieferhohle. Handb. d. Zahnheilk., 1892, ii, 2. Abt.,
420-438.
Pearce (R. M.). The bacteriology of the accessory sinuses of the nose in diphtheria and
scarlet fever. J. Bost. Soc. M. Sc., 1898-99, Hi, 216-223.
Skillern (R. //,). The catarrhal and suppurative diseases of the accessory simises of the
nose. Philadelphia & London [1913], J. B. Lippincott Co. 389 p. 8°.
Stark (H. H.). Sudden blindness due to suppuration of the accessory nasal sinuses, with
report of three cases. J. Am. M. Ass., Chicago, 1915, Ixv, 1513-1520.
Stimson (G. W.}. Empyema of frontal and ethmoidal sinuses- J Am. M. Ass., Chicago,
1915, Ixv, 418-41S,
DISEASES OF THE PAKANASAL SINUSES 565
Symposium; disease of the accessory sinuses. Ann. Otol., Rhinol. & LaryngoL, St. Louis.
1905, xiv, 431-528.
Tilley (//.)• Diseases of the accessory sinuses. In: Syst. Med. (Allbult & Rolleston). 8°.
London, 1909, iv, pt. 2, 72-91.
Turner (A. L.}. The accessory sinuses of the nose; their surgical anatomy and the diagnosis
and treatment of their inflammatory affections. Edinburgh, 1901. 8°.
Watson-Williams (P.). Cerebro-spinal rhinorrhea with subsequent ethmoiditis and frontal
sinus suppuration. J. LaryngoL, London, 1913, xxviii, 623-625.
Intranasal operations for frontal.sinus suppuration. J. LaryngoL, London.
1914, xxix, 225-242. 8 pi.
Note on the technique of the intranasal operation for antral sinus suppura-
tion. J. LaryngoL, London, 1914, xxix, 113-116.
Zuckerkandl (E.). Normale und pathologische Anatomie der Nasenhohle und ihrer pneu-
matischen Anhdnge. 2. Aufl. Wien & Leipzig, 1893. 8°.
2. Maxillary Sinusitis
(Maxillary Antritis, Antrum Disease)
Definition. — An inflammation (catarrhal or suppurative) of the sinus
maxillaris, due to infection, arising usually by extension from the nose,
or from the root of a tooth, most often from the second bicuspid or the
first molar tooth, the roots of which are nearest to the floor of the antrum.
Symptoms. — The patient may complain of a foul-smelling discharge
from one side of the nose, or of pain, either directly over the antrum or
radiating from it into the side of the face. If the pus has been swallowed
for some time, there may be digestive disturbances or anemia ; metastatic
infections involving the kidneys or the joints are not uncommon complica-
tions. In one of Crowe's cases, the pus from an infected antrum had
passed backward ?long the !N". maxillaris into the skull cavity and given
rise to an extradural abscess over the temporal lobes and to a meningitis.
When the antritis is secondary to rhinitis, an examination of the nose will
reveal the primary condition; when it is secondary to an infected tooth,
there may be pain in the teeth on the affected side, and a dental rontgeno-
gram may reveal the particular tooth at fault.
Transillumination of the antrum (q. v.) will reveal a shadow if there
be an exudate in the antrum, if its walls be thickened, or if the cavity
be filled by polypoid excrescences. Occasionally, a darkening is due to
thickened bone or to the absence of an antrum on one side. Similarly, a
rontgenogram of the two antra will reveal differences in density on the
two sides. The x-ray photograph should be so taken that the frontal sinuses,
the ethmoidal cells, and the antra of the two sides shall show on the same
plate, as it is necessary to compare the two sides. The x-ray operator
should avoid any superimposition of the foramen magnum and of the
base of the skull over the antra.
Occasionally, after a menthol or a cocain spray, the antrum will be
seen to drain into the nose (middle meatus) ; but sometimes it is necessary
to open the antral wall, either through the nose, or from the mouth through
566 DISEASES OF THE EESPIKATORY APPARATUS
the alveolar process. In passing a trocar into the antrum, great caution
should be observed, since examiners before now have passed it into the
Pig. 164. — Rontgenogram in Influenzal Inflammation of Antrum. E. P., Age 18 — Infection
of Right Antrum of About One Year's Duration Following an Attack of Influenza. Symp-
toms : General Lassitude, Occasional Headaches, Discharge in the Nasopharynx. Con-
firmed by Operation. Pure Culture of B. influenzae. (By courtesy of S. J. Crowe.)
orbit, or into the tissue on the far side of the antrum ! When a chronic
purulent condition has lasted for some time, fistula formation may occur,
with necrosis of bone and the development of polypoid growths. It should
not be forgotten that a purulent discharge originating in a frontal sinus
or in the anterior ethmoidal cells may drain into an antrum, thus giving
rise to a pyosinus.
Differential Diagnosis. — In ACUTE: CASES, there may be swelling of the
cheek, lip and eyelids on the affected side. One may at first suspect (1)
facial erysipelas,, but examination and the anamnesis should exclude it,
since in erysipelas the swelling is in the skin itself, not in the deeper
parts; the patient may have had several earlier attacks, and the swelling
will have begun at the nose.
We next rule out (2) furuncle of the upper lip with infection of the
facial veins ; the anamnesis and the site of the original furuncle are usually
decisive.
DISEASES OF THE PAKANASAL SINUSES 567
It is sometimes difficult to differentiate (3) a maxillary periostitis
from an acute flare-up of antral disease; in both there may he swelling of
the face, and tenderness on pressure in the canine fossa. But the anam-
neses differ; in ordinary periostitis, the patient will have had a preced-
ing toothache, and on examination a carious tooth, or a tooth tender on
pressure, will he found, while in acute maxillary sinusitis, a history of a
preceding coryza or influenza will he elicitable ; or if there is an exacerba-
tion of chronic antral disease, there will be a history of periodic discharge
of pus and perhaps of blood from the nose. The soft parts of the face are
less swollen in sinus disease than in maxillary periostitis ; the tenderness
in the former is diffuse over the maxilla, reaching as far as the lower
margin of the orbit, often accompanied by infra-orbital neuralgia, whereas
in periostitis, the tenderness is most marked at the alveolar process of
the upper jaw.
In CHRONIC CASES, rhinoscopy reveals hypertrophy of the mucosa of
the middle concha, and often polypi in the nose. If there be no obstruc-
tion to the orifice of the sinus, the purulent outflow can be observed at
times below the middle concha. When there is retention, transillumina-
tion and rontgenograms will reveal the darkened sinus.
Now and then, there is a possibility of confusing disease of the antrum
with (4) acute dacryo cystitis, in which there is swelling and tenderness
in the naso-orbital angle. But in this case there will be epiphora, due to
blocking of the lacrimal duct, and the patient will probably give a history
of earlier attacks, and, perhaps, of previous treatment of the duct.
Other conditions, occasionally confused with antral disease, especially
in children, are (5) maxillary tuberculosis, and (6) acute parotitis.
3. Frontal Sinusitis
The frontal sinus, on one or on both sides, may be the site of an
acute catarrhal, or an acute purulent inflammation, or, more often still,
of a chronic empyema. Occasionally, cysts, polyps, and hydrops of the
cavities are met with. The sinuses are often the site of anatomical varia-
tion, as x-ray pictures show. The sinuses of the two sides are usually
separated by a septum; either sinus may be subdivided into several com-
partments.
Symptoms. — On the subjective side, the local symptoms consist of head-
ache and discharge from the nose ; in some patients, there are complaints
of disturbances of the sense of smell, obstruction of the nose, epistaxis, and
eczema of the nostrils. The patients often present neurasthenic symptoms
(incapacity for mental work, irritability, intolerance for alcohol and
tobacco). Neuralgic pains in the domain of the ~N. ophthalmicus may
occur. On the objective side, in suppurative disease of the frontal sinus,
568 DISEASES OF THE KESPIKATOKY APPARATUS
the pus appears in the middle meatus, often under the anterior end of
the middle concha. Sometimes polyps or hypertrophied mucosae prevent
inspection of the most anterior part of the middle meatus. When this
is not the case, removal of the pus with a swab will be followed by the
appearance of a streak of pus running down from above and in front.
When the patient sits upright the flow may be continuous, in contrast with
the periodic flow in antrum disease. In latent stages, however, the flow
need not be continuous; it is then most often visible in the early morning
hours.
The continuous flow is often converted into a periodic flow through the
presence of polypi or of hypertrophied mucous membrane. Such hyper-
Left
Side
of
Skull
Right
Side
of
Skull
Fig. 165. — Rontgenogram Showing Clouding of Sinuses in S'nusitis. Patient. Age 30; Chronic
Infection of the Right Frontal Sinus and the Right Antrum. Symptoms : Headache,
Purulent Discharge, Nasal Obstruction, Indigestion (Hyperacidity). Confirmed by
Operation. (By courtesy of S. J. Crowe.)
trophies usually involve the anterior end of the middle concha, and extend
to the most anterior part of the hiatus and of the infundibulum, whereas
in antral disease the polyps and hypertrophy are limited more to the
posterior part of the hiatus in the immediate neighborhood of the ostium
maxillare.
In disease of the frontal sinus, the most anterior part of the middle
meatus is often narrowed on the diseased side owing to edema of the
mucous membrane on the most anterior part of the concave side of the
middle concha.
DISEASES OF THE PAKANASAL SINUSES 569
There is often tenderness over the anterior wall of the frontal sinus
on percussion with the index finger, or with the percussion hammer. There
may be tenderness on pressure at the root of the nose, on the orbital
surface of the frontal sinus, especially at two spots; namely, (1) the
inner upper angle of the orbit, and (2) the region behind the supra-orbital
notch.
Occasionally, a slight edema of the soft parts of the forehead over the
frontal sinus and of the upper eyelid can be made out ; such an edema is
prone to come and go; it is usually most marked in the morning.
Chronic infection of a frontal sinus occasionally gives rise to extradural
abscess over the frontal lobe of the cerebrum and to meningitis.
Diagnosis. — This depends upon the history, the demonstration of in-
creased discharge in the middle meatus of the nose, the exclusion of antrum
disease, and upon the methods of transillumination and, especially, of
x-ray examination of the sinuses. In some instances, the passage of a
sound into the sinus and washing it out may be necessary ; as a rule, such
sounding should be avoided, since one may easily infect a healthy sinus,
or may perforate the cribriform plate.
4. Ethmoidal Sinusitis
The ethmoid cells are divisible into two groups, an anterior and a
posterior. The number of cells in each group is variable. It is impor-
tant to remember that those of the anterior group chiefly empty into the
middle meatus, and those of the posterior group for the most part
into the superior meatus. Clinically, this division of the ethmoid cells
into those that empty into the middle meatus and those that empty info
the upper meatus is very convenient. The posterior group of cells stands in
close relation to the nasal wall of the orbit, and, occasionally, an infection
of the cells may lead to perforation of the orbital wall and give rise to
unilateral exophthalmos and visual disturbances.
The ethmoid cells are often the site of inflammation, acute or chronic ;
the condition is, unfortunately, frequently overlooked.
Symptoms. — In latent cases, there may be no symptoms except those of
a general run-down condition. In acute cases, and in acute exacerbations
of chronic cases, there is usually headache, dull aching pain in the eyes
and at the root of the nose, purulent discharge from the nose, disturbance
of the sense of smell, nasal obstruction, and often secondary inflammations
of the middle ears, tonsils, cervical glands, pharynx and larynx. The
disease is sometimes the primary focus of infection in chronic arthritis ; in
all cases of chronic arthritis, the paranasal sinuses should be carefully
examined. Various diseases of the eye and disturbances of the eye-
muscles have been observed as sequelae of ethmoidal sinusitis.
Diagnosis. — Chronic empyema of the ethmoid cells includes many of
570 DISEASES OF THE EESPIKATORY APPARATUS
the cases formerly described as recurring polyp formation, and as fetid
blennorrhea or ozena. Not infrequently the ethmoidal cells are involved
simultaneously with other paranasal sinuses.
It is not uncommon to have one part of the ethmoid cells involved while
the others remain healthy.
Occasionally, mucocele of the ethmoid develops, owing to retention of
serum or mucus in the cells. It may appear as a mass, yielding parch-
mentlike crepitation. It should not be mistaken for a meningocele, a
dermoid, or a neoplasm.
An empyema of the ethmoid cells may be either open or closed. In
the open cases, the pus flows into the nasal cavity and polypi are common.
In the closed cases, this flow of pus is prevented, owing to obstruction at
the opening into the nose; the patient complains of headache; sometimes
external swellings appear owing to dilatation of the cells; such swellings
may project into the skull cavity or into the orbit.
In latent cases, the diagnosis can be made only by rhinoscopic study
or by x-ray examination. In manifest cases, it may be suspected even in
the absence of a rhinoscopic examination. Many patients complain of
dry ness of the throat, due to atrophy of the secreting glands of the pharynx.
Whenever suspected, a careful rhinoscopic study should be made by a
specialist, and an x-ray examination of the various paranasal sinuses re-
sorted to. The x-ray is more helpful in the diagnosis of disease of the
anterior group of ethmoidal cells than of disease of the posterior group.
The bulla ethmoidalis, situated just beneath the anterior end of the
middle concha, is sometimes large and it may then look like a polyp;
touched with a probe, however, it is found to be hard (bony), while a polyp
is soft and mobile.
Operative measures on the ethmoid are especially dangerous, owing to
the thinness of the lamina cribrosa, and to the fact that sheaths of dura
surround the filaments of the olfactory nerves; meningitis has occurred
after operation in a number of instances.
5. Sphenoidal Sinusitis
The sphenoidal sinus on either side is less often affected than the
other sinuses, but it is sometimes the site of inflammatory changes,
or of disease of its bony walls. The sinus is related anatomically to the
N. opticus, the sinus cavernosus, the dura mater, and the A. carotis ; hence
the occasional complications of blindness from retrobulbar neuritis, of sinus
j thrombosis, of meningitis, and of erosion of the A. carotis with fatal
hemorrhage.
Symptoms. — The symptoms are very inconstant, but include headache,
stiffness of the neck, nasopharyngeal catarrh, subjective disturbances of
,the sense of smell, vertigo, and general neurasthenic symptoms,
DISEASES OF THE PAKANASAL SINUSES 571
On objective examination, the discharge is found to empty either into
the anterior part of the olfactory fissure, or, much more often, backward
into the nasopharynx at the part of its roof that lies close to the superior
meatus. It is sometimes associated with ozena.
The mucous membrane bounding the olfactory fissure becomes hyper-
trophied, and it is sometimes the site of polypi. Catarrhal inflammations
of the pharynx and larynx are more common in sphenoidal sinusitis than
in inflammations of the other paranasal sinuses. Occasionally, the bony
walls of the sinus become diseased, in which event there is danger of cere-
bral complications (sudden unilateral blindness, due to compression of
the optic nerve in the foramen opticum, or to perineuritis). Sometimes
Fig. 166. — Method of Showing Right and Left Sphenoidal Sinuses. The Upper Arrows Point
to the Foramen magnum and the Odontoid Process ; the Four Lower Arrows to the
Sinuses. (By courtesy of Drs. Baetjer and Waters, X-ray Dept., J. H, H.)
572 DISEASES OF THE KESPIKATOKY APPAKATUS
the retrobulbar tissues of. the eye become invaded, with resulting exoph-
thalmos. Occasionally, the lateral superior wall of the sinus is perforated,
injuring the sinus cavernosus, and causing thrombosis or fatal hemorrhage.
Diagnosis. — The presence of pus in the olfactory fissure should excite
suspicion ; the nose should be .thoroughly cleansed, and then be watched for
the return of pus. The diagnosis may be aided (1) by x-ray examination,
and (2) by the demonstration of the origin of the discharge from the
sphenoidal cells, (a) by direct observation of the outflow from the open-
ing of these cells, or (b) by the passage of a sound, and irrigation of
the cells.
6. Mastoiditis
The mastoid is not a paranasal sinus, but an accessory cavity of
the middle ear. For convenience, however, inflammation of the mas-
toid will be mentioned here. Secondary to otitis media, acute mastoiditis
or mastoid disease frequently develops, and the condition should never
be overlooked. Many cases when neglected go over into a suppurative
process or into a chronic mastoiditis.
A purulent otitis media usually causes rupture of the drum with dis-
charge to the outside. As long as the inflammation is confined strictly
to the tympanic cavity, the main danger is impairment of hearing, but
when it extends beyond this, serious complications often arise. Mas-
toiditis is, as a rule, the connecting link between purulent otitis media
and its graver complications (Reik).
Symptoms. — Following upon the signs of an acute otitis media (local
pain, fever, bulging of the ear drum, perforation^ otorrhea), the pain
may change its location and be assigned by the patient either to the
region just over the mastoid, behind the ear, or to the depth of the ear
itself. There is localized tenderness on firm pressure over the mastoid,
or higher up over the mastoid antrum at the level of the upper border
of the external auditory meatus. There may be no swelling nor redness ;
when these are observable over the mastoid, they indicate that the abscess
has already broken through the bone and has given rise to a periostitis,
or perhaps to a subperiosteal abscess. Another important sign of mas-
toiditis is swelling of the inner end of the posterior cutaneous wall of
the external auditory canal, so that this portion droops just in front
of the tympanic membrane. The posterior cervical lymph glands under-
go enlargement. In acute mastoiditis there is fever, but in the chronic
cases the temperature may be normal; there is a moderate leukocytosis.
Diagnosis. — Since otitis media is a common complication of scarlet
fever, typhoid fever and influenza, the symptoms due to a developing
mastoiditis are not infrequently attributed to the primary infection, the
important local process being overlooked especially in children. In all
DISEASES OF THE PARANASAL SINUSES 573
acute infections, especially in children, the mastoids should be regularly
examined. Spontaneous pain, in or behind the ear, accompanied by
tenderness over the mastoid is diagnostic, even in the absence of otorrhea
and of local swelling or edema of the soft tissues over the mastoid.
In chronic otorrhea, an involvement of the mastoid by the chronic
suppurative process is' very common. Eecently, x-ray examinations have
been found helpful in the diagnosis of this condition.
Complications of Mastoiditis. — The intracranial complications are the
Fig. 167. — Rontgenogram of Mastoid Disease. The Large Clear Area (See Arrows) Near
the Tip of the Left Mastoid Indicates the Situation of a Sequestrum and Extradural
Abscess. (It is Necessary in Taking an X-ray of the Mastoid to Have the External and
Internal Auditory Meatus Superimposed — See Arrows, 2 Left Upper Ones.) In this Case
the Right Mastoid Was Normal; Left Mastoid, Infection of Two Months' Duration
Pure Culture Streptococcus mucosus. Symptoms : Left-sided Headache, Purulent Dis-
charge from the Ear, Local Tenderness Over the Mastoid, Edema of the Walls of the
External Auditory Canal. X-ray Confirmed at Autopsy. (By courtesy of S. J. Crowe.)
most serious. Any one of the following may occur: (1) pachymenin-
gitis, (2) extradural abscess, (3) leptomeningitis, (4) cerebral or cere-
bellar abscess, (5) thrombosis of the lateral sinus, or (6) purulent laby-
rinthitis.
574 DISEASES OF THE EESPIKATOKY APPAKATUS
References
Bezold (F.). Die Krankheiten des Warzentheiles. Handb. d. Ohrenheilk. (Schwartze).
Leipzig, 1893, ii, 299-351.
Bishop (S. £.)• Diseases of the masioid process. Internal. Clin., Philadelphia, 1897, 7. s.,
i, 327-331. 1 pi.
Caldwell (G. W.}. Transillumination of the mastoid cells as a means of diagnosis of mas-
toiditis interna suppurativa. Canada Lancet, Toronto, 1892-93, xxv, 357.
Also: N. York M. J., 1893, Iviii, 66.
Dench (E. /?.)• The diagnosis and treatment of mastoiditis. J. Am. M. Ass., Chicago, 1901,
xxxvii, 247-254.
Fraser (J. S.) & Dickie (J. K. M.). An analysis of 123 consecutive cases in which opera-
tions were performed for the relief of mastoid, labyrinthine and intracranial
complications of suppurative otitis media. J. Laryngol., London, 1912,
xxvii, 133; 191.
Friedenwald (H.). A case of extensive caries and cholesteatoma of the mastoid process with-
out local signs of inflammation; death from thrombosis of the lateral sinus
and meningitis. Arch. Otol, New York, 1891, xx, 1-10.
Hagedorn (M.). Ursachen undFolgen der Erkrankungen des Warzenleils und ihreBehand-
lung. Samml. zwangl. Abhandl. a. d. Geb. d. Nasen-, Mund- u. Halskr.,
Halle a. S.t 1900, Hi, 12. Hft., 1-65.
Katz (L.}, Preysing (H.) & Blumenfeld (F.). Handbuch der speziellen Chirurgie des
Ohres und der oberen Luftwege. Wurzburg, 1912.
Lamacq & Dormoy. Semeiologie des ganglions mastoldiens et pre-auriculaires. Gaz. hebd.
d. sc. med. de Bordeaux, 1904, xxv, 162-164.
McKernon (J. F.}. The differential diagnosis between diffuse circumscribed external otitis,
or furuncle, and acute mastoiditis. Post-Graduate, New York, 1904, xix,
1001-1005.
Oppenheimer (S.}. The venous system of the temporal bone and its relation to the compli-
cations of mastoid disease. Tr. Am. Laryngol., Rhinol. & Otol. Soc., 1902,
New York, 1903, viii, 295-306.
Mastoid disease and cerebellar abscess. Ann. Otol., Rhinol, & Laryngol.,
St. Louis, 1903, xii, 705-724.
Woods (H.) Jr. Cases of Mastoid disease. Maryland M. J., Baltimore, 1898-99, xL
147-150.
C. Diagnosis of Diseases of the Larynx
Four main groups of diseases of the larynx have to be considered:
1. Inflammatory (acute, chronic, specific) ;
2. Circulatory (edema of the glottis) ;
3. Paralytic;
4. ISTeoplastic (papillary fibro-epithelioma, fibroma, carcinoma) ;
5. Stenotic.
References
Harwell (H.). Diseases of the larynx. 2. ed. London, 1910, H. Frowde. 266 p. 8°.
Chiari (O.). Die Krankheiten der oberen Luftwege. 3. Teil. Die Krankheiten des Kehl-
kopfes und derLuftrohre. Leipzig u. Wien, 1905, F. Deuticke. 404 p. 8°.
'Gottstein (/.)• Die Krankheiten des Kehlkopfes mit Einschluss der Laryngoskopie und der
local-therapeulischen Technic fur praktische Aerzte und Studierende.
4. Aufl. Leipzig & Wien, 1893. 8°.
DISEASES OF THE LAKYNX 575
Grant (D.). Some common errors in diagnosis and treatment of diseases of the pharynx,
larynx and naso-pharynx. Clin. J., London, 1904, xxiv, 305-310.
Laurens (Georges). Oto-rhino-laryngologie du medecin practiden. Paris, 1912, Masson
& Cie. 418 p. 8°.
Meyer (/?.). Die Erkrankungen des Kehlkopfes. Handb. d. inn. Med. (Mohr & Staehelin).
Berlin, 1914, ii, 107-159.
Semon (F.) & Williams (P. JF.). Diseases of the larynx. In: Syst. Med. (Allbutt &
Rolleston). 8°. London, 1909, iv, pt. 2, 179-282.
[For other references, see under (1) Methods of Examination of the Larynx and (2)
Diseases of the Nose.]
1. Inflammatory Diseases of the Larynx
These are met with especially in the members of certain professions :
singers, lawyers, preachers, politicians, auctioneers. The use of alcohol
and especially of tobacco predisposes.
(a) Acute Laryngitis
(Laryngitis acuta)
Two main forms are met with : a catarrhal and a diphtheritic.
i. Acute Catarrhal Laryngitis
(Laryngitis catarrhalis acuta, False Croup)
The attack comes on after "catching cold," with hoarseness, cough,
and sometimes fever. On laryngoscopic examination, redness and swell-
ing of the laryngeal mucous membrane is visible ; occasionally, small ero-
sions or hemorrhages can be seen. The secretion may be only slightly in-
creased ; it is mucous or mucopurulent.
In small children, an acute laryngitis may be associated with paroxysms
of stenosis of the glottis, in the night; these attacks are known as afalse
croup." Waking suddenly, they startle their parents with the signs of
an attack of suffocation; there is barking, crouplike cough, and diffi-
cult, whistling, inspiration, accompanied by retraction of the jugulum and
of the epigastrium ; expiration is also difficult and the voice is hoarse. After
a short time, the respiration usually becomes easier; the acute symptoms
pass off in a few hours, though the child may remain hoarse for several
days. One must make absolutely sure at once that the child has not
diphtheria ; if there be any doubt, antitoxin should be administered. In
false croup, intubation is occasionally, though very rarely, indicated.
Reference
Rice (C. C.), Some of the unusual manifestations of so-called catarrhal laryngitis. N. York
M. J., 1896, Ixiv, 445-449. [Discussion] 467.
576 DISEASES OF THE KESPIEATOKY APPAKATUS
ii. Acute Pseudomembranous Laryngitis
(Laryngitis* pseudomembranacea, Diphtheritic Laryngitis, True Croup)
The epiglottis is most often affected, but the whole laryngotracheal tube
may be involved. The disease is rarely primary ; it is usually secondary
from the pharynx. A dirty, grayish- white, pseudomembrane (fibrin,
leukocytes, necrotic epithelium) exists on the surface of the mucosa. The
adjacent mucous membrane is deeply injected and swollen. Casts of the
larynx and of the trachea are sometimes coughed up.
Etiology. — In most cases true croup is due to the diphtheria bacillus,
though in the form complicating scarlet fever, measles, sepsis, etc., strepto-
cocci may be the cause. When a true false membrane is present in the
pharynx, or larynx, antitoxin should be promptly administered without
waiting for a bacteriological diagnosis. There is great danger of suffoca-
tion ; intubation or tracheotomy may soon be indicated, and someone
capable of performing them should be present with an outfit at hand.
References
Meltzer (S. /.)• Intubation in cases of foreign bodies in the air-passages; with remarks
concerning feeding after intubation. Med. Rec., New York, 1889, xxxvi,
811-313.
Northrup (W. P.). Some points concerning intubation of the larynx. Med. Rec., New
York, 1887, xxxi, 26.
O'Dwyer intubation instruments; added small tubes for infants under one
year; exhibition of modern complete set. Arch. Pediat., New York, 1903,
xx, 519-522.
O'Dwyer (/.). Intubation of the larynx. Tr. 9th Internal. M. Cong., Washington, 1887,
Hi, 516-527.
The evolution of intubation. Tr. Am. Pediat. Soc., New York, 1896, viii,
9-19. 1 pi.
(b) Chronic Laryngeal Catarrh
(Laryngitis catarrhalis chronica)
Etiology. — The condition is most often due to chronic irritation from
dust, smoke, etc. It is common in singers, public speakers, cigarette
smokers, millers, stone-cutters, and metal-workers. It is sometimes
secondary to nasopharyngitis or to pulmonary disease.
Symptoms. — The cough is often slight; the voice is feeble or hoarse,
and tires easily, growing weaker on talking. On laryngoscopic examina-
tion, one can make out moderate injection and swelling of the mucous
membrane. Often, visible thickenings of the epithelium of the true
vocal cords can be made out; the horny layer becomes milk-white, or of
a dull blue color, is detachable with forceps, and often presents papillary
nodules (pachydermia laryngis) ; this is the condition in the so-called
"singer's nodes" (trachoma of the vocal cords).
DISEASES OF THE LAKYNX 577
The secretion from the larynx is tenacious and grayish-white in color ;
or it may be brownish, due to admixture of blood.
Diagnosis. — Before making the diagnosis of simple chronic laryngeal
catarrh, one should exclude tuberculosis and lues, and should examine care-
fully the nose, the pharynx, and the lungs. Use may be made of the
Wassermann reaction, the Calmette test, and, if necessary, of histological
examination of a particle of tissue excised, for the differential diagnosis.
The whole body should be carefully gone over in the search for signs of
lues or of tuberculosis.
References
Chiari (O.). Beitrag zur Kenntniss des Baues der sogennannten Sdngerknotchen. Arch. f.
LaryngoL u. RhinoL, Berlin, 1900-01, xi, 415-422. 2 pi.
Discussion on "the utility or non-utility of local applications in chronic catarrhal laryngitis."
Arch. LaryngoL, New York, 1883, iv, 140-144.
Frdnkel (Z?.). Pachydermia laryngis, ihre Geschichte, pathologische Anatomie und Patho-
logic. Arch. f. LaryngoL u. RhinoL, Berlin, 1894, ii, 106-122.
Giittich (A.}. Die Sdngerknotchen in pathologisch-anatomischerBeziehung. Arch. f. exper.
u. klin. Phonet.,. Berlin, 1913-14, i, 361-371.
Hautiere (E.}. Contribution a I' etude des nodules vocaux chez les chanteurs; pathogenic et
traitement. Paris, 1901. 8°.
MacDonald (G.). The forms of epithelial hypertrophy in the larynx. Internal. Clin.,
Philadelphia, 1895, 5. s., Hi, 321; 1896, 6. s., i, 296; 1897, 6. s., iv, 306.
M' Bride (P.}. Pachydermia of the larynx. Tr. Med.-Chir. Soc., Edinburgh, 1892-93, n. s.,
xii, 108-121. 1 pi.
Miller (F. E.). Chorditis cantorum; a contribution to the study of the etiology, pathology and
treatment of singers' nodes, or nodules on the vocal cords. Laryngoscope,
St. Louis, 1902, xii, 809-839.
Shurly (E. L.)« Chronic laryngitis, simple and traumatic, Syst. Dis. Ear, Nose and
Throat (Burnett}. Philadelphia, 1893, ii, 457-499.
(c) Specific Inflammations of the Larynx
These include the tuberculous, the syphilitic, the typhoidal and other
specific inflammations.
i. Tuberculosis of the Larynx
(Tuberculosis laryngis)
The symptoms and signs are, at first, those of simple catarrh; they
include hoarseness, cough, reddening of the mucous membrane, erosions,
and paresis of the vocal muscles. Later, visible tuberculous infiltration
develops, usually appearing first in the interarytenoid region; this subse-
quently breaks down to give rise to ulcers (flat, sharp margins; granular
base). Sometimes, only a single ulcer develops ; or two symmetrical ulcers
may appear on the vocal cords ; sometimes, there are several groups of
confluent, "lenticular," ulcers. The edge of the epiglottis is often involved.
578 DISEASES OF THE KESPIKATOEY APPARATUS
An infiltrating form, involving especially the adenoid tissue (epi-
glottis, aryepiglottic folds, vocal cords), giving rise to firm swelling, is some-
times seen. Later, caseation and ulceration occur; this form is often
combined with arytenoid perichondritis.
A third form of tuberculous laryngitis is lupus of the larynx; small
gray nodules with a red periphery appear ; they do not undergo ulceration.
In advanced cases of laryngeal tuberculosis, there is pain on swallow-
ing, and occasionally symptoms of stenosis.
The disease is nearly always secondary to pulmonary tuberculosis.
About one-third of the patients suffering from pulmonary tuberculosis
have also tuberculosis of the larynx. Primary tuberculosis of the larynx
is exceedingly rare.
References
Casselberry (W. E.}. The recognition of early changes in the larynx in tuberculosis. J. Am.
M. Ass., Chicago, 1913, Ixi, 1789-1791.
Glas (E.) & Kraus (E.~). Einfluss der Schwangerschaft auf die Tuberkulose des Kehlkopfes*
Med. Klin., Berlin, 1909, v, 963; 1008.
Greene (/. B.). Laryngeal tuberculosis. South. M. J., Nashville, Tenn., 1915, viii, 973-
978.
Hajek (M.). Tuberkulose Larynxtumoren. Internal, klin. Rundschau, Wien, 1893, vii,
1385; 1428.
Kast (A.} & Rumpel (T.). Tuberkulose des Kehlkopfs. In: Path.-anat. Tafeln, Hamb.
Staatskrankenh., Wandsbek-Hamb., 1896, xiv, pi. R 9, 10, 11 with text.
Killian (G.). Ueber die Behandlung der Kehlkopftuberkulose. Deutsche med. Wchnschr.,
Leipzig u. Berlin, 1912, xxxviii, 585-589.
Kyle (D. B.}. Initial forms of tubercular laryngitis. Internal. M. Mag., New York, 1900,
ix, 202-205.
Lake (R.}. Laryngeal phthisis, or consumption of the throat. London, 1901. 8°.
Levy (R.). Laryngeal tuberculosis. J. Am. M. Ass., Chicago, 1913, Ix, 1518-1523.
Minor (C. L.). The diagnosis and treatment of the earlier changes in the larynx in pul-
monary tuberculosis. J. Am. M. Ass., Chicago, 1910, Iv, 1806-1808.
Semon (F.). A clinical lecture on laryngeal tuberculosis. Clin. J., London, 1893-94, Hi,
154-167.
Steiner (R.). Zur Kenntniss der primdren Kehlkopftuberkulose. Arch. f. Laryngol. u.
Rhinol, Berlin, 1912, xxvi, 424~435.
Swain (H. L.). Tubercular laryngitis. N. York M. J., 1887, xlvi, 675-682.
Thomson (Sir St. C.). Three years' sanatorium experience of laryngeal tuberculosis.
Brit. M. J., London, 1914, i, 801-803.
Wat son- Williams (P.). Note on the treatment of laryngeal tuberculosis by tuberculin.
Bristol M.-Chir. J., 1914, xxxii, 136-138.
ii. Syphilitic Laryngitis
(Laryngitis syphilitica, Laryngeal Lues)
Symptoms. — The voice is hoarse ; there is sometimes actually aphonia.
Cough and pain are slight, or absent. In secondary syphilis, the laryngeal
picture may be that of subacute catarrh, accompanied by papules and
DISEASES OF THE LARYNX 579
erosions. In the tertiary stage (more important), gummata may occur
in any part of the larynx ; in the trachea, they appear only at the bifurca-
tion. Arising in the suhmucosa, or in the perichondrium, the gummata
may form firm infiltrations, often narrowing the lumen. These infiltra-
tions, breaking down, give rise to ulcers with firm, punched out, reddened
margins. On healing, they leave white scars, which cause deformations
(especially of the epiglottis), and often stenosis of the larynx, with per-
manent hoarseness. Ulceration and scar formation at the bifurcation of
the trachea are not uncommon. It is important to recognize this condi-
tion before the retraction of the luetic infiltration has begun since in the
later stages it is entirely resistant to ordinary specific treatment and not
infrequently ends fatally through stenosis of the larynx.
Diagnosis. — The laryngeal picture is often characteristic. The an-
amnesis helps out. The occurrence of lesions elsewhere in the body should
be looked for. The Wassermann reaction is positive.
References
Hope (C. W. M.). Unusual form of syphilitic laryngitis. Proc. Roy. Soc. M., London,
1913, vi, Laryngol Sect., 71-73.
Martin (H. //.). Syphilis of the nose and throat. South. M. J., 1913, vi, 19. [Discussion],
32-35.
Robertson (C. Af.). Syphilis of the larynx. J. Am. M. Ass., Chicago, 1903, xl, 162-164.
Schrotter (L.). Veranderungen im Larynx bei Syphilis. Jahresb. d. Klin. f.Laryngosk.
a. d. Wien. Univ. (1870), 1871, 61-72. 1 pi.
iii. Typhoidal Laryngitis
This is a rare complication of typhoid fever; the lymphoid tissue of
the larynx, like that of the intestine, is affected and undergoes ulceration.
In some cases, the laryngeal complication is a secondary infection due to
other bacteria (cocci). Perichondritis is a frequent complication; both
arytenoid cartilages were expectorated by one of my patients.
2. Circulatory Diseases of the Larynx
(a) Edema of the Glottis
Definition. — In this condition, a serous infiltration of the soft tissues
of the larynx arises gradually, or, more often, suddenly, with suifocative
phenomena (cyanosis, dyspnea). The soft tissues of the epiglottis, the
aryepiglottic folds, and the false vocal cords are chiefly involved.
Occurrence. — It is met with most often in acute inflammations of the
larynx or its neighborhood; it may occur also in the general anasarca of
cardiopathies and nephropathies, and is then sometimes responsible for
exitus. Earely, edema glottidis is a fatal complication of angioneurotic
580 DISEASES OF THE KESPIKATOEY APPAEATUS
edema ; occasionally, it occurs along with urticaria as a part of the "serum
disease" following injection of antitoxin.
Symptoms. — There is a sudden appearance of dyspnea without apparent
cause; it increases rapidly, the patient gasping for breath and quickly
becoming cyanotic. There is aphonia. Expiration is easier than in-
spiration. The patient feels no pain. Unless relief is quickly obtained,
death occurs from asphyxia.
References
Hajek (M.). Anatomische Untersuchungen uber das Larynxodem. Arch. f. klin. Chir..
Berlin, 1891, xlii, 46-93. 2 pi.
Roy (/>.)• A case of angio-neurotic oedema of the larynx. N. York Polyclin., 1896, viL
140-143.
3. Paralytic Diseases of the Larynx
(a) Paralyses of the Laryngeal Muscles
To understand these, one must be acquainted with the muscles of the
larynx and their functions, as well as their nerve supply.
The most important movements of the larynx are those determining
the position of the vocal cords, that is, those altering the width and form
of the vocal slit (rima glottidis). The .vocal cords are farthest apart on
deep inspiration, whereas they are closest together in the middle line On
phonation. The change of position is brought about, mainly, by move-
ment of the arytenoid cartilages; these can be moved away from the
middle line, and can also be rotated on their perpendicular axes.
The Muscles of the Larynx
The three principal functions of the laryngeal muscles are:
(1) Closure of the glottis.
(2) Opening of the glottis.
(3) Tightening of the vocal cords.
Muscles closing the glottis: M. arytenoideus transversus, M. arytenoideus
obliquus, M. crico-arytenoideus lateralis, M. thyro-arytenoideus (externus) and
M. vocalis.
Muscles opening the glottis: M. crico-arytenoideus posterior.
Tensors of the vocal cords: M. cncothyroideus, M. thyro-arytenoideus internus
(or M. vocalis).
The Nerves of the Larynx
The nerves of the larynx all arise from the N. vagus. The N. laryngeus superior
supplies the mucous membrane of the upper half of the larynx as far as the margin
of the vocal cords, the musculature of the epiglottis and the M. cricothyroideus,
whereas the N. laryngeus inferior (or N. recurrens) innervates all the other laryn-
geal muscles (openers and closers of the glottis) and the mucous membrane down-
ward from the vocal cords.
DISEASES OF THE LARYNX
581
Complete Recurrens Paralysis. — The most important form of laryngeal
paralysis is the so-called recurrens paralysis. It is sometimes bilateral,
more often unilateral. All the laryngeal muscles except the M. crico-
thyroideus are paralyzed, the vocal cords assuming the so-called "cada-
veric" position, a sort of middle position, dependent entirely upon their
elasticity and corresponding, approximately, to the position occupied dur-
ing normal respiration (i. e., midway between the phonation position and
the inspiration position) (Fig. 168).
In unilateral recurrens paralysis, the healthy vocal cord is capable, on
intonation, of crossing the median line and so closing the glottis. As a
result, the voice is not aphonic, but only poor in clang.
The commonest cause of recurrens paralysis is injury of one or both
nerves at the upper aperture of the thorax (aortic aneurism, carcinoma
esophagi, mediastinal tumors). Occasionally, it is due to neuritis or to
disease of 'the central nervous system (e. g., bulbar paralysis).
Partial Recurrens Paralysis (Posticus Paralysis). — Among the fibers
Pig. 168. — Diagrammatic Representation of the Position of the Vocal Cords in Different Forms
of Laryngeal Paralysis, a and b — Normal Larynx ; a — Phonation Position ; b — Respira-
tion Position; c — Cadaveric Position in Bilateral Recurrens Paralysis ; d and e — Left-
sided Recurrens Paralysis ; d — Respiration Position ; e — Phonation Position ; f — Paralysis
of the Tensors of the Vocal Cords ; g — Paralysis of the Mm. Thyroarytenoidei and of
tfie Mm. Interarytenoidei. (After Seifert & Miiller, "Klin. Diagnostik," published by
J. F. Bergmann, Wiesbaden.)
running in the N. recurrens are those supplying the M. crico-arytenoideus
posterior (opener of the glottis), and these, of all the fibers of the nerve,
are the most easily injured; thus, a recurrens paralysis always begins
with "posticus paralysis," and, when recovery occurs from recurrens
paralysis, the posticus muscle recovers its function last ( Semon-Rosenbach
law).
Bilateral posticus paralysis is a very dangerous condition, for, since
the glottis cannot be opened, the stenosis results in inspiratory dyspnea".
increasing to suffocation, though phonation is retained. The condition is
not infrequently met with in postdiphtheritic neuritis.
Unilateral posticus paralysis causes standstill of the paralyzed cord
582 DISEASES OF THE EESPIKATOEY APPARATUS
near the middle line, but since the other vocal cord is movable, there
may be no clinical symptoms, and, unless a laryngoscopic examination be
made, the lesion may go undiscovered.
A condition similar to bilateral posticus paralysis sometimes results
from spasm and contracture of the adductor muscles.
Paralysis of the Adductor Muscles (Closers of the Glottis). — When
the M. crico-arytenoideus lateralis and the M. inter arytenoideus are
paralyzed the vocal cord on the paralyzed side cannot be approximated to
the middle line. In bilateral paralysis of these adductors, the vocal slit
stands open, in the form of a large triangle ; aphonia results, and cough-
ing is unaccompanied by sound ; respiration is normal.
In paralysis of the interarytenoid muscle alone, the arytenoid carti-
lages can be brought together in the region of the vocal processes, but not
at their bases; on phonation, a triangular opening is then seen opposite
the posterior third of the vocal cord. The voice is hoarse and there may
be partial aphonia.
Paralysis of the Internal Thyro-arytenoid Muscle or Vocal Muscle.—
This muscle is a tensor of the vocal cord, and paralysis of it leads to imper-
fect closure of the glottis on phonation, owing to insufficient tension of the
vocal cord, which looks concave on the paralyzed side. If the paralysis
be bilateral, one sees, on phonation, a lancet-shaped cleft between the
cords. When the interarytenoids are simultaneously involved, the respira-
tory glottis remains open and the vocal processes project medialward;
when the interarytenoids are not involved, the respiratory glottis closes
normally.
Paralysis of the N. laryngeus superior. — Paralysis of this nerve causes
unilateral ^immobility of the epiglottis, and anesthesia of the mucous
membrane of the larynx (loss of reflexes, with "swallowing the wrong
way"). Owing to the paralysis of the M. cricothyroideus, the vocal cord
on the side of the lesion occupies a lower position than on the healthy
side ; the voice is deep, rough, and impure, and the patient cannot produce
high tones.
Paralysis of the N. vagus as a Whole. — This gives rise, not only to the
phenomena referable to the N. laryngeus inferior (recurrens) and the
IN", laryngeus superior, but also to paralysis of the muscles of the pharynx
on the side of the lesion.
Hysterical Aphonia. — The aphonia here is usually due to a defective
function of the adductor muscles; on attempting to phonate, the glottis
is not closed. Cough, however, is accompanied by sound, showing that
the glottis can be closed. This involvement of the function of speech
without simultaneous involvement of the function of cough is character-
istic of hysterical paralysis of the larynx.
The tensors of the vocal cords are often weakened in acute and in
chronic laryngitis.
DISEASES OF THE LAKYNX 583
References
Cadet (A.). Lies paralysies laryngees du tabes. Lyon, 1898. 8°.
Casselberry (W. E.). Recurrent and abductor paralysis of the larynx; diagnosis and treat-
ment. Med. Rec., New York, 1908, Ixxiv, 803-307.
Dorendorff (H.). Ein Beitrag zur Frage des Zustandekommens linksseitiger Rekurrensldh-
mung bei Mitralstenose. Berl. klin. Wchnschr., 1913, i} 912-914'
Elsberg (L.). Paralysis of muscles of the larynx. Arch. LaryngoL, New York, 1882, iii,
195-203.
Fetterolff (G.) & Norris (G. W.}. The anatomical explanation of the paralysis of the left
recurrent laryngeal nerve found in certain cases of mitral stenosis. Tr.
Coll Phys., Philadelphia, 1911, 3. s., xxxiii, 66-82.
Garrod (A. E.). A case of paralysis of the abductors of the vocal cords with lesions of several
cranial arteries. St.Barth. Hosp. Rep., London, 1886, xxii, 209-211.
Hofbauer (L.). Recurrensldhmung bei Mitralstenose. Wien. klin. Wchnschr., 1902, xv,
1065-1067.
Lian (C.) & Marcorelles (E.}. De la paralysie recurrentielle gauche dans le retrecissement
mitral. Arch. d. mal. du cceur [etc.], Paris, 1913, vi, 869-384.
Macintyre (/.)• Nervous diseases of the larynx; abductor paralysis. J. LaryngoL, London,
1899, xiv, 385-392.
Meillon (A.}. Contribution d V etude des paralysies du larynx d? origins centrale. Paris,
1897. 8°.
Onodi (A.}. Die Anatomic und Physiologie der Kehlkopfnerven. Mil ergdnzenden patho-
logischen Beitragen. Berlin, 1902. 8°.
Semon (Sir F.}. Die Nervenkrankheiten des Kehlkopfes und der Luftrohre. Handb. d.
LaryngoL u. Rhinol. Wien, 1897, i, 587-768.
Semon (Sir F.) & Horsley (V.). Paralysis of laryngeal muscles and cortical center for
phonation. Lancet, London, 1886, i, 1045.
Sobernheim (W.) & Caro (A.}. Rekurrensldhmung bei Erkrankung des Herzens. Arch,
f. LaryngoL u. Rhinol., Berlin, 1913, xxvii, 410-420.
Wishart (D. J. G.}. Abductor paralysis of the larynx. Canad. Pract. & Rev., Toronto,
1902, xxvii, 380-385.
4. Neoplasms of the Larynx
Tumors of the larynx may be benign or malignant. Benign growths
include singer's nodes, polyps, and papillomata, though only the latter and
some of the polyps are to be regarded as true tumors (neoplasms). Malig-
nant growths of the larynx include sarcomata and especially carcinomata.
Symptoms of Tumors of Larynx. — These may be slight at first, but
when present should lead to laryngoscopic examination. Hoarseness and
tiring of the voice on use are, as a rule, the first symptoms. Cough is not
common. Benign growths do not cause pain ; malignant growths may excite
pain, radiating to the ear of the affected side. Dysphagia may appear
early in the course of a malignant growth. Dyspnea, continuous or par-
oxysmal, may accompany any kind of growth.
Inspection of Laryngeal Growths. — A thorough examination of all
parts of the larynx should be made with the laryngoscope. The commonest
site of neoplasm is at the anterior commissure of the vocal cords. If a
growth be visible, we note its size, form, color, site, surface, consistency
584 DISEASES OF THE RESPIRATORY APPARATUS
(probe), mobility, attachments, and surroundings. If there be doubt as to
the nature of the growth, a fragment should be excised for microscopical
diagnosis.
In malignant growths, the tumor as a rule is not pedunculated ; the
neighboring tissues are red and infiltrated; there is early interference
with the mobility of the vocal cord; the tumor bleeds easily and tends to
ulcerate; dysphagia and dyspnea are complained of; and sometimes the
regional lymph glands are enlarged.
(a) Polyps of the Larynx,
These are very common. They appear as red, soft masses, usually
situated on the anterior third of one vocal cord. They occur in adults of
middle age, almost never in children. Histological examination of an
excised fragment may be necessary for diagnosis. Once properly re-
moved, such polypi do not tend to recur.
(b) Papilloma of the Larynx
Papilloma is rarer than polyp, but more common than other tumors
of the larynx. It is met with most often in children, and appears as a
cauliflowerlike excrescence, usually on one of the vocal cords. The cord
moves -normally. The growth shows no sign of ulceration or of inflamma-
tion. On removal, papilloma tends to recur, though it almost never
undergoes malignant change. This tumor does not show histologically
any areas of round-celled infiltration such as are seen in tubercle, lues,
or singer's nodes ; it differs from the papillary form of carcinoma, in that
the latter bleeds easily, tends to ulcerate, and is associated with infiltra-
tion of the adjacent mucosa and with enlargement of the regional lymph
glands. It is interesting that papilloma of the larynx, like papilloma of
the bladder, can be satisfactorily treated with the high-frequency current.
(c) Carcinoma of the Larynx
Cancer usually begins on one of the vocal cords, occasionally on one
of the false cords or in the ventricle, exceedingly rarely on the interary-
tenoid fold. It is rare before middle life.
Seen in the early stage, intrinsic cancer of the larynx appears as a
small nodule on one vocal cord, bleeding easily, and tending to recur after
removal. The histological diagnosis may not be easy, but if strands of
epithelial cells invade surrounding tissue with no basal membrane, malig-
nancy is certain. If allowed to remain, the tumor grows steadily, causes
hoarseness and may ulcerate, though ulceration does not occur until the
mass is twelve or eighteen months old. As it increases in size, it causes
DISEASES OF THE LAKYNX 585
dysphagia and dyspnea. In the late stages, the regional lymph glands
and the base of the tongue may become involved. Metastases occur late.
By extrinsic cancer of the larynx is meant a cancer beginning in the
epiglottis, on an arytenoid cartilage, in the recessus pyriformis, on an
aryteno-epiglottidean fold, or on the pharyngeal surface of the posterior
wall of the larynx. In this form, the early symptoms include dysphagia
and pain radiating to the ear of the same side. The outlook is even graver
than in intrinsic cancer.
(d) Other Tumors of the Larynx
These can only be mentioned here. They include cysts, angiomata,
and sarcomata. Neoplasm may be simulated by leukemic nodules, by in-
growths of thyroid gland, by gummata, and by tuberculous nodules.
References
Sevan (A. Z>.). Carcinoma of the larynx. Ann. Surg., Philadelphia, 1903, xxxvii, 632.
Chiari (O.). Beitrdge zur Diagnose und Therapie des Larynxkrebses. Arch. f. Laryngol. u.
RhinoL, Berlin, 1898, vii, 67-127.
Crile (G. W.). Laryngectomy for cancer. Laryngoscope, St. Louis, 1912, xxii, 1317-1330.
Frdnkel (B.). Der Kehlkopfkrebs, seine Diagnose und Behandlung. Deutsche med.
Wchnschr., Leipzig u. Berlin, 1889, xv, 1; 28; 50; 68; 87; 109.
Mackenzie (J. N.). A plea for early naJ$ed-eye diagnosis and removal of the entire organ
with the neighboring area of possible lymphatic infection in cancer of the
larynx. Johns Hopkins Hosp. Bull, Bait., WOO, xi, 323-325.
Schrotter (L.). Neubildungen im Larynx. Jahresb. d. Klin. f. Laryngosk. a. d. Wien.
Univ. (1870), 1871, 38-56. 1 pi.
Semon (Sir F.). A clinical lecture on benign growths in the larynx. Clin. J.t London,
1894-95, v, 261-268.
Clinical lectures on malignant diseases of the lojrynx. Clin. J., London,
1895-96, vii, 265-278.
Smith (H.). Papilloma of the larynx. J. Am. M. Ass., Chicago, 1914, Ixiii, 2207-2211.
Wolfenden (R. N.) & Martin (S.). Studies in pathological anatomy, especially in relation
to laryngeal neoplasms. I. Papilloma. London, 1888. 8°.
5. Stenosis of the Larynx
Stenosis of the larynx and trachea may be due to (1) acute croupous
or phlegmonous laryngitis, (2) gumma, (3) scars of earlier necrotic in-
flammations, (4) neoplasms, (5) aneurisms, or (6) foreign bodies.
References
Ingals (E. F.). Stenosis of the larynx. Internal. Clin., Philadelphia, 1894, 4. s., U, 326-
330.
Jones (W. S.). Chronic stenosis of the larynx, with Jive illustrative cases. J. Am. M. Ass.t
Chicago, 1898, xxx, 606.
Woods (H. R.). On the treatment of laryngeal stenosis. Tr. Roy. Acad. M. Ireland, Dublin,
1911, xxix, 145-157. 1 pi.
586 DISEASES OF THE KESPIKATOEY APPAEATUS
D. Diagnosis of the Principal Diseases of the
Trachea and Bronchi
(The Tracheopathies and the Bronchopathies)
Here we have to deal especially' with. : 1, inflammations (tracheitis
and bronchitis) ; 2, dilatations (bronchiectasias) ; and 3, stenoses (tracheal
and bronchial stenoses).
References
Claisse (P.), Mosny (E.} [et al.]. Maladies des poumons, des branches et de la trachee.
Paris, 1910, J. B. Bailliere et fils. 860 p. 8°. [Nouv. Traite de Med.
de Therap., xxix.]
Freund (A.). Ueber Tracheopathia osteoplastica. Beitr. z. Anat., PhysioL, Path. u.
Therap. d. Ohres [etc.]. Berlin, 1914-15, viii, 11-40.
McPhedran (A.). Diseases of the bronchi. Mod. Med. (Osier). 8°. Philadelphia &
New York, 2. ed., 1914, ii, 881-944-
Roe (J. O.). Phlegmons of the upper respiratory tract. N. York M. J. [etc.], 1914, c, 1049-
1052.
Staehelin (/?.). Die Bronchitis; die Bronchiektasie ; Stenose der Trachea und der Bronchien ;
das Asthma bronchiole. In: Handb. d. inn. Med. (Mohr & Staehelin}.
Berlin, 1914, ii, 314-878.
Tendeloo (N. P.). Die mechanische Bedeutung der Bronchien. Mittheil. a. d. Grenzgeb. d.
Med. u. Chirurg., Jena, 1913, xxvi, 247-255.
1. Inflammations of the Trachea and Bronchi
(Tracheitis j Tracheobronchitis, Bronchitis)
Of the acute inflammatory processes, the more important are (a)
acute catarrhal tracheobronchitis, (b) acute capillary bronchitis (or
bronchiolitis), and (c) acute fibrinous bronchitis. There are several
forms of (d) chronic bronchitis. Closely allied, and therefore considered
in this section, are (e) bronchial asthma and (f) acute anaphylactic
shock ; they are, however, neuromyogenic disturbances rather than inflam-
matory processes.
(a) Acute Catarrhal Tracheobronchitis
Etiology. — Three groups of factors may exert a causative influence:
(1) mechanical and chemical irritants, like dust and gases, and certain
drugs administered internally (e. g., KI) ; (2) infections, some of them
affecting the respiratory mucosa primarily (coryza, influenza, measles,
pertussis), others affecting it secondarily (typhoid, lues, tuberculosis,
diphtheria, etc.), and (3) circulatory disturbances, as in the various
bronchial catarrhs due to stasis (cardiopathies, nephropathies, obesity).
Symptoms. — Here only the trachea and the larger bronchi are involved.
The symptoms include cough, a feeling of tickling, tightness, burning,
DISEASES OF THE TKACHEA AND BKONCHI 587
and soreness behind the sternum; there may or may not be slight fever,
and slight expectoration.
The sputum is usually scanty in the beginning, and may be entirely
absent ; if there be any, it is thick, tenacious mucus ; later, it usually be-
comes thinner, and generally mucopurulent. Cover-slip preparations and
a sputum culture are desirable to determine the etiology (Bacillus influ-
enzae, pneumococcus, streptococcus, staphylococcus, etc.). The sputum
should always be stained for tubercle bacilli, especially when the physical
signs are local, or when the sputum contains blood.
Physical Signs. — Inspection and percussion may be negative. On pal-
pation, sometimes rhonchial fremitus can be fe}t. On auscultation, the
breathing is vesicular and accompanied by coarse snoring sounds (sono-
rous rhonchi) over the upper chest, especially in the interscapular regions
behind. If the medium sized and smaller bronchi become narrowed, from
swelling of the mucous membrane and the accumulation of mucus, owing
to extensions of the tracheobronchitis downwards, dry, piping, whistling
sounds are heard (sibilant rhonchi). The condition then becomes one of
diffuse bronchial catarrh (see below). As the bronchitis resolves and the
secretion becomes more abundant and more fluid, moist, non-consonating,
medium sized, or even bubbling, rales become audible. The abnormal
sounds can then usually be heard over the whole thorax, though, as a rule,
they are most numerous at the bases, behind. A localized bronchitis,
especially if it be apical, is highly suggestive of tuberculosis, but influenzal
infections sometimes give rise to similar signs.
Loud rales in the trachea, due to the accumulation of secretion there
that remains unexpectorated, are often met with in agonal states (hence
sometimes spoken of as the "death rattle").
References
Hart (C.). Ueber akute idiopathische Tracheobronchitis necroticans. BerL Min. Wchnschr.,
1915, Hi, 402-404.
Kerley (C. G.). Recurrent bronchitis in children. Pediatrics, New York, 1915, xxvii, 175-
183.
Llopart (P.). Erfahrungen iiber Vergiftungen durch " Nitrose-Gase " ; nach dem Material
des gerichtlichmedizinischen Institutes in Zurich, 1912, J . J . Meier. 140 p.
8°.
Meltzer (S. /.). How deep should the tube be introduced in intra-tracheal insufflation? J.
Am. M. Ass., Chicago, 1914, Ixii, 1547-1549.
Schdfer (Sir Edw.}. On the immediate effects of the inhalation of chlorine gas. Brit. M. /.,
London, 1915, ii, 245-247.
(b) Acute Diffuse Bronchial Catarrh
(Capillary Bronchitis or Bronchioliti$),
Definition. — A form of bronchitis, prone to occur in small children, in
it is. an. extremely dangerous. disease owing to the occlusion, Q£
588 DISEASES OF THE KESPIEATOKY APPAKATUS
numerous small bronchioles by swelling. of the mucous membrane, accumu-
lation of secretion, and spasm of the walls.
Symptoms. — When due to cold or to stasis, there is usually only slight
fever; when due to influenza or other specific infections, there may be
high fever. The paroxysmal cough is distressing, and often causes tachy-
cardia and pain in the side, the latter not being due to pleuritis, but to
violent contractions of the muscles on coughing. The patients feel chilly
and suffer from general malaise. The respirations are accelerated ; there
is marked dyspnea, and often cyanosis and sweating. On inspiration, the
force may be insufficient to overcome the resistance, so that no new air can
enter the alveoli; as a result, there is often extensive atelectasis (tympa-
nitic percussion sound), with inspiratory retraction of the lower thorax
in adults, and of the sternum in children. In other cases, the expiration
may be too feeble to expel the air from the alveoli, in which 'event the
air sacs become overdistended, the superficial cardiac dullness is di-
minished, and; the lower limits of the lung come to occupy a lower level
than normal on percussion.
The sputum is scanty at first, consisting of tough mucus (sputum
crudum) ; later, it is thinner and more abundant (sputum coctum). In
influenza, the sputum is often of a greenish color, and may be nummular,
not unlike that from phthisical cavities. Stained smears and sputum
cultures will reveal the etiological agent.
On auscultation, besides $ibilant and sonorous rhonchi, there are many
fine moist rales to be heard over both lungs. Vesicular breathing is
enfeebled or roughened, and expiration is prolonged; the inspiratory
and the expiratory sounds are absent over atelectatic areas.
Capillary bronchitis is often fatal, especially in young children.
Bronchopneumonia is a common complication.
Diagnosis. — It is important, besides recognizing the bronchitis, to seek
for an underlying disease (typhoid, pertussis, influenza).
Obliterating Bronchitis. — A rare form of involvement of the small bronchioles
(bronchiolitis obliterans) sometimes follows aspiration of caustic vapors, which
give rise to violent acute inflammation; the exudate undergoes organization, and
leads to progressive obliteration of the bronchioles, and to death by slow asphyxi-
ation.
Reference
Jehle (L.). Die Bronchialerkrankungen im Kindesalter. Beihefte z. Med, Klin., Berlin u.
Wien, 1914, x, 49-80.
(c) Acute Fibrinous Bronchitis
(Pseudomembranous or Croupous Bronchitis)
Besides the form due to true diphtheria, an acute fibrinous bronchitis
may occur in pneumonia or as a primary disease of chronic course and of
unknowni etiology ("essential form").
DISEASES OF THE TEACHEA AND BEONCHI 589
'. .'
Symptoms. — An acute and a chronic form are distinguished.' r In both
the patients cough up casts of the bronchial tree. Before expectoration of
the cast, the breath sounds are enfeebled in the part of the lung affected,
and expansion is diminished. There is marked cyanosis and dyspnea,
sometimes attacks of suffocation. The normal sounds return after evacua-
tion of the cast. The acute cases are serious, often ending fatally.
Chronic membranous bronchitis may recur over long periods.-
Reference
Bettmann (M.). Fibrinous bronchitis. Johns Hopkins Hosp. Bull., Baltimore, 1901 .
xii, 299-300.
(d) Chronic Bronchitis
Several forms are distinguished, among them: (1) dry bronchitis
(bronchitis sicca), with scanty secretion of tough mucus; (2) broncho-
blennorrhea, in which the sputum is abundant, thin, mucopurulent and
separates, on standing, into three layers, just as in bronchiectasia ; (3)
serous bronchorrhea, or pituitous catarrh, in which the expectoration is
fluid, seromucous, poor in protein, and very abundant (1 to 1J liters in
twenty-four hours). It is often accompanied by marked dyspnea, and is
sometimes described as wet asthma (asthma humidum) ; and (4) putrid or
fetid bronchitis, with abundant, stinking, purulent sputum, separating into
three layers, and containing, in the bottom layer, Dittrich's plugs. When
the bronchitis is due to stasis, the sputum contains many "heart-failure
cells."
Etiology. — The disease is due, usually, to recurring attacks of acute
bronchial catarrh, dependent upon inhalation of dust (mineral or vege-
table), upon extension of inflammation from the nose or throat, or upon
stasis in the pulmonary circulation as in cardiac and renal disease, in
atherosclerosis, in emphysema, in cirrhosis of the lung, in kyphoscoliosis,
and in certain metabolic diseases, especially obesity and gout. Certain
families seem to be definitely predisposed.
Chronic bronchitis may also occur as an accompaniment of chronic
infections of the lung (pneumococcus, tubercle bacillus), and of bron-
chiectasis.
Symptoms.: — The patients are usually afebrile ; they suffer from a
chronic cough, worse in winter ("winter cough"), with more or less expec-
toration. The physical signs in chronic bronchitis vary according to the
amount of the secretion; when it is scanty ("dry catarrh"), there are
sibilant and sonorous rhonchi; when it is abundant, moist rales, of vari-
able size, but non-consonating, are audible. The signs are present in both
lungs and are most marked in the lower lobes. The different forms of
chronic bronchitis are distinguishable by the characters of the sputum,
above.) The patients are more or less cyanotic, and exhibit an
590 DISEASES OF THE RESPIRATORY APPARATUS
expiratory dyspnea. After the disease has lasted for some time, the
patients all show signs of pulmonary emphysema. In this disease, the
general state of the patient may not be much affected ; in acute exacerba-
tions, however, there may be fever and increased dyspnea. In such
acute exacerbations it is common to find at one or both bases posteriorly
an area of impaired resonance on percussion with a diminution in the
breath sounds and numerous coarse rales; the presence of such evidence
of a complicating hypostatic pneumonia should be especially looked for in
older people.
Diagnosis. — An important clew lies in the fact that in uncomplicated
chronic bronchitis, the physical signs indicate a diffuse involvement of
both lungs, though they may be more marked in some parts than in others.
One must carefully exclude tuberculosis (family history, stain for bacilli,
physical study of apices, x-ray). The frequent association of chronic
bronchitis with emphysema, with heart disease, and with nephritis should
be kept in mind. Putrid bronchitis is commonest in association with
bronchiectasia, and with pulmonary gangrene.
Reference
Florand (Antoine Leon), Francois (Max Leopold) & Flurin (Henri). Les bronchites
chroniques; leur traitement. Paris, 1913, Masson & Cie. 359 p. 8°.
(e) Bronchial Asthma
(Asthma bronchiale; Nervous Asthma)
Definition. — A condition in which paroxysmal attacks of marked dysp-
nea (chiefly expiratory) occur, due to sudden bronchospasm and to swell-
ing of the bronchial mucous membrane, and apparently dependent
sometimes upon a reflex neurosis, sometimes upon anaphylactic chemical
stimulation of the autonomic nervous system.
Etiology. — Among the sites of irritation in the cases due to reflex neu-
rosis may be mentioned (1) the nose, especially enlarged conchae and nasal
polypi (nasal asthma) ; (2) the genitals (asthma sexuale), especially the
uterus in the female, the posterior urethra in the male; and (3) the
trachea and bronchi. Heredity plays an important role. Rickets and gout
seem to be predisposing factors. The asthma due to hay fever has already
been described.
In the anaphylactic cases, the patients seem to be susceptible to various
proteins that act as "asthmogenic substances" ; among these may be
mentioned horse serum and egg albumen.
Symptoms. — During an attack, respiration is labored, though not neces-
sarily accelerated; cyanosis and orthopnea are common. An acute pul-
monary emphysema (volumen pulmonum auctum), with descent of the
diaphragm, develops also during the attack.
DISEASES OF THE TKACHEA AND BKONCHI 591
Attacks are common at night; they usually last several hours, some-
times days.
In an attack, the lower limits of the lung are depressed and but little
mobile; the superficial cardiac dullness is diminished; a boxlike tone is
elicitable on percussion. The respiratory murmur is obscured by loud
snoring and whistling sounds, especially during expiration. At the end
of an attack, a tough mucus, containing Charcot-Leyden crystals, eosino-
phils, and Curschmann's spirals, may be expectorated. Inspiration may
be roughened, and expiration prolonged, for a period after the subsidence
of the attack; later, these signs and the rhonchi disappear. In long-
standing cases, permanent pulmonary emphysema develops.
The disease is more common in men than in women, and in "nervous"
people than in the phlegmatic.
Diagnosis. — True bronchial (or "neurogenic" ) asthma is to be dis-
tinguished (1) from cardiac asthma; (2) from the dyspnea of emphy-
sema; (3) from renal asthma; (4) from spasm of the glottis (here the
dyspnea is inspiratory, not expiratory) ; and (5) from hysterical pseudo-
asthma (absence of cyanosis, violent thoracic movements, "barking").
In this country attention has been paid of late to bronchial asthma
considered as an anaphylactic phenomenon. The matter has been dis-
cussed by Meltzer, by Matthews, by Koessler and others. Some asthmatic
patients seem to be especially sensitive to certain proteins. One of my
patients recently gave a sharp reaction to serum protein, another a violent
reaction to milk protein. Many asthmatic patients are said to be sen-
sitive to egg-white, a few to meat proteins. The tests for sensitization
are easily made by intradermic injection of a minute quantity of the
protein.
References
Abbott (W. /.). Bronchial asthma and the relation of nasal conditions to it. Ann. OtoL,
Rhinol. & LaryngoL, St. Louis, 1914, xxiii, 83-92.
Adam (James). Asthma and its radical treatment. New York, 1914, P. B. Hoeber.
184 P- 8°.
Andrews (E. W.). Chondrectomy or operative treatment of bronchial asthma. J . Am. M.
Ass., Chicago, 1914, Ixiii, 1065-1069.
Babcock (R. H.}. An inquiry into the cause of bronchial asthma. Illinois M. J., Chicago,
1913, xxiv, 5-9.
Berkart (J. B.}. On bronchial asthma, its pathology and treatment. 3. ed. London,
1911, H. Frowde. 150 p. 8°.
Borchardt (L.). Asthmabehandlung mit Hypophysenextrakten. Therap. d. Gegenw., Ber-
lin, 1913, liv, 536-541.
Brugelmann (W.}. Das Asthma, sein Wesen und seine Behandlung aufGrund siebenund-
zwanzigjdhriger Erfahrungen und Forschungen. 4- Aufl. Wiesbaden,
1905, J. F. Bergmann. 260 p. 8°.
Cloetta (M.}. Zur experimentellen Pathologic und Therapie des Asthma bronchiole. Arch,
f. exper. Pathol. u. Pharmakol, Leipzig, 1913, Ixxiii, 233-250.
Curschmann (H.). Zur Frage der " Bronchotetanie" der Erwachsenen und ihre Behandlung
mit Kalzium. Munchen. med. Wchnschr., 1914, Ixi, 289-298.
592 DISEASES OF THE EESPIEATOKY APPAKATUS
Davies (B. C.). A clinical study of asthma. J. Am. M. Ass., Chicago, 1914, Ixii, 1006-
1008.
Dorn (M.). Ein asthmatischer Anfall im Rontgenbilde. Berl. klin. Wchnschr., 1896,
xxxiii, 1046-1048.
Dudley (W. H.}. The consideration of nasal conditions causing asthma. J. Ophth. & Oto-
Laryngol., Chicago, 1915, ix, 14~19.
Fraenkel (A.}. Ueber Bronchialasthma. In: Deutsche Klinik, Berlin u. Wien, 1907, iv,
25-60.
Fukushi (M.). Ueber das Verhalten der Bronchialmuskulatur bei akuter und chronischer
Bronchitis. Virchow's Arch. f. path. Anat. [etc.], Berlin, 1914, ccxvii, 16-
55. 1 pi.
Gibson (G. A.). Asthma: its varieties and treatment. Lancet, London, 1911, ii, 867-368.
Goodale (J. L.). Studies regarding anaphylactic reactions occurring in horse asthma and
allied conditions. Tr. Am.Laryngol. Ass., New York, 1914, xxxvi, 95-110.
Also: Ann. Otol, Rhinol. & Laryngol., St. Louis, 1914, xxiii, 635-341.
Goodhart (J. F.} & Spriggs (E. /.). Asthma and hay-fever. In: Syst. Med. (Allbutt &
Rolleston). 8°. London, 1909, v, 45-71.
Golla (F. L.) & Symes (W. L.). The reversible action of adrenaline and some kindred
drugs on the bronchioles. J. Pharmacol. & Exper. Therap., Baltimore,
1913-14, v, 87-103.
Hofbauer (L.). Die Summtherapie des Bronchialasthmas. Deutsche med. Wchnschr., Leip-
zig u. Berlin, 1914, xl, 1106-1109.
Januschke (H.). Asthma bronchiole. Ergebn. d. inn. Med. u. Kinderheilk., Berl., 1915,
xiv, 231-286.
Joppich (O.). Die Behandlung des Asthma bronchiole. Beitr. z. Klin. d. Tuberk., Wiirz-
burg, 1914, xxxi, 247-260.
Kayser (C.). Klinische und experimentelle Studien zur Kalktherapie, speciell beim Asthma
bronchiole. Ztschr.f. exper. Path. u. Therap., Berlin, 1915, xvi, 369-378.
Keiper (G. F.}. The bronchoscopic treatment of spasmodic asthma. Ann. Otol., Rhinol. &
Laryngol., St. Louis, 1914, xxiii, 53-58.
Koessler (K. K.). Bronchial asthma due to hypersusceptibility to hens' eggs. Illinois M.
J., 1913, xxiii, 66-71.
Lemann (I. /.)• The treatment of bronchial asthma. Am. J. M. Sc.} Philadelphia & New
York, 1911, clxii, 865-869.
Marcinowski (/.)• Die Heilung eines schweren Falles von Asthma durch Psychoanalyse.
Jahrb. f. psychoanal. u. psychopathol. Forsch., Leipzig u. Wien, 1913, v.
2. Halfte, 529-620.
Matthews (/.)• Anaphylaxis and asthma. Med. Rec., New York, 1913, Ixxxiv, 512-514.
McCord (C.). The rationale of the use of adrenalin in the treatment of asthma. Med.
Rec., New York, 1913, Ixxxiii, 431-433.
Meltzer (S. /.)• Bronchial asthma as a phenomenon of anaphylaxis. J. Am? M. Ass.,
Chicago, 1910, Iv, 1021-1024.
Park (E. A.). The physiological action of epinephrin on the bronchi. J. Exper. M., Lan-
caster, Pa., 1912, xvi, 558-566.
Schlesinger (E.). Beitrag zur endobronchialen Behandlung des Asthmabronchiale. Arch,
f. Laryngol. u. Rhinol., Berlin, 1914, xxviii, 310-823.
Staehelin (R.). Entstehung und Behandlung des Asthma bronchiole. Jahreskurse f.
aerztl. Fortbild., Munchen, 1912, 2. Heft, 25-39.
Talbot (F. B.). Asthma in children. Its relation to " egg poisoning " (anaphylaxis).
Boston M. &S.J., 1914, clxxi, 708-712.
Ullman (J. S.). The relation between surgical infections of the gastro-intestinal tract and
asthma; a preliminary report. South. M. J., Nashvillet Tenn.} 1915, viii,
DISEASES OF THE TKACHEA AND BKONCHI 593
War f el (F. C.). Report of seven cases of bronchial asthma treated with pituitary body anterior
lobe. Indianapolis M. J., 1915, xviii, 287-290.
Warren (L. F.). An orthodiagraphic study of a case of bronchial asthma. Am. J. M. Sc.,
Philadelphia & New York, 1913, cxlvi, 711-716.
Weber (E.}. Neue Untersuchungen uber experimentelles Asthma und die Innervationen der
Bronchialmuskeln. Arch. f. Physiol, Leipzig, 1914, 63-154.
Widal (F.) & Lermoyer (N.) [et al.]. Les phenomenes d'ordre anaphylactique dans Vasth-
me; la cause hemoclasique initiale. Presse med., Paris, 1914, xxii, 525-
527.
Winter. 1st es gerechtfertigt, ah Ursache des bronchialasthmatischen Anfalls eine Ver-
engerung der feineren Luftwege, sei es in Form von Schleimhautschwellung,
anzunehmen? Med. Klin., Berlin, 1914, x, 1319-1321.
2. Dilatation of the Bronchi
(Bronchiectasia or Bronchiectasis)
The bronchi may undergo (1) diffuse (cylindrical) dilatation, or (2)
circumscribed (saccular, or spindle-shaped) dilatation; the condition is
known as bronchiectasia or bronchiectasis. One, several, or all of the
bronchi may be involved.
Etiology. — Brorichiectasias are usually the result of chronic inflamma-
tions that weaken the walls of the bronchi, diminishing their elasticity
and increasing their distensibility. A localized form may follow those
cicatricial processes in the lungs or pleura that lead to traction upon the
walls of the bronchi from without (after pneumonia or pleurisy). A
very important factor, in many cases, is increased pressure within the
lumen of the bronchus through increased (expiratory) air pressure, or
through accumulated secretions.
Cylindrical bronchiectasia is common in children after capillary
bronchitis, bronchopneumonia or pertussis ; in adults it is often a sequel to
chronic bronchitis. Saccular bronchiectasia may be the sequel of a
bronchiostenosis due to pressure from aneurism or neoplasm or to scars
from ulceration of the bronchial wall in lues or in tuberculosis ; occasion-
ally it follows aspiration of a foreign body. In chronic indurative
processes in the lung (e. g., in Corrigan's pulmonary cirrhosis), and in
thickened pleura, bronchiectasis sometimes develops.
Symptoms. — Paroxysmal c^gh,, with expectoration by "mouthfuls"
in the morning, especially on change of posture, is the characteristic diag-
nostic sign.
The sputum is abundant, and usually putrid (due to a complicating
putrid bronchitis) ; it separates typically into three layers (frothy, serous,
and purulent), the lowermost layer containing Dittrich's plugs. Tissue
fragments are not present in the sputum in simple bronchiectasia ; when
found, they point to abscess, or to gangrene, of the lung. The albumin
content of the sputum is not abnormally increased.
In the saccular form, the physical signs of a cavity (q. v.) may be dis-
594 DISEASES OF THE RESPIRATORY APPARATUS
tinguishable after expectoration. The auscultatory findings may differ
markedly before and after expectoration. The persistence of rales in a
definite area of the thorax often permits one to localize a bronchial dilata-
tion in the absence of cavernous symptoms. Exquisite pictures of the
bronchial tree on both sides, and of any dilatations existing, are obtainable
by stereoscopic rontgenography.
There is, in cases of long standing bronchiectasis, a marked tendency
to recurring attacks of acute infection of the diseased bronchi. In the
more severe of these attacks there is considerable elevation of temperature,
the amount of sputum in the first days may be diminished, and signs of
bronchopneumonia appear over the portions of the lungs affected. Dif-
fuse impairment of the percussion note is observed, and patches of tubu-
lar breathing and moist rales are found. The repetition of these acute
attacks gives to the disease its progressive character.
Hemoptysis is common, and may, erroneously, excite the fear of
tuberculosis. Bulbous enlargement of the finger-tips is often present in
bronchiectasia. Rontgenograms show the change in the tips of the
phalanges, and often also subperiosteal bony deposits along; the shafts of
the phalanges and metacarpal bones (toxicogenic osteoperiostitis).
Complications. — The accompanying putrid bronchitis may give rise to,
or follow, gangrene of the lung. Metastatic infections (brain abscess,
arthritis) are not so very uncommon as complications of bronchiectasia.
Inflammatory infiltrations of the parenchyma of the lung near the cavity
are common ; occasionally pleuritis or empyema, develops, the latter often
becoming putrid.
Diagnosis. — Before the x-ray could be applied, diagnosis was often very
difficult. Even now there may be difficulty, especially in the pure
bronchitic forms with simply general cylindrical ectasia. In saccular
ectasia, if cavity symptoms are present, the localization is easy through
the physical signs and through stereoscopic rb'ntgenograms ; sometimes
rales audible over a circumscribed area are the only localizing signs.
The sputum raised by mouthfuls in the morning is often more decisive
than the physical signs over the lungs. In ruling out tuberculosis,
chronic lung abscess, and pulmonary gangrene, our diagnostic resources
are sometimes taxed to the utmost; the same is true of liver abscess and
of subphrenic abscess rupturing into the lung. A careful consideration of
the anamnesis, the physical signs and the x-ray findings will usually per-
mit us to arrive at a correct diagnosis. Bronchoscopy may be resorted to
in doubtful cases, and probably should always be applied before advising
surgical therapy.
References
Batzdorff (E.). Die chirurgische Behandlung der Bronchiektasie. Centralbl. f. d. Grenzgeb.
d. Med. u. Chir., Jena, 1913, xvi, 1-18.
Boggs (T. /?.)• The influenza bacillus in bronchiectasis. Am. J. M. Sc., Philadelphia &
New York, 1905, cxxx, 902-911.
DISEASES OF THE TEACHEA AND BRONCHI 595
Davies (H. M.). Bronchiectasis treated by ligature of branch of pulmonary artery. Proc.
Roy. Soc. Med., London, 1914-15, viii, Clin. Sect., 30-32.
Ewart (W.). Bronchiectasis and bronchiolecta-sis. In: Syst. Med. (Allbutt & Rollestori).
8°. London, 1909, v, 127-172.
Howard (C. P.). The etiology and pathogenesis of bronchiectasis. Am. J. M. Sc., Phila-
delphia & New York, 1914, cxlvii, 313-332.
Kawamura (/£.). Experimentelle Studien uber die Lungenexstirpation. Deutsche Ztschr. f.
Chir., Leipzig, 1914, cxxxi, 189-222.
Lilienthal (H.}. Extirpation of the right lower pulmonary lobe for septic bronchiectasis.
Ann. Surg., Philadelphia, 1915, Ixi, 103-105.
Meyer (W.). On bronchiectasis. Ann. Surg., Philadelphia, 1914, Ix, 7-28. [Discussion],
122-124.
Resection of the lung for bronchiectasis. Ann. Surg., Philadelphia, 1915,
Ixi, 114-116.
Mumford (J. G.) & Robinson (S.). The surgical aspect of bronchiectasis. Tr. Am. Surg.
Ass., Philadelphia, 1914, xxxii, 688-696.
Wydler (A.). Zur radikalen Behandlung der Bronchiektasien. Mitt. a. d. Grenzgeb. d. Med.
u. Chir., Jena, 1914, xxviii, 1J+1-1J+9.
Zinn (JF.) & Muhsam (R.). Ueber extrapleurale Thorakoplastik bei Lungentuberkulose
und Bronchiektasen. Berl. klin. Wchnschr., 1915, liii, Ifi; 71.
3. Stenosis of the Trachea and of the Bronchi
(Tracheostenosis, Bronchiostenosis, Foreign Bodies in the Bronchi)
Stenosis of the trachea or bronchi may result from (1) inflammatory
exudate (e. g., diphtheria, fibrinous bronchitis) or cicatrix (lues) ; (2)
foreign bodies, especially in children (peas, beans, buttons, coins, bone),
and in adults under anesthesia (tooth) ; and (3) pressure from without
(aneurysm, goiter, carcinoma, enlarged glands, etc.).
The dyspnea is often extreme, with stridor on inspiration and on
expiration. The diagnosis of bronchiostenosis depends upon (1) the an-
amnesis, (2) decreased movement of the affected side, and (3) enfeeble-
ment of the respiratory murmur in the area supplied by the bronchus.
When the cause of the bronchiostenosis is unknown, it may sometimes be
discovered by rontgenography or by bronchoscopy (q. v.}. Moreover,
rontgenography and rontgenoscopy reveal a characteristic lung area in
bronchiostenosis.
References
Conner (L. A.}. Syphilis of the trachea and bronchi; an analysis of 128 recorded cases and
report of a case of syphilitic stenosis of the bronchi. Am. J. M. Sc., Phila-
delphia, 1903, n. s., cxxv, 57-95.
Hommel (IF.). Die Syphilis der Trachea und der Bronchien und ihre Diagnose durch die
Tracheobronchoskopie. Monatschr. f. Kinderh. [etc.], Berlin u. Wien,
1914, xlviii, 783-809.
Jacobsohn (O.). Zur Rontgenologic der Bronchostenose. Fortschr. a. d. Geb. d. Ront-
genstrahl, Hamburg, 1913, xx, 294-298.
Killian (G.) . Ueber die Leistungen der directen Bronchoskopie bei Fremdkdrpern der Lungen.
Munch, med. Wchnschr., 1899, xlvi, 723-726.
596 DISEASES OF THE RESPIRATORY APPARATUS
Large (S. H.}. The removal of an open safety pin, point up, from the left bronchus of a seven-
year-old child. Cleveland M. J., 1915, xiv, 517-618.
Schwyzer (A.). On bronchoscopy, with report of a case in which a foreign body was removed
from the right lower lobe of a lung through a bronchoscove. Ann. Surg.,
Philadelphia, 1904, xxxix, 194-206. 2 pi.
Thornton (W. L.) & Pratt (J. />.)• The relation of bronchial stenosis to bronchieciasis.
Johns Hopkins Hosp. Bull., Baltimore, 1908, xix, 230-232.
Ziegler (/.)• Beilrag zur Rontgendiagnostik der Bronchostenose. Deutsche med. Wchnschr.,
1913, xxxix,
E. Diagnosis of the Principal Diseases of
the Lun£s
(The Pneumopathies)
For clinical purposes the principal diseases of the lungs may be
divided into five main groups:
1. Pneumopathies of inflammatory origin (pneumonias).
2. Pneumopathies due to alteration of the air content of the alveoli
(atelectasis, emphysema).
3. Pneumopathies of circulatory origin.
4. Pneumopathies due to the presence of foreign bodies and of
parasites.
5. Pneumopathies due to neoplasms (tumors of the lung).
References
Babcock (R. //.). Diseases of the lungs. New York & London, 1907, D. Appleton &
Co. 828 p. 8°.
Barlow (T. W. N.). Administrative measures for the control of respiratory diseases other
than phthisis. J. Roy. San. Inst., London, 1914, xxxv, 346-348.
Carrel (A.}. On the technique of intrathoracic operations. Surg., Gyn. & Obstet., Chicago,
1914, xix, 226-228.
Claisse (P.), Mosny (E.} [et al.]. Maladies des Poumons, des Bronches et de la Trochee.
Paris, 1910, J. B. Bailliere & fits. 860 p. 8°. [Nouv. Traite de Med.
et de Therap., xxix.]
Clark (Sir A.). Clinical lectures on some obscure affections of the lung. Med. Press &
Circ., London, 1893, n. s., Ivi, 573; 655; 1894, n. s., Mi, 187.
Frankel (A.). Spezielle Pathologic und Therapie der Lungenkrankheiten. Berlin & Wien,
1904, Urban & Schwarzenberg. 996 p. 8°.
Garre (Karl) & Quincke (Heinrich). Surgery of the lung. 2. ed. Translated from the
German by D. M. Bancroft. London [1913], J. Bale Sons & Daniellson.
279 p. 2pl 4°.
Hofbauer (L.). Therapie der Krankheiten der Respirationsorgane (ausschliesslich der
Pneumonic und der Lungentuberkulose] . Therap. Monatsch., Berlin, 1915,
xxix, 237-244.
Hoffmann (F. A.}, Rosenbach (O.) & Aufrecht (E.}. Diseases of the bronchi, lungs and
pleura. Edited, with additions, by John H. Musser. Authorized trans-
lation from the German, under the editorial supervision of Alfred Stengel.
Philadelphia & London, 1902, W. B. Saunders Co. 1029 p. 8°.
Nothnagel's Encyclopedia of Practical Medicine. Amer. ed.
DISEASES OF THE LUNGS 597
Lindsay (/. A.). Lectures on diseases of the lungs. 2, ed. London, 1906, Bailliere,
Tindall & Cox. 518 p. 8°.
Lord (F. 7\). Diseases of the bronchi, lungs and pleura. Philadelphia & New York.
1915, Lea & Febiger. 632 p. 8°.
Meltzer (S. /.). Simple devices for effective artificial respiration in emergencies. J. Am.
M. Ass., Chicago, 1913, Ix, 1407-1410.
Moritz (F.). Ueber Lungenerkrankungen im Kriege. Ztschr. f. drztl. Fortb., Jena, 1915,
xii, 321-331.
Pincussohn (L.). Chemie der Lunge. In: Handb. d. Biochem. (Oppenheimer), Jena,
1909, ii, 2. Hlfte., 369-376.
Powell (Sir R. Z>.) & Horton-Smith-Hartley (P.). Diseases of the lungs and
pleurae. 5. ed. London, 1911, H. K. Lewis. 740 p. 29 pi. 8°.
Sauerbruch (F.). Fortschritte in der chirurgischen Behandlung der Lungenkrankheiten.
Munch, med. Wchnschr., 1913, Ix, 1890; 1944.
Sauerbruch (F.) & Schumacher (E. D.}. Technik der Thoraxchirurgie. Berlin, 1911,
J. Springer. 101 p. 4°.
Staehelin (R.). Die Erkrankungen der Trachea, der Bronchien, derLungen und der Pleuren.
In: Handb. d. inn. Med. (Mohr & Staehelin) t Berlin, 1914, ii, 205-810.
Tendeloo (N. /*.). Studien liber die Ursachen der Lungenkrankheiten. Wiesbaden, 1900,
xi, Teil I, Bergmann. 118 p. 8°.
West (S.). Diseases of the organs of respiration. 2. ed. London. 1909, C. Griffin & Co.
974 P> 8°.
1. The Inflammatory Pneumopathies or Pneumonias
These are divisible into three great groups:
I. The parenchymatous pneumonias:
(a) Genuine lobar pneumonia (fibrinous).
(b) Lobular or bronchopneumonia (catarrhal).
(c) Metastatic pneumonia (embolic).
(d) Chronic pulmonary abscess and gangrene.
(e) Gangrene of lung.
II. The interstitial pneumonias.
III. The "specific" pneumonic processes:
(a) Tuberculous pneumonia.
(b) Luetic pneumonia.
(c) Actinomycotic pneumonia, etc.
L THE PAKENCHYMATOUS PNEUMONIAS
(a) Genuine Lobar Pneumonia
(Fibrinous or Croupous Pneumonia)
Definition. — An acute infectious disease of sudden onset (violent chill,
high fever, tachypnea, and stitch in the side), usually without prodromata,
and leading to consolidation of one or more lobes of the lung.
Etiology. — The disease is caused by infection with the pneumococcus
(Micrococcus lanceolatus) ; rarely with the Bacillus mucosus capsulatus
598 DISEASES OF THE KESPIRATOKY APPAKATUS
(Friedlander's pnenmobdcillus) . For the several strains of pneumococci
concerned, see the Section on Infectious Diseases in which Cole and
Dochez's work is referred to (Part IV).
The disease may occur at any time of year, but is commonest in
the United States during the winter months. According to Keller, the
incidence of lobar pneumonia is inversely proportional to the rain-fall.
Conditions that predispose a person to the infection include exposure
to cold and wet, trauma, and irritation of inhaled gases or dust. One
that has once had an attack is likely to have another or several attacks
later on in life. Children and old people are often affected. Women
suffer less often than men. Contagion seems to play a part sometimes,
especially in pneumonia epidemics.
Symptoms. — Clinically, lobar pneumonia runs its course in three
stages :
1. The initial stage (corresponding histologically to the stage of
ENGORGEMENT and of beginning infiltration).
2. The stage of demonstrable CONSOLIDATION of the lung tissue (cor-
responding histologically to red hepatization and gray hepatization).
3. The stage of CONVALESCENCE, with fall of temperature (often by
crisis, sometimes by lysis) and return of the physical signs to normal
(corresponding histologically to the stage of RESOLUTION, or absorption, of
the exudate after autolysis).
On inspection, the patients usually look very ill. The respiration is
accelerated (30-60 per minute) and shallow, partly owing to the pleural
pain. There is cyanosis, marked dilation of the nostrils during respiration,
coughing, and diminished expansion of the thorax on the side affected.
The face is flushed but sometimes only on the side of the affected lung.
The patient may lie on the affected side in order to lessen the pain by
restricting movement.
On palpation, the vocal fremitus is increased over the affected lobe as
long as the bronchus is patent. Expansion of the side affected is dimin-
ished. A friction fremitus due to the accompanying dry pleurisy may
be palpable.
On percussion over the affected lobe (most frequently the lower right)
the note, in the initial stage, may be slightly higher pitched and somewhat
tympanitic (Skoda's resonance). When consolidation has taken place, the
note is dull, but not absolutely flat, retaining usually a slight tympanitic
quality. On resolution, the note gradually grows less dull, but it remains
higher pitched than normal, and slightly tympanitic, for a long time
(weeks or months) after convalescence has begun. In central pneumonia,
outspoken dullness may be absent for days after the onset of the disease.
When the lower lobe is involved, the percussion-note over the upper front
of the chest is often lowered in pitch and sometimes slightly tympanitic,
due to relaxation of the air-containing lung.
DISEASES OF THE LUNGS 599
On auscultation, during the first twenty-four hours, that is, during
beginning infiltration, fine crepitation is audible on inspiration (crepitatio
indux). During the stage of consolidation, this fine crepitation disappears
and loud bronchial breathing and bronchophony become audible over the
dull area. Rales may be absent at this stage ; if present, owing to a marked
bronchitis, they are consonating. During resolution, the bronchial breath-
ing gradually disappears, fine crepitation (crepitatio redux) reappears,
and, later, coarser sounds (moist rales) become audible, especially on
expiration ; should the fine crepitation persist long, it is a sign of delayed
resolution. Pleuritic friction is often audible. If the bronchus to the
diseased lobe become plugged, the bronchophony and the increased vocal
fremitus, otherwise present, may not be observable. It should be borne
in mind that in the earlier stage of lobar pneumonia the breath sounds
may be suppressed.
The sputum is scanty, very tenacious, and is often, though not always,
of a rusty tint; many lancet-shaped diplococci and red blood corpuscles
are present. Sometimes, small fibrin casts are visible. On resolution, the
sputum becomes purulent, and later mucoid.
On rontgenoscopy one sees a clear lung field for several hours after the
initial chill ; then an even shadow appears over, as a rule, one whole lobe,
growing gradually darker as hepatization proceeds ; during resolution, the
shadow grows less intense, but some shadow remains for from two to eight
weeks after the attack.
The fever, at onset, rises rapidly to its height (103°-105° F.), and
remains very constant during the fastigium or stadium acmes. The maxi-
mal temperatures are seen between the fourth and the sixth days. During
the fastigium, the fever is, as a rule, slightly remittent, but it may be
continuous, or, in rare cases, intermittent. The fever commonly ends by
crisis (5th to llth day), with sweats and slowing of the pulse and res-
piration; sometimes, a pseudocrisis precedes, by a day or two, the real
crisis. Or, the fever may terminate by lysis.
The rate of the pulse is ordinarily from 100 to 116 ; in cases in which
the pulse rises above 120, the mortality is high. Dilatation of the right
heart sometimes occurs. The excretion of chlorids in the urine is sup-
pressed. Herpes labialis, a frequent accompaniment, appears on the sec-
ond or third day of the disease. There is nearly always a leukocytosis
of from 12,000 to 60,000 or more; in the differential count the increase
is seen to be in the polymorphonuclear neutrophils. In very grave in-
fections, there may be a leukopenia instead of a leukocytosis. The fibrin-
content of the blood and the blood platelets are increased. In many cases,
a blood culture will reveal the presence of the pneumococcus.
In children, the initial chill may be replaced by a convulsion. The
symptoms may simulate meningitis (delirium, vomiting, rigidity) ; while
a true meningitis may complicate the disease, these symptoms are usually
600 DISEASES OF THE RESPIKATOEY APPARATUS
due to intoxication (meningismus) . Similar grave nervous symptoms
may also be met with in adults. Drunkards may develop delirium
tremens in pneumonia.
The spleen is probably always a little enlarged, but it becomes palpable
in less than a quarter of the cases.
Vomiting is common in children at the onset ; it is sometimes present
Temperature
Leukocytes
Respiration
Pulse
Pig. 169. — Pneumonic Crisis. Diagrammatic Chart Representing Relation of Temperature,
Pulse, Respiration, and Leukocytes at Temperature Crisis in a Large Number of Cases
of Acute Lobar Pneumonia. There is Also a Group of Cases in Which the Leukocytes
and Respirations Come Down to Normal More Rapidly and Synchronously with the
Temperature Crisis. (Compiled by Messrs. Tredway, Vanorden, Weinberg and Whitcraft ;
Med. Clinic, J. H. H.)
in adults, especially in apical pneumonia. In asthenic pneumonia gastro-
intestinal symptoms (diarrhea, vomiting, slight icterus) may be marked.
Special Forms of Lobar Pneumonia. — When the upper lobe is involved
(APICAL PNEUMONIA) the mortality is high. One lobe after another may
become affected (wandering pneumonia or PNEUMONIA MIGRANS). Pneu-
monia is an especially fatal disease in drunkards (delirium tremens, heart
failure, gangrene), in the aged, in the very young, and in patients suffering
DISEASES OF THE LUKGS 601
from obesity, emphysema, or cardiac disease. Pneumonia involving both
lungs is known as DOUBLE PNEUMONIA.
In CENTRAL PNEUMONIA, the physical signs usually present on percus-
sion and on auscultation may be absent; there may even be no rusty
sputum. The diagnosis has to be made as a probability diagnosis from
the mode of onset, the febrile course, the tachypnea and the leukocytosis ;
in some cases, a positive blood culture (pneumococcus), or a central shadow
on rontgenoscopy will be decisive.
In ASTIIENIC PNEUMONIA, the course may be nearly afebrile and the
physical signs atypical; the nervous and gastro-intestinal symptoms are
often pronounced ; the patients are markedly prostrated from the beginning,
and may show the signs of what is often called a "typhoid state" ; the
course is often protracted and the mortality very high.
In so-called MASSIVE PNEUMONIA, there is dullness on percussion ex-
tending over the whole of one side of the thorax, accompanied by a feeling
of great resistance on percussion. The bronchi are plugged with exudate
and no sounds may be audible on auscultation. It is but little wonder that
in such cases of massive pneumonia the condition is sometimes mistaken
for a huge pleural effusion ; but the heart is not displaced and Grocco's
triangle of dullness is not present.
Complications. — These include empyema, pericarditis, endocarditis,
meningitis ; more rarely arthritis, nephritis or peritonitis. Abdominal pain
is not uncommon at the onset of pneumonia ; an acute surgical condition
in the abdomen has often been suspected and exploratory laparotomy done !
Sequelae. — Abnormal terminations of lobar pneumonia include abscess
of the lung, gangrene, tuberculosis, and chronic pneumonia (unresolved
and organizing exudate).
Diagnosis. — In frank cases of lobar pneumonia little difficulty in
diagnosis is experienced ; the sudden onset with chill, fever, pain in the
side, rapid breathing, cough, rusty sputum, and herpes, combined with the
physical signs above described, is conclusive. Some difficulty may be
experienced in the early stage of the disease in cases in which the sub-
jective symptoms are masked by the presence of complicating conditions.
Thus in cases of meningitis, of delirium tremens, in surgical accident
cases, etc., the presence of a lobar pneumonia can readily be overlooked
unless the investigation of the case and the analysis of the findings be
thorough. At times the symptoms at onset may suggest other conditions ;
thus abdominal pain, vomiting, distention . and frequently jaundice may
lead to suspicion of the existence of peritonitis ; or meningitis may be
diagnosed because of the delirium, headache, fever and leukocytosis.
The slow development of the physical signs of consolidation often
leads to confusion. The whole condition may erroneously be thought
to be due to a simple pleurisy; or the slight impairment of resonance
and the diminution in breath sounds that are found may be considered
602 DISEASES OF THE BESPIKATOKY APPAKATUS
insufficient evidence of pulmonary involvement. A rontgenogram of the
chest may be of value, in obscure cases, at this time, for central pneu-
monias, or an early lobar consolidation may thus be clearly demon-
etrable.
The atypical physical signs observed over a massive pneumonia
(absence of tubular breathing and vocal fremitus due to plugging of
bronchi) have frequently led to confusion with pleurisy with effusion,
or with an empyema. Should doubt exist, it is always wise to explore
the chest thoroughly with a needle. Acute lobar pneumonia, especially
when situated at one apex, may readily be confused with acute tuberculous
bronchopneumonia. The further course will differentiate between these
conditions readily but an early diagnosis often requires great skill in the
interpretation of the data (history; physical signs; rontgenogram; sputum
examinations including cultures; blood culture; leukocyte count, includ-
ing a differential count). Caseous pneumonia involving a whole lobe
and the pseudolobar form of bronchopneumonia are two conditions often
mistaken for true lobar pneumonia of pneumococcal origin.
On entering a sick-room in winter when pneumonia is prevalent, an increase
in the patient's respirations per minute may at once call attention to the possi-
bility of a pulmonary involvement. I have been surprised to find how common
it is for students and even for physicians of considerable experience to neglect
this simple observation and to fail to think of the possibility of the developing
pneumonia to which a tachypnea frequently points.
References
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Boyd (H.). Blood-letting in pneumonia. South. M. J., Nashville, 1914, vii, 799-802,
DISEASES OF THE LUNGS 603
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Cole (R. /.). Treatment of pneumonia by means of specific serums. J. Am. M. Ass.,
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Cross (/. G.). Analysis of four-hundred cases of lobar pneumonia. J. Am. M. Ass.,
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Doming (/.)• Abdominal symptoms in pleurisy and pneumonia. Tr. Am. Pediat. Soc.,
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Dreschfeld (/.)• On creeping pneumonia (pneumonia migrans) and its relation to epidemic
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Edgeworth (F. H.}. On the cerebral symptoms of lobar pneumonia in children. Bristol
Med.-Chirurg. J., 1913, xxxi, 308-317.
Emerson (C. P.). The termination of pneumonia in cases with recovery. Johns Hopkins
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Fleischner (E. C.). Some sources of error in the diagnosis and treatment of lobar pneumonia
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Fraenkel (A.~). Optochin bei Pneumonie. Therap. d.Gegenw., Berlin, 1915, Ivi, 1-5.
Hare (H. A.)» The ratio of blood-pressure to pulse-rate in croupous pneumonia from a
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xxxiv, 387-390.
Herrick (J. B.}. Abdominal pain in pleurisy and pneumonia. J. Am. M. Ass., Chicago,
1903, xli, 535-540.
Holt (L. E.). The temperature in acute primary pneumonia of children. Arch. Pediat.,
N. Y., 1891, mii, 881-899.
Hoover (C. F.). Fluid in the pleural cavity simulating pneumonia. Cleveland J. M., 1904,
Hi, 441-446.
Howell (A. A.). The use of pituitary extract in the control of some of the associated symptoms
of pneumonia which favor hypotension. Am. J. M. Sc., Philadelphia,
1914, cxlviii, 563-567.
Koplik (H.}. The frequency, prognosis and treatment of lobar pneumonia in infants and
children. Boston M. & S. J., 1905, clii, 741-744.
Lambert (Alex.}. The blood pressure in pneumonia. J. Am. M. Ass., Chicago, 1911,
Ivii, 1827-1829.
Lapinski (/.)• Ueber die Wirkung des Aethylhydrocupreins (Optochins) bei krupposer
Pneumonie. Therap. Monatsch., Berlin, 1915, xxix, 103-114-
Mays (T. J.}. The treatment of acute pneumonia. Internal. Clin., Philadelphia, 1914, 24. s.,
iv, 28-38.
Nammack (C. E.). The differential diagnosis of lobar pneumonia. Med. Rec., New
York, 1913, Ixxxiii, 611-613.
Newburgh (L. H.). The vasomotor mechanism in pneumonia. Am. J. M. Sc., Philadel-
phia, 1915, cxlix, 204-209.
Newburgh (L. H.} & Minot (G. R.}. The blood-pressure in pneumonia. Arch. Int.
Med., Chicago, 1914, xiv, 48-5$,
604 DISEASES OF THE EESPIKATOKY APPARATUS
Norria (G. W.). Lobar pneumonia. A study of 445 cases, with special reference to the de-
creased mortality since the institution of fresh-air treatment. Am. J. M.
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Northrup (W. /*.)• The early diagnosis and treatment of pneumonia in infants. Chicago
M. Recorder, 1904, xxvi, 688-705.
Osier (Sir W.}. On certain features in the prognosis of pneumonia. Am. J. M. Sc., Phila-
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Parkinson (/.)• ^ clinical trial of aethylhydrocuprein in pneumonia. Ztschr. f. Chemo-
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Porter (W. T.), Newburgh (L. H.} & Newburgh (/.)• The state of the vasomotor appara-
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Rohdenburg (G. L.} & Vander Veer (A.}, Jr. The spinal fluid in pneumonia. J.
Am. M. Ass., Chicago, 1915, Ixiv, 1227-1228.
Steell (G.)« A clinical lecture on certain physical signs met with in a case of pneumonia.
Lancet, London, 1893, i, 980-983.
Sutherland (G. A.). Lobar pneumonia in childhood. Clin. J., London, 1905-06, xxvii,
26; 44-
Taylor (F.). Pneumonia in children. Brit. J. Child. Dis., London, 1907, iv, 873-394.
Weill (M. E.) & Mouriquand (G.). Les foyers d'hepatisation pneumonique "silencieux"
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West (5.). Observations upon the pulse-respiration ratio in croupous pneumonia. St. Barth.
Hosp. Rep., London, 1892, xxviii, 231-233.
Williams (W. R.) & Youland (W. E.), Jr. On the therapeutic use of aqueous extract of
leucocytes (Hiss) in lobar pneumonia. J. Med. Research, Boston, 1914-
15, xxxi, 391-407.
Williamson (C. 5.). The onset in pneumonia, typical and atypical. Illinois M. J., Spring-
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Willson (R. N.). The heart in the pneumonias. J. Am. M. Ass., Chicago, 1914, Ixii, 982-
984.
Wynkoop (E. /.)• Some thoughts on the atypical pneumonias of infancy and childhood.
N. York State J. M., New York, 1914, xiv, 437-44*.
3. Blood in Pneumonia
Chatard (J. A.). The leucocytes in acute lobar pneumonia. Johns Hopkins Hosp. Rep.,
Baltimore, 1910, xv, 89-98.
Dochez (A. R.). Coagulation time of the blood in lobar pneumonia. J. Exper. M., Lan-
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Swing (/.)• A. study of the leucocytosis of lobar pneumonia. N. York M. J., 1893, Iviii,
713-718.
Futcher (T. B.). The blood in pneumonia. J. Pract. Med., New York, 1897-98, viii, 811-
313.
Hastings (T. W.) & Boehm (E.}. A study of cultures from sputum and blood in lobar
pneumonia. J. Exper. M., Lancaster, Pa., 1913, xvii, 239-251.
Miller (J. A.) & Reed (Margaret A.). Studies of the leukocytes in pulmonary tuberculosis
and pneumonia. Arch. Int. Med., Chicago, 1912, ix, 609-636.
Mouriquand (G.) & Dufourt (A.). Le chimisme humoral de la pneumonie. Progres
med., Pans, 1914, 3. s., xxx, 109-111.
Peabody (F. W.}. The carbon dioxide content of the blood in pneumonia. J. Exper. M.,
Lancaster, Pa., 1912, xvi, 701-718.
The oxygen content of the blood in lobar pneumonia. J. Exper. M., Lan-
caster, Pa.. 1913, xviii, 7-17.
Rosenow (E. C.). The blood in lobar pneumonia; with remarks concerning treatment.
J. Am. M. Ass., Chicago, 1905, xlix, 871-873,
DISEASES OF THE LUNGS 605
Stitt (E. /£.)• Leukopenia of a marked degree in a fatal case of pneumonia. U. States Nav.
Bull., Washington, 1915, ix, 275.
4. Metabolic
Cook (H. W.). Nitrogen excretion in pneumonia and its relation to resolution. Johns
Hopkins Hosp. Bull, Baltimore, 1902, xiii, 307-316.
Lambert (A.} & Wolf (C. G. L.}. The metabolism of nitrogen and sulphur in pneumonia.
J. Biol. Chem., New York, 1907-08, Hi, p. xix.
Medigreceanu (F.). On the mechanism of chlorin retention in pneumonia. J. Exper. M.,
Lancaster, Pa., 1911, xiv, 289-297.
Peabody (F. W.}. Studies of the inorganic metabolism in pneumonia, with especial refer-
ence to calcium and magnesium. J. Exper. M., Lancaster, Pa., 1913,
xvii, 71-82.
Wolf (C. G. L.) & Lambert (Alex.}. Protein metabolism in pneumonia. Arch. Int.
Med., Chicago, 1910, v, 406-448.
5. Complications and Sequelae
Cary (C.) & Lyon (I. P.). Pseudomembranous inflammation of the mucous membranes
caused by the pneumococcus'; review of the literature and report of a case of
pneumococcic pseudomembranous exudation on the mucous membranes of
the mouth, tongue, throat, nose, eyes, glans penis, anus, [etc.], complicating
acute lobar pneumonia. Am. J. M. Sc., Philadelphia, 1901, n. s., cxxii,
298-309.
Edsall (D. L.} & Pemberton (R.}. The use of the X-rays in unresolved pneumonia. Am.
J. Med. Sc., Philadelphia & New York, 1907, n. s., cxxxiii, 286-297.
On the use of the X-ray in unresolved pneumonia and on the nature of the
general toxic reaction after X-ray exposure. Tr. Ass. Am. Phys., Phila-
delphia, 1906, xxi, 618-640.
Edsall (D. L.) & Robertson (W. E.}. A case of postpneumonic endocarditis. Proc. Path.
Soc., Philadelphia, 1903-04, n. s., vii, 199.
Forchheimer (F.). Cardiac and vascular complications of pneumonia. J. Am. M. Ass.,
Chicago, 1909, liii, 1449-1454.
Fraenkel (E.) & Reiche (F.). Beitrdge zur Kenntniss der acuten fibrinosen Pneumonic,
insbesondere der Nierenverdnderungen bei derselben. Ztschr. f. klin. Med.,
Berlin, 1894, xxv, 230-284.
Fussell (Af.). Acute dilatation of the stomach in pneumonia. Am. J. M. Sc., Phila-
delphia & New York, 1911, cxlii, 794-803.
Gerhardt (D.). Ueber parapneumonische Empyeme. Mitteil. a. d. Grenzgeb. d. Med. u.
Chir., Jena, 1913, xxvi, 695-700.
Goldie (Wm.). On the occurrence of fluid exudate in cases of lobar pneumonia. Canad.
M. Ass. J., Toronto, 1915, v, 503-507.
Guthrie (L. G.}. Pneumonia and encephalitis cerebelli. Proc. Roy. Soc. Med., London,
1913-14, vii, Sect. Stud. Dis. Child., 120-122.
Holt (L. E.}. Meningitis complicating pneumonia in young children. Arch. Pediat., New
York, 1893, x, 1011-1023.
von Kalden (C.). Ueber Lungeninduration nach crouposer Pneumonic. Centralbl. f. allg.
Path. u. path. Anat., Jena, 1897, viii, 561-582.
McCrae (T.). Delayed resolution in lobar pneumonia. Johns Hopkins Hosp. Rep.,
Baltimore, 1910, xv, 277-305.
Empyema in acute lobar pneumonia. Johns Hopkins Hosp. Rep.,
Baltimore, 1910, xv, 167-188.
McPhedran (F.). Notes on jaundice in pneumonia. Johns Hopkins Hosp. Bull., Bal-
timore, 1911, xxii, 408-409.
606 DISEASES OF THE EESPIKATOKY APPAKATUS
Newburgh (L. H.}. The heart muscle in pneumonia. J. Exper. M., Lancaster, Pa., 1915,
xxii, 123-128.
Osier (W.). Parotitis in pneumonia. Univ. Mag., Philadelphia, 1893-94, vi, 245-247.
Cerebral features of pneumonia. Maryland M. J., Baltimore, 1897-98,
xxxviii, 381-383.
Ribbert (H.). Ueber den Ausgang der Pneumonic in Induration. Arch. f. path. Anat.
[etc.], Berlin, 1899, clvi, 164-180.
Steiner (W. R.}. Peripheral venous thrombosis in pneumonia, with report of three cases
and a review of those previously recorded. Johns Hopkins Hosp. Rep.,
Baltimore, 1910, xv, 189-227.
Stockton (C. G.). Relapsing lobar pneumonia, with absence of leucocytosis. Phila. M. J.,
1898, i, —
Vaughan (V. C.}, Jr. Pleuritic effusions and empyema subsequent to or coincident with
pneumonic attacks. J. Mich. M. Soc., Grand Rapids, 1914, xiii, 698-695.
Weichselbaum (A.}. Ueber endocarditis pneumonica. Wien. med. Wchnschr., 1888,
xxxviii, 1176; 1209
White (W. H.). A clinical lecture on empyema following on lobar pneumonia. Lancet,
London, 1902, ii, 1331-1335.
Winslow (R.}. Thoracotomy in unresolved pneumonia. Surg. Gynec. & Obst., Chicago, 1915,
xx, 350.
Withington (C. F.}. Cerebral complications in pneumonia. Boston M. & S. J., 1913,
clxviii, 945-950.
Pneumonic hemiplegias. Am. J. M. Sc., Philadelphia & New York,
1914, cxlvii, 203-213.
6. Etiological; Immunological; Experimental
Clark (J. M.). Diseases of the lungs associated with the presence of Friedldnder's bacillus.
Bristol M.-Chir. J., 1914, xxxii, 2-12.
Cole (R. /.). Types of pneumococci and their characteristics. Arch. Pediat., New York,
1915, xxxii, 53-60.
Pneumococcus infection and lobar pneumonia. Arch. Int. Med., Chicago,
1914, xiv, 56-93.
Cole (JR.) & Dochez (A. R.}. Report of studies on pneumonia. Trans. Ass. Am. Phy-
sicians, Philadelphia, 1913, xxviii, 606-616.
Dochez (A. R.). The presence of protective substances in human serum during lobar pneu-
monia. J. Exper. M., Lancaster, Pa., 1912, xvi, 665-679.
The occurrence and virulence of pneumococci in the circulating blood during
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692.
Dochez (A. JR.) & A very (O. T.). The occurrence of carriers of disease-producing types of
pneumococcus. J. Exper. M., Lancaster, Pa., 1915, xxii, 105-113.
Varieties of pneumococcus and their relation to lobar pneumonia. J. Exper.
M., Lancaster, Pa., 1915, xxi, 114-132.
Hanes (F. M.). The biologic classification of pneumococci and the serum treatment of lobar
pneumonia. Old Dominion J. M. & S., Richmond, 1915, xx, 134-148>
Kline (B. S.) & Winternitz (M. C.). Studies upon experimental pneumonia in rabbits.
VII. The production of lobar pneumonia. J. Exper. M., Lancaster, Pa.,
1915, xxi, 304-310.
Lamar (R. V.) & Meltzer (S. /.). Experimental pneumonia by intrabronchial insuffla-
tion. J. Exper. M., Lancaster, Pa., 1912, xv, 133-148.
Meltzer (S. J.). Ueber eine Melhode zur experimentellen Erzeugung von Pneumonic und
liber einige mil dieser Methode erzielte Ergebnisse. Berl. klin. Wchnschr.,
1914, li, 1351-1353.
DISEASES OF THE LUNGS 607
Neufeld (F.) u. Handel. Ueber Herstellung und Prufung von Anlipneumokokkenserum
und uber die Aussichten einer spezifischen Behandlung der Pneumonie.
Ztschr. f. Immunitatsforsch. [etc.], I. Teil, Orig., Jena, 1909, Hi, 159-171.
Roque (G.}, Cordier (V.) & Levy (L.). Pneumonie a pneumobacille de Friedlaender et a
pneumocoques. Lyon Med., 1914, cxxii, 1391—1396.
Rosenow (E. C.) & Hektoen (L.}. Treatment of pneumonia with partially autolyzed
pneumococci. J. Am. M. Ass., Chicago, 1913, Ixi, 2203-i
Smith (T.). Some bacteriological and environmental factors in the pneumonias of lower
animals, with special reference to the guinea-pig. J. M. Research, Boston,
1913, xxix, 291-323.
Strouse (5.). Phagocytic immunity in pneumococcus infections and in pneumonia, with
relation to the crisis. J.Exper.JM., Lancaster, Pa., 1911, xiv, 109-115.
Wadsworth (A.}. Experimental studies on the etiology of acute pneumonitis. Am. J. M.
Sc., Philadelphia & New York, 1904, cxxvii, 851-877.
Wassermann (A.). Ueber differentielle Diagnostik von entzundlichen Lungenaffectionen.
Deutsche med. Wchnschr., Leipzig u. Berlin, 1893, xix, 1201-1205.
Wells (E. F.}. Pneumonia, etiology and epidemiology. Med. News, New York, 1905,
Ixxxvi, 930-934.
Winter nitz {M. C.) & Hirschf elder (A. />.)• Studies upon experimental pneumonia in
rabbits. Parts I to III. I. The production of lobar pneumonia. II.
Pneumonia in animals rendered aplastic. III. Intro, vitam staining.
J. Exper. M., Lancaster, Pa., 1913, xvii, 657-665, 4 pi.
Wollstein (Martha) & Meltzer (S. /.)• Pneumonic lesions made by intrabronchial in-
sufflation of non-virulent pneumococci. J. Exper. M., Lancaster, Pa., 1913,
xvii, 353-361.
Y. Mortality
Bollinger (O.). Ueber Todesursachen bei crouposer Pneumonie. Munch, med. Wchnschr.,
1895, xlii, 745-748.
Brown (A. G.}, Jr. The present-day mortality of pneumonia. Atlanta Jour.-Rec. Med.,
1902-03, iv, 586-591.
Burkhart (J. L.). Pneumonia mortality and prevention. Pub. Health Mich., Lansing,
1915, Hi, 16-21.
Davis (N. S.). The increased prevalence and mortality of pneumonia during the last sixty
years, with reference to its prevention and treatment. Internal. Clin.,
Philadelphia, 1904, 14. s., i, 41-49.
Mackenzie (H.}. The mortality and frequency of pneumonia as affected by age, sex, seasons
and habits. Practitioner, London, 1900, Ixiv, 34~45.
Pleasants (J. H.}. The increasing mortality from pneumonia in Baltimore, and its causes.
Maryland M. J., Baltimore, 1904, xlvii, 177-183.
NOTE. — For other references on Pneumonia see under Pneumococcus in Part IV.
(b) Bronchopneumonia
(Caiarrhal Pneumonia, Lobular Pneumonia, Focal Pneumonia)
Definition. — This is usually an extension of a bronchitis to the lobules
of the lung supplied by the single bronchioles — hence the term lobular
pneumonia. A lobar infiltration may be simulated by the confluence
of numerous bronchopneumonic foci. But focal pneumonia is not always
secondary to a bronchiolitis ; sometimes the bronchioles and the parenchyma
608 DISEASES OF THE RESPIRATORY APPAEATUS
of the lung are simultaneously involved; or bacteria may be aspirated
directly into the alveoli, causing a pneumonia not preceded by a bron-
chitis; sometimes, the focal process arises because of bacteria arriving
by way of the blood vessels (see Embolic Pneumonia) or by way of the
lymph channels.
Occurrence. — The disease is most common in childhood, frequently fol-
lowing measles, whooping-cough and influenza. Recurring attacks are
often seen in children suffering from infected tonsils and adenoids. Many
of the cases designated capillary bronchitis are really instances of broncho-
pneumonia with numerous small foci scattered through both lungs.
Bronchopneumonia is not uncommon in the aged and enfeebled; it may
occur also after operations ("ether pneumonia'7), in some comatose
patients (apoplexy, uremia), and in patients that vomit much (carcinoma
ventriculi, peritonitis).
Etiology. — The infection is usually due to the pneumococcus, the strep-
tococcus, Friedlander's -bacillus, or the staphylococcus ; occasionally, it is
due to the Bacillus influenzae, the Bacillus coli, the meningococcus, the
Bacillus pestis, the Micrococcus catarrhalis, or other bacteria. The broncho-
pneumonia is usually secondary to a preceding bronchitis of a descending
type.
One form of bronchopneumonia, known as ASPIRATION PNEUMONIA or
FOREIGN-BODY PNEUMONIA, follows the aspiration of food or other particles
into the trachea and bronchi ; it involves, usually, the lower lobes and is
especially prone to become purulent or putrid.
In HYPOSTATIC PNEUMONIA, occurring in bed-ridden patients with
faulty circulation, there is usually a slight bronchopneumonia with atelec-
tasis. Indeed, in most bronchopneumonias, there are usually signs of
more or less widespread atelectasis accompanying the focal infiltrative
process.
Symptoms. — The clinical picture is far more variable than that seen in
genuine lobar pneumonia. The patients show remittent fever, tachypnea,
dyspnea, tachycardia and cyanosis. As a rule, both lungs are involved.
When the foci of infiltration are close together, the diseased portion of
the lung being as large as a silver dollar, a dull or slightly tympanitic note
may be demonstrable; only rarely is there outspoken dullness.
On auscultation, numerous small and medium-sized 'rales, often con-
sonating, can be made out over circumscribed areas, first, as a rule, over
the lower lobes. Over larger infiltrations, bronchial breathing, broncho-
phony and increased vocal fremitus may become demonstrable. ^In in-
fluenzal pneumonia, many foci may appear simultaneously or successively ;
the physical signs (rales, roughened breathing, bronchophony) may be
very different over different foci ; the foci of infiltration may, later, fuse
and causo consolidation of a whole lobe (pseudolobar pneumonia) ; the
"jumping" of the inflammatory process from one spot to another may be
DISEASES OF THE LUNGS 609
a striking feature, the bronchial breathing and crepitant rales soon dis-
appearing from one spot and becoming audible at another.
The sputum, absent in young children, is in adults mucopurulent, and
occasionally blood-stained. Cultures made on blood-agar, by Luetscher's
method, from a washed ball of fresh sputum, will usually reveal the causal
microorganism in pure, or in nearly pure, culture. Blood-agar is essential
for the demonstration of the presence of hemoglobinophil bacteria like the
Bacillus influenzae. The fever is more irregular than in lobar pneumonia ;
it often lasts three weeks or longer, and it ends by lysis.
There is always danger of circulatory failure either from failure of
vasomotor tone or from weakening of the right heart owing to the obstruc-
tion in the pulmonary circulation.
Pleuritis, pericarditis, and otitis media are common complications.
Tuberculosis often follows in persons predisposed to the disease. Abscess
and gangrene of the lung occasionally occur as complications, especially
in aspiration pneumonia. Severe diarrhea sometimes sets in, probably
a toxic symptom. In the old, in the feeble, and in rachitic children, the
outlook is grave.
Differential Diagnosis. — We must distinguish bronchopneumonia (1)
from atelectasis (enfeebled breath sounds, absence of consonating rales,
sometimes sudden disappearance of dullness after deep inspirations) ; (2)
from genuine lobar pneumonia (onset, duration, crisis, and quick resolu-
tion) ; (3) from pleuritis duplex (exploratory puncture when in doubt) ;
(4) from pulmonary tuberculosis, with or without complicating pyogenic
infection.
References
Demmer (F.). Ueber katarrhalische Lungenkomplikationen bei chirurgischen Erkrankungen
und deren Behandlung mil Oxygen-adrenalin-Inhalation. Deutsche Ztschr.
f. Chir., Leipzig, 1913, cxxv, 257-293.
Larrabee (R. C.). A localized, subacute form of bronchopneumonia. Boston M. & S. J^
1915, clxxii, 257-260.
Riesman (/).)• A lobar form of bronchopneumonia of long duration, occurring in children
and young adults. Am. J. M. Sc., Philadelphia & New York, 1913,
cxlvi, 313-321.
Schottmuller (H.). Staphylomykose der Luftwege und Lunge im Kindesalter. Beitr. z.
Klin. d. Infektionskr., Wurzburg, 1914, Hi, 361-375.
Suner (E.~). Untersuchungen uber den bronchopneumonischen Pseudokrupp. Jahrb. f.
Kinderh., Berlin, 1914, n. f., Ixxx, 579-600. t
Willson (R. N.). The incidence of fibrinous and broncho-catarrhal pneumonia in the Phila-
delphia General Hospital. Tr. Coll. Phys., Philadelphia, 1914, xxxvi,
54-59.
Wollstein (3f.) & Meltzer (S. /.). Experimental bronchopneumonia by inlrabronchial
insufflation. J. Exper. M., Lancaster, Pa., 1912, xvi, 126-138.
The character of the pneumonic lesions produced by intrabronchial insuffla-
tion of virulent streptococci. J. Exper. Med., Lancaster, Pa., 1913,
xviii, 548-555.
610 DISEASES OF THE RESPIRATORY APPARATUS
(c) Metastatic (Embolic) Pneumonia
This is always a part of some septic process, usually a phlebitis,.' some-
where in the body. Septic emboli, arriving through the pulmonary artery,
cause septic infarcts, which may lead to embolic pneumonia, to lung
abscess, or to gangrene. The pleura is often involved, and empyema or
pneumothorax may follow.
The diagnosis rests upon the local signs combined with the demonstra-
tion of the existence of the primary infectious process elsewhere in the
body.
(d) Abscess of the Lung
Definition. — A suppurative inflammation involving the lung substance.
Etiology. — In the acute and subacute forms, the pyogenic infection (1)
may follow trauma, with tear of the lung; (2) may be due to septic emboli
(in puerperal fever, thrombosis of cerebral sinuses, ulcerative endocarditis,
phlebitis, etc.) ; (3) may result from rupture of an abscess into the lung
(from the liver, subphrenic area, or retroperitoneum) ; (4) may follow
aspiration of a foreign body; (5) may be a sequel to genuine lobar pneu-
monia, or to an influenzal or other form of bronchopneumonia ; (6) may
occur as a secondary process in cancer of the esophagus, tuberculosis, r.c-
tinomycosis, .or glanders.
In the so-called chronic abscess of the lung, we have to deal, as Friinkcl
has shown, less with actual abscess formation (in which a cavity arises
from purulent softening) than with a necrosis followed by ulceration,
the condition occurring in the course of subacute indurative pneumonia or
in cirrhosis of the lung where necrosis may result from insufficient blood
supply in the indurated tissue. Such a process should scarcely be desig-
nated "chronic abscess" ; it would seem preferable to use the terms sug-
gested by Charcot, namely "chronic ulcerative pneumonia" or "chronic
ulcer of the lung."
Symptoms. — When abscess occurs as a sequel of lobar pneumonia, there
is (1) delayed resolution of the pneumonic exudate, and (2) a continuance
of the fever with the development of a "choppy" temperature chart due
to morning remissions and evening exacerbations of the fever — always
strongly suggestive, after pneumonia, of either empyema or lung abscess.
At first the sputum may be of a greenish color, as in most cases of delayed
resolution. Should the abscess rupture into one of the larger bronchi,
the sputum becomes more abundant and is often coughed up in mouthfuls.
This sputum is usually devoid of odor and is yellowish or brownish-yellow
in color ; on standing, the pus sinks in the form of a homogeneous yellow
sediment, the supernatant fluid being gray and turbid. Sometimes par-
ticles or fragments of pigmented lung tissue are visible to the naked eye.
As the abscess empties itself, the temperature may fall, and the physical
signs of a cavity become demonstrable. Cavernous breathing appears
DISEASES OF THE LUNGS 611
over the circumscribed area, the breath sounds often having an amphoric
or a 'metallic character. Coarse bubbling rales may be heard, and some-
times metallic rales. A stereoscopic rontgenogram will reveal the exact
size and position of such a cavity. In favorable cases, the inflammatory
process gradually subsides, the signs of a cavity grow less distinct, the
sputum diminishes in amount and becomes mucopurulent. As cicatriza-
tion proceeds, retraction of the chest wall may gradually develop.
The patients usually recover. In rare cases, gangrene of the lung may
complicate the process ; sometimes, an abscess of the lung ruptures into
the pleural cavity and causes empyema ; still more rarely, abscess of the
lung may be followed by a general septicemia or pyemia.
Differential Diagnosis. — We must distinguish abscess of the lung (1)
from perforated interlobar empyema; (2) from bronchiectasis ; and (3)
from pulmonary tuberculosis with cavity formation. We may derive
much help from rontgenography and from bronchoscopy in cases difficult
of diagnosis. V
References
Barring ton- War dJ^L. E.). Pneumococcal abscess of the lung in children. Lancet, Lon-
don, 1913, 1090-1091.
Kiilbs (F.). Ueber Lungenabszesse und Bronchiektasen. Mitt. a. d. Grenzgeb. d. Med. u.
Chir., Jena, 1913, xxv, 549-567.
Lemann (I. /.) & Maes (U.). Artificial pneumothorax in the treatment of lung abscess.
N. Orl. M. & S. J., 1914-15, Ixvii, 321-327.
Lilienthal (//.)• Abscess of the lung; incision and drainage; thoracotomy. Ann. Surg.,
Philadelphia, 1914, lix, 309-311.
Pulmonary abscess and bronchiectasis. Tr. Am. Surg. Ass., Philadelphia,
1914, xxxii, 491-529.
Lord (F. T.). The diagnosis and treatment of abscess and gangrene of the lungs, with special
reference to operation. Internal. Clin., Philadelphia, 1906, 16. s., ii,
57-70.
Manges (Morris}. Non-tuberculous pulmonary suppurations. Their medical and sur-
gical relations. J. Am. M. Ass., Chicago, 1915, Ixiv, 1554-1559.
Murphy (F. T.). The choice of anesthetic in operating for abscess of the lung; report of two
cases operated upon under local anesthesia. Tr. Am: Surg. Ass., Phila-
delphia, 1915, xxxii, 484-490.
Norris (G. W.) & Landis (H. R. M.). The diagnosis of pulmonary abscess. Tr. Ass.
Am. Physicians, Philadelphia, 1913, xxviii, 302-308.
Pitie (H.}. Pulmonary abscess. Surg., Gynec. & Obst., Chicago, 1914, xix, 549-552.
(e) Gangrene of the Lung
(Pulmonary Gangrene)
Definition. — A condition in which a portion of the lung undergoes
necrosis and putrid softening, the production of the foul-smelling substances
being due to the presence of certain anaerobic bacilli. Gangrene may
affect a solitary area, or it may, especially in chronic cases, involve several
areas (multiple gangrene).
612 DISEASES OF THE RESPIRATORY . APPARATUS
Etiology. — Pulmonary gangrene may have (1) a vascular origin due to
septic and putrid emboli from gangrenous processes elsewhere in the body ;
(2) a bronchial origin as in the instances in which it follows putrid bron-
chitis and bronchiectasis, the aspiration of a foreign body (from the mouth,
from an esophageal lesion, or, a lymph gland perforating a bronchus) ;
or (3) a pulmonary origin owing to the presence of some destructive lesion
in the lung (acute abscess, chronic ulcerative pneumonia, pulmonary tuber-
culosis, trauma). It is most often secondary to bronchiectasis and putrid
bronchitis, but it occurs not infrequently also after influenzal pneumonia,
aspiration pneumonia, and in carcinoma of the esophagus.
Symptoms. — As in putrid Bronchitis, the sputum is inexpressibly foul
ai.d contains Dittrich's plugs. But in gangrene, particles or fragnu'i.ts
of lung tissue are also present in the sputum, at least at times ; in acute
gangrene, large fragments may appear, whereas in chronic gangrene
coarser fragments may be entirely absent over a period of months. Elas-
tic fibers may or may not be present ,**they tend to disappear owing to the
presence of a trypsinlike ferment.
There is some fever ; the face looks pale and emaciated.
When a cavity has formed, there is paroxysmal coughing with mouth-
ful expectoration, as in bronchiectasis ; the patient instinctively assumes the
posture in which the coughing spells are least frequent.
On physical examination, the findings depend upon the size of the
cavity and its proximity to the surface of the lung. One may find a
tympanitic area (surrounded by an area of dullness), exhibiting Wintrich's
change of pitch on opening ar.d closing the mouth; over the same area,
amphoric breathing may be audible. The exact size and position of the
cavity and the surrounding infiltration are most accurately determined by
stereoscopic rontgenography ; in a case of chronic gangrene that I saw
with Dr. Holtzapple of York, Pa., the dimensions and the precise situa-
tion of the diseased area were easily demonstrable by this method.
Diagnosis. — This is easy when large fragments of lung tissue are present
in foul sputum, exceedingly difficult when they are absent. As Frankel
emphasizes, the presence of dullness over the lower lobes with loud bronchial
breathing does not suffice for a diagnosis of gangrene, no matter how
foul the sputum may be, for such findings are not uncommon in putrid
bronchitis with concurrent chronic pneumonia ; an associated tympany may
be due to relaxation of lung tissue near the infiltrated areas. The presence
of amphoric breathing, however, speaks in favor of gangrene and often
gives the clew to the position of the gangrene cavity. It is important to
remember that in chronic gangrene, fragments of lung tissue may not
be discoverable in sputum, even when regularly examined for months.
The x-ray may be very helpful in the localization of a process believed
to be gangrenous.
DISEASES OF THE LUNGS 613
References
Blecher. Ueber Lungengangran bei Bronchialsleinen. Mitt. a. d. Grenzgeb. d. Med. u.
Chir., Jena, 1915, xxviii, 619-626.
Conte (R.)» The medical and surgical aspects of gangrene of the lung. Am. J. M. Sc.,
Philadelphia, 1902, n. s., cxiii, 375-393.
Kast (A.} & Rumpel (T.). Lungengangran. In: Path.-anat. Tafeln. Hamb. Staats-
krankenh., Wandsbek- Hamburg, 1896, xiii, pi. R. 5, with text.
Ophtils (W.). Acid-proof bacilli in five cases of pulmonary gangrene. J. M. Research,
Boston, 1902, vii, 242-2,54.
P err in (M.). Gangrene pulmonaire fuso-spirillaire, guerie par I'arseno-benzol. (Rap. de
Caussade, p. 237.} Bull, et mem. Soc. med. d. hop. de Paris, 1914, 3. s.,
xxxvii, 238-241.
Schrbtter (//.). Beitrag zur Aetiologie der Lungengangran, nebst Bemerkungen zur Anatomic
der grossen Bronchien. Wien. klin. Wchnschr., 1890, Hi, 867-870.
Shaw (L. E.). Gangrene of the lung. Guy's Hosp. Gaz., London, 1893, n. s., vii, 157-161.
II. THE INTERSTITIAL PNEUMONIAS
Occasionally, in man, an acute interstitial pneumonia results from purulent
pleuritis (pleurogenous pneumonia), not unlike the pleuropneumonia of cattle.
Chronic forms of interstitial pneumonia are met with in the pneumonoconioscs
(q. v.}, and sometimes in tuberculosis (q. v.).
III. THE SPECIFIC INFLAMMATORY PNEUMOPATHIES
Under this heading are included (a) pulmonary tuberculosis, (b)
syphilis of the lung, and (c) certain other processes such as actinomycosis,
streptothricosis, glanders, blastomycosis, and aspergillosis.
(a) Pulmonary Tuberculosis
(Phthisis pulmonum)
Definition. — A chronic disease of the lungs and bronchi due to infection
with the tubercle bacillus.
Historical. — The disease was known to the ancients, and there are easily
recognizable descriptions of it in the works of Hippocrates. Sylvius in
the seventeenth century thought the nodules (tubercles) were enlarged
lymph glands. Baillie at the end of the eighteenth century discovered the
miliary tubercle; he distinguished also between conglomerate tubercles
and caseous pneumonia. Great advances in clinical and pathological
knowledge of the -disease were made by the French physicians (Bayle,
Laennec, Broussais) early in the nineteenth century. Virchow (1847-
1852) made careful studies of the histology of tubercle, and Villemin
(1865-1868) by a series of brilliant experiments on animals, established
the transmissible and infectious character of the disease, showed the
especial susceptibility of guinea-pigs, and asserted that the disease was
transmitted from man to man by a virus present in the sputum. Vii-
614 DISEASES OF THE RESPIRATORY APPARATUS
lemin's views were at first disputed, but were soon corroborated by many
workers, and notably by Cohnheim and Salomonsen, who devised the
method of demonstrating the presence of the virus in pathological mate-
rials by inoculation of the anterior chamber of the rabbit's eye. The
common nature of the virus in pulmonary tuberculosis, joint tuberculosis,
gland tuberculosis, etc., was next established.
In 1882, the proof of the bacterial nature of the virus was brought
by Robert Koch ; he discovered, stained, and grew the Bacillus tuberculosis,
and reproduced the disease by inoculation of pure cultures. A simple
differential stain for this "acid fast" bacillus, very important as a diag-
nostic aid, was devised by P. Ehrlich. Extracts of the bacilli, known as
tuberculin, were made by Koch, and used both for diagnostic and thera-
peutic purposes. Soon thereafter began the great campaign for the pre-
vention and cure of tuberculosis (dispensaries, sanatoria, national and
international conferences).
Pathology. — Tuberculous inflammations of the lung occur in two forms :
(1) tuberculous granulation (with tubercle formation), and (2) caseous pneu-
monia. The former is a productive, the latter an exudative inflammation. The
former develops in the interstitial tissue; the latter fills the alveoli with exudatc.
Both are due to the same bacillus, and the two processes may go on together in
the same lung. Formerly, one out of every six or eight deaths was due to tuber-
culosis; but in recent years the mortality rate from the disease has begun to
decrease.
Of the main types of pulmonary tuberculosis may be mentioned:
1. ACUTE DISSEMINATED MILIARY TUBERCULOSIS (distribution of bacilli through
the blood; usually part of a general iniliary tuberculosis; where only one lung or
one lobe is involved, the distribution may be bronchogenous from coughing).
2. CHRONIC PULMONARY TUBERCULOSIS (beginning usually in the apices, and
gradually extending to the lower portions of the lungs and to the pleurae, healing
with induration in some places, extending, or softening, in others).
3. ACUTE TUBERCULOUS PULMONARY PHTHISIS (like 2, with signs of rapid
cavity formation, or with extensive caseous pneumonic processes, in the most rapid
cases giving rise to galloping consumption).
Etiology. — Pulmonary tuberculosis is due to reactions of the lungs to
infection with Koch's Bacillus tuberculosis; the disease is, however, often
complicated by mixed infections with other bacteria (influenza bacilli,
streptococci, pneumococci, etc.), these mixed infections accounting for
much of the fever and cachexia, and, perhaps, for the amyloid degeneration
of the organs that sometimes occurs. To understand hpw the disease de-
velops (phthisiogenesis), it is necessary to study not only modes of infec-
tion, but also the conditions of disposition. Tuberculous infection occurs
in everyone that lives to become an adult; the progressive disease that
leads to pulmonary phthisis develops in not over one-tenth of these.
Modes of Infection. — The bacilli reach the lung in various ways, sometimes
by aspiration or aerogenous infection (droplet infection, laryngeal tuberculosis,
DISEASES OF THE LUNGS 615
tonsillar tuberculosis), sometimes by lymphogenous or hematogenous infection,
through the lymph channels or the blood channels (secondary to tuberculous otitis,
tuberculous enteritis, tuberculous adenitis, tuberculous pleuritis, etc.).
When the Bacillus tuberculosis was first discovered, it was thought that aspi-
ration of the bacilli explained the source of human infection in nearly all cases.
Later studies have led to the consideration of many other modes of infection.
Experimental studies on animals have been extensively made, and the effects
of intravenous, subcutaneous, intra-ocular, and intraperitoneal inoculation, as well
as of feeding experiments and inhalation experiments, have been carefully watched.
And, in general, it may be said that, aside from direct inoculation into the blood
stream, there is always first, no niatter what the portal of entry, an involvement
of the regional lymph glands, this involvement of the lymphatic apparatus often
occurring without signs of pathological change at the actual portal of entry.
Studies of tuberculous human beings indicate that human infection does, in
reality, occur in several different ways. CONGENITAL INFECTION is rare, but has
been indisputably proven to take place;, it is not a germinal infection, but comes
always from the mother through placental tuberculosis. INTESTINAL INFECTION,
as primary, has recently, through the studies of Behring, of Heller, and of Coun-
cilman, Mallory and Pearce, assumed considerable importance. In children, pre-
viously apparently healthy, dying of diphtheria, about 6 per cent are found to
show signs of primary intestinal tuberculosis (in the mesenteric lymph glands).
About half the cases of primary infection through the intestine are due to the
bovine type of bacillus, the other half to the human type. TONSILLAR AND
MOUTH INFECTION, as shown by tuberculosis of the cervical lymph glands, is very
common in childhood; how often it leads to pulmonary tuberculosis is not known;
when it does so, the bacilli reach the lungs in all probability by passing from the
cervical glands to the lung, neither by way of the bronchial glands nor by way
of the lymphatics to the pleura, but rather by entrance, first, into the venous
system and thence through the right heart to the lungs. INHALATION INFECTION
OR AEROGENOUS INFECTION is held by many to be the commonest mode of contract-
ing pulmonary tuberculosis. The evidence is strongly in favor of this view for
chronic pulmonary tuberculosis beginning in the apices, the apices being especially
predisposed on account of (1) the minimal energy of the movement' of the air
during expiration there, and the corresponding lessened energy of the lymph
current in the same situation (Tendeloo), and (2) the predisposing influence of
stenosis of the upper aperture of the thorax in persons of the habitus
plithisicus due to congenital shortening and ossification of the cartilage of the
first rib (W. A. Freund), this peculiarity of the first rib giving rise to a groove-
like constriction of the apex of the lung (Schmorl) and to a faulty development
of the bronchial tree at the apex (Birch-Hirschfeld), conditions that, when
experimentally simulated, predispose strongly to both aerogenous and hema-
togenous tuberculous infection of the apices in animals (Bacmeister). Acute
pulmonary tuberculosis, (acute or galloping consumption) arises, however, in a
different way; thus in the lobar or pseudolobar caseous pneumonia, the cause is
most often found to be the aspiration of large numbers of tubercle bacilli either
from a tuberculous lymph gland perforating into a bronchus, or from a tuber-
culous cavity due to a preexisting chronic tuberculosis, and in the disseminated
form of acute tuberculosis the miliary tubercles may arise either through a
bronchogenous distribution of the bacilli (through coughing or through aspira-
tion) or through a hematogenous distribution (through rupture of a caseating
focus into one pulmonary artery).
The tubercle bacilli have their source chiefly in tuberculous human beings,
partly in tuberculous animals (cows). Infected human beings may give off
616 DISEASES OF THE RESPIRATORY APPARATUS
bacilli in various ways ; by far the most important discharge is tuberculous sputum,
though urine, feces, pus, discharge from lupus, etc., may occasionally be respon-
sible. The bacilli of sputum may reach other persons by direct contact (fingers,
kissing), by the spray produced by coughing (droplet infection of Fliigge), and by
dust containing dried sputum (careless expectoration), especially in dwelling-
houses, hotels, theaters, factories, and shops, since street-dust seems rarely to be
responsible.
Uncooked inilk, cream, and butter may spread the bovine type of the bacillus;
meat is less often responsible. About half the cases of tuberculosis of the intestine
and the mesenteric glands are due to the bovine type; it is rare, however, to find
the bovine type in human pulmonary tuberculosis.
Conditions of Disposition. — Most people — probably all — that live to be
thirty years of age become infected with the tubercle bacillus. Fortu-
nately, the infection does not cause sickness in the majority. As has often
been emphasized, every infectious disease is the product of infection and
disposition. In order that the disease occur, the relations of infection
and disposition must be such "that the sum of both is larger than in patients
that do not sicken" (Staehelin). There appears to he a l»»ral (iixj><>xili<>n
to pulmonary phthisis as well as a constitutional predisposition to tuber-
culous infection ; all men Lave some of the latter, but the former is often
a family affair. Thus, one predisposed to pulmonary phthisis may have
a long narrow thorax (thorax phthisicus) with short and early-ossified
first-rib cartilage (see above), hypoplasia of the heart and of the aorta,
and visceroptosis (habitus asthenicus). Besides the hereditary local pre-
disposition, there are other accidental predisposing factors: namely (1)
certain infectious diseases (measles, whooping-cough, influenza) ; (2) the
pneumonoconioses (anthracosis, siderosis, chalicosis, etc.) ; (3) prolonged
physical or mental over-exertion; (4) prolonged under-nutrition and life
under non-hygienic conditions; (5) diabetes; and (6) pregnancy. On
the other hand, pulmonary tuberculosis is rare in persons that suffer
from emphysema or from chronic heart disease. On the side of expo-
sure, frequent contact with infected persons, leading to multiple reinfec-
tions, is undoubtedly of great importance in the development of the disease.
When tuberculosis is suspected, therefore, the anamnesis should be taken with
especial care. One should gather data on the following points:
1. Is there any history of tuberculosis, pleurisy, scrofula, meningitis, or hip-
joint disease in the family (parents, sibs, husband or wife, children), or has the
patient lived in a house or worked in a shop with infected persons?
2. Has the patient himself previously suffered from hemoptysis, pleurisy,
hoarseness, cough or enlarged glands?
3. Has the patient been exposed to great hardship or overwork, or, if a
woman, to many pregnancies or to prolonged lactation?
4. Does the occupation of tire patient predispose (exposure to dust, wet and
cold; alcoholism, etc.)?
5. Has the patient recently lost weight or suffered from cough, with sweats
or with unexplained digestive disturbances?
Clinical Examination. — Tuberculous patients often present a character-
DISEASES OF THE LUNGS 617
istic appearance, the so-called phthisical constitution (habitus phthisicus).
They may look pale, thin and feeble, have a delicate bony framework, with
a long, narrow, flattened thorax with wide intercostal spaces (thorax par-
alyticus, expiratory type of thorax). The pulse and the respiration are
often accelerated. There may be intermittent fever (febris hectica), with
tendency to night sweats. The hair may look unhealthy, the sclerae bluish,
and there is often a skin infection, pityriasis versicolor. Search should
always be made for signs of previous scrofula or of infantile tuberculosis
(scars in the neck, corneal opacity, bone and joint lesions).
i. Ordinary Chronic Forms of Pulmonary Tuberculosis
^.
For convenience, it is customary to distinguish three stages or degrees
of the ordinary form of pulmonary tuberculosis.
Stage 1. — Initial, incipient or developmental period (phthisis incipiens).
Staged. — Stage of well established infiltration (phthisis confirmata).
Stage 3. — Terminal stage, with signs of cavity formation (phthisis
consummata, stadium colliquationis).
In referring patients to sanitaria or to other physicians for treatment,
it is customary to speak of three grades, or classes, of patients.
1. Mild cases, in which the disease is limited to a small area in one lobe,
especially at one apex, but not extending below the clavicle or the spine
of the scapula, and with or without fine rales that are non-consonating.
2. Cases of medium severity, the disease extending beyond the limits
of 1 but not as far as 3.
3. Advanced 'cases with involvement of one whole lobe or of several
lobes, or with signs of cavity formation.
EPITOME OF THE PHYSICAL SIGNS. — Stage 1 (Phthisis incipiens, Api-
cal Catarrh). — Rales are usually audible at one apex in front or behind;
these may be either fine crepitant rales or rhonchi. The respiratory mur-
uni r is either enfeebled or roughened, with prolongation of the expiratory
sound, cog-wheel breathing or indefinite breathing. The percussion note
may be normal, or only slightly shorter and a little higher pitched than nor-
mal; usually there is demonstrable narrowing of the area of apical reso-
nance. Occasionally, a slight lagging of the movement of the affected side
can be made out on inspection. Dry cough is a common symptom, especially
in the early morning, with scanty sputum or none; tubercle bacilli are
occasionally demonstrable in the sputum, but by no means always. Hemop-
tysis is not uncommon.
The student should remember that a, chronic catarrh of one apex is
most often tuberculous in nature. This is an extremely common disease,
though in the majority of instances it heals, leading only relatively rarely
to a progressive phthisis.
Several varieties of phthisis incipiens have been distinguished. Thus
Staehelin includes (a) a catarrhal form, resembling at onset an ordinary
618 DISEASES OF THE KESPIKATOKY APPAKATUS
bronchitis after catching cold; (b) an anemic form, in which anemia,
palpitation and tachycardia are striking symptoms ; (c) a dyspeptic form,
in wjhich disturbances of digestion bring the patient to the physician; (d)
a febrile form, in which an obscure fever may last for some time before
the pulmonary origin becomes recognizable ; (e) a pleuritic form, in which
either a dry or a wet pleurisy is the first recognizable change ; (f ) a hemop-
toic form, in which the first sign is the spitting of blood ; and, finally, (g) a
traumatic form, in which the signs of pulmonary tuberculosis develop a
few weeks or months after a contusion of the chest.
Stage 2 (Phthisis confirmata, Stage of Definite Infiltration). — At this
stage, the disease extends beyond the apex. The dullness in front, above
the clavicle, is continuous with dullness as far down as the second or the
third rib, and, behind, there is dullness in the fossa supraspinata ; usually
slightly tympanitic resonance can be made out in the corresponding upper
Anterior View. Posterior View.
Fig. 170. — Regions of the Thorax Over Which Percussion and Auscultation ShOuld Be Carried
Out Systematically In Suspected Tuberculosis
/
chest on light percussion. Over the dull area, even bronchial breathing,
with dry and moist rales, often consonating, is audible. Whispered voice
sounds are markedly increased in affected areas. When, on the right, rales
are audible as low as the third intercostal space or the fourth rib, the mid-
dle lobe has become involved as well as the upper. There is diminished ex-
pansion, or lagging, on the affected side, often with signs of retraction
of the upper lobe. As the disease extends gradually downward in the
lung first affected, the apex of the other lung usually becomes involved.
The sputum is more abundant than in the first stage, is mucopurulent,
and usually contains tubercle bacilli. There may, or may not, be fever.
Usually there is a gradual, sometimes a rapid, loss of body-weight. Hem-
optysis is not uncommon.
This stage of pulmonary tuberculosis must -be differentiated from (1)
simple chronic bronchitis, (2) bronchiectasis, (3) the pneumonoconioses,
and (4) chronic non-tuberculous pneumonias.
DISEASES OF THE LUNGS 619
Stage 3 (Phthisis consummates, Advanced Tuberculosis with Cavity
Formation). — This last stage is characterized by widespread infiltration
of both lungs, and, especially, by the formation of cavities. The extent
of the infiltration can be determined by demonstration of the areas over
which tympanitic dullness, bronchial breathing, increased fremitus, rales
and bronchophony exist. Both lungs are involved; sometimes the lower
lobes as well as the upper are infiltrated. Retraction of the upper lobes,
"due to fibroid change, causes contraction of the upper thorax with deepening
of the supra- and inf raclavicular fossae and of the upper intercostal spaces.
Signs of cavity formation are usually present (bubbling rales, metallic
tinkling, loud bronchial or amphoric breathing, cracked-pot resonance,
change of pitch on percussion). The sputum is mucopurulent, free from
air bubbles, often nummular or coin-shaped, and loaded with tubercle
bacilli ; sometimes it contains elastic fibers or blood.
In this terminal stage, the fever is often high, due to mixed infection
with pyogenic cocci, but it may be subnormal. Night sweats are a trouble-
some symptom. The emaciation may become extreme.
The diagnostic tuberculin tests (von Pirquet, Calmette, etc.) and other
points bearing upon diagnosis are described in the section on Infectious
Diseases.
Acute Form of Pulmonary Tuberculosis
(Phthisis florida. Galloping Consumption)
Under this heading we include (a) the pneumonic form, and (b) the
multiple focal form.
(a) PNEUMONIC FORM, INCLUDING CASEOUS PNEUMONIA. — In the
peracute cases, the onset may resemble that of ordinary lobar pneumonia,
except that there is rarely any chill, the fever is less regular" and the sputum
not rusty. Death may occur within two weeks (primary alveolar pul-
monary tuberculosis of Heller and Hedinger).
In less acute cases, the onset may be similar, suggesting croupous pneu-
monia, but the course is somewhat less rapid than in the peracute cases
above described. The sputum may be gelatinous, greenish, though some-
times it is rusty. Tubercle bacilli may be present at first, though as a rule
they are not found until later. Pneumococci may be present in considerable
numbers and help to mislead the diagnostician. An early and intense
diazo-reaction in the urine speaks for caseous pneumonia rather than for
ordinary lobar pneumonia. The practitioner may first have his eyes
opened by the failure of a crisis to appear and the persistence of the infil-
tration beyond the ordinary period of lobar pneumonia. Coarse rales de-
velop and a little later perhaps typical cavernous symptoms. The sputum
becomes nummular; the fever becomes irregular; and the patient goes
rapidly down hill. Death often occurs at the end of six weeks just as
620 DISEASES OF THE RESPIRATORY APPARATUS
cavities are beginning to form.. Some patients, linger on until large cavi-
ties form ; in such instances, the disease may become temporarily arrested,
and the patients regain some health and strength, but, as a rule, even then,
cure does not occur, the patients dying ultimately with the signs of chronic
cavernous pulmonary tuberculosis.
(b) DISSEMINATED FORMS OF ACUTE TUBERCULOSIS. — Galloping con-
sumption, instead of taking the pneumonic form above described, may be
due to the simultaneous development of multiple foci, usually involving
both lungs. Three main types may be distinguished: (1) a disseminated
ulcerating form, most often met with in diabetes and in chronic alcoholism ;
(2) a hemoptoic form, in which the bacilli are distributed with the blood
in the alveoli, death often occurring within a month after the hemorrhage ;
and (3) an acute peribroncJiitic or nodular form, due to aspiration of
bacilli into many small bronchi.
The patients may, on the one hand, have been apparently entirely
healthy before; on the other hand, such an acute disseminated focal tuber-
culosis may develop in patients that have had a simple apical tuberculosis
or in those that have suffered for some time from ordinary chronic pul-
monary phthisis. Such acute outbreaks are most common in persons that
have but little or no immunity to tuberculosis, either because they have not
suffered from earlier mild infections (doubtless responsible for the rela-
tive immunity of most adults), or because immunity has in some way been
greatly lowered (diabetes, influenza, pregnancy, lactation, alcoholism).
The diagnosis may be especially difficult in the acute peribronchitic
form in persons apparently healthy before. The condition is often
wrongly diagnosed as a persistent influenza, as typhoid fever, or as acute
miliary tuberculosis. We have to rely upon most careful physical exami-
nations frequently repeated, bacteriological studies of the sputum and
blood, immunological tests (Widal, Calmette), the presence or absence of
changes in parts of the body other than the lungs (meninges, choroid, intes-
tines, etc.), and rontgenographic studies.
In the ulcerative form the diagnosis soon becomes clear, and in the
hemoptoic form there is rarely difficulty.
Complications of Pulmonary Tuberculosis. — Among the complications
of pulmonary tuberculosis may be mentioned pleuritis, laryngeal tubercu-
losis, intestinal tuberculosis, peritoneal tuberculosis, and general miliary
tuberculosis. Spontaneous pneumothorax occasionally occurs. In advanced
cases there may be amyloid degeneration of the organs (splenomegaly,
diarrhea, albuminuria). Tuberculosis is often made worse, by pregnancy.
Acute respiratory infections complicating tuberculosis are prone to lower
resistance (influenza, pneumonia, measles, pertussis).
Causes of Death. — In fatal cases, death may occur from asphyxia-
tion due to extensive involvement, from hemorrhage (hemoptysis), or from
pleural complications (empyema, pyopneumothorax) ; occasionally, it
DISEASES OF THE LUNGS
621
results from cardiac failure (chronic intoxication, pulmonary obstruc-
tion). In a few cases, death is due to general miliary tuberculosis or to
general amyloid degeneration. Not infrequently, in advanced stages, death
is due to an intercurrent infection (lobar pneumonia, influenza, strepto-
coccus sepsis).
Rontgenography and Rontgenoscopy in Pulmonary Tuberculosis —
Examinations by means of Rontgen rays are less important for the diagnosis
of the existence of pulmonary tuberculosis than for the recognition of the
extent of the disease and the distribution of the pathological foci in the
Fig. 171. — Pulmonary Tuberculosis. Extensive Infiltration Found in a Medical Student, Who
Had Worked Up to a Few Days Before, Unaware of Infection. (X-ray Dept., J. H. H.)
lungs. In x-ray plates of the lungs, infiltrations throw a shadow, whereas
cavities appear as clear areas.
The shadows due to infiltration are not evenly diffuse, but arc mottled.
Some experience is necessary in interpreting the x-ray plates, since nor-
mally the hilus of the lung and the bronchial tree cause some mottling.
Mere enlargement or increased intensity of the hilus shadows, even with
strandlike shadows radiating toward the apices, are to be very cautiously
interpreted. The meaning of the hilus shadows is only gradually being
worked out. Changes in these hilus shadows are undoubtedly sometimes
due to tuberculosis, but they may also follow upon non-tuberculous proc-
esses (chronic lymphadenitis simplex, chronic passive congestion, chronic
622 DISEASES OF THE RESPIRATORY APPARATUS
bronchitis, etc.). When, however, the mottling is asymmetrical, or is seen
in the periphery of the lung area, or extends downward from a diffuse
shadow at one apex, it is to be regarded as very suspicious of tuberculosis.
Rontgenoscopy alone is insufficient for the study of pulmonary tubercu-
losis, though it is often very helpful for a general preliminary orientation.
Rontgenography is, as a rule, necessary, and soft tubes yielding good con-
trasts should be used. It is best to take (1) a view of the whole chest on a
large plate (30 X 40 or 40 X 50 cm.) at a focal distance of 50-60 cm., the
Fig. 172. — Tuberculosis; Thickened Pleura on Left; Cavity on Right. Which Was Obscured
by Thickened Pleura, as Was Shown at the Post Mortem; Adhesions on Right Side.
The Arrows Indicate Pleural Thickening on the Right Side Over a Cavity. (X-ray 1 >••]>!.,
J. H. H.)
rays being passed through in the dorsoventral direction, so as to avoid too
much bone shadow, and (2) a partial view of an apex down to the
hilus on a smaller plate (24 X 30 cm.), using a tube or diaphragm and a
focal distance of 40 cm. Stereoscopic plates are especially helpful.
Pleural thickenings may be recognizable as diffuse shadows. Adhe-
sions to the diaphragm may give rise to projections or puckerings of the
upper surface of the diaphragm as seen in the x-ray plate. Calcification
of the cartilage of the first rib should always be looked for. Often intense
circumscribed shadows will be found near the hilus or toward one apex;
DISEASES OE THE LUNGS
623
they usually indicate calcified lymph glands or lime deposits in healed foci
of tuberculosis in the lung.
A cavity appears in an x-ray plate as a clear, round area, surrounded
by a ring-like shadow. The' latter is well brought out if the exposure be
made through a narrow diaphragm. Of course, if the cavity be filled with
sputum, it will 'give rise to a shadow in the rontgenogram instead of to a
clear area. Irregularities in the wall of a cavity, or subdivision of the
cavity into several chambers, can occasionally be made out.
The respiratory movements are changed in pulmonary tuberculosis ;
Fig. 173. — Generalized Tuberculosis of the Lungs. Arrows Show Cavity in Left Upper Lobe.
(X-ray Dept, J. H. H.)
less air is taken into the diseased lung on inspiration and the diaphragm
excursion is less (Williams' symptom) ; this phenomenon is often demon-
strable by rontgenoscopy in incipient apical tuberculosis. This symptom
is, however, less valuable for diagnosis than was formerly thought, since it
is demonstrable in only a minority of the cases, and, moreover, may be
present in cases of healed tuberculosis.
Valuable as x-ray examinations are in the study of pulmonary tubercu-
losis, it must be emphasized that there are often marked discrepancies
624 DISEASES OF THE KESPIRATOKY APPARATUS
between x-ray findings and the general physical findings (F. H. Baotjor
and L. Hamman). Either may help to a positive diagnosis when the
other is almost negative. As a rule, however, the x-ray examination reveals
in positive cases, a wider distribution of the tuberculous process than
would be suspected from the examination by percussion and auscultation.
In the third stage of pulmonary tuberculosis, with extensive infiltra-
tion and cavities, the x-ray plate gives a better idea of the extent of the
process than any other method of examination.
During the treatment of pulmonary tuberculosis by production of arti-
Fig. 174. — Artificial Pneumothorax. Arrows Indicate Collapsed Lung ; Crosses Indicate Pneu-
mothorax. (X-ray Dept., J. II. H.)
ficial pneumothorax (Forlanini), x-ray examinations offer an excellent
method of control.
For other facts regarding pulmonary tuberculosis see Section on In-
fectious Diseases.
References
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626 DISEASES OF THE KESPIKATOEY APPAKATUS
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DISEASES OF THE LUNGS 627
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DISEASES OF THE LUNGS 629
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Colliver (J. A.). Cutaneous regional variation in the Pirquct reaction. Arch. Pediat., New
York, 1915, xxxii, 92-95.
Crow (G. /?.)• Sime prevailing ideas regarding the treatment of tuberculosis. U. Navy M.
Bull., Washington, 1914, viii, 541-554.
Davies (H. M.). The indications for surgical intervention in pulmonary tuberculosis. Brit.
J. Tuberc., London, 1915, ix, 12-16.
Dearholt (H. E.} & Cheadle (C. M.). Are physicians square with their tuberculosis
patients? Wisconsin M. J., Milwaukee, 1914-15, xiii, 333-345.
Debains (E.) & Jupille (F.}. Sur le sero-diagnostic dc la tuberculose. Ann. de Vlnst.
Pasteur, Paris, 1915, xxix, 182-189.
Devoto (L.)* Le lejioni non tubercolari dett'apice polmonarc. Atiualitd Med., Milano, 1914,
in, 625-650.
Dobbie (W. J.}. The diagnosis of intra-thoracic tuberculosis in children. Nat'l Ass. Study
& Prcv. Tuberc., Baltimore, 1915, 93-100.
Dunham (Kennori) . Stereoroentgenography: Pulmonary tuberculosis. Troy, N. Y.,1915,
The Southworth Co. 83 p. 4°-
Pulmonary tuberculosis as studied by the stereo-roentgenogram. Lancet-
Clinic, Cincinnati, '1912, cvii, 514-517.
Ferrannini (L.). Contributo allo studio delle lesioni non tubercolari delVapice polmonare.
Riforma Med., Napoli, 1915, xxxi, 113; 141.
Fetterolf (G.}. The larynx in one hundred cases dying of pulmonary tuberculosis: a clin-
ical post-mortem study. Tr. Am. Laryngol. Ass., New York, 1914,
xxxvi, 258-272.
Forbat (A.). Ueber "Splitter" im Sputum von Phthisikern. Deutsche med. Wchnschr.,
Leipzig, 1913, xxxix, 949-750.
630 DISEASES OF THE EESPIEATOEY APPAEATUS
Forlanini (C.). Zur Behandlung der Lungenschwindsucht durch kunstlich erzeugten Pneu-
mothorax. Deutsche med. Wchnschr., Leipzig u. Berlin, 1906, xxxii, 1401-
1405.
Frdnkel (M.). Die Rontgenstrahlen im Kampf gegen die Tuberkidose, speziell der Lungen.
I. Fortschr. a. d. Geb. d. Rontgenstrahlen, Hamburg, 1914-15, xxii, 482-
501.
Friedenwald (//".)• The dangers of the ophthalmic tuberculin test. Am. Med.) Burlington,
Vt. & New York, 1914, n. s., ix, 568-572.
Giffin (H. Z.) & Sheldon (W. D.). Clinical and radiologic findings in pulmonary tuber-
losis; the value of cooperative diagnosis. Journal-Lancet, Minneapolis,
1915, xxxv, 223-229.
Glover (E. <7.)« The early diagnosis of pulmonary tuberculosis. Quart. J. Med., Oxford,
1915, viii, 839-355.
Gorse (P.) & Dupuich (A.). Tuberculose pulmonaire et chirurgie. Rev. d. chirurg.,
Paris, 1913, xxxiii, 221-262.
Gray (E. A.) & Pickmann (Olga). Pancreatic ferment determination in pulmonary tuber-
culosis. J. Am. M. Ass., Chicago, 1915, Ixv, 1271-1273.
Hamman (L.) & Baetjer (F. H.). Pulmonary physical signs and Roentgen ray findings
in healthy adults. Arch. Int. Med., Chicago, 1914, xiv, 7 57-768.
Hamman (//.) & Sloan (M. F.). Induced pneumothorax in the treatment of pulmonary
disease. Johns Hopkins Hosp. Bull., Baltimore, 1913, xxiv, 53-62.
Hart (C.). Ucber Muskelatrophie und Muskelstarre am Brustkorb dcs Phthisikcrs. Med.
Klin., Berlin, 1914, x, 1689-1692.
Hartshorn (W. M.). The Roentgen ray in the diagnosis of pulmonary conditions in chil-
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Hawes (J. B.), Jr. Under what conditions is the diagnosis of " tuberculosis" in children,
justified? Boston M. cfc S. J., 1914, ctxx, 7S4-786.
Intrathoracic tuberculosis in infancy and childhood, including bronchial
gland tuberculosis. Interstate M. J., St. Louis, 1914, xxi, 300-3().>.
Hawes (J. /?.). The problem of infection in tuberculous families. Boston M. & S.J., 1914,
clxxi, 217-220.
Remarks on the diagnosis and treatment of early pulmonary tuberculosis.
Boston M. & S. J., 1914, clxxi, 346-349.
Henschen (C.). Results and prospects of surgical treatment of tuberculosis of the lungx <tn,<l
of bronchiectasis. Tr. Am. Surg. Ass., Philadelphia, 1914, xxxii, 547-
591.
Holzknecht (G.)» Die rocntgcnologische Diagnostik der Erkrankungcn der Brusleingcweide.
Hamburg, 1901, Grafe & Silleur. 229 p.
Jordan (A. C.). Some points in the diagnosis of pulmonary tuberculosis by the X-rays.
Lancet, London, 1914, i, 963-964.
Kinghorn (H. M.) & Twichell (D. C.). A clinical stwly of (he complement-fixation test
in the diagnosis of pulmonary tuberculosis. Ztschr. f. TuberkuL, Berl.t
1913, xx, 11-21.
Klotz (W. C.). A study of Kroenig's isthmus in pulmonary tuberculosis. Tr. Nat'l Ass.
Study & Prev. Tuberc., Baltimore, 1915, 88-92.
Kohler (A.}. Rontgenbefunde bei chirurgischcr Tuberkulose. Tuberculosis, Berlin, 1915,
xiv, 25-27.
Kovacs (/.)• Ueber einige Streitfragen hinsichtlich der Bedeutung der latenten Lungen-
tuberkulose. Arch. f. path. Anat., etc., Berlin, 1913, ccxiii, 405-411.
Kraus (F.~). Die Erkennung der Tuberkulose, mit vorwiegender Berucksichtigung der Friih-
diagnose. ' Ztschr. f. arztl. Fortbild., Jena, 1904, i, 60-68.
Kuhn (E.). Weitere Erfahrungen mit der Hyperdmiebehandlung der Lungen vermittels der
Lungen-Langmaske. Munchen. med. Wchnschr., 1907, liv, 782-786.
Kiipferle (L.). Ueber Rontgentiefentherapie der Lungentuberkulose. Strahlentherapie, Ber-
lin u. Wien, 1914-15, Orig., v, 655-667.
DISEASES OF THE LUNGS 631
Kuthy (D. O.) & Wolff-Eisner (A.}. Die Prognosenstellung bei der Lungentuberkulose
mit eingehender Beriicksichtigung der physikalischen und serologischen
Befunde und der therapeutischen Prognostik. Berlin & Wien, 1914, Urban
& Schwarzenberg. 588 p. 8°.
Lampe (A. E.) & Cnopf (/.)• Serologische Untersuchungen bei Lungentuberkulose mit
Hilfe der oplischen Methode. In: Fermenlforschung (Abderhalden) Leip-
zig, 1915, 269-310.
Landis (H. R. M.) & Kaufman (/.)• The diagnosis of tuberculosis in early life. Am. J.
M. Sc., Philadelphia, 1914, cxlviii, 530-539.
Lapham (Mary E.). The surgical treatment of pulmonary tuberculosis. Boston M. & S. J.,
1913, clxix, 676.
Lau (H.}. Ueber menstruelle Temperatursteigerungen bei Lungentuberkulose. Ztschr. f.
Tuberk., Leipzig, 1914, xxii, 534-546.
Leslie (R. M.). Hilus tuberculosis (root phthisis). Brit. J. TubercuL, London, 1913,
vii, 160-170; Tr. Internal. Cong. Med., 1913, London, 1914, Sect. VI,
Medicine, pt. 2, 485-492.
Locke (E. A.). The nutrition of anemic and tuberculous children. Boston M. & S. J., 1913,
clxix, 701-707.
Maragliano (V.). La rontgendiagnosi nella tuberculosi polmonare. Tuberculosi, 1913,
v, 217-221.
Mircoli (Stefano}. Sul determinismo delle alterazioni nevro-psichiche nei tubercolosi; re-
sponsabilild dei tubercolosi. Napoli, 1914, V. Idleson. 330 p. 4°.
Moore (A. B.}. Radiography in the diagnosis of pulmonary tuberculosis. Interstate M. «/.,
St. Louis, 1914, xxi, 326-329. 2 pi.
Morton (R.). Skiagrams of early pulmonary tuberculosis in children. West. Lond. M. J.,
1915, xx, 121-124.
Niles (W. L.). The clinical index of the thorax associated with pulmonary tuberculosis.
J. Am. M. Ass., Chicago, 1909, Hi, 1916-1918.
Osier (W.). Acute tuberculous pneumonia. Brooklyn M. J., 1905, xix, 57-61.
Overend (W.}. The incipient pulmonary phthisis of school children. Brit. M. J., London,
1914, ii, 1009-1014.
Owen (S. A.}. The value of radiography in the early detection of tuberculosis of the lungs
from the standpoint of the physician. Tr. Internal. Cong. Med., 1913,
London, 1914, Sect, xxii, Radiol, pt. 2, 113-127.
Owen (S. A.} & Morton (E. R.). The value of radiography in the early detection of tuber-
culosis of the lung and mediastinum. Arch. Roent. Ray, London, 1913-14,
xviii, 87-97, 101-103.
Par fit t (C. D.) & Crombie (D. W.). Artificial pneumothorax in the treatment of phthisis.
Canad. M. Ass. J., Toronto, 1915, v, 277; 373; 489.
von Pirquet (C.). Die traumatische Cutanreaktion. Ztschr. f. d. ges. exper. Med., Berlin,
1914, iv, 181-209.
Pottenger (F. A/.). Tnspektion, Palpation, Perkussion und Auskultation bei der Fruh-
diagnose der Lungentuberkulose. Beitr. z. Klin. d. Tuberk., Wurzburg,
1914, xxiii, 49-76.
Rach (E.). Radiologisch erkennbare anatomische Typen der kindlichen. Lungentuberkulose.
Miinch. med. Wchnschr., 1914, Ixi, 642-G45.
Radcliffe (J. A. D.}. Complement fixation in pulmonary tuberculosis. J, Hyg., Cambridge,
1915, xv, 36-50.
Ranke (K. E.}. Zur Diagnose der kindlichen Tuberkulose. Munchen. med. Wchnschr.,
1914, Ixi, 2099; 2134.
Ritter (/.)• Early 'recognition of pulmonary tuberculosis by study of lymphocytic picture and
albumin contents of sputum. J. Am. A. Ass., Chicago, 1914, Ixiii, 2283-
2285.
Sachs (T. B.). Artificial pneumothorax in the treatment of pulmonary tuberculosis. Nat'l
Ass. Study & Prey. Tuberc., Washington, 1915, 150-158.
632 DISEASES OF THE RESPIRATORY APPARATUS
Schrotter (L.). Veranderungen im Larynx bei Tuberculose der Lungen. Jahresb. d. Klin.
f.Laryngosk. a. d. Wien. Univ. (1870} , 1871, 56-61.
Schut (//.)• Die Lungentuberkulose im Rontgenbilde. Beilr. z. Klin. d. Tuberk., Wurz-
burg, 1912, xxiv, 145-191.
Sergent (E.}. The tendency of current medical opinion at the present time to unduly extend
the domain of tuberculosis; being a criticism of certain methods of diagnosing
tuberculosis. Monde med., Paris, 1915, xxv, 5-21.
Skinner (E. H.}. Roentgentherapy in tuberculosis; a review of recent literature. Interstate
M. J., St. Louis, 1914, xxi, 483-489.
Sluka (E.}. Ubcr die Haufigkeit der SpUzenluberkulose im Kin.dc sailer. Wien. Iditi.
Wchnschr., 1914, xxvii, 173-179.
Slyfield (F.). Essential points in the early determination of tubercle. Nat'l Ass. Study <fc
Prey. Tuberc., Baltimore, 1515, 132-139.
Stiles (//. /.)• Treatment of tuberculosis in childhood from (he surgical pain.t of view, with
special reference to the bones, joints and glnn.:!*. 7V. I nt''nn<t. Co/,1.'/. Med.,
1913, London, 1914, Sect. X, Dis. Child., 39-91. [Discussion], 7-11.
Stoll (H. F.). Tuberculosis in the aged and the diagnostic value of increased whisper in, I he.
interscapular space. Boston M. & S. J., 1912, clxvii, 869-874-
Stone (A. K.}. Subnormal temperature in tuberculosis. Boston M. & S. ,/., 1914, clxxi,
1008-1011.
Tanszk (F.~). Die asfhmaiischcn Formen der Lungentuberkulose. Ztschr. f. Tuberktd.,
BerL, 1913, xxi, 110-1 .>..'.
Thompson (E.) & Gall (II. L.). A possible m-w X-ray sign of tuberculosis. lr.
Nav. M. Bull., Washington, 1915. ix, 436-43S. 3 pi.
Tidy (H. J.}. Tlic relation of tnbercnloxix to ollur J/'.sr'/.srx, including pregnancy. Prac-
titioner, London, 1914-15, xc.iii, 359-3(17.
Tuffier (T.}. Immobilisation ct compression fA-.s- deux sommets du poumon pour
j>:/!>ni>n(!.irc. Decollemeni plciiro-itnrn-lal. ct r<-/i//)!ixxqge retro-pi cu nil par
du tissu adipcux d droilc, dc la ptirajjirn bismuthSe'd yauc/u'. Hull, et
in/'tn. Soc. d. chirurg., Paris, 1913, xx.ri.r, 11 ^0-1 IS//.
J.'!<;! (iclnd dc la chiruryic iidrathoradquc . Paris, 1914. 182 p. 8°.
White (W. C.) <& Van Norman (K. H.}. /////;rmA/m'a of the skin overlying active lesions
in pt/ltnoniiri/ lulu rctdoxix. Arch. Int. Med., Chicago, 1309, iv, 1-7.
An in'Hriduiil (//id/tHlal/rc index to tu'tcrcidin dosage in treatment. Arch.
Int. Mai., Chicago, 1910, vi, 4.'t»-',(',S.
Wood (F. C.). Prognostic value of the diazo-rcaction in pulmonary tuberculosis. Med.
News, New York, 1903, Ixxxii, 631-6 J,;.
(b] Syphilis of the Lung
(Lues pulmonum)
A rare, condition in adults, met with sometimes in the tertiary stage (gum-
mata). Besides tlie gummatous form, a chronic, sclerotic, interstitial pneumonia
may be due to lues. It is rarely met with in the apices; gummata most often
develop in the lower lobes or in the middle lobe on the right side. A dry cough
with mucoid sputum and dyspnea are usually the first symptoms. A few rales
over an area of circumscribed dullness may be discoverable, most often in the
middle lobe on the right side.
Lung syphilis may closely simulate tuberculosis. Indeed, most cases of lung
syphilis are treated for a long time for tuberculosis before the true nature is dis-
covered. The differential diagnosis is all the more difficult since (1) pulmonary
tuberculosis may occur in luetic patients that have no syphilis of the lung, and
DISEASES OF THE LUNGS 633
(2) pulmonary tuberculosis and pulmonary syphilis may coexist in the same
patient !
Cavity formation is rare. There is no single, absolutely certain, criterion for
diagnosis, arid the disease may be confused not only with tuberculosis, but also
with bronchiectasia, with abscess, with neoplasm, or with chronic pneumonia. A
probable diagnosis can be made if the disease be thought of, if the Wassermann
be positive, if the x-ray reveal a large hilus shadow with outrunners, if tubercle
bacilli are permanently absent from the sputum, if there be but little fever, if
the process involve especially the middle of the lung, and if there are signs of
syphilis in other ^organs. If the symptoms and signs disappear under specific
anti-luetic therapy, the diagnosis is confirmed, though it should be borne in mind
that the sclerotic form of pulmonary syphilis will be but little influenced by
therapy. In association with syphilis of the lung, the existence of laryngeal
syphilis or of syphilis of the trachea or bronchi may bo demonstrable. Amyloid
degeneration of the organs may complicate the clinical picture.
I have seen one case in which a luetic infiltration widespread throughout one
lung cleared up entirely under salvarsan therapy. Hereditary syphilis of the
lung is not uncommon in the fetus and in the new-born. Most often it takes the
form of an interstitial pneumonia; a catarrhal pneumonic form, known as pneu-
monia alba (Virchow), abo occurs; in rare instances, one sees circumscribed
gummata.
References
Councilman (W. T.). Syphilis of the lung. Johns Hopkins Hosp. Bull., Ball., 1891, ii,
34-37.
Dieulafoy (G.). Syphilis du poumon et de la plevre. Gaz. hebd. de med., Paris, 1889, 2. s.t
xxvi, 285; 303; 317; 335; 348; 367.
Downing (A. F.). Syphilis and luny disease. Boston M. & S. J., 1915, clxxii, 898-901.
Fowler (J, K.}. Syphilitic disease of the lungs. In: Syst. Med. (Allbutt). New York &
London, 1898, v, 311-322.
Hoffman (C. G.}. Syphilis of the lung; report of a case. Kentucky M. J., Bowling Green,
1915, xiii, 197-201.
Hollman (C.). Pulmonary syphilis. Urol & Cutan. Rev., Si. Louis, 1915, xix, 181-185.
Landis (H. R. M.} & Lewis (P. A.}. Latent syphilitic infection of (he lungs. Am. J. M.
Sc., Philadelphia, 1915, cl, 195-200.
Satterthwaite (T. E.}. Pulmonary syphilis in the adult. Boston M. & Surg. J., 1891,
cxxiv, 573; 600.
Schlesinger (//.'). Syphilis der Bronchien und der Lungen. Handb. d. Geschlechtskrankh.
.(Finger, Jadassohn, et al.). Wicn & Leipzig, 1912, Hi, 559-583.
Syphilis der Pleura. Handb. d.Geschlechtskrank. (Finger, Jadassohn, et al.).
Wien & Leipzig, 1912, Hi, 584-589.
Stengel (A.}. Syphilis of the lungs simulating pulmonary tuberculosis. Univ. Penn. M.
Bull., Philadelphia, 1903-04, xvi, 89-99.
(c) Other Specific Inflammations of the Lung
Actinomyces, glanders, blastomyces^ and aspergillum may affect the lungs, but
such infections are rare. (See Infectious Diseases.) Streptothricosis of the lung
is occasionally met with; it may resemble pulmonary tuberculosis closely clinically.
Infiltrations of the lung also occasionally occur in leukemia, and in the several
pseudoleukemias, including Hodgkin's disease.
634 DISEASES OF THE EESPIRATOEY APPARATUS
References
Bauer (W.). Chirurgische Behandlung der Lungenaktinomykose. Mitt. a. d. Grenzgeb. d.
Med. u. Chir., Jena, 1913, xxv, 135-144-
Bridge (N.). Slreptothricosis (actinomycosis) of the lungs. J. Am. M. Ass., Chicago,
1911, Mi, 1501-1506.
Flexner (S.). Actinomycosis of the human lung. Proc. Path. Soc., Philadelphia, 1899-
1900, n. s., Hi, 141-145.
Huber (F.) & Berkowitz (S.}. Primary pulmonary aclinomycosis in a ch'ld aged ten, with
post-mortem examination. Am. J. Dis. Child., Chicqgo, 1914, viii, 113-
119.
Karewski (F.). Die Aktinomykose der Lunge und der Pleura. Ergcbn. d. Chir. u. Orthop.,
Berlin, 1914, viii, 424-470.
Kato (Y.). Ueber die bei den Erkrankungen der Lunge vorkommende Leptothrix und ihre
Reinkuliur. Mitt. a. d. med. Fakult. d. k. Univ. zu Tokyo, 1915, xiii',
441-477. 4pl.
L'edoux & Lebard (R.}. Les aspects radiologiques de Vactinomycose pulmonaire. Bull, et
mem. Soc. med. d. hop. de Paris, 1914, 3. s., xxxviii, 219-222.
Pearson (L.) & Ravenel (M. P.}. A case of pneumonia due to the Aspergillus futniyntns.
Proc. Path. Soc., Philadelphia, 1900, n. s., Hi, 241-256. 2 pi.
Schottmiiller (H.). Ueber Lungenmilzbrand. Munch, med, Wchnschr., 1898, xlr, 1231-
1235.
Warthin (A. S.) & Olney (H. S.}. Pulmonary streptothricosis. Am. J. M. Sc., Phila-
delphia & New York, 1904, cxxviii, 637-649.
2. Pneumopathies Characterized by Alterations of
the Alveolar Lumen
Under this heading we include (a) atelectasis, and (b) emphysema
pulmonuni.
(a) Atelectasis
Definition. — When the pulmonary alveoli are empty of air, and their
opposite walls come into apposition, so as to resemble the fetal state of tlio
lung, the condition of atelectasis or collapse exists.
Etiology. — Atelectasis, or apneumatosis, may be congenital or acquired.
In CONGENITAL ATELECTASIS, areas of thf. lung substance fail to take in
air and remain in their fetal state owing to insufficient expansion of the
chest because of feeble muscles or faulty innervation. In ACQUIRED ATE-
LECTASIS, lung that formerly contained air becomes devoid of air and
the alveoli collapse and reassume a state similar to the fetal. Such
acquired atelectasis may be due (1) to enfeeblement of the inspiratory
muscles, (2) to compression of the lungs owing to encroachment upon the
intrathoracic space, .or (3) to stenosis of the air-tubes.
In ATELECTASIS DUE TO FEEBLE CONTRACTION OF THE MUSCLES OF IN-
SPIRATION, or so-called "marant-ic atelectasis," the cause is to be sought in
some prostrating disease (e. g.7 rickets, diarrhea, typhoid fever or sepsis).
DISEASES OF THE LUNGS 635
COMPRESSION ATELECTASIS may be due to accumulation of fluid or gas
in the pleura or in the peritoneal sac, or to the growth of mediastinal
tumors, aneurisms, or intrathoracic strumata, to such an extent that the
pressure on the adjacent lung is equal to or greater than the inspiration
pressure. Again, compression atelectasis may follow encroachment upon
the intrathoracic space and interference with the contractions of the dia-
phragm from below, as by meteorism, ascites, or large abdominal tumor.
The atelectasis seen in kyphoscoliosis is also a compression atelectasis.
STENOTIC OK OBSTRUCTIVE ATELECTASIS depends upon the complete
plugging of a bronchus by inflammatory secretion, by an aspirated body,
or by a tumor, with subsequent absorption of the air from the correspond-
ing lobule of the lung. This form of collapse is commonest in the capillary
bronchitis of children complicating measles, whooping-cough and other,
infections.
Symptoms. — In atelectasis of the new-born, the symptoms consist of
dyspnea, cyanosis, distention of veins, retraction of the lower thorax dur-
ing inspiration in the form of a deep furrow at the level of the 6th and
7th costal cartilages. Fever and cough may be absent. The pulse is slow,
the right heart is labored and the pulmonic second sound accentuated. In
severe cases, attacks of asphyxia may occur. Occasionally there is sinus
thrombosis due to stasis ; the child becomes drowsy and shows paresis of
one side of the face and distention of the jugular veins of the same side.
Prolonged bilateral atelectasis after birth may be the cause of a peculiar
deformity of the thorax known as the wasp-waist (Wespentaille) of
Francke, in which the anteroposterior diameter of the chest is increased
above, and the lower thorax is separated from the upper by a groovelikc
constriction.
In acquired atelectasis, the condition is always an accompaniment of
some other pathological process (see etiology), and the physician may
experience much difficulty in deciding which of the signs are due to atelec-
tasis and which to the primary process. Thus atelectasis is common in the
periphery of a bronchopneurnonic focus. Over atelectatic areas, say at the
bases of the lungs, we find dullness and suppression af the breath sounds ;
after a forced inspiration, the dullness may lessen and the breath sounds
become louder. At the upper margin of an atelectatic area, crepitant rales
often become temporarily audible on inspiration deep enough to overcome
the bronchial obstruction.
Diagnosis — The main difficulty lies in distinguishing acquired atelec-
tasis from a pneumonic process. When atelectasis and bronchopneumonia
are simultaneously present, the diagnostic acumen of the most skilled is
severely taxed. Fever is absent in uncomplicated atelectasis, but fever may
be absent in pneumonia in a feeble child or in an aged person. The
sudden lessening of dullness and the loudening of the breath sounds after
deep inspirations are perhaps the most important criteria in the diagnosis
636- DISEASES OF THE RESPIRATORY APPARATUS
of atelectasis. As acquired atelectasis is a secondary phenomenon, it may
sometimes be suspected from the character of the primary disease.
Reference
Heller. Klinische und experimentelle Beitrdge zur Kenntniss der akuten Lungenatelek-
tase durch obturierenden Fremdkorperverschluss der Bronchien. Ztschr.f. d.
ges, exper. Med., Berlin, 1913-14, ii, 453-484.
(b) Vesicular Emphysema of the Lungs
(Emphysema pulmonum)
Definition. — A condition in which there is enlargement of the lungs with
an increased air content. In ACTIVE LUNG DISTENTION (simple lung dislcn-
tion, volumen pulmonum acutum) there is an abnormal distention of the
alveoli with temporary or permanent loss of elasticity ; in many instances
there is a return to normal when the cause is removed. It may be diffuse,
involving both lungs as in bronchial asthma, or it may affect certain parts
only; in the latter instance, it is usually a vicarious (or collateral) em-
physema, due to interference with the function of other parts (through
atelectasis, tuberculosis, pneumonia, or compression).
In CHRONIC, TRUE, OR SUBSTANTIAL, VESICULAR EMPHYSEMA the in-
creascd air content of the lungs is associated with an actual atrophy of the
lung substance, neighboring alveoli or even large groups of alveoli fusing
to form larger air cavities. The lungs become permanently dilated, their
margins overlap the heart, and those of the two lungs may meet in front,
obliterating the superficial cardiac dullness.
Etiology and Pathogenesis. — An acute lung distention is a common
accompaniment of attacks of bronchial asthma, of acute capillary br n-
chitis, and of exacerbations of a chronic bronchitis.
( 1 ironic vesicular emphysema seems to depend upon mechanical influ-
ences acting upon lungs of abnormally low resistance, rspcrialK of their
elastic fibers. In most cases the emphysema is secondary ton chronic bron-
chitis. It is often inet with in horn-blowers, glass-blowers, singers, public
speakers, and men that do heavy lifting or much stair-climbing. That
there may be a congenital weakness of the elastic tissue of the lungs in
those affected is favored by the fact that "emphysematous families are
known." Still, the main cause seems to lie in the bringing of the thorax,
over a long period, into an exaggerated position, secondary to which a
distention-atrophy of the alveolar walls develops (Tendeloo). Men are
twice as often affected as women. Asthma, chronic bronchitis, and bron-
chiectasis are common accompaniments.
The thorax becomes barrel-shaped and immobile in the position of deep
inspiration. The ribs and the sternum are displaced forward and upward,
so that the anteroposterior diameter of the chest is increased. The inter-
costal spaces are widened ; there is premature ossification of the rib carti-
DISEASES OF THE LUNGS 637
lages. Ereund believes that the emphysema is secondary, like the deform-
ity of the thorax, to changes in the costal cartilages, but Frankel opposes
this view. Owing to the fact that many of the alveolar walls with their
capillaries are destroyed, hypertrophy, and, later, dilatation of the right
ventricle occur; ultimately, myocardial insufficiency develops and may be
the cause of death.
Symptoms. — In pronounced cases, the barrel-shaped thorax (see above)
is a characteristic feature. Slight grades of emphysema may cause no dis-
tressing symptoms except when complicated by bronchitis or asthma. In
severer cases, chronic bronchitis is almost always present and is associated
with dyspnea and cyanosis. The respiration, which is chiefly abdominal,
is accelerated, and the expiratory character of the dyspnea is marked. The
cyanosis may reach a high grade; it becomes more marked on muscular
exertion, or during a complicating bronchitis, or when myocardial insuffi-
ciency sets in. The veins of the neck and head are usually distended, and
there is often venous ectasis of the skin opposite the attachment of the
diaphragm.
On percussion there is hyperresonance, the tone being louder and of
loAver pitch than normal (box! ike tone) ; the lower limits of the lungs
extend below the normal level ; and there is diminished dislocation of the
lower limits on inspi ration. The superficial cardiac dullness is diminished
or obliterated.
On auscultation, the inspiratory murmur is feeble, and is followed by a
prolonged, difficult, expiratory sound ; rhonchi, sibilant and sonorous, due
to the complicating bronchitis, often replace the inspiratory breath sound.
During attacks of bronchial catarrh, moist rales may be audible. Though
the position of the right margin of the heart may be hard to determine on
account of the emphysema unless rontgenoscopy be resorted, to, the hyper-
trophy of the right ventricle is usually indicated by accentuation of the
pulmonic second sound. The heart sounds, on the whole, seem distant on
auscultation. The most important disturbance, in emphysema is undoubt-
edly the hindrance to the circulation and the strain on the right side of
the heart.
The sputum varies with the complicating conditions (dry catarrh,
moist catarrh, bronchiectasis).
On x-ray examination, the abnormal clearness of the pulmonary areas,
the low position of the diaphragm and the enlargement of the cardiovascu-
lar stripe to the right are striking features.
Diagnosis. — This ought not to be difficult if what has been said above be
attended to. In the differential diagnosis, it is necessary to distinguish
emphysema (1) from pneumofhorax (metallic phenomena, process uni-
lateral, rb'ntgeno^raphy) ; and (2) from bilaterally adherent pleurae with
myocardial insufficiency (higher position of the diaphragm, rontgenog-
raphy).
638 DISEASES OF THE KESPIEATOEY APPARATUS
Genuine chronic vesicular emphysema will scarcely be confused with
acute lung distention if the history of the patient be studied and the course
of the disease be observed.
References
Armbruster (G.). Physiologische Studien iiber Lungenemphysem mil neuen Anschauungen.
Aerztl. Rundschau, Milnchen, 1915, xxv, 81-83.
Baumann (A.). Un nouveau traitement de I 'emphyseme pulmonaire. Bull. gen. de therap.
[etc.], Paris, 1914, clxviii, 102-105.
Boothby (W. M.) & Berry (F. H.). Distension of the lungs; its effect on the respiration in
man and in normal and vagotomized dogs. Am. J. Physiol., Baltimore,
1915-16, xxxvii, 433-451.
Christiansen (J.) & Haldane (J. S.). The influence of distention of the lungs on human
respiration. J. Physiol., London, 1914, xlviii, 272-277.
Fowler (J. K.}. Emphysema. In: Syst. Med. (Allbutt & Rolleston). 8°. London,
1909, v, 474-497.
Freund (W. A.}. Zur operaiiven Behandlung gevrisser Lungenkrankheiten, insbesondere des
auf starrer Thoraxdilatalion beruhenden alveoldren Emphysema (///// einem
Operationsfatte). Ztschr.f. exper. Path. u. Therap., Berlin, 1906, Hi, 479-
498.
Der heutige Stand der Frage von tli-ni Zuxammenhang primdrer Thorax-
anomalien mil gewissen Lungenkrankheiten. Berl. Idin. UY/m.sr ///•., 1912,
xlix, 1695-1699.
Goppert (F.). Ueber manifeste und /«/»•///«• Inxuffizienz der Expiration im Kindesalter.
Berl. klin. Wchnschr., 1914, U, 49-53.
neuter (C.). Ueber angeborene Bronchiektasien und (int/t'hnn'tir \Yu1nnhinge. Beitr. z.-
path. Anal. u. z. allg. Path., Jena, 1914, fix, 5.^^-538.
Hofbauer (L.)« Zur Pathogenese desLunge-nemphysems. Deutsche med. Wchnschr.. Leipzig
u. Berlin, 1912, xxxviii, 1534.
Hoover (C. F.). The minute volume and alveolar air in pulmonary emphysema. Arch.
Int. Med., Chicago, 1913, xi, 52-65.
Hoover (C. F.) & Taylor (Lester). The venlilatory function of the lung in emphysema
and asthma. Arch. Int. Med., Chicago, 1915, xv, 1-15.
Kahler (().)• The scabard trachea and pulmonary emphysema. J. Laryngol, London,
1914, xxix, 7-12.
Staehelin (R.). Pathologie, Pathogenese und Thcrapie des Lungenemphysems. Ergcbn.
d. inn. Med. u. Kindtrheilk., Berl., 1915, xiv, 516-575.
Tendeloo (N. Ph.). Lungcndehnung und Lungenemphysem. Ergebn.' d. inn. Med. u.
Kinderh., Berlin, 1910, vi, 1-28.
3. Pneumopathies of Circulatory Origin
Under this heading we include :
(a) Chronic passive congestion of the lungs and stasis bronchitis.
(b) Pulmonary hemorrhage and hemoptysis.
(c) Pulmonary embolism, hemorrhagic infarction of the lung
and thrombosis of the pulmonary artery.
(d) Edema of the lungs.
(a) Chronic Passive Congestion of the Lungs and Stasis Bronchitis
Definition. — A condition met with in diseases leading to prolonged
stasis in the pulmonary veins and resulting in hyperemia and induration of
the lungs.
DISEASES OF THE LUNGS 639
Etiology and Pathogenesis. — Stasis in the pulmonary veins may
occur in .any condition that causes directly or indirectly a dilatation of
the left atrium of the heart. Thus it is common in mitral lesions, and in
conditions causing dilatation of the left ventricle, for example, aortic in-
sufficiency and the myocardial insufficiency of myocarditis, adhesive peri-
carditis, and the chronic cardiopathies of renal and of thyrotoxic origin.
The stasis leads to engorgement of the pulmonary capillaries and to a
gradual increase in the consistency of the lung substance due to increase
of fibrous tissue. The pathological anatomists describe a "red induration"
(earlier stages) and a "brown, induration" of the lungs (later stages).
The alveoli contain a few desquamated alveolar epithelial cells, a few
white and red blood corpuscles, and the characteristic hemosiderin-con-
taining "heart-failure cells."
Symptoms. — The patients complain of shortness of breath, especially
on exertion, arid there is usually cough with mucoid sputum containing
desquamated alveolar epithelium filled with a yellow to a blackish-brown-
colored ferruginous pigment ("heart-failure cells"). The sputum is
occasionally streaked with blood.
On percussion over the lungs, the note may be slightly impaired. On
auscultation, the breath sounds are usually impure ; they mayHbe feebler
than normal or somewhat accentuated, and, owing either to slight edema
or to a complicating bronchitis, usually fine and medium-sized moist rales
can be heard, especially over the lower lobes, though the findings vary
much from day to day.
Kontgenograms show lung areas that are bilaterally and throughout
less clear than normal, owing to the general slight condensation of the
lung-substance ; the hilus shadows are larger and denser than normal.
Chronic passive congestion of the lungs is often complicated by other
phenomena common in myocardial insufficiency (e. g., edema of the lungs,
atelectasis, hypostatic congestion, hydrothorax, and infarction).
(6) Pulmonary Hemorrhage and Hemoptysis
Blood in the respiratory tubes may be aspirated -from above (nose,
pharynx), or result from hemorrhage due to erosion of vessels in the walls
of a cavity .or of an ulcer (phthisis, lues, paragonimiasis, bronchiectasia,
gangrene) ; from passive hyperemia of the lung (in cardiac stasis, in com-
pression of the pulmonary veins by neoplasms, enlarged glands or aneu-
risms) ; from active hyperemia of the lung (in tuberculosis, cancer, echi-
nococcus, or malaria); from rupture of an aneurism or from trauma;
from hemorrhagic diathesis (scurvy, hemophilia, purpura, acute leu-
kemia) ; rarely from vicarious menstruation. In hemoptysis or coughing
up of blood, these various possible sources as well as hemorrhagic infarc-
tion should be considered.
640 DISEASES OF THE RESPIRATORY APPARATUS
The amount of blood expectorated may vary from a minute quantity,
streaking the sputum, to large amounts (100 c.c. ; 1 liter; even 3 liters!).
The blood is bright red and frothy. There may be fever for 2-3 days after
a hemoptysis, due to absorption of blood, or to a complicating inflam-
mation.
In pulmonary tuberculosis a hemoptysis may lead to an extension of
the tuberculous process to other parts of the lung, and either a caseous
pneumonia or an acute disseminated tuberculosis of the lungs may follow.
In the differential diagnosis of hemoptysis, we must rule out epistaxis,
hematemesis, and buccal, pharyngeal and laryngeal hemorrhages.
References
Baweletz (A.}. Der derzeilige Stand der Befiandlung der Hdmoptysen. Therap. d. Gegenw.-,
Berlin, 1914, Iv, 468-475.
Burns (N. B.). Treatment of hemoptysis in pulmonary tuberculosis. Boston M. & S. J.,
1914, dxxi, 437-440.
Rolleston (J. D.) & Robert son- Ross (J. E.). Fatal haemoptysis in a child aged four
years. Proc. Roy. Med. Soc., London, 1913-14, vii, Sect. Stud. Dis. Child.,
171-174.
(c) Pulmonary Embolism; Hemorrhaglc Infarction of the Lung ;
Pulmonary Thrombosis
Embolism of the main stem or of a branch of the pulmonary artery is by
no means uncommon ; over half of all cases of embolism involve this domain.
The most common form of embolus is a blood clot embolus, that is, a frag-
ment of a thrombus, detached from its site of formation in the right heart
(mitral stenosis, myocardial insufficiency, etc.), or, more often, in one of
the body veins (saphenous, femoral, prostatic, uterine, etc.) in acute infec-
tions, in the puerperium, and after operations. Other forms of emboli, such
as fat embolus, gas embolus, and cell embolus, are only occasionally met
with. The so-called bland emboli are sterile; emboli that contain patho-
genic bacteria are known as septic emboli.
i. Fmbolism of the Pulmonary Artery or of One of Its Large Branches
Symptoms. — A patient of mine, a young woman, who had suffered for
years from mitral stenosis, was talking quietly to her mother while out
driving, when suddenly she broke off in the middle of a sentence; the
mother, on looking around, saw that her daughter's head had dropped
forward and that she was unconscious; in a few moments she was dead.
Such a sudden death, due to embolism of the main trunk of the A. pul-
monalis, is not uncommon in long-standing cardiac disease, in convales-
cence from pneumonia, or in the puerperium. The patients may be either
very pale when the death is sudden, or cyanotic when they live a little
longer. In some instances, the first symptom is extreme dyspnea, accom-
DISEASES OF THE LUNGS 641
panied by a feeling of anxiety ; the patients struggle for breath, and may
even cry out; then they become unconscious, the breathing stops and the
pulse becomes imperceptible.
When the embolus lodges in the right or, less frequently, the left
branch, having passed through the main trunk, death is sometimes just as
sudden, but, more often, the patient lives for a few hours ; there is marked
dyspnea, great anxiety, and, soon, cyanosis ; the patient breaks out into a
colcl sweat, and may remain conscious for a time complaining of headache
and vertigo; the pupils dilate, and the eyes protrude; later, patients be-
come comatose and convulsive seizures may precede death. Occasionally,
a patient recovers, but often when recovery has begun to seem probable,
the symptoms become worse, due to further embolism or to the conversion
of a partial obstruction into a complete one from thrombus formation at
the site of the embolus.
On examination of the chest, there may be a lagging of the right side
of the chest on inspiration, and the breath sounds may be feebler on that
side; the area of cardiac dullness usually becomes enlarged to the right.
Diagnosis. — The diagnosis cannot be made with certainty, but it is
made very probable if the symptoms above mentioned occur in a patient
that is known to have venous thrombosis, or has recently had an
operation (laparotomy, prostatectomy), or one in the puerperium, or
in the convalescent stage of pneumonia, or under treatment for severe
chlorosis. A loud whistling systolic murmur in the second left intercostal
space or along the right side of the sternum can occasionally be made out
(Litten) ; it is believed to be a sign of incomplete occlusion of the A.
pulmonalis.
ii. Embolism of a Medium-sized Branch of the Pulmonary Artery Causing
Infarction of the Lung
The immediate effects of embolism of a medium-sized branch may be
slight, or, if the patient suffer from myocardial insufficiency, may be so
severe as to resemble those due to embolism of the right or left main
branch. In case death does not occur from the embolism there is a danger
not incident to embolism of the larger trunks, namely, that of hemorrhagic
infarction. This occurs only when the pulmonary capillaries are abnormal,
either owing to preexisting passive congestion, or to damage from a septic
embolus without previous stasis. The filling of the infarcted area with
blood may be due either to collateral flow from neighboring pulmonary
capillaries, or to retrograde inflow from, the bronchial veins, since, as is
well known, the latter empty into the pulmonary veins.
Symptoms. — An embolism not followed by infarct may cause no symp-
toms during life, as we know from post-mortem examinations of well-
studied clinical cases. If infarction occur, the patient complains of a
642 DISEASES OF THE KESPIKATOEY APPAKATUS
"stitch in the side/' due to the dry pleurisy over the infarct, and of diffi-
culty in breathing. A little later, the sputum becomes streaked with
blood or rusty, or there may be an outspoken hemoptysis ; on microscopic
examination, one sees not only red blood corpuscles, but, also, nearly
always, "heart-failure cells." There is usually some fever, and sometimes
a chill, and these symptoms may lead to the false diagnosis of croupmis
pneumonia. The fever may occur even when the infarction is due to a
bland embolus ; it may then be the result either of absorption of bloocl or
of a secondary infection.
On percussion and auscultation, there is dullness over the infareted
area ; the breath sounds, at first indefinite, soon become bronchial in type ;
crepitant rales are audible; and, frequently, a pleuritic friction sound can
be heard. In the rontgenogram, a shadow, usually sharply circumscribed,
can be made out, though if the passive congestion be extreme, or if there
be associated edema of the lung, the outlines of the shadow may not be
sharp.
Ilemorrhagic infarction occurs more often in the lower lobe of the
right lung than in any other part.
In favorable cases, tbe temperature may soon become normal, the
sputum ceases to be bloody, and the physical signs gradually disappear.
In the unfavorable cases, death may occur from cardiac failure, from
abscess formation or from gangrene. Occasionally, an empyema develops,
or a pneumothorax occurs. A patient doing well, after an embolism, may
succumb later from repeated embolic attacks.
Differential Diagnosis. — AYe must try to distinguish infarction (1)
from simple dry pleurisy; (2) from lobar pneumonia; (3) from pulmo-
nary tuberculosis (anamnesis, sputum, Calmette, x-ray) ; (4) from tumor
of the lung (rontgenogram) ; (5) from echinococcus cyst (x-ray, situation
in upper lobe or in left lung, complement-fixation test).
iii. Embolism of the Smaller Branches of the Pulmonary Artery
A single embolus in a small branch does no harm and causes no symp-
toms, except, of course, when it carries pathogenic bacteria or tumor cells,
in which event a metastatic abscess or a local neoplasm may develop.
Multiple embolisms of small branches of the A. pulrnonalis are most
often due either to air bubbles (opening of a large vein at surgical opera-
tion), or to fat droplets (after bone injury) ; they may be very serious
indeed, often causing death either suddenly or after a few hours.
Symptoms. — In air embolism, there may be a sudden attack of dyspnea
with cyanosis after opening a large vein; the surgeon may hear the gas
enter the vein. The patient quickly becomes unconscious and may have
convulsions. Death may occur at once, or after a few hours. Recovery
is rare. A bubbling murmur may be audible over the right heart, since
DISEASES OF THE LJJNGS 643
the right ventricle may be full of air or bloody froth; in the area of
cardiac dullness the percussion note may become tympariitic.
In fat embolism, though the emboli lodge in the smaller branches of
the pulmonary arteries, the symptoms resemble those of gradual occlusion
of the main trunk of the A. pulmonalis. (See above.) The patient, a
few hours after a bone injury, or after a severe burn, begins to have
dyspnea, which gradually increases in severity. There is a general cya-
nosis. The patient has an anxious look. On physical examination of the
lungs, there may be nothing to make out, except slight signs of pulmonary
edema (q. v.). Recovery is not uncommon if the emboli be not too numer-
ous. In the severer cases, death occurs in a few hours or days. Now and
then, fat droplets pass through the lungs, enter the general circulation,
and may give rise to embolism of the cerebral, retinal, or renal arterioles.
In cases that recover, the emboli disappear, partly through saponification
of the fat by the blood, partly through ingestion by phagocytes.
iv. Thrombosis of the Pulmonary Artery or of Its Branches
Autochthonous thrombosis of the main trunk or of the right or left branch
is rare, twit does occur occasionally, especially in children after severe intestinal
catarrh (Beneke) or after measles (Staehelin) ; the lesion also may occur as an
agonal phenomenon. During life, the signs are usually believed to be due to a
bronchopnenmonia and only at autopsy is the true nature of the lesion revealed.
Most of the described thromboses of the artery were not primary, but were either
thrombotic extensions of emboli, or were only the emboli themselves derived from
distant thrombi in veins (Lubarsch). Multiple thrombi are sometimes found in
the smaller branches of the pulmonary artery after inhalation of poisonous gases
(e. g., phosgen) ; the diagnosis cannot be made with certainty during life.
References
*
Alwens & Frick (4;). Ueber die Lokalisation von Embolien in der Lunge. Frankfurt.
Ztschr. f. Path., Wiesbaden, 1914, xv, 315-326. 2 pi.
Beneke (R.). Die Embolie. In: Handb. d. allg. Pathol. (Krehl & Marchand), Leipzig,
1913, ii, Abt. ii, 300-371.
Conner (L. A.). A type of pulmonary attack simulating primary lobar pneumonia, seen in
apparently healthy persons and caused by pulmonary embolism and infarc-
tion from a latent venous thrombosis. Tr. Internal. Cong. Med., 1913,
/ London, 1914, Sect. VI, Medicine, pi. 2, 545-548.
Fischer (#.)• Experimenielle Untersuchungen uber den Mapillarkreislauf der Lungen und
die Fettembolie. Verhandl. d. deutsch. path. Gesellsch., Jena, 1914, xvii,
279-281.
Heller (/?.), Mager (W.} & von Schrotter (#.). Ueber arterielle Luftembolie aus den
Untersuchungen uber Luftdruckerkrankungen. Ztschr. f. klin. Med., Ber-
lin, 1897, xxxii, Supplhft., 113-162.
Karsner (H. T.) & Ghoreyeb (A. A.). Studies in infarction. III. The circulation in
experimental pulmonary embolism. J. Exper. Med., Lancaster, Pa.,
1913, xviii, 507-511.
Kretz (R.}. Ueber experimentelle Lokalisalion der Lungenembolie. Beilr. z. pathol. Anal.,
etc., Jena, 1913, Iv, 371-372.
Moritz (F.). Anomalien im Lungenkreislauf. Handb. d. allg. Pathol. (Krehl & Mar-
chand), Leipzig, 1913 , ii, 2, 87-93.
644 DISEASES OF /THE RESPIRATORY APPARATUS
Novak (E.). Fatal post-operative pulmonary embolism. Interstate M. J., St. Louis, 1915,
xvii, 565-568.
Schumacher (E. D.} & Jehn (W.). Experimented Untersuchungen uber die Ursache
des Todes durch Lungenembolie. Ztschr. f. d. ges. exper. Med., Berlin,
1914, m, 340-376.
Tigerstedt (R.). Der kleine Kreislauf. Ergebn. d. Physiol, Biophysik, 1903, ii, 528-584.
(d) Edema of the Lungs
In edema of the lungs, serum escapes from the capillaries and not only
saturates the interstitial tissue but also enters the pulmonary alveoli. It
may be (1) inflammatory, as in pneumonia; or (2) non-inflammatory or
mechanical, due to cardiac failure, especially when the left ventricle fails
before the right (W. H. Welch) ; the latter is often agonal, and is espe-
cially common in mitral stenosis, in acute intoxications and infections,
and in diseases associated with hydremia (chronic nephropathies, per-
nicious anemia, etc.). According to Sahli, an increased permeability of
the vessel walls is even more important than the failure of the left heart ;
in some cases, neural influences appear to play a part. Clinically, we may
be unable to distinguish the mechanical, the inflammatory, and tlje ncimil
edemas from one another. Acute edema of the lungs occasionally follows
thoracentesis.
Symptoms ajid Signs. — The onset is usually heralded by dyspnea and
cyanosis; the extremities are cold and the patient breaks out into a cold
sweat, the face assuming an anxious appearance. In outspoken cases of
acute and peracute edema, the sputum is very characteristic, being copious,
thin, frothy and tinged pink owing to the admixture of blood. Loud
tracheal rfiles (the "death-rattle") may be audible. The frothy, blood-
stained fluid may well up into- the month and out through the lips in large
quantities; this fluid is rich in protein and may coagulate spontaneously
in the sputum cup.
The percussion note varies according to the degree of edema. When
this is slight there may be no change, or only slight tympany. If it be
marked, and especially if the edema be chronic, the note may be dull.
Crepitant or loud moist rales are nearly always audible on auscultation;
sometimes there is only l^nd roughened breathing without rales. In the
rontgenogram, the lung area is not as clear as normal, being diffusely
clouded or indistinctly mottled.
In inflammatory edema, there is fever, a strong pulse, and usually a
polymorphonuclear leukocytosis.
In non-inflammatory edema, fever is absent, the pulmonary second
sound is exaggerated, and the pulse is usually small and frequent. The
history of the case (cardiac disease, renal disease, arterial hypertension)
helps in the diagnosis. A recurring form of acute pulmonary edema is
not uncommon in mitral stenosis and in arteriolar nephropathy.
DISEASES OF THE LUNGS 645
Diagnosis. — This is easy when dyspnea is associated with frothy, blood-
tinged sputum, rich in protein. When the typical sputum is absent, the
diagnosis may be difficult and the condition may be confused with hypo-
static congestion or with atelectasis. When the condition of a patient
favors the development of a pulmonary edema, a close watch should be
kept on the lungs ; should crepitation appear and begin to spread rapidly,
prompt and energetic therapy may prevent an attack.
References
Coplin (W. M. //.)• Pulmonary oedema, with analysis of 405 cases occurring in 2,030
autopsies. Proc. Path. Soc., Philadelphia, 1906, n. s., ix, 77-95.
Davies (L. G.). Acute oedema of the lungs treated with belladonna. Brit. M. J., London,
1910, ii, 257.
Giraud (Mar the) & Giraud (C.). Retentions azotees et serum glycose hypertonique (fails
cliniques); oedeme pulmonaire aigu consecutif d une injection inlraveineuse
de glycose en solution hypertonique. Par. med., 1913-14, xv, 194-201.
Grober (J. A.). Bchandlung des Lungenodems. Deutsche med. Wchnschr.. Leipzig u. Berlin.
1914, xl, 1097-1099.
Jores (L.). Uber experimentelles, neurotisches Lungenodem. Deutsches Arch. f. klin.
Med., Leipzig, 1906, Ixxxvii, 389-401.
Klemensiewicz (R.). Lungcnoedem. In: Handb. d. allg. Pathol. (Krehl & Marchand).
Leipzig, 1912, ii, 1, 424-430.
Kraus (F.). Ucbcr Lungenoedem. L Ztschr. f. expcr. Path. u. Thcrap., Berlin, 1913, xiv,
402-412. 5 pi.
Miller (J. L.) & Mathews (S. A.). A study of the mechanical factors in experimental
acute pulmonary edema. Arch. Int. Med., Chicago, 1909, iv, 856-376.
Modrakowski (G.). Beobachtungen an der uberlebenden Sctugetierlunge. II. Uebcr die
experimentellc Erzeugung von Lungenodem. Arch.f. d. ges. Physiol.,Bonn,
1914, clviii, 527-554.
Nicholls (A. G.). Acute oedema of the lungs. Canadian M. Ass. J., Toronto, 1915, v, 981-
994.
Riesman (/).)• Acute pulmonary oedema, with special reference to a recurrent form. Am.
J. M. Sc., Philadelphia & New York, 1907, n. s., cxxxiii, 88-100.
Sahli (//.). Zur Pathologie und Therapie des Lungenodems. Arch. f. cxpcr. Path. u.
Pharmakol., Leipzig, 1885, xix, 433-482.
Zur Pathologie des Lungenoedems. Ztschr. f. klin. Med., Berlin, 1887,
xiii, 482-487.
Welch (W. //.)• Zur Pathologie des Lungenodems. Arch. f. path. Anal, [etc.], Berlin,
1878, Ixxii, 375-412.
4. Pneumopathies Due to Foreign Bodies and Parasites
Under this caption may be included (a) the pneumonoconioses and
(b) parasitic invasions of the lungs.
(a) The Pneumonoconioses
Definition. — The diseases of the lungs due to inhalation of dust of
various sorts are called the pneumonoconioses. "The dust gives rise to
chronic bronchitis and to interstitial inflammations of the lung that lead
646 DISEASES OF THE RESPIRATORY APPARATUS
to fibrosis (cirrhosis puhnoiiuin}. Bronchiectasis and emphysema often
develop. The diseases are often complicated by tuberculous infection.
Varieties of Pneumonoconiosis. — Three main varieties are distinguish-
able, namely;
(1) Anthracosis pulmonum, due to carbon or coal-dust, met with* in
coal-miners, chimney-sweeps, stokers, and workers in graphite.
(2) Chalicosis pulmonum, due to stone-dust, and met with in stone-
cutters, slate-workers, polishers, etc. The gold-miner's phthisis of South
Africa seems to belong here.
(3) Siderosls pulmonum, due to iron-oxid-dust, met with in file
workers, iron-workers, scissors-grinders, mirror-makers, workers in wall-
paper factories, etc.
Similar lung diseases occur in persons following other occupations
(millers, bakers, carpenters, weavers, cigar-makers, potters, fertilizer-
makers, etc.).
Disposition. — It is a remarkable fact that certain only of the workers
become affected. There would seem, therefore. In lie a special disposition
to attack. This disposition is increased by any previous affection of the
bronchi or of the lungs. The disease h:is been experimentally studied by
Arnold (1885) and by Tenddoo (HM)^). One of the best accounts in
English will be found in Oliver's "Diseases of Occupation" (1908).
Symptoms. — While the dust is bein»- inhaled, the symptoms of bron-
chitis develop and the sputum contains the dust particles. As a rule the
bronchitis ceases soon after removal of the patient from the harmful
opcupation, but it may continue even after mimval, especially if bron-
chiectasis and emphysema have already developed. Occasionally, a putrid
bronchitis complicates the picture. When the disease has led to chronic
interstitial inflammation of the lungs, there is dullness on percussion, and
moist rales are audible on auscultation, the upper Inlx-s being symmetric-
ally involved on the two sides (the reverse of what occurs in fibroid tuber-
culosis, in which one side is more involved than the other). The patients
are usually pale, suffer from cough, and may have "asthmatic'' attacks.
Many of them are erroneously believed to be • tuberculous, especially if
there be cavity formation with nummular sputum. It must not be forgot-
ten, however, that pneumonoconiosis and tuberculosis not infrequently
coexist.
Rontgenograms show a coarsely granular, evenly distributed, mottling
of the upper parts of the lung areas, the two lungs being equally affected.
The appearance is not unlike that of miliary tuberculosis, but the mark-
ings are coarser.
In the later stages, the signs of cirrhosis of the lung can be made out,
namely, retraction of the chest on the affected side, increased vocal frem-
itus, dullness on percussion, and bronchial breathing with moist rales.
The right heart is hypertrophied and the pulmonic second sound accentu-
DISEASES OF THE LUNGS 647
ated. In the severer forms, the right ventricle dilates and relative
tricuspid insufficiency develops. The bronchial lymph glands become
filled with dust transported through the lymph channels ; sometimes these
glands soften and break down, rupturing into the bronchi, the blood ves-
sels, the pericardium or the esophagus. Cicatrix formation may lead to
traction-diverticulum of the esophagus, or to tracheal or bronchial stenosis.
Occasionally a fibrous mediastinopericarditis develops as a result of pneu-
monoconibsis.
References
Armbruster (G.). Naturlicher Schutz der Lunge gegen Staub und Bakterien. Monatsbl f.
Gesundhtspflg., Braunschweig, 1914, xxxvii, 94~99.
Arnold (/.)• Untersuchungen ilber Staubinhalation und Staubmetastase. Leipzig, 1885,
F. C. W. Vogel. 204 p. 8°.
Cabot (R. C.). The functions of hospitals and clinics in the prevention of industrial diseases.
Am. Labor. Legisl. Rev., New York, 1912, ii, 293-296.
Collis (E. L.}. , The effects of dust in producing diseases of the lungs. Tr. Internal. Cong.
Med., London, 1913, Sect. XVIII, Hyg. & Prevent. Med., 1-34.
Corrigan (D. J.)« Cirrhosis of the lung. Proc. Path. Soc., Dublin, 1852-58, 247-249.
Entin (M.). Ueber Pneumonokoniosen. Fortschr. a. d. Geb. d. Rontgenstrahlen, Hamburg,
1915, xxiii, 19-30. 1 pi.
Hay thorn (S. R.}. Some histological evidences of the disease importance of pulmonary
anthracosis. J. M. Research, Boston, 1913, xxix, 259-279.
Heim (F.) & Agasse-Lafont. Effet des poussieres industrielles dans la production des
affections broncho-pulmonaires. Tr. Internal. Cong. Med., 1913, London,
1914, Sect. XVIII, Hyg. & Prevent. Med., pt. 2, 1-26.
Kast (A.} & Rumpel (T.). Kohlenpigmentlunge mit Bronchialerweiterung. In: Path.-
anat. Tafeln. Hamb. Staatskrankenh., Wandsbek- Hamburg, 1903, xvi.
1 pi. with text.
Klotz (O.). Pulmonary anthraco^is— a community disease. Am. J. Pub. Health, Boston,
1914, iv, 887-916.
McCrae (John}. The ash of silicotic lungs. Johannesburg, 1913, W. E. Hortor & Co.
6 p. 8°.
Pitch ford (W. W.~). The gross characters of the silicotic lung. Med. J. S. Africa, Johan-
nesburg, 1914-15, x, 167-174-
Steell (G.). Two cases of cirrhosis of the lung. Med. Chron., Manchester, 1887-88, vii,
95-104.
Thorel (C.). Die Specksteinlunge ; ein Beitrag zur pathologisch^n Anatomie der Staublungen.
Beitr. z. path. Anat. u. z. allg. Path., Jena, 1896, xx, 85-101.
Wainwright (J. M.) & Nichols (H. J.}. The relation between anthracosis and pulmonary
tuberculosis. Am. J. M. Sc., Philadelphia & New York, 1905, cxxx,
403-414.
White (W. H.). Fibroid disease of the lung. Guy's Hosp. Gaz., London, 1899, xiii, 21-27.
(b)' Parasites of the Lung
Aside from bacterial invasions of the lungs, invasions by actinomyces,
streptothrix, aspergillus, mucor, thrush fungi, etc., may occur. Pigeon-
feeders are especially prone to pseudotuberculosis aspergillina, described
by French authors as maladie des ganeurs des pigeons.
648 DISEASES OF THE RESPIRATORY APPARATUS
Of the animal parasites that invade the lung, 'echinococcus and para-
gonimus are the more important.
Echinococcus cyst is most often met with in the right lower lobe. The
parasite usually reaches the lung as an embolus, having reached the right
heart either through the vena cava superior or through the vena hypo-
gastrica. Sometimes a cyst of the liver breaks into the right pleural cavity
and then involves the lung. The diagnosis depends on (1) the rontgeno-
gram, (2) the complement-fixation test, or (3) upon finding membrane or
booklets in the sputum.
The Paragonimus westermanni is the cause of the endemic liemopiy-
sis of Japan and other Oriental countries. (For a description, see section
on Sputum.)
An amebic abscess of the liver is sometimes emptied through the lung
and the Entameba histolytica is discoverable in the sputum.
References
Beclere (A.). Un cas de kyste hydatique du poumon gauche. Butt, ct mem. Soc. med. d. hop.
de Paris, 1903, 3. s., xx, 763-767.
Bles (C.). Echinokokkus der Lunge. Forlschr. a. d. Geb. d. Rontgenstrahlen, ^Hamburg, 1915,
xxiii, 56-68.
Dieulafoy (G.). Sur un cas de kyste hydatique du poumon. J. de med. et chir. prat., Paris,
1902, Ixxiii, 414-418.
Miura (M.) & Nakanishi (K.}. Lungendislomen in Formosa [Japanese text]. Ztschr. d.
.med. Gesellsch. z. Tokio, 1897, xi, 767-769.
Ward (H. B.). The Asiatic lung-distome in the United States. Med. News, Philadelphia,
Weinberg (M.). Die Echinococcen und die Serumdiagnostik der Echinococcenkrankheit.
In: Handb. d. pathog. Mikroorg. (Kolle ct* Wassermann), 2. ed., Jena,
1913, viii, 123-184.
Wovschin (W.)» A case of saccharomycete infection of the lungs. Med. Rec., New York,
1913, Ixxxiv, 388-389.
5. The Neoplastic Pneumopathies
(Tumors of the Lung)
Tumors of the lung may be primary in the lung substance or bronchi
(carcinoma) ; more often they are metastatic through the blood stream
(sarcoma), or reach the lung by extension directly, or through the lymph
channels (sarcoma of the thymus, lymphosarcoma, carcinoma esophagi).
Benign tumors (teratoma, dermoid cyst, fibroma, adenoma, lipoma, os-
teoma, chondroma) are clinical and pathological rarities.
CANCER of the lung, when primary, arises most often from the mucous
glands of a bronchus, occasionally from the surface epithelium of a
DISEASES OF THE LUNGS 649
bronchus or of a pulmonary alveolus. When a cancer begins at the hilus
of a lung it may extend as a compact mass into the adjacent lung tissue,
or it may grow out into the lymphatics (either those ensheathing the
bronchi, or those in the interstitial tissue of the lung). But cancer may
begin in the middle of a lobe and form a sharply circumscribed mass
there, or it may diffusely infiltrate a lobe, roughly resembling the involve-
ment in a caseous pneumonia. Metastases may involve the pleura, the
bronchial glands, or, sometimes, the mediastinal and the 'supraclavicular
glands.
Primary LYMPHOSAECOMA of the lung is not uncommon among miners.
Secondary (metastatic) tumors of the lung are much more common than
primary tumors. They are usually multiple and often involve both lungs.
Symptoms. — At onset the symptoms m^y not be at all characteristic.
The patient may complain of pain or discomfort in the thorax, of- cough
and sputum, or of an inexplicable dyspnea. Occasionally, the signs of
pleurisy, of dysphagia, or of hoarseness and paralysis of a recurrent
laryngeal nerve first excite attention. There may or may not be fever of
low grade.
On physical examination, there may be lagging of one side of the
chest on inspiration, or signs either of a pleural effusion or of retraction
on one side. Pressure signs may be visible on inspection (collateral
circulation).
On palpation, percussion and auscultation, we may find dullness, with
enfeebled breath sounds, and lessened vocal fremitus, without rales. Not
infrequently, the signs of a pleural effusion, of a mediastinal mass, or of
a bronehiostenosis will be demonstrable.
The sputum may or may not be characteristic. Raspberry- jelly like
sputum is very suspicious. Hemoptysis occasionally occurs. Large fat
droplets in the sputum are suggestive (degeneration of tumor cells).
Sometimes actual tumor-particles can be found in the sputum. If tumor
be suspected, some of the sputum should be hardened, sectioned and
stained, and areas of carcinoma- or sarcoma-tissue looked for.
When pleural effusion is present, the fluid obtained by exploratory
puncture should be carefully examined. A hemorrhagic effusion usually
indicates either tuberculosis or carcinoma. (See Tumors of the Pleura.)
Cytological study of the sediment may reveal the presence of tumor cells
(sheets of cells, "seal-ring" cells).
In rb'ntgenograms the findings may be characteristic and decisive,
especially in tumors beginning at the hilus. One sees a spherical or irreg-
ularly-shaped mass from which jagged processes radiate out into the sur-
rounding lung area. In metastatic carcinoma, multiple shadows may bo
scattered through both lungs, usually most numerous in the right lower
lobe.
Diagnosis and Differential Diagnosis. — Many mistakes are made. The
650 DISEASES OF THE KESPIKATOEY APPARATUS
FJU. l(.l. — Tumor of Lung. (X-ray Dept., J. H. H.)
condition is often overlooked when present; a positive diagnosis of neo-
plasm is sometimes made when no tumor exists.
Errors of omission are less likely if the clinician will think of the
possibility of tumor of the lung in obscure intrathoracic disease. A
persistent pleurisy, especially if the effusion be hemorrhagic, a gradually
developing bronchiostenosis, a raspberry- jelly sputum in an old person, a
mediastinal growth, or a progressive cachexia associated with cough and
dyspnea, should certainly excite suspicion. This suspicion will be
strengthened if the physical signs above described (circumscribed dullness,
suppression of breath sounds, diminished fremitus, absence of rales) be
found, or if the rontgenogram be characteristic. The occurrence of en-
larged supraclavicular glands may be helpful in the diagnosis. I was
once called to Texas, to try to give relief to an elderly miner, who was
supposedly suffering from pulmonary tuberculosis, and who had begun to
have severe neuralgic pains in the neck. On examination, I found a
hemorrhagic pleural effusion on one side, suggestive lung signs, and
enlarged supraclavicular glands that rapidly grew in size. On excision
of one of the glands for diagnosis, the histological study revealed a lympho-
sarcoma. On another occasion, I saw in Virginia an elderly miner, sup-
posedly suffering from uremic asthma. His blood pressure was only
DISEASES OF THE LUNGS
651
slightly elevated, there was a trace of albumin and a few casts in the urine,
and his heart was negative ; a routine physical examination brought to
light a chain of enlarged lymph glands in the right neck, and suspicious
lung signs. The glands rapidly enlarged and the patient died a few weeks
later.
In some cases, a positive diagnosis becomes possible through finding
particles of tumor in a pleural effusion or in the sputum, through histo-
logical examinations of a supraclavicular gland, or through actual broncho -
scopic inspection.
If neoplasm be thought to be present, we should try to determine its
site and its origin, whether it be single or multiple, whether primary or
secondary, and, when possible, its exact nature.
In the differential diagnosis we must rule out: (1) aneurism of the
Fig. 176. — Intrathoracic Tumor ; Probably a Teratoma.
(X-ray Dept, J. H. H.)
Note the Smooth Contour.
aorta (rontgenoscopy, positive Wassermann) ; (2) mediastinal tumors
(q. v.) ; (3) pulmonary tuberculosis (search for bacilli, absence of tumor
cells and fat droplets from sputum, rontgenography ; histology of excised
gland) ; (4) echinococcus cyst (rontgenography, complement-fixation test).
The possibility of confusion with (5) infarct of the king, (6) syphilis of
652 DISEASES OF THE RESPIRATORY APPARATUS
the lung, (7) actinomycosis, and (8) chronic abscess and gangrene should
also be borne in mind.
In the United States, Dr. I. Adler of New York has had a large expe-
rience with tumors of the lung, the results of which, together with a
review of the literature, are recorded in his excellent monograph.
References
Adami (J. G.). A case of malignant intra-bronchial growth associated with a misleading
train of symptoms. Montreal M. J., 1895-96, xxiv, 510-513.
Adler (/.)• Primary malignant growths of the lungs and bronchi. New York, 1912, Long*
mans, Green & Co. 325 p. 8°.
Bard (£.)• La lymphangite pulmonaire cancereuse generalisee. Sctnaine med., Paris,
1906, xxvi, 145-157.
Buscinco (A.) & Trogu (G.). Richerche istogenetiche sui cancri primitivi del polmone
Tumori, Roma, 1914-15, iv, 662-682.
Domfaguez (M.). Sarcoma primitivo del pulmon. Arch, de la Soc. estud. din. de la
Habana, 1914, xxi, 130-136. -
Edlavitch (B. M.). Primary carcinoma of the lung. Second communication. J. Am.
M. Ass., Chicago, 1914, Ixiii, 1364-1367.
Fraenkel (-4.)* Ueber Komplikationen und besondere klinische Verlaufsweisen dcr Lungen-
geschwiilste. Med. Klin., Berlin, 1913, ix, 572-575.
Hellendall (H.). EinBeitrag zur Diagnostik der Lungengeschwiilste. Ztschr. f. klin. Med.,
Berlin, 1899, xxxvii, 435-455.
Kast (A.) & Rumpel (7\). . Primdres Lungenkarcinom mit Durchbruch in dcr Bronchus.
In: Path.-anat. Tafeln. Hamb. Staatskrankenh., Wandsbek- Hamburg,
1896, xi'ii. PL R 6 with text.
Killian (G.). Zur diagnostichen Verwerthung der oberen Bronchoskopie bei Lungencarcinom.
Berl. klin. Wchnschr., 1900, xxxvii, 437-440.
Lakin (C. /?.)• Primctry chondroma of the lung. Arch. Middlesex Hosp., London, 1912,
xxv, 37-39.
Le Count (E. R.). Primary carcinoma of the lungs. Tr. Chicago Path. Soc., 1899-1901,
iv, 67-71.
Lemann (I. /.). Carcinoma of the lung apparently primary. N. Orl. M. & S. J., 1914-15,
Ixvii, 786-789.
Lubarsch (O.). Zur Kenntniss der Knochenbildungen in Lunge und Pleura. Verhandl.
d. Gesellsch. deutsch. Naturf. u. Aerzte, 1900, Leipzig, 1901, Ixxii, pt. 2,
ii, 15-17.
McPhedran (A.). Carcinoma of the lung and pleura with occlusion of superior vena cava.
Canad. Pract. & Rev., Toronto, 1900, xxv, 17-21.
Otten (M.). Die Rontgendiagnose der Lungengeschwiilste. Fortschr. a. d. Geb. d. Ront-
genstrahlen, Hamburg, 1910, xv, 1-31.
Pdssler (H.). Ueber das primdre Carcinom der Lunge. Arch. f. path. Anat. [etc.], Berlin,
1896, cxlv, 191-278. 1 pi.
Rolleston (H. D.) & Trevor (R. S.}. A case of primary sarcoma of the lung simulating
empyema; with remarks on the nature of primary malignant disease of the
lung. Brit. M. J., London, 1903, i, 361-363.
Schmidt (R.}. Zur klinischen Diagnostik der Miliarcarcinose der Lungen. Med. Klin.,
Berlin, 1913, ix, 2059-2061.
Stevens (A. A.}. Malignant disease of the lung, with special reference to sarcoma. Am.
J. M. Sr.., Philadelphia & New York, 1912, cxliv, 193-202.
Taylor (F.). A case of cancer of the lung and mediastinum. Guy's Hosp. Gaz., London,
1901, xv, 177-184.
DISEASES OF THE PLEUKA 653
Weil (A.). Drei Fdlle von Lungentumoren mil ungewohnlichem rontgenologischen Befund.
Fortschr. a. d. Geb. d. Rontgenstrahlen, Hamburg, 1912, xix, 142-148.
Welter (C. V.). Primary carcinoma of the larger bronchi. An analysis of 90 cases with
regard to pathology, symptomatology and diagnosis, and a report of a new
case. Arch. Int. M., Chicago, 1913, xi, 314-333.
West (£.)• New growths of the lung and pleura. St. Earth. Hosp. Rep., 1897. London,
1898, xxxiii, 109-137.
F. Diagnosis of the Principal Diseases of
the Pleura
The principal diseases of the pleura include :
1. Inflammations of the pleura (pleuritis) ;
2. Circulatory disturbances involving the pleura (hydrothorax and
hemothorax) ; 4
3. Air or gas in the pleural cavity (pneumothorax) ; and
4. Tumors of the pleura.
1. Inflammations of the Pleura (Pleuritis, Pleurisy)
Pathology. — Inflammations of the pleura may be (a) simple (due chiefly to
pyogenic microorganisms— streptococci, pneumococci, influenza bacilli, etc.), in
which case they may be acute or chronic; or (b) specific (tuberculosis, luetic, etc.).
The exudate in acute pleuritis may consist chiefly of fibrin (dry pleurisy or
pleuritis sicca), or of fluid (pleurisy with effusion or pleuritis exudativa). In
the latter case, the exudate may be serous, serofibrinotis, hemorrhagic or purulent.
A purulent effusion is sometimes spoken of as an empyema or pyothorax.
Such pleuritides may have their origin in:
(1) Inflammations or infarcts of the lung, with extension to the pleura;
(2) Inflammations of neighboring organs extending through (pericardium,
bronchial lymph glands, peritoneum), or perforations from abscess of the liver
or spleen, from ulcer of the stomach, or from carcinoma of the stomach or of the
esophagus ;
(3) A general infection (septicemia, pyemia, articular rheumatism, scurvy,
smallpox; or
(4) A metastatic infection from some local focus (tonsillitis, sinusitis, etc.).
An acute pleurisy may end in complete absorption of the exudate, in the for-
mation of adhesions (organization of the exudate), or, in chronic pleurisy with
thickening. Sometimes we meet with encapsulation of an exudate. Calcification
or ossification of the pleura occasionally occurs.
Of the specific pleurisies, tuberculosis is by far the most common. Tuberculous
pleuritis usually arises by extension from the lungs or from the bronchial glands.
Syphilis and actinomycosis of the pleura are rare.
The clinical recognition of the existence of pleurisy depends chiefly upon the
results of physical examination, less upon the subjective symptoms present. The
diagnostic procedure is divisible into two parts; (1) the detection of the signs of
anatomical lesion; and (2) the etiological or bacteriological diagnosis.
654 DISEASES OF THE BESPIKATOKY APPAKATUS
For clinical purposes, three main types of anatomical lesion are dis-
tinguishable :
(a) Dry or plastic pleurisy (pleuritis sicca) ;
(b) Pleurisy with effusion (pleuritis exudativa) ;
(c) Chronic pleurisy with adhesions or with pleural thickening
(pleuritis chronica productive).
(a) Dry or Plastic Pleurisy
(Pleuritis sicca)
Definition. — Ah inflammation of the pleura in which the exu,date con-
sists chiefly of fibrin.
- Etiology. — By far the most common cause
of dry pleurisy is a tuberculous infection. But
it may follow trauma, or may occur temporarily
at the onset of a lobar or a lobular pneumonia,
in carcinoma, or as a forerunner of a sub-
phrenic abscess.
Symptoms and Signs. — The patient usually
complains of pain in the chest on the side
affected, most often in the lower axilla, and
tries to lessen it by diminishing the respiratory
movements on that side. There may be a little
cougli, with slight fever. Friction fremitus
may be palpable. On auscultation, a friction
rub (q. v.) of variable intensity is audible, and
is the main criterion in diagnosis. Such pleural
friction is usually loudest in regions in which
the excursion made by the visceral pleura over
the parietal pleura during respiration is great-
est, that is, at the lower margins of the lung
and in the axillary line. The sound is a more
or less interrupted one and is usually-, audible
during both expiration and inspiration. It is
increased by pressure on the stethoscope.
Occasionally, a dry pleurisy may be demon-
strable at one apex (though a rub here is rare
owing to the minimal movement), or in the
diaphragmatic pleura (friction rub occasion-
ally, though rarely, audible near diaphragmatic
attachment ; hiccough common ; pain at the
lower margin of the thorax, especially on cough-
ing or on retching, sometimes referred to the
Fig. 177. — Areas in Which
Pain and Hyperalgesia \\'<MV
Present in a Case of Dia-
phragmatic Pleurisy. Shaded
Area on Left Shoulder is in
the Cutaneous Distribution
of the Fourth Cervical
Nerve, and is an Evidence of
the Conduction of a Stimu-
lus from the Diaphragm by
the Phrenic Nerve, Which
Leaves the Spinal Cord with
the Fourth Cervical Nerve.
Phrenic Nerve Contains Af-
ferent Fibers as Well as
Efferent (Motor), and it is
in all Probability by the
Former that the Stimulus
is Conveyed to Center of
Fourth Cervical Nerve in
Cord. Shaded Area in Ab-
domen is in Region of Dis-
tribution of Eighth and
Ninth Thoracic Nerves.
(After J. Mackenzie, "Symp-
toms and their Interpreta-
tion," published by Shaw &
Son, London.)
DISEASES OF THE PLEUKA 655
abdomen; s.udden contraction of upper part of M. rectus abdominis on
diseased side on deep inspiration, or so-called "respiratory abdominal
reflex" of R. Schmidt; pain on pressure at certain points, namely, (1)
between the sternal and the clavicular attachment of the M. sternocleido-
mastoideus, (2) the sternal margin of the first intercostal space, (3) the
junction of the parasternal line with a line corresponding to the course of
the 10th rib, (4) line of the diaphragmatic attachment, and (5) the spines
of the 4th and 5th cervical vertebrae).
Care should be taken not to confuse a friction rub with (a) skin
sounds, from slipping of the stethoscope, (b) muscle sounds, or (c) atelec-
tatic crackles.
A dry pleurisy may disappear in a few days, or it may last for weeks
or even for months. It is always important to search for what "lies behind
it."
(b) Pleurisy with Effusion
(Pleuritis exudativa)
Definition. — An inflammation of the pleura associated with a fluid exu-
date ; the fluid may be serous, serofibrinous, serohemorrhagic, purulent, or
putrid.
i. Pleurisy with Serous or Serofibrinous Effusion
(Pleuritis serosa and Pleuritis serofibrinosa)
Etiology. — The majority of cases are due to tuberculous infection. Bac-
teriological examinations of the centrifugate by means of stained smears
or by cultural methods in the tuberculous cases may be negative, but in-
oculation of a guinea-pig with the sediment is usually positive. Even
when bacteria other than tubercle bacilli are demonstrable in the cen-
trifugate, the possibility of a mixed infection should not be lost sight of.
Certainly 80 per cent or more of all serofibrinous pleurisies have a tuberculous
basis. In the 20 per cent (or less) that are non-tuberculous, any one of several
varieties of bacteria may be responsible. Most often, perhaps, the pneumococcus
is found. Streptococcus and staphylococcus pleuritides are also not uncommon.
More rarely, the B. typhosus, the B. diphtheriae, the meningococcus, Friedlander's
bacillus, or other bacteria may be met with.
When the pleuritis is the only local manifestation of the infection it is said to
be "primary" or "idiopathic" ; when, however, it is discoverably due to propaga-
tion from an inflammation in the neighborhood of the pleura, or to metastatic
deposition in the pleura of bacteria brought by the ' blood current from some
distant focus of infection, it is said to be "secondary." In the last analysis, we
must believe that all pleuritides are secondary; we call them "primary" only when
we cannot discover the mode of infection of the pleura.
Symptoms and Signs. — In some instances, the onset is acute, with stitch
in the side, chill, fever, tachycardia and dyspnea; in other instances,
656 DISEASES OF THE RESPIRATORY APPARATUS
the onset may be insidious, the patient complaining of nothing but a little
shortness of breath, though physical examination may reveal the presence
of a pleural effusion of considerable size.
The GENERAL SYMPTOMS may or may not be pronounced. The fever is
rarely high; it may be continuous or remittent, and the temperature
usually falls by lysis. Sometimes, especially in the aged, there may be no
fever at all. When fever is present, the axillary temperature may be a
little higher on the affected than on the healthy side.
The most constant general symptom is pain. It is sometimes severe
at the beginning, and is increased by any movement, but especially by
attempts at deep inspiration, by coughing, or by sneezing. The pain is
usually referred to the side or the back of the thorax, though it may radiate
into the shoulders and arms, or into the abdomen. The pain may errone-
ously be thought to be due to intercostal neuralgia, to muscular rheuma-
tism, or to an acute surgical condition within the abdomen. As the
effusion develops, the pain may disappear.
. If cough or sputum be present, we must blame an accompanying
bronchitis rather than the pleuritis itself. Chills may occur. Sweats are
common, especially during remissions of the fever. Digestive disturb-
ances, including anorexia, nausea, and vomiting are frequently present
As. the effusion develops, the output of urine is diminished (oliguria) }
during convalescence, as the exudate is absorbed, there is often polyuria.
The urine may contain a trace of protein and a few casts, owing to an
accompanying toxic nephropathy. During an attack of pleurisy, the
patient may grow very weak, and may suffer a considerable loss in body-
weight.
The LOCAL SYMPTOMS are those upon which the diagnosis depends.
On inspection, the posture of the patient may give a clew; the patient's
tendency is to lie on the side affected, rather than on his back, assuming a
"diagonal'' lateral position so as to give more freedom for expansion of
the lung of the healthy side. When the effusion is large, there may be
orthopnea, and the sitting posture is assumed; if it- be small, the dorsal
decubitus may be comfortable. Xow and then, there is an exception to
the general rule and the patient insists on lying on the healthy side, assert-
ing that this position is the least painful. While the effusion is being-
formed there is some enlargement of the whole half of the thorax on
the side affected, the bulging being most marked in the region of the fluid.
The scapula of the diseased side stands a little high and there is a little
lateral curvature of the spine with concavity toward the healthy side. The
skin over the region of the effusion may be slightly turgid. On inspira-
tion, there is visible lagging on the diseased side and the expansion is less ;
the lagging is noticeable, also, at the beginning of expiration. The inter-
costal spaces are widened on the diseased side; they may retract slightly
on inspiration. Litten's phenomenon is absent. The veins of the neck
DISEASES OF THE PLEUEA 657
are overfull, and the apex beat of the heart, if visible, can be seen to be
displaced toward the side opposite the effusion.
On palpation, the vocal fremitus will be found to be absent, or greatly
diminished, over an effusion ; just above the level of the fluid, it may be
exaggerated owing to the proximity of compressed lung; still higher, it
may be normal. In testing the vocal fremitus in a woman, we ask her to
pitch her voice low when counting "one, two, three" or saying "ninety-
nine," since the fremitus is most marked when the pitch of the voice corre-
sponds to the Eigenton of the lung (F. v. Miiller). It should be remem-
bered that in emphysema, and in old people with rigid thorax, the vocal
fremitus is often indistinct even when the pleurae are normal. Should the
pleura become thickened, the vocal fremitus may remain absent or feeble
even after the absorption of the effusion.
Dislocation of the heart to the right or to the left by an effusion in a
pleural cavity can often be suspected through determination of the position
of the apex beat by palpation.
On percussion, if the effusion reach any considerable size (say 400-600
c.c.), dullness or flatness, with total absence of tympany, can be-made out
over it. The upper limit of flatness (light percussion) and increased re-
sistance on percussion assumes a typical curved form (except when the
effusion is so large as to cause dullness over the whole side from base almost
to apex). Thus, in medium-sized effusions, the upper limit of dullness
extends from the spine upward and lateralward to reach its highest level
in the posterior axillary line, whence it curves downward and forward
toward the middle line in front (Ellis' line, Damoiseau's curve). Some-
times the line takes the form of a letter S turned on its side.
In the lower back, close to the spine on the healthy side, there is a
triangular area of relative dullness with base below and apex in the spine
above the level of the effusion. This is known as the paravertebral tri-
angle of dullness (Grocco's triangle, v. Koranyis triangle). Authors vary
in their explanations of the origin of this dullness, but the evidence seems
to favor the view that it is due to dislocation of the posterior inferior
mediastinum and compression of the healthy lung. The sign is of some
value in the differential diagnosis of pleural effusion from pneumonia of
the lower lobe.
In the lower back, close to the spine on the diseased side, there can be
demonstrated a triangular area of relative resonance after the patient has
coughed and breathed deeply; the apex of the triangle is below and the
base above (Garland's triangle). The note is not perfectly clear owing
to the fact that the lung is compressed and, besides, there may be a very
thin layer of fluid over it (Sahli), but it is relatively clear in contrast with
the flat note lateral from it (below Ellis' line). Garland's triangle is
not present when the exudate is large. In lobar pneumonia such a tri-
angle of relative resonance near the spine is never met with.
658 DISEASES OF THE EESPIEATOEY APPAKATUS
Fig. 178. — Greece's Sign — Aortic Aneurism ; Hydrotborax on Right Side.
(Mod. Service, J, II. II.)
/
Dullness or flatness on light percussion in the upper part of Traube's
semilunar space is an important diagnostic sign of beginning accumula-
tion of fluid in the left pleural cavity. On the right side, dullness due to
effusion may fill up the cardiohepatic angle and, on superficial examina-
tion, mislead the physician into thinking it is due either to an effusion
into the pericardial cavity, or to a dilatation of the right side of the
heart.
The upper limit of dullness due to pleural effusion changes a little on
deep inspiration, and on change of posture, unless it be encapsulated ; the
change is rarely great, however.
One striking feature on more forcible percussion over an effusion de-
serves especial mention, namely, the increasing intensity of the dullness
(flatness) and of the feeling of resistance on percussing from above down-
ward ; on immediate percussion with the finger tips, the increased feeling
of resistance may be most easily experienced.
On percussing over the lung just above the upper level of the effusion,
a zone of loud tympanitic resonance is met with (Skodaic resonance). If
an effusion is large, Skoda's resonance may be elicitable in the infra-
clavicular region, owing to the relaxation of the lung. Sometimes the
pitch changes with the phases of respiration (Williams' "tracheal tone"),
or on strong percussion a "cracked-pot sound" may come out.
DISEASES OF THE PLEUEA 659
When the effusion is on the right side, the lower edge of the liver may
be found, on percussion, to lie lower than the costal margin.
Changes in the size of an exudate during absorption are best followed
by mensuration with a tape, rather than by percussion (Staehelin). Four
measurements should be carefully made, namely, that of each half of the
thorax above the nipple and also at the level of the xiphoid. As an effu-
sion diminishes in size, both halves of the thorax grow smaller, but the
reduction is much more marked on the side of the effusion. In the late
stages of a pleuritis, the dimensions of the diseased side may be less than
those of the healthy side, owing to retraction > of the thorax.
On auscultation, a friction-rub may be audible at the very beginning ;
even after an effusion has developed, a rub may be audible near its upper
limit; as the fluid becomes reabsorbed a rub may become audible at the
former site of an effusion as soon as the visceral and parietal layers of
the pleura again come into contact.
Over an effusion the breath sounds may be diminished or entirely
absent according to the thickness of the layer of fluid. Occasionally, dis-
tant bronchial breathing, bronchophony, and rales are audible through an
effusion, especially in children. On the healthy side, the breath sounds
may be exaggerated owing to "vicarious emphysema." The voice sounds
are usually distant behind an effusion; as an effusion is developing, a
strange, high-pitched, bleating or nasal quality may characterize the voice
sounds auscultated at the upper margin of the effusion (egophony). It
has been asserted that the whispered voice grows ever less distinct as an
exudate grows richer in cells (Baccelli's sign of empyema) ; but the sign
is notoriously UP reliable, and it is better to study the cell count of fluid
obtained by exploratory puncture.
It is nearly always, if not always, advisable to make an exploratory
puncture when pleuritis with effusion is either known, or suspected, to
exist. The chemical, bacteriological, serological, and cytological methods
of studying the fluid obtained are described in the section on Exploratory
Punctures (q. v.).
On rontgenoscopy, it is sometimes possible to discover small pleural
effusions not demonstrable by percussion. If the effusion be confined to
the pleural sinus, it is necessary carefully to adjust the tube and the
direction of the transillumination if the shadow is to be discovered. It is
best to have the patient assume a sitting or a standing posture, if he be not
too ill. In larger effusions, the shadow is seen to be highest in the lateral
part of the thorax and lowest and most intense near the spine behind and
near the sternum in front. The upper limit of an effusion appears in the
rontgenogram as an indistinct concave border to the shadow, very differ-
ent from the margin of a pneumonic infiltration or of a tumor.
The dislocations of the organs (heart, mediastinum) are easily visible
fluoroscopically. The lung area on the healthy side may be less clear than
660 DISEASES OF THE RESPIRATORY APPARATUS
normal if an effusion be large, owing partly to compression, partly to
hyperemia. When the effusion is small, the lung on the affected side may
be unusually clear owing to "vicarious emphysema."
Several ATYPICAL FORMS of serofibrinous pleurisy must be mentioned,
including (1) the diaphragmatic form, (2) the interlobar form, (3) the
mediastinal form, and (4) the pleurisy that is a part of a polyserositis.
In diaphragmatic pleurisy with serofibrinous effusion, the fluid ac-
cumulates between the lower surface of the lung and the diaphragm. The
symptoms at onset resemble those of dry pleurisy in this situation. (See
Pleuritis sicca.) On x-ray examination, the shadow due to the effusion
may be visible.
In interlobar pleurisy with serofibrinous effusion, the fluid may be
poured out in the cleft between two lobes, and, owing to adhesions, be
prevented from reaching the general pleural cavity. A zone of dullness
varying in width with the volume of the effusion can be made out on the
surface of the chest in regions corresponding to the junctions of the lobes.
There may be Skodaic resonance above and below the narrow zone of
dullness, owing to relaxation (or compression) of the adjacent lung tissue.
The breath sounds are feeble over the zone of dullness, whereas above and
below it the breathing may be almost bronchial in type. Moist rales may
be audible in the adjacent lung. The condition may be mistaken for
tumor of the lung, pneumonic infiltration, lung abscess, or interlobar
empyema. The rontgenogram is of great aid in distinguishing an inter-
lobar effusion from tumor or pneumonia, as is also exploratory puncture
with a long needle in the axillary line over the zone of dullness; the laller
will also differentiate between a serofibrinous and a purulent exudate.
(See Interlobar Empyema.) Occasionally, an interlobar exudate breaks
through into the general pleural cavity at one end of an interlobar cleft,
but remains circumscribed there, owing to adhesions in the neighborhood ;
in this way arises the so-called "shirt-stud-shaped effusion" of Sabourin.
In mediastinal pleurisy with serofibrinous effusion, the fluid collects
between the mediastinal and the pulmonary pleura and recognition may
be very difficult. It may be located in the anterior or in the posterior
region of the chest, on either the right or the left side. Good accounts
of this form of pleuritis will be found in the articles of Frick and of
Savy.
In serofibrinous pleurisy as a part of a polyserositis, there may be
fluid also in the pericardial cavity, in the peritoneal cavity, or in both.
Such a polyserositis is most often tuberculous, but a non-tuberculous form
does occur. (See also Pick's Syndrome.)
Diagnosis. — The local signs of pleurisy with effusion are very character-
istic. (See above.) A serofibrinous exudate can be distinguished from
(1) the purulent exudate of an empyema, and (2) from the transudate of
a hydrothorax, by study of the fluid obtained by exploratory puncture ; the
DISEASES OF THE PLEUKA 661
etiological diagnosis can also often be made from the study of this fluid,
and from the study of the body as a whole.
In the differential diagnosis, we must also rule out (3) pneumonia
(vocal fremitus usually increased, topography of dullness and its slightly
tympanitic character, crepitant rales, no marked dislocation of adjacent
organs, "dry tap," rontgenograrn ; sometimes a pneumonia and a pleurisy
with effusion coexist) ; ^nd (4) pleural thickening. (See below.)
ii. Pleurisy with Serohemorrhagic Effusion
The local signs are like those of pleurisy with serofibrinous effusion.
On exploratory puncture, the serohemorrhagic character is discovered.
Such an exudate points nearly always to either a tuberculous or a neo-
plastic etiology, just as do chylous and pseudochylous pleural exudates.
In rare instances, we may meet with a serohemorrhagic exudate in pneu-
mococcus pleuritis or in a pleurisy from any cause occurring in association
with a hemorrhagic diathesis.
iii. Pleurisy with Purulent Exudate
(Plem'ili* pnrulenta, Pleuritis suppurativa, Empyema pleurae)
Etiology. — Pleuritis with purulent exudate is usually secondary to lobar
pneumonia (pneumococcus infection) or to pulmonary phthisis (tubercu-
lous infection) ; sometimes, especially in children, it is secondary to a
bronchopneumonia due to streptococcus infection. In the careful studies
by Dr. F. T. Lord of Boston of the pus from empyema cases, the pneu-
mococcus was found to be the cause in 39.4 per cent, the streptococcus in
20.4 per cent, the staphylococcus in 3.6 per cent, and mixed infections in
16 per cent; in 1'8.2 per cent the pus was sterile. When no bacteria grow
on media suitable for the pneumococcus and for ordinary pyogenic organ-
isms, the etiological agent may have been the B. tuberculosis (guinea-pig
inoculation), or an anaerobic organism (see Putrid Empyema) ; or a
pneumococcus may have been present and been killed off before the culture
was made.
Symptoms and Signs. — Empyema pleurae is always the result of a
severe infection; either the microorganism causing the pleuritis is espe-
cially virulent or the patient's resistance is low, or both conditions simul-
taneously obtain. The severity of the general symptoms is further
dependent upon the absorption of the disintegrating leukocytes of the pus
shut up in the pleural cavity. It is very important to distinguish clini-
cally between a purulent and a nonpurulent effusion in cases of pleuritis,
for, in empyema, the pus cavity should be promptly evacuated, and pro-
vision made for thorough drainage.
The GENERAL SYMPTOMS may be so severe as to excite suspicion of a
purulent exudate. Intermittent fever, tachycardia^, sweats, and chilly
662 DISEASES OF THE KESPIKATORY APPARATUS
sensations are common, and there are often repeated severe chills. The
patients grow rapidly pale and begin to emaciate. There is usually an
outspoken hyperleukocytosis with marked relative increase in the poly-
morphonuclear neutrophils in the blood. It should be remembered, how-
ever, that in children, in the aged, and in decrepit patients of any age, the
onset of empyema may be insidious and without symptoms directing the
physician's attention to the respiratory apparatus; in such cases, the
thorough routine examination alone saves the clinician from overlooking
the important local physical signs.
On PHYSICAL EXAMINATION, the findings, except on exploratory punc-
ture, may be indistinguishable from those described above for pleurisy
Fig. 179. — Pleurisy and Empyema. (X-ray Dept, J. II. H.)
with serofibrinous effusion (q. v.). Occasionally, there is edema of the
wall of the chest opposite the exiidate, or a pulsating bulging (empyema
pulsans) may be visible, the latter when it occurs being almost always on
the left side. An encapsulated empyema, or an interlobar empyema, may
be small and yield but few physical signs ; here, a rontgenogram is of the
greatest help in the recognition of the exact position and size of the
exudate, and gives us the clew to the proper site for exploratory puncture.
The same is true of diaphragmatic and of mediastinal empyema. In the
DISEASES OF THE PLEURA 663
rontgenogram the "hanging shadow" extending from the region of one
shoulder toward the heart is characteristic of interlobar exudate.
Bilateral empyema is rare, but does occasionally occur.
Empyema in connection with pneumonia (see Gerhardt's studies) may
either accompany the pneumonic process (parapneumonic empyema) , or
it may be a sequel to it (metapneumonic empyema).
A tuberculous empyema is usually secondary to pulmonary tubercu-
losis, but it may be met with as a complication of caries of a rib or of the
spine. It is very often accompanied by pneumothorax (pyopneumo-
tliorax) .
Empyema should be suspected whenever in the course of pneumonia there is a
change in the patient's condition with appearance of a paroxysmal, non-produc-
tive cough, chills, sweats and a more remittent type of fever. The physical signs
may readily permit one to localize the purulent accumulation; but in interlobar
or other encapsulated forms the diagnosis is often difficult. Exploratory puncture
should be resorted to early. Rontgenograms may yield valuable information. Fre-
quently, however, the condition is first thought of when, at the end of the usual
duration of the pneumonia, the fever and leukocytosis persist. Delayed resolution
explains a number of such cases, but this diagnosis should never be made until
every effort has been put forth conclusively to rule out the possibility of an empy-
ema or of a tuberculous pneumonia.
If is a great pity that an empyema should ever be overlooked, for it is
rare that the pus undergoes spontaneous absorption; except in the para-
pneumonic form, and occasionally in the empyemas of children. It is not
uncommon to receive in hospitals patients that have had an undetected
empyema for weeks, and who, through the long-continued infection and
high fever, have become extremely prostrated and emaciated. Such pa-
tients may have already suffered general amyloid change (spleen, kid-
neys, intestines) ; some of them have metastatic infections (arthritis,
endocarditis, meningitis, brain abscess). Occasionally, the pus breaks
through the wall of the pleural cavity, either into the lung, or through the
wall of the chest (empyema necessilatis} ; in rare instances, there may be
perforation into the pericardial cavity, the mediastinum, the esophagus,
the trachea, or a large blood vessel.
Diagnosis. — As soon as signs of effusion into the pleural cavity have
been discovered, an exploratory puncture should be made, even though one
may believe the exudate to be non-purulent. In obscure/ infections, the
possibility of a small empyema should be kept in mind, even in the ab-
sence of symptoms referable to the chest ; a rontgenogram of the whole
chest may reveal an encapsulated effusion, an interlobar, a supradia-
phraginatic, or a mediastinal shadow.
In cases' of pneumonia and of pulmonary tuberculosis, the possibility
of empyema, either as a complication or as a sequel, should be thought of.
When a pleural effusion has been shown to be serofibrinous, it should
664 DISEASES OF THE RESPIEATOKY APPARATUS
be remembered that it may become purulent later, and, also, that a pleu-
ritis may have a serous exudate in one region and a purulent exudate in
another.
I have been astonished to find how often diagnosis is delayed through
failure to make exploratory puncture with a long needle of wide lumen.
It is well to keep a vacuum in the syringe during withdrawal of the
needle, and, after withdrawal, to drive any droplet of fluid out of the
needle for examination for pus. A single "dry tap" by no means excludes
empyema. When negative, repeated puncture at several sites may be
necessary before a conclusion that there is no empyema is warranted.
In the differential diagnosis from conditions simulating empyema,
great difficulties are sometimes encountered. Even the most experienced
consultant may at times be at a loss to distinguish a mediastinal enipv-
ema from other mediastinal masses, a diaphragmatic empyema from a sub-
phrenic abscess, an interlobar empyema from a lung tumor, or an encap-
sulated empyema from a pulmonary abscess extending to the surface of the
lung. If, however, the anamnesis be carefully considered, a thorough
general physical examination be made, the leukocytes counted, an explora-
tory puncture done, and rontgenograms utilized, there should be but few
errors, either of omission or commission, made.
iv. Pleurisy with Putrid Exudate
(Putrid Empyema, Fetid Pleurisy, Ozenous Pleuritis, Gangrenous
Empyema)
Etiology. — The foul odor is due to the presence of putrefactive bacteria ;
these are nearly always, if not always, anaerobic.
A putrid empyema may follow pulmonary gangrene, putrid bronchitis,
or bronchiectasis. Or it may be due to some perforative lesion of the
esophagus or to extension from a subphrenic process.
Symptomatology. — The patients deteriorate more rapidly than in non-
putrid empyema. They emaciate quickly and look badly; the pulse is
small and frequent, there is complete anorexia and the prostration may be
extreme.
On exploratory puncture, the punctate yields a putrid odor, and on
this the diagnosis depends. Sometimes gas develops. (See Pyopneumo-
thorax).
(c) Pleural Thickening
(Pleuritis chronica product iva)
Definition. — A chronic inflammation of the pleura with formation of
new fibrous tissue and with adhesions between the two layers._ There may
be (1) obliteration of a whole pleura! cavity on one side with retraction
DISEASES OF THE PLEURA 665
of the thorax, (2) partial but extensive obliteration, or (3) circumscribed
adhesions.
Etiology. — Delicate pleural adhesions and slight thickening may follow
simple pleurisies, but great thickenings are most often due to tuber-
culous pleurisy.
Symptoms and Signs. — The patients may be slightly cyanotic, and they
often show dyspnea on exertion. In obliteration of one pleural cavity
with retraction of the thorax (retrecissement thoracique), one side of the
chest is narrower and shorter than the other, there is scoliosis with con-
cavity toward the shrunken side, the shoulder is lower than its fellow
(as is also the nipple), and the intercostal spaces are narrowed. There
is diminished expansion, dullness on percussion, and enfeeblement of
breath and voice sounds and of vocal fremitus. Litten's phenomenon is
absent. As the side becomes shrunken, the mediastinum and the heart
are drawn over. If there be much thickening, an exploratory needle meets
characteristic resistance and may have to be shoved through a thick layer
of tough fibrous tissue before the resistance is overcome (Rosenbach's
"palpatory puncture").
On x-ray examination, the whole lung area is darker than normal, the
dislocation of the heart and mediastinum is obvious, and the changes in
the form of the bony thorax are visible. More circumscribed pleural
thickenings may be recognizable as broad shadows or as cords. These
may be difficult to distinguish from exudates unless it be remembered
that when a pleural thickening is close to the rb'ntgenoscopic screen or
the x-ray plate, the shadow is deeper than when the examination is made
in the opposite direction, whereas with exudates, the difference does not
exist at all or is only very slight.
When a pleural thickening is calcified, remarkable x-ray pictures are
obtained (circular or radiating shadows). Adhesions to the diaphragm
are often exquisitely demonstrable by the x-ray. A plate exposed on deep
inspiration shows the distortion of the upper surface of the diaphragm
at the point of adhesion. When patients complain of pain on deep inspira-
tion, especially with change of weather, pleural adhesions should be sus-
pected; even if a rontgenogram be negative, one should insist upon
thorough rontgenoscopy in different directions before ruling out pleural
adhesions ; many supposed simulants have, in reality, adhesions.
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Gee (5.). Revised byT.J. Harder. Pleurisy. In: Syst. Med. (Allbult & Rolleston). 89.
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666 DISEASES OF THE KESPIKATOKY APPARATUS
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Experimentelle Beilrdge zur Lehre vom Lungenkreislauf und von der
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DISEASES OF THE PLEUKA 667
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3. Symptoms
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to the tubercular form. Med. &Surg. Rep. Presbyterian Hosp., New York,
1904, vi, 201-220.
Coriat (I. H.}. The occurrence of the Bence-J ones albumin in a pleuritic effusion. Am. J.
M. Sc., Philadelphia & New York, 1903, n. s., cxxvi, 631-643.
Courmont (P.) & Nicholas (/.)• Formule urinaire dans la pleuresie tuberculeuse (poly-
urie, hypochlorurie, et albuminurie de la convalescence}. Bull. Soc. de
med. de hop. de Lyon, 1904, Hi, 266-280.
668 DISEASES OF THE KESPIKATOKY APPAKATUS
Damoiseau (//.)• Recherches chniques sur plusieurs points du diagnostic des epanchemenis
pleuretiques. Arch. gjsn. de med., Paris, 1843, 4. s., Hi, 129; 408.
Dieulafoy (G.). Means of telling whether an attack of serofibrinous pleurisy is tuberculous.
Internal. Clin., Philadelphia, 1902, 12. s., in, 87-106.
Earl (H. C.). The cytology of serous and serofibrinous effusions of the pleural and other
serous cavities, and of the cerebrospinal fluid. Tr. Roy. Acad. M. Ireland,
Dublin, 1904, xxii, 285-307.
Eastman (J. /?.)• Diagnosis of supra- and subdiaphragmatic suppuration. Lancet-Clinic,
Cincinnati, 1904, n. s., liii, 1-7.
Ewart (W.}. A rapid method for the diagnosis and estimation of pleural effusions. Poly-
clin., London, 1906, x, 13-16.
Floyd (C.). The interrelationship of dry pleurisy, pleurisy with effusion and empyema.
J. M. Research. Boston, 1914-15 , xxxi, 261-275.
Gerhardt (C.). Zur Geschichte des Bruststiches. Berlin, 1890. 8°.
Gougerot (H.). Note sur revolution des reactions cellulaires dans les epanchements s6ro-
fibrineux, d propos d'un cas de pleuresie typhoidiquc. Arch, de med. exper.
et d'anat. path., Paris, 1906, xviii, 593-608.
Greene (C. L.}. A fluoroscopic and percussion sign of pleuritic effusion hitherto unde-
' scribed. Report of two illustrative cases. New York M. J ., 1902, Ixxvi,
240.
Rhythmic lateral displacement of tJie heart as a sign of unilateral pleuritic
exudate. Am. J. M. Sc., Philadelphia & New York, 1906, cxxxi, 519-522.
Gulland (G. L.}. Cytodiagnosis of pleural effusions. Tr. M.-Chir. Soc., Edinburgh, 1901-
02, n. s., xxi, 229-239. 1 pi.
Herrick (J. B.). Some points concerning (he diagnosis of pleurisy with effusion, with particu-
lar reference to misleading physical signs. Medicine, Detroit, 1898, iv,
705-716.
Huchard (H.) & Flessinger (N.}. La valeur diagnostique de la ponction pleuralc chez les
cardiaques et les renaux. Rev. gen. de din. et de therap., Paris, 1906,
xx, 565-567.
von Koranyi (A.). The differential diagnosis of pleuritic effusions. Med. Press & Circ.,
London, 1902, n. s., Ixxiv, 33.
Lord (F. T.}. An air-tight trocar for thoracentesis. J. Am. M. Ass^, Chicago, 1908, i, 122.
Montgomery (C. M.} & Eckhardt (E. A.}. Factors involved in some cases of pleural
fluid associated with normal or increased vocal resonance. Arch. Int.
Med., Chicago, 1915, xv, 1040-1045.
Morse (J. L.). The leucocyte count in serous pleurisy. Am. J. M. Sc., Philadelphia &
New York, 1900 f n. s., cxx, 658-661.
Oliver (T.). A clinical lecture on pleurisy. Clin. J., London, 1892-93, i, 161-165.
Pat on (/.)• Calcareous masses removed from the pleural cavity during life. Tr. Glasq.
Path. & Clin. Soc., 1884-86, ii, 71-76.
Pfender (C. ^4.)- Autoserotherapy in serofibrinous pleurisy. Wash. M. Ann., 1914. xiii-
83-113.
Renon (L.). La pleuresie droite des cardiaques. Bull, med., Paris, 1905, xix, 453-455.
Rubino (C.) & Vattuone (A.). L'autosieroterapia nelle pleuriti essudative (Osservazione
cliniche e ricerche fisico-chimiche sui versamenti) . Gazz. Internaz. di Med.,
Napoli, 1914, xvii, 929-935.
Schlesinger (H.}. Die entzundlichen Pleuraergiisse im Alter; nach Literaturangaben und
unter Benutzung eigenerBeobachtungen. Ergebn. d. inn. Med. u. Kinderh..
Berlin, 1914, xiii, 138-150.
Schmidt (A.}. Offene Pleurapunktion. Munchen. med. Wchnschr., 1915, xxvi, 873-874.
Sears (G. G.)» Hemorrhagic pleurisy; a study of thirty cases. Boston M. & S. J., 1896 f
cxxxv, 283-286.
DISEASES OF THE PLEUEA 669
Smith (G. E.}. On the displacements produced by pleural effusion. Lancet, London, 1907,
ii, 890-892.
Tuffier (T.), Jardry (//.) & Gy (A.}. De la calcification pleurale. Rev. de chirurg.,
Paris, 1907, xxxv, 329-346.
West (S.). A case in which the pleura contained several pints of calcareous, mortar-like fluid.
Tr. Clin. Soc., London, 1905-06, xxxix, 42-45.
Widal (F.) & Ravaut (P.). Applications cliniques de V etude histologique des epanchements
serofibrineux de la plevre (pleuresies mecaniques). Compt. rend. Soc. de
biol., Paris, 1900 , 11. s., ii, 201-224.
von Ziemssen (//.)• Symtomatologie und Diagnose der Pleuritis. Leipzig, 1889. 8°.
4. Grocco's Triangle
Beall (K. H.}. The paravertebral triangle of dullness in subphrenic abscess (Grocco's sign}.
J. Am. M. Ass., Chicago, 1907, xlix, 2148-2149.
Blumer (G.}. Some observations on Grocco's sign. Proc. Connect. M. Soc., New Haven,
1908, 239-247.
Calvert (W. J.}. The posterior median pleural boundary, with reference to Grocco's sign.
Am. J. M. Sc., Philadelphia & New York, 1907, cxxxiv, 579-581.
Displacement of the heart by pleural pressures. Johns Hopkins Hosp.
Bull., Baltimore, 1907, xviii, 444-446.
Ewart (W.}. Grocco's triangle; physical and anatomical explanation. Lancet, London, 1907,
ii, 49; 188.
Gordinler (H. C.). The paravertebral triangular area of dullness in pleural effusions
(Koranyi-Grocco sign), with the report of a case of solitary abscess of the
right lobe of the liver presenting this sign, but without an exudate in the
pleural space. Albany M. Ann., 1909, xxx, 314-324.
Grocco (P.). Triangolo paravertebrale opposto nella pleurite essudativa. Lavori d. Cong,
di med. int. 1902, Roma, 1903, xii, 190.
Also: A proposito del triangolo paravertebrale opposto. Riv. internaz. di
din. e terap., Napoli, 1909, iv, 16-18.
Hamburger (F.). Die Pertyssionsbefunde neben der Wirbelsdule bei Pleuritis. Mitt. d.
Gesellsch. f. inn. Med. u. Kindh. in Wien, 1906, v, 76-81.
von Koranyi (A.). Ein Beitrag zur Differentialdiagnostik pleuritischer Ergiisse. Wien.
klin. Rundschau, 1902, xvi, 300-302.
Der diagnostische Wert des Perkussionstones der Wirbelsdule. Pest. M.-
Chir. Presse, Budapest, 1906, xlii, 910-912.
Ueber den Perkussionschall der Wirbelsdule und dessen diagnostische Ver-
wertung; nebst einer Berichtigung beziiglich des pleuritischen (paraverte-
bralen} Dreiecks. Ztschr. f. klin. Med., Berlin, 1906, Ix, 295-313. 1 pi.
Rauchfuss (C.). Die paravertebrale Ddmpfung auf der gesunden Brustseite bei Pleuraer-
giissen. Verhandl. d. Versamml. d. Gesellsch. f. Kinderh. deutsch. Naturf.
u. Aerzte, 1904, Wiesbaden, 1905, xxi, 202-211. 1 pi.
Thayer (W. S.} & Fabyan (M.). The paravertebral triangle of dullness in pleural effusion
(Grocco1 s sign). Am. J. M. Sc., Philadelphia & New York, 1907, cxxxiii,
14-28.
Rdntgenological
Barjon (F.). La courbe de Damoiseau et Vexamen radioscopique des epanchements pleuraux.
Lyon med., 1904, di, 783-789.
Beclere (A.). Vexamen radioscopique des plevres interlobaires et la diagnostic de la sclerose
de I'interlobe. Ann. d'electrobiol. [etc.], Paris, 1902, xli, 491-505.
Bergonie (J.) & Carriere (G.}. Etude fluoroscopique des epancfiements pkuretiques.
Arch, electric, med., Bordeaux, 1899, vii, 301-332.
Eisler (F.). Die interlobare pleuritische Schwarte der kindlichen Lunge im RontgenbUd.
Munch, med. Wchnschr., 1912, ii, 1899-1902.
Engelbach ( W.} & Carman (R. D.) . X-ray studies of serofibrinous pleuritis. Am. J. M.
Sc., Philadelphia & New York, 1911, cxliii, 838-851.
670 DISEASES OF THE RESPIRATORY APPARATUS
Greene (C. L.). A fluoroscope and percussion sign of pleuritic effusion hitherto undescribed;
report of two illustrative cases. N. York M. J., 1902, Ixxvi, 240.
Kohler (A.~). Zur rontgenoskopischen Diagnostik der Pleuritis adhcesiva. Fortschr. a. d.
Geb. d. Rontgenstrahlen, Hamburg, 1903-04, vii, 123-125.
Lehmann & Stapler. Pleuritis exsudaliva im Rontgenogramm; kurze Mitteilung eines
in diagnostischer Hinsicht eigenlumlichen Falles. Fortschr. a. d. Geb. d.
Rontgenstrahlen, Hamburg, 1905-06, ix, 202-204. 1 pi-
Rack (E.). Zur Radiologie pleuraler Ergusse bei Kindern. Ztschr. f. Kinderh., Berlin,
1914, Orig., xii, 1-3. 1 pi.
Stuertz. Zur Diagnose der Pleura-Adhdsionen an Pericard und Zwerchfell. Fortschr. a. d.
Geb. d. Rontgenstrahlen, Hamburg, 1904, vii, 265-272. 1 pi.
Weill & Gar der e. Valeur semeiologique de V ombre radioscopique "en bande transversale"
de la region moyenne du poumon. Bull. Soc. med. d. hop. de Lyon, 1914,
xiii, 262-266.
I
6. Empyema
Ballance (H. A.}. Seven cases of thoracoplasty performed for the relief of chronic empyema.
Brit. M. J., London, 1904, ii, 1561-1566.
Baur (J.), Levy (L.) & Petzetakis (M.). .Un cas d'epanchement puriforme aseptique de
la pleirre a eosinophiles. Arch, de med. exper. et d'anat. path., Paris,
1913, xxv, 581-594. 1 pl>
Beckman (E. H.). Decortication of the lung for old empyema. Northwest Med., Seattle,
1914, n. s., vi, 68-72.
Bovaird (D.}, Jr. Empyema in infants. Med. News, Nciv York, 1899, Ixxv, 825-827.
Broadbent (Sir W.}. Interlobar empyema. Practitioner, London, 1905, Ixxiv, 145-148.
Calvert (W. J.}. The causes of pulsations in empyema. Am. J. M. Sc., Philadelphia &
New York, 1905, n. s., cxxx, 890-893.
Traube's semilunar space in empyema. J. Am. M. Ass., Chicago, 1907,
xlix, 1027.
Carr (J. W.}. A lecture on empyema. Clin. J., London, 1915, xliv, 105-110.
Comby (Jules). De Vempyeme. Paris, 1895, Rueff & Cie. 216 p. 12°.
Cowan (J. M.)« Some notes on empyemata in childhood. Glasgow Hosp. Rep., 1901, Hi,
814-327.
Edington (G. H.}. Shell-like deformity of the ribs from a case of empyema. Glasgow M. J.,
1903, Ix, 121-125.
Thickening of the ribs in chronic empyema. Glasgow M. J., 1905, Ixiii,
836-840.
Faisans & Audusfere. Pleuresie purulente toleree pendant pres de quarante ans. Bull,
et mem. Soc. med. d. hdp. de Paris, 1901, 3. s., xviii, 605-614.
Gefhardt (D.). Ueber parapneumonische Empyeme. Mittheil. a. d. Grenzgeb. d. Med. u.
Chirurg., Jena, 1913, xxvi, 695-700.
Hall (J. N.}. Empyema, with a report of thirty cases. Internal. Clin., Philadelphia, 1906,
15. s., iv, 48-60. 2 pi.
Hamilton (W. F.). Empyema; a study of thirty cases from clinical and bacteriological
standpoints. Montreal M. J., 1900, xxix, 757-765.
Hartwell (J. A.}. Empyema. M. & S. Rep. Presbyterian Hosp., New York, 1900, iv,
131-149.
Henry (F. P.). Report of a case of pulsating empyema necessitates, with three strongly pul-
sating tumors. T~r. Ass. Am. Phys., Philadelphia, 1903, xviii, 71-80.
Koplik (H.). Empyema in infants and children; its frequency, etiology, symptomatology
and prognosis. Med. News, New York, 1902, Ixxxi, 481-483.
Laache (S.}. Zur Kasuistik des doppelseitigen Empyems. Berl. klin. Wchnschr., 1906 „
xliii, 65-67.
DISEASES OF THE PLEUEA 671
•
Lilienthal (#.). Intercostal thoracotomy in empyema; an. original method. N. York M J
[etc.], 1915, ci, 191-193.
Mayo (C. H.) & Beckman (E. H.). Visceral pleurectomy for chronic empyema. Ann.
Surg., Philadelphia, 1914, lix, 884-890. 3 pi. [Discussion], Ix, 126.
Moore (Sir J.}. Empyema or hypophrenic abscess. Tr. Roy. Acad. M., Ireland, Dublin,
1906, xxiv, 75-80.
Morgan (A. C.) & Funk (E. H.). Perforation of the chest wall in empyema (empyema
necessitatis) . Publications from Jefferson M. Coll. & Hosp., Philadelphia,
1915, vi, 127-135.
Murphy (J. /?.)• Empyema. Surg. Clin., Chicago, 1914, Hi, 194-206. 1 pi.
Netter & Boiigault. Acidite du pus des pleuresies a pneumocoques, ses relations avec la
duree de Vepanchement; reaction acide dans un cas d'epanchement puri-
forme amicrobien de la plevre. Compt. rend. Soc. de BioL, Paris, 1914,
Ixxvii, 266-268.
Primrose (A.~). The treatment of chronic empyema. Canad. J. M. & S., Toronto, 1903,
xiv, 77-86.
Robinson (5.). The surgical aspects of those diseases of the thorax that are amenable to
surgical interference. Penn. M. J., Athens, Pa., 1912-13, xvi, 527-531.
Sauer (L. W.}* Twd cases of parapneumonic empyema in children. Arch. Pediat., New
York, 1915, xxxii, 207-209.
Simmons (D. G.). Empyema in country practise. Kentucky M. J., Louisville, 1904-05,
ii, 192-194.
Sinkler (F. W.}. Interlobar empyema. J. Am. M. Ass., Chicago, 1914~~, Ixii, 687-689.
Talley (J. E.). A case of interlobar empyema following pneumonia. Tr. Phila. Pediat.
Soc., New York, 1904-05, i, Papers, 43-46.
Tyrie (C. C.). Atypical empyema in general practice, with illustrative cases and critical
notes. Lancet, London, 1901, ii, 448-450.
Widal (F.) & Gougerot (//.). Pleuresies puriformes aseptiqucs mice polynucleaires intacts
chez les pneumoniques el les cardiaques; benignile du pronostic. Bull.
Acad. de med., Paris, 1907, 3. s., Mii, 36-45.
Wilensky (A. O.}. Empyema of the thorax; a critical study of 299 cases of acute empyema
of the thorax, treated at Mount Sinai Hospital, New York, in the last ten
years. Surg., Gynec. & Obst., Chicago, 1915, xx, 501-514-
Withington (C. F.). A clinical study of 135 cases of empyema based upon the bacteriological
findings in the exudate. Tr. Ass. Am. Physicians, Philadelphia, 1902,
xvii, 222-242.
Zybell (F.). Das Empyem im Sduglingsalter. Ergebn. d. inn. Med. u. Kinderh., Berlin,
1913, xi, 611-639.
7. Putrid Effusions
Dieulafoy (G.}. Les pleuresies ozeneuses; pleuresies f elides, putrides, gangreneuses. Se-
maine med., Paris, 1900, xx, 375-379.
Guillemot (L.}, Halle (/.) & Rist (E.). Recherches bacteriologiques' et experimentales
sur les pleuresies putrides. Arch, de med. exper. et d'anat. path., Paris,
1904, xvi, 571; 677. 2 pi.
8. Interlobar, Diaphragmatic and Mediastinal Pleurisies
Bar ion (F.). Les pleuresies, enkystees de la region du hile; cam-four hilaire de la-ptevre.
fitude dinique et radiologique. J. d. radiol. et d'eleclrol, Paris, 1914, i,
177-182.
Beclere (A.). L'examen radioscopique des plevres interlobaires et la diagnostic de la sclerose
de Vinterlobe. Bull, et mem. Soc. med. d. hop. d. Paris, 1902, 3. s., xix,
157-169.
672 DISEASES OF THE RESPIRATORY APPARATUS
Belot (/.)• Un cas de pleuresie mediastine. Bull, et m£m. Soc. de radiol. med. de Par.,
1914, vi, 194-196.
Bois (G.). Les pleurisies enkystees de la region du hile. Lyon, 1914, Waltener & Cie.
47 p. 8°.
Chauffard (A.). Des pleuresies sereuses mediastines. Presse med., Paris, 1902, i, 363-
365.
La pleuresie interlobaire. Rev. g&n. de din. et de therap., Paris, 1914,
xxviii, 420-422.
Claude (H.) & Armande-Delille (P.}. Pleuresie diaphragmatique; luberculose du
diaphragme. Bull, et mem. Soc. med. d. hop. d. Paris, 1901, 3. s., xviii,
1289-1294.
Collier (W.). Two cases of diaphragmatic pleurisy simulating perforation of the stomach.
Birmingh. M. Rev., 1900, xlviii, 219-221.
Cooper (C. M.). A case of diaphragmatic pleurisy simulating an acute abdominal condition.
Occidental M. Times, San Francisco, 1903, xvii, 282-284.
Dexter (R.). The pain distribution in diaphragmatic pleurisy. Cleveland M. J., 1914 ,
xiii, 102-106.
Dietlen (Hans'). Ueber interlobdre Pleuritis. Ergebn. d. inn. Med. u. Kinderh., Berlin,
1913, xii, 196-217.
Dieulafoy (G.}. Les pleuresies inlerlobaires. Rev. prat, de trav. de med., Paris, 1898, lv,
409-412.
Frick (A.). The different forms of mcdiastinal pleurisy, with report of three cases. J. Am.
M. Ass., Chicago, 1910, lv, 2042-2048.
Manges (M.). A case of cholcsterin pleurisy. Mt. Sinai Hosp. Rep., New York, 1903,
Hi, 53-58.
Sabourin (C.). Interlobitss seches et pleurites en bouton de chemise chez les phlhisiqucs.
Arch. gen. de med., Paris, 1912, cciii, 5-16.
Savy (P.)- Les pleuresies mediastines. Progrcs med., Paris, 1910, 371-375.
Sergent (/?.)• Les fausses guerisons par vomique dans la pleuresie interlobaire metapneu-
monique. Presse med., Paris, 1900, ii, 129-131.
Shaw (L. E.). Some cases of diaphragmatic pleurisy. Guy's Hosp. Gaz., London, 1892,
n. s., vi, 258-263.
Stone (A. K.). Interlobar exudates. Boston M. & S. J., 1911, clxv, 124-127.
9. Pulsating Pleural Effusions; Accidents in Tlwracentcsis
Beclere (A.}. Pathogenic des pleuresies pulsatiles. Cong, internal, de med., C. r., Paris,
1906, Sect, de path, int., 268-272.
Dayton (H.). Accidents and deaths from exploratory puncture of the pleura. Surg., Gyn.
& ObsL, Chicago, 1911, xiii, 607-625.
Hamilton (W. F.). Accidents in thoracentesis. Montreal M. J., 1907, xxxvi, 749-756.
Janeway (E. G.)» Two attacks of temporary hemiplegia occurring in the same individual
as the result of the use of peroxide of hydrogen in a sacculated empyema
(pleural). Am. J. M. Sc., Philadelphia & New York, 18.98, n. s., cxvi,
420-424.
Levi (E.). Pulsierende Pleuraergiisse. Centralbl. f. d. Grenzgeb. d. Med. u. Chir., Jena,
1914, xviii, 286-314.
McPhedran (A.}. A case of pulsating serous pleural effusion. Tr. Ass. Am. Phys., Phila-
'delphia, 1903, xviii, 334-336.
Osier (W.}. Pulsating pleurisy. Am. J. M. Soc., Philadelphia, 1889, xcvii, 43-50.
Sears (G. G.). Accidents following thoracentesis; pneumothorax ; sudden death from ex-
ploratory puncture. Tr. Ass. Am, Phys., Philadelphia, 1906, xxi, 177-
186.
DISEASES OF THE PLEUEA 673
Wilson (J. C.). Pulsating pleural effusion. Tr. Ass. Am. Phys., Philadelphia, 1893, viii.
-195-212.
10. Pleural Adhesions
Banks (C. E.). The frequency of pleuritic adhesions as shown in 1,356 necropsies. Rep.
Superv. Surg.-Gen. Mar. Hosp., Washington, 1889-90, xviii, 147-149.
Cassarini (D.). Anatomia patologica e patogenesi delle aderenze pleuriche. Osp. Maggiore,
Milano, 1915, 2. s., Hi, 194-198.
Taylor (F.}. On combined pleural and pericardial adhesion. Lancet, London, 1898, ii,
• 1109-1113.
11. Prognosis in Pleurisy
Cabot (R. C.). Prognosis of pleurisy with serous effusion. Tr. Ass. Am. Phys., Phila-
delphia, 1902, xvii, 156-160.
Chauffard (A.}. L'avenir des pleuretiques. Rev. gen. de din. et de therap., Paris, 1893,
vii, 97-99.
2. Circulatory Disturbances Involving the Pleura
Under this heading are included (a) hydrothorax, (b) hemothorax,
and (c) chjlothorax.
(a) Hydrothorax
Definition. — A collection of thin, clear, yellowish fluid, poor in cells, in
the pleural cavity — a transudate, not an inflammatory exudate.
Etiology. — Hydrothorax is most often secondary to the general circula-
tory disturbance of cardiac or renal disease, being a part of a general
dropsy or anasarca, but occasionally it is due to local obstructions to the
circulation of the blood or lymph from the pressure of tumors or of
enlarged mediastinal or bronchopulmonary lymph glands. Often bilateral
(as in general anasarca), it may, when due to dilatation of the right heart
and pressure upon the azygos vein, be unilateral (usually right-sided),
and independent of general hydrops.
Symptoms and Signs. — The fluid obtained by exploratory puncture has
the characters of a transudate (specific gravity usually below 1.012, no
precipitate with 3 per cent acetic acid in the -cold) rather than those of
an exudate (specific gravity usually above 1.018). (See Exploratory
Punctures.) Fever and pain are usually absent; if present, they are not
due to the hydrothorax. Dyspnea is a prominent symptom. The physical
signs are those of pleural effusion (q. v.). It was formerly believed that
shifting dullness may be more marked in hydrothorax than in pleurisy
with effusion, but in my experience this has not been so. Small amounts
of iodin, or of KI, given by mouth, can, it is said, be demonstrated in
transudates but not in exudates.
674 DISEASES OF THE BESPIRATOKY APPAKATUS
References
Anders (J. M.}. Myocardial hydrothorax, with reports of cases. Am. J. M.*Sc., Phila-
delphia & New York, 1913, cxlvi, 15-28.
A statistical study of hydrothorax; its diagnosis and treatment. Penn.
M. J., Athens, 1913-14, xmi, 345-349.
Fetterolf (G.) & Landis (H. R. M.). Compression of the pulmonary veins, the pressure
factor in the etiology of cardiac hydrothorax. Am. J. M. Sc., Philadelphia
& New York, 1909, n. s., cxxxviii, 712-727.
Jones (F. A.}. Hydrothorax in its relation to cardiorenal lesions. South. M. J., Nashville,
1913, vi, 631-633.
(b) Hemothorax
Definition. — An accumulation of blood in one pleural cavity.
Etiology. — Hemorrhages into the pleural cavity occur from rupture of
an aneurism, from erosion of intercostal vessels (tumor, caries of rib),
or from trauma ; the latter is by far the most common cause and hemo-
thorax is accordingly more often met with in the surgical than in the
medical wards.
Hemothorax is to be distinguished from a hemorrhagic pleuritic effu-
sion, which, as has already been pointed out, most often points to a
tuberculous pleuritis, occasionally to a carcinoma, now and then to a
pyogenic pleuritis (pneumococcus), or to a hemorrhagic diathesis.
Symptomatology. — In addition to the ordinary signs of a rapidly de-
veloping effusion, pressure symptoms may appear, with increasing dyspnea
and dislocation of the heart and of the mediastinum. There are also signs
of anemia due to internal hemorrhage (pallor, tachycardia, sweating, syn-
cope) ; fever is usually present after the first or second day. The
physical signs are, of course, like those of pleural effusion, but an explora-
tory puncture reveals J)lood, and it is interesting that the blood shows,
as a rule, no tendency to coagulate, owing, perhaps, to a change that
h'brinogen undergoes when it comes into contact with the endothelial cover-
ing of the pleura.
Reference
Pagenstecher (E.}. Klinische wid experimentelle Untersuchungen uber den Hdmothorax.
Beitr. z. klin. Chir., Tubingen, 1895, xiii, 264-288.
Das Verhalten traumatischer Blutergiisse speziell in den Gelenken und der
Pleura. Mitt. a. d. Grenzgeb. d. Med. u. Chir., Jena, 1913 , xxv, 663-681.
(c) Chylothorax
Definition. — An accumulation of a milky fluid in the pleural cavity.
The fluid may consist of pure chyle (chylothorax proper), or of a serous
or serofibrinous fluid containing fat droplets not derived. from the lymph
channels (pseudochylous effusion).
Etiology. — Chylothorax proper depends upon a break in the continuity
of the thoracic duct with escape of its chyle ; the lesion may be due to
DISEASES OF THE PLEUEA 675
trauma, to carcinoma of the pleura, to thrombosis of the left subclavian
vein, to compression of the thoracic duct by tumors or enlarged glands,
or to blocking of the duct by a parasite.
Pseudochylous effusions are pleural exudates (due usually either to
tuberculosis or to carcinoma) in which the fluid becomes milky owing to
the escape of fat droplets from the disintegrating cells (endothelium,
leukocytes).
Symptomatology. — The physical signs are those of a pleural effusion.
On exploratory puncture, the milkiness of the fluid indicates either a
chylous or a pseudochylous nature. Microscopic examination usually
quickly differentiates between the two, since in chylous effusions cells are
absent and the fat droplets are minute and equal in size, while in pseudo-
chylous effusions many cells undergoing fatty degeneration are present and
the free fat droplets vary in size.
If the fat be extracted, it will be found to be present in large amounts
(up to 10 per cent) in true chylothorax, and in only small amounts
(rarely over 0.5 per cent) in pseudochylous effusions; this explains why,
when allowed to stand, a thick cream rises on the surface of a chylous
effusion, whereas only a thinner layer will form upon a pseudochylous fluid.
References
Bargeduhr (Arnold). Chylose und chyliforme Ergiisse im Pleura- und Pericardialraum.
Deutsches Arch. f. klin. Med., Leipzig, 1895, liv, 410.
Dock (G.)- Chylous ascites and chylous pleurisy in a case of lymphocytoma involving the
thoracic duct. Am. J. M. Sc., Philadelphia, 1907, n. a., cxxxiv, 634-643.
Hartley (P. H. S.}. Chylothorax, with notes of a case of the pseudochylous variety. St.
Earth. Hosp. J., London, 1914-15, xxii, 58-62.
Nieriker (Armin). Ueber Chylothorax und Chyloperikard; drei Falle von chylosen Ansamm-
lungen. Zurich, 1911, Gebr. Leemann & Cie. 68 p. , 8°.
3. Gas in the Pleural Cavity; Pneumothorax
Under this heading, we have to consider three conditions: (1) pure
pneumothorax, in which there is gas only in the pleural cavity; (2) sero-
pneumothorax, in which besides the gas there is serous fluid due to a
complicating pleuritis serosa ; and (3) pyopneumothorax, in which besides
the gas there is pus, due to an associated pleuritis purulenta.
When the gas enters through the external wall of the chest, for example,
after a pleural tapping, or during a surgical operation for resection of a
rib, we speak of an external pneumothorax ; when the gas enters the pleural
cavity from the lung itself, or is formed in the pleural cavity as a result
of putrefaction, we speak of an internal pneumothorax. When the per-
foration in the wall of the pleural cavity is patent during both inspira-
tion and expiration, we speak of an open pneumothorax; if the opening
become closed after its formation, so as to be patent neither during
676 DISEASES OF THE RESPIRATORY APPARATUS
inspiration nor expiration, we speak of a closed pneumothorax ; and when
the perforation is patent during inspiration but is wholly or partially
closed during expiration, as is commonly the case in spontaneous pneumo-
thorax, we speak of a valvular pneumothorax (see below).
Etiology. — From 80 to 90 per cent of all cases of pneumothorax are due
to pulmonary tuberculosis, the rupture of the lung in this disease occurring
about four times as often in men as in women. In the remaining 10-20
per cent of the cases, pulmonary gangrene, empyema pleurae, trauma, pul-
monary abscess, bronchiectasis and pulmonary emphysema are moct often
responsible. Among the conditions that may more rarely be compli-
cated by pneumothorax may be mentioned thoraceritesis, pulmonary in-
farction, perforating ulcer of the stomach or esophagus, echinococcus
invasion, subphrenic abscess, and caries of a rib or of the sternum.
Since the method of treating pulmonary tuberculosis by injecting air
or nitrogen into the pleural cavity (artificial pneumothorax) has come
into vogue, much new light has been thrown upon the pathological physi-
ology of pneumothorax by clinical and experimental study.
In spontaneous (internal) pneumothorax, the perforation of the lung
most commonly occurs in the lower part of the upper lobe; at autopsy,
the perforation is usually found in an area between the mammillary and
the axillary line at a level between the second and the fourth rib.
In seropneurnothorax, the pleuritis is due to bacterial infection; in
pyopneurnothorax, putrefactive (anaerobic) as well as pyogenic (aerobic)
bacteria are present.
Symptomatology. — Pneumothorax usually occurs suddenly, with pain,
•dyspnea, and feeling of constriction ; there is often collapse with marked
cyanosis. In the stormiest type, death may occur in a few hours or even
in a few minutes from asphyxia. More often, however, the phenomena are
less severe ; the patient feels some pain in his chest and notices that he has
become short of breath without apparent cause. In a few instances, the
occurrence of pneumothorax has caused no symptoms recognized by the
phthisical patient, and the physician has found the signs of it on making
one of his regular routine examinations.
When air enters the pleural cavity, there is sudden retraction of the lung to
the region of the hilus, exquisitely demonstrable by the x-ray. The heart and
the whole mediastinum are drawn over to the healthy side where the pleura is still
under negative pressure.
In open pneumothorax (rarely seen) the internal pressure is equal to the
external pressure; respiration is ineffective and death from asphyxia may occur.
In closed pneumothorax, the internal pressure increases as soon as an inflam-
matory exudate develops; here there is less danger of asphyxia but there is risk,
as in exudative pleuritis, of circulatory disturbances. In so-called valvular
pneumothorax (the commonest form), air enters the pleural cavity on inspiration,
but cannot get out during expiration; this may lead to extreme distention and to
-dangerous interference with the circulation.
DISEASES OF THE PLEUKA 677
On physical examination, the affected side is usually distended and
immobile, or nearly immobile, on respiration. Litten's phenomenon is
absent on the affected side. The apex beat of the heart is displaced
toward the normal side. Vocal fremitus is absent or greatly enfeebled on
the side of the pneumothorax. When the mediastinal tissues are markedly
dislocated, the larynx and trachea may also be palpably displaced in the
same direction. On percussion over the pneumothorax, there is usually
hyperresonance, often tympanitic or amphoric in quality; the per-
cussion note varies, however, markedly, according to the tension of the gas
in the pleural cavity; there may occasionally be actual dullness! The
coin sound (bruit d'airain) is very .characteristic; thus on listening at
the back of the chest, while an assistant taps one coin on another in
front, a distinct, metallic, echoing sound is heard. A similar metallic
sound can be heard if one taps on a pleximeter with the end of a
lead pencil or with the handle of a percussion hammer. The sound
is sometimes elicitable only when certain circumscribed areas are thus
percussed.
If fluid or pus be present (seropneumothorax, pyopneumothorax)
there is dullness bounded by a horizontal line above, and the dullness shift-
ing on any change of posture is found still to be horizontal, in contradis-
tinction to what happens in simple pleural effusions without pneumothorax.
On shaking the patient, a metallic splashing sound may be audible (Hip-
pocratic succussion splash). Sometimes the sound can be heard at some
distance; a patient may hear such a sound himself, and voluntarily pro-
duce it by shaking his trunk, to the astonishment of bystanders. In such
cases, too, the metallic sound of a falling drop (gutta cadens) may be
audible. When the lung fistula is patent and lies below the surface of the
fluid in the pleural cavity, a gurgling sound like that due to gas bubbles
passing through fluid may be heard; this is the so-called "water-whistle"
sound, or "fistular murmur."
On auscultation over a pneumothorax the breath sounds are usually
markedly enfeebled or entirely suppressed. In some cases, loud amphoric
breathing may be audible.
If pneumothorax be suspected, an x-ray examination should, if possi-
ble, be made. The findings in the lung areas in complete unilateral
pneumothorax are very characteristic. There is abnormal clearness on the
affected side; the normal lung markings are absent; the lung is retracted
to its root. The diaphragm stands low, though it may be normally curved.
The displacement of the cardiovascular stripe is striking. The horizontal
level of any fluid present is clearly visible. On Hippocratic succussion,
waves in the fluid may be rontgenoscopically observed. On rontgenoscopy,
too, a so-called "paradoxical movement of the diaphragm" may be visible,
the diaphragmatic shadow moving upward on inspiration and downward
on expiration on the affected side ; since the opposite occurs on the normal
678 DISEASES OF THE KESPIBATOBY APPAKATUS
side a peculiar "teeterlike" or "see-saw" movement of the two halves of
the diaphragm is observable.
In the artificial pneumothorax used in the treatment of chronic pul-
monary tuberculosis, retraction of the lung may be only partial, owing to
Fig. 180. — Artificial Pneumothorax with Pleural Adhesions. The Arrows Indicate the Margin
of the Collapsed Lung ; the Cross Shows the Portion of the Lung Held by Pleural
Adhesions. (X-ray Dept, J. H. H.}
pleural adhesions. Spontaneous partial pneumothorax is not an uncommon
finding in rontgenograms of phthisical lungs.
Diagnosis. — The recognition of PURE PNEUMOTHORAX is, as a rule, not
difficult if the possibility of its existence be thought of. Too often, unless
dyspnea have come on suddenly, the physician fails to suspect it. This
fact emphasizes again the importance of thorough physical examination
of the chest in every dyspneic patient. The physical signs are usually
characteristic enough if the physician systematically studies them. A lag-
ging side on respiration, with diminished vocal fremitus and enfeebled
or suppressed breath sounds, even without much change in the note on per-
cussion, should always arouse suspicion and lead the examiner to test
the coin sound, to look for the displacement of organs, and to study a
rontgenogram of the chest.
In the DIFFERENTIAL DIAGNOSIS, we must distinguish total unilateral
pneumothorax (1) from unilateral emphysema (coin-test negative, x-ray
decisive) ; we must distinguish partial pneumothorax (2) from diaphrag-
matic hernia (anamnesis, auscultation, rontgenogram) ; (3) from gaseous
distention of stomach (passage of stomach tube, x-ray) ; and (4) from an
DISEASES OF THE PLEUKA 679
intrapulmonary cavity; in the last instance, a rontgenogram may be in-
conclusive, but the onset of pneumothorax is usually sudden, and the inter-
costal spaces opposite it bulge, whereas an intrapulmonary cavity develops
slowly and there is often retraction of the intercostal spaces over it
(Staehelin).
In SEROPNEUMOTHORAX the diagnosis is very easy if Hippocratic
succussion be practiced, and if the x-ray reveal the presence of fluid with
horizontal level below the gas. To distinguish it from pyopneurnothorax,
exploratory puncture should be made below the level of the surface of
the fluid. Should pus be found, a careful bacterio-diagnostic study should
follow, since the therapy of tuberculous pyopneumothora s differs from
that of non-tuberculous forms. Even in the tuberculous form, the possi-
bility of a mixed infection should not be forgotten. Occasionally, an
artificial pure pneumothorax of phthisicotherapeutic origin may be con-
verted into a PYOPNEUMOTHORAX through secondary infection, or through
the rupture of a tuberculous cavity into it. When the pus of a pyopneumo-
thorax is putrid, anaerobic bacilli will usually be demonstrable in it.
Subphrenic pyopneumothorax may clinically resemble a partial super-
phrenic pyopneurnothorax. It is due to the collection of gas below the
diaphragm in gaseous subphrenic abscesses, or to rupture of the stomach
or of the lower end of the esophagus in cancer. Here the x-ray plate will
differentiate, since in the subphrenic cases the cavity will be bounded
above by the shadow of the diaphragm (pushed up into the thorax) ;
moreover, Litten's sign may still be present, and, sometimes, the punctate
has a feculent odor.
References
Andres (Andre). De I' 'aspect radiologique du pneumothorax. Lyon, 1913. 50 p. 13 pi.
No. 115. 8°.
Arnsperger (H.). Ueber Pneumothorax im Rontgengebilde. Mitt. a. d. Grenzgeb. d. Med.
u. Chir., Jena, 1901, viii, 367-376. 2 pi.
Beclere (A.). Le diagnostic et le traitement du pneumothorax a soupape. Bull, et mem.
Soc. med. d. hop. de Paris, 1900, 3. s.} xvii, 445-453.
Bovaird (D.}, Jr. Pneumothorax in children. Arch. Pediat., New York, 1903, xx, 817-
826.
Brauer (L.) & Spengler (L.). Erfahrungen und Ueberlegungen zur Lungenkollapstherapie.
IV. Klinische Beobachtungen bei kunstlichem Pneumothorax. Beitr. z.
Klin. d. Tuberk., Wurzburg, 1911, xix, 1-335.
'Bushby (T.). A case of spontaneous hoBmopneumothorax. Brit. M. J., London, 1913, ii,
1624.
Calvert (W. J.}. MovaUliiy of the heart in pneumothorax. Johns Hopkins Hosp. Bull,
Baltimore, 1905, xvi, 300-303.
de la Camp (O.). Zur Differentialdiagnose von Pneumothorax und grossen Knrcrtn-n.
Fortschr. a. d. Geb. d. Rontgenstrahlen, Hamburg, 1904, vii, 21-26. 1 pi.
Carr (J. W.}. A lecture on pneumothorax. Clin. J., London, 1913, xlii, 337-343.
Cummer (C. L.}. Recurrent pneumothorax; report of case, with review of the literature.
Am. J. M. Sc., Philadelphia, 1915, cl, 222-227.
680 DISEASES OF THE EESPIKATOEY APPAEATUS
Elsberg (C. A.}. Pneumothorax and posture. J. Exper. M., Lancaster, Pa., 1909, xi,
444-452.
Emerson (C. P.). Pneumothorax: an historical, clinical and experimental study. Johns
Hopkins Hosp. Rep., Baltimore, 1903, xi, 1-450.
Ewart (W.). Abstract of a clinical lecture on cardiac and hepatic percussion in the diagnosis
between pneumothorax, subphrenic pneumothorax, and gastric gaseous dis-
tension. Clin.J., London, 1894, iv, 201-207.
Finlay (D. W.). Pneumothorax. In: Syst. Med. (Allbutt & Rollestori). 8°. London,
1909, v, 575-585.
Finley (F. G.). Pneumothorax from gas-producing bacteria. Montreal M. J., 1899,
xxviii, 759-763.
Fussell (M. If.) & Riesman (/>.)• Spontaneous non-tuberculous pneumothorax. Tr. Ass.
Am. Phys., Philadelphia, 1902, xvii, 332-355.
Hofbauer (L.)» Die Dyspnoe beim Pneumothorax. Zentralbl. f. inner e Med., Leipzig,
1905, xxvi, 161-170.
Hoover (C. F.). Some observations on the physical signs of pneumothorax and its treat-
ment. Cleveland J. M., 1898, Hi, 45-55.
Jochmann (G.). Zur Radiologie der Heilungsvorgdnge beim unkomplizierten Pneumo-
thorax. Ztschr. f. Elektrother., Leipzig, 1906, viii, 57-64.
Kidd (/*.)• Pneumothorax in a child aged 23 months; recovery. Tr. Clin. Soc., London,
1902-03, xxxvi, 251.
Lapham (Mary E.). Artificial pneumothorax, technic and results. N. York M. J. [etc.],
1913, xcvii, 582-584.
The pleural effusions of artificial pneumothorax. South. M. J., Nashville,
1915, viii, 108-116.
Lord (F. T7.). Pneumothorax. Mod. Med. (Osier & McCrae). 2. ed. Philadelphia &
New York, 1914, ii, 1071-1092.
Minerbi (C.). Un segno fisico nuovo del pneumotorace saccato. Riv. crit. di din., Firenzi,
1914, xv, 357-359.
Moss (W. L.). Traumatic pneumothorax. J. Am. M. Ass., Chicago, 1908, 1971-1972.
Peters (L. S.). Exudatcs in artificial pneumothorax. Nat1 1 Ass. Study & Prev. Tuberc.,
Washington, 1915, 186-192.
Sabourin (C.). Sur le pneumothorax scissural. Arch. gen. de med., Paris, 1905, i, 1089-
1096.
Siciliano (L.). L'aspetto radioscopico del pneumotorace. Radiol. med., Torino, 1914, i,
302-310.
Tobiesen (F.). Die Zusammensetzung der Pneumothoraxluft. Deutsches Arch. f. klin.
Med., Leipzig, 1914, cxv, 399-406.
Webb (G. B.), Gilbert (G. B.}, James (T. L.) & Havens (L. C.). Artificial pneumo-
thorax. Arch. Int. Med., Chicago, 1914, xiv, 883-896.
4. Tumors of the Pleura
Primary tumors of the pleura are rare (endothelial cancer; sarcoma). Sec-
ondary tumors are much more common, especially metastases from cancer of the
breast, lungs, stomach, esophagus, or thymus. In secondary cancer of the pleura,
the membrane is often studded over with nodules, which at autopsy remind one
of tubercles; the condition is known as carcinosis pleurae.
Cancer of the pleura usually develops with the signs of pleural effusion. The
malignant nature may be first suspected from the bloody character of the punctate,
the presence of cancer cells in it, the resistance of the "pleuritis" to ordinary treats
DISEASES OF THE PLEUEA 681
ment, the enlargement of glands above the clavicle and in the axilla, the develop-
ment of cachexia, or the persistence of an intercostal neuralgia.
Tumors of the pleura -must be distinguished from carcinoma or lymphosarcoma
of the lung (q. v.) and from mcdiastinal masses (sarcoma, aneurism, echinococcus,
esophageal carcinoma). X-ray examinations may help in the differentiation.
I have now under observation a man aged 39, referred to me for study by Dr.
A. D. Parrott of Kinston, N. C., who for more than a year has suffered from
pain in the back and right side of the chest. The pain begins in the right hypo-
chondrium and radiates into the back. This pain is often so severe as to prevent
sleep. Its location led a very good surgeon to explore the gall-bladder region.
Some adhesions were found between the gall-bladder and the liver and these were
severed, but without relief to the pain. Later the pain radiated also into the
region of the right scapula and into the right side of the neck. Returning to his
surgeon, x-rays were made of the kidney regions and a small shadow was found
in the rontgenogram of the left kidney. A stone was removed, but without relief to
the pain. A few months before consulting me the patient began to have out-
spoken dyspnea and a dry cough, and retraction of the right thorax became
noticeable. On physical examination, I found retraction of the whole right side
of the chest and outspoken dullness in the lower half of the chest, with flatness
at the base. In the hospital over a liter of fluid was drawn off. This fluid was
turbid and contained a large number of endothelial cells rich in fat droplets. No
tubercle bacilli were present. A rontgenogram revealed a mass in the lower right
pleura. There can be but little doubt that we are dealing here with a primary
tumor of the pleura — so-called pleural endothelioma or pleural cancer.
References
Biggs (H. M.}. Endothelioma of the pleura. Proc. N. Y. Path. Soc., 1891, 119.
Butler (G. R.). Endothelioma of the pleura. N. York M. J., 1898, Ixvii, 247-249.
Fraenkel (A.}. Ueber primdren Endothelkrebs (Lymphangitis prolifera) der Pleura. Berl.
klin. Wchnschr., 1892, xxix, 497; 534.
Harris (T.). A contribution to the pathology and clinical features of primary malignant dis-
ease of the pleura. J. Path. & BacterioL, Edinburgh & London, 1893-94,
ii, 174-189. 1 pi.
Kast (A.} & Rumpel (T.). Carcinom-Metastasen der Pleura. In: Path.-anat. Tofeln.
Hamb. Staatskrankh., Wandsbek- Hamburg, 1896, xiii, pi. R 7.
Le Monnier (Jean}. La pleuresie hemorragique cancereuse; contribution a V etude cyto-
scopique. Paris, 1903. 75 p. 8°.
Lewis (D. D.). Endothelioma of the pleura, with report of a case. Tr. Chicago Path. Soc.,
1903-04, vi, 256-260.
Napier (A.) & Anderson (/.)• Case of sarcoma of the right pleura and lung, with involve-
ment of the mediastinal glands and extension through the diaphragm to the
liver. Glasgow M. J., 1907, xlvii, 345-351. [Discussion], 402.
Rosenbaum (S.). Beitrag zur Frage der onkologischen Stellung des sogenannten Endothel-
krebses der Pleura. Ztschr. f. Krebsforsch., Berlin, 1914, xiv, 543-565.
Sprunt (T. P.). Primary carcinoma of the pleura. Johns Hopkins Hosp. Bull., Baltimore,
1911, xxii, 289-293.
Stewart (/.) & Adami (J. G.}. Case of primary angiosarcoma of the upper portion of
the left pleura. Montreal M. J., 1893-94, xxii, 909-914.
Warthin (A. S.}. The diagnosis of primary sarcoma of the pleura from the cells found in
the pleuritic exudate. Med. News, New York, 1897, Ixxi, 489-494.
Witzel (Wilhelm Friedrich), Ueber den Pleurakrebs. Giessen, 1912, O. Kindt. 54 p.
682 DISEASES OF THE KESPIKATOKY APPAEATUS
5. Parasites of the Pleura
The most common parasite to invade the pleural cavity is echinococcus. A
good many cases are reported in the literature under the name hydatid of the
pleura. Such echinococcus cysts may be mistaken for tumors or cysts of the liver.
References
Gary (C.) & Lyon (I. P.}. Primary echinococcus cysts of the pleura. Report of a case of
primary exogenous echinococcus cysts of the pleura, showing hyaline de-
generation of the cuticle without lamellation, with notes from the literature.
Am. J. M. Sc., Philadelphia & New York, 1900, cxx, 402-413.
Duffey (G. F.). Hydatid cyst of the pleura. Dublin J. M. Sc., 1891, xci, 281-287.
Also: Lancet, London, 1891, i, 777.
Georgesco-Carpatiano (M.). Des kystes hydatiques primitifs de la plevre. 8°. Paris,
1899.
Luff (A. P.). Large hydatid tumor of the left pleural cavity simulating hydatid disease of the
liver; operation; recovery. Lancet, London, 1896, i, 1134-
Purser. Cysts in the cavity of the right pleura. Proc. Path. Soc., Dublin (1871-73),
1874, n. s., 158-161.
Whitelocke (R. H. A.). A case of hydatid cyst in the right pleura treated successfully by
operation. Brit. M. J., London, 1901, ii, 1159.
G. Diagnosis of the Principal Diseases of
the Mediastinum
The mediastinum subserves three main functions :
It is a septum between the two lungs, making each lung and pleural
cavity independent of the other, so that the intrathoracic pressure may
under pathological conditions differ on one side from that on the other.
This septum may be displaced lateralward as a whole, or at either one
of its two weak spots. One weak spot in the septum is situated in the
anterior part of the upper mediastinum in the region of the thymus fat
(Kitsch). Here the mediastinum is often reduced to a thin membrane
consisting of the adherent layers of the mediastinal pleura. If one pleural
cavity be blown up in the cadaver, this weak spot of the mediastinal
septum will balloon out into the opposite half of the thorax.
Another weak spot in the mediastinal septum lies in the posterior part
of the inferior mediastinum. It is bounded in front by the esophagus
and the heart, and behind by the spine and aorta. Here, again, in the
cadaver, inflation of one pleural cavity leads to ballooning out of this
second weak spot of the septum into the opposite half of the thorax
(Mtsch). This weak spot has, however, nothing to do with the region of
the para vertebral triangle of dullness in pleural effusion (q. v.)
The second main function of the mediastinum is to serve as an area
lodging important channels of communication (heart and great vessels,,
DISEASES OF THE MEDIASTINUM 683
trachea and larger bronchi, esophagus, nerve trunks, including the N.
vagus, ~N. sympathicus, N. phrenicus, and Nn. intercostales).
The third main function of the mediastinum is to serve as an impor-
tant area of the lymphatic system (ductus thoracicus, mediastinal lymph
glands, lymph spaces of mediastinal connectfve tissue communicating with
the peritoneum below). The lymph spaces in the mediastinum are often
the site of inflammatory processes (acute and chronic mediastinitis), and
the lymph glands here are frequently the site of important pathological
changes (tuberculosis, Hodgkin's disease, lymphosarcoma). Since the
advent of rontgenographic methods a flood of new light has been thrown
upon these pathological processes that involve the mediastinal lymph glands
and lymph spaces.
References
von Bergmann (€?.)• Die Erkrankungen des Mediastinum. In: Handb. d. inn. Med.
(Mohr & Staehelin), Berlin, 1914, ii, 163-204.
Christian (H. A.). Diseases of the mediastinum. Mod. Med. (Osier & McCrae). 2. ed.
Philadelphia & New York, 1914, ii, 1093-1112.
Meltzer (S. J.). On the respiratory changes of the intrathoracic pressure, measured in the
mediastinum posterior. J. PhysioL, London, 1892, xiii, 218-238.
Nitsch (G.). Die schwachen Stellen des Mediastinums und ihre klinische Bedeutung bei
pleuritischem Exsudat und Pneumothorax. Beitr. z. Klin. d. Tuberk.,
Wiirzburg, 1910, xviii, 1-20. 3 pi.
Roberts (F. T.}. Diseases of the mediastinum. In: Syst. Med. (Allbutt & Rollestori).
8°. London, 1909, v, 595-322.
CLASSIFICATION OF DISEASES OF THE MEDIASTINUM
The most convenient classification at present is that suggested by G. von
Bergmann :
1. Displacement of the mediastinum through pressure or traction from the
outside (disturbances of the septal function).
(a) Total displacements.
(b) Partial displacements.
2. Space-occupying processes in the mediastinum (disturbances of the chan-
nels of communication in the mediastinum).
(a) Small masses.
(b) Large masses.
3. Diseases involving the lymph spaces of the mediastinum (disturbances of
the lymphatic function).
(a) Acute mediastinitis.
(b) Chronic mediastinitis.
(c) Mediastinal hemorrhage.
(d) Mediastinal emphysema.
Diseases of the heart, of the pericardium, of the esophagus, of the aorta, etc.,
though strictly speaking they belong to the mediastinum, are considered elsewhere.
684 DISEASES OF THE KESPIKATOEY APPAEATUS
1. Displacements of the Mediastinum Through Pressure
or Traction
(a) Total Displacements
The mediastinum is more or less movable and distensible. At every
breath the distance between the sternum and the spine is increased during
inspiration and diminished during expiration. Again, changes in the
pressure in each half of the thorax can lead to concavity or convexity of
the mediastinum toward the opposite side, according as a negative or
positive pressure is greater in one half of the thorax than in the other
(pleural effusion, pneumothorax, bronchiostenosis). The degree of dis-
placement is also affected by the degree of rigidity of the mediastinal
septum, which varies much in different persons ; in chronic mediastinitis
the septum may become quite rigid.
The septum is less often pressed over to the opposite side by an exudate
or by a pneumothorax than drawn over by the negative pressure of the
actively-breathing half of the thorax (Brauer).
Chronic cicatricial processes (pleuromediastinitis, pleuropericar-
ditis externa) may pull the mediastinum far to one side. Such a process
on the right may pull the heart far to the right, simulating the dextro-
cardia of situs inversus.
(b) Partial Displacements
The two weak spots of the mediastinum have been described above;
in pneumothorax they may balloon out into. the opposite side (Brauer),
and in pleuritis they may bulge into the healthy side like a mediastinal
hernia (Spengler). Such partial displacements can be recognized by
rontgenography and sometimes by percussion. In cicatricial contraction of
one lung there may be a dislocation of a "weak spot" toward the diseased
side.
2. Space-occupying Processes in the Mediastinum
Symptoms. — Certain symptoms are common to pathological processes
that occupy space in the mediastinum (tumors, hemorrhages, abscesses,
mediastinal pneumothorax, mediastinal emphysema, aneurisms, esophageal
diverticula, enlarged lymph glands). These symptoms arise chiefly from
the compression of structures in the mediastinum (veins, arteries, air
passages, esophagus, nerves).
Two types of collateral venous circulation are met with in mediastinal
disease. In the first type there is general dilatation of the small cutaneous
veins over the whole chest, back and upper abdomen. On pressing upon
such dilated veins, one finds that they swell above the point of compression
and collapse below it, indicating that the current is flowing from the vena
DISEASES OF THE MEDIASTINUM
685
cava superior to the vena cava inferior. This is the condition seen when
the collateral circulation is fairly sufficient. In the second type the dilated
veins may not be easily visible, but, instead,
there is a general cyanosis of the skin of the
upper half of the body, with pitting on pressure
and obliteration of the normal contours of the
neck and thorax, the swelling extending down-
ward as far as the level of the diaphragm.
This second type is known, as the "collar of
Stokes.7'
Sometimes one sees a unilateral edema due
to compression or thrombosis of one innomi-
nate vein. The varying clinical picture, ac-
cording to the number of veins involved in
the compression (superior cava, innominates,
V. azygos, V. hemiazygos, Vv. pulmonales),
has been described by Dieulafoy. In case the
V. azygos is free when the superior cava is
compressed distal from it, the collateral cir-
culation is carried on not only by the inferior
cava, but also through the Y. azygos, in which
event there is less dilatation of the cutaneous
veins. According to the degree of insufficien-
cy of compensation by collateral circulation
one sees every transition from a normal skin
with dilated vehis, through moderate turgor
and definite edema, to the most marked edema
that stretches the skin and makes it shiny.
Along with this edema of the upper half of the
body, one sees also in the marked cases deep
cyanosis of the lips and face, and injection of
the conjunctiva! vessels; such patients suffer
from headaches and vertigo, and often from severe epistaxis. Blood counts
from blood drawn from the upper half of the body may show an outspoken
polyglobulia, while a count made from blood from the toe may be normal.
A unilateral hydrothorax may be due to compression of the Y. azygos
or the Y. hemiazygos alone ; when the thoracic duct is also pressed upon,
the fluid of the hydrothorax becomes chylous.
Compression of the aorta or of the pulmonary artery in the medias-
tinum may give rise to a systolic stenosis-murmur. Should the aorta be
compressed at the site of origin of the innominate artery or of the left
subclavian artery, the pulse at one wrist may be. feebler than that at the
other (pulsus differens).
When the air passages are compressed by masses in the mediastinum,
Pig. 181. — Collateral Circula-
tion Between the Superior
and the Inferior Vena Cava
in a Case of Mediastinal
Tumor. (By courtesy of Dr.
Rowntree.)
686 DISEASES OF THE EESPIRATOKY APPARATUS
important diagnostic symptoms may arise ; thus in compression of the
trachea the signs of tracheal stenosis appear (difficult breathing, audible
stridor, retraction of the thorax). When one main bronchus is compressed
there is tachypnea, lessened expansion, enfeebled breath sounds, and en-
feebled vocal fremitus on the affected side. The percussion note may
remain clear. Sometimes stenosis murmurs may become audible.
If the lung itself be compressed, the physical signs vary according
to the site of the compression ; usually the breath sounds are enfeebled,
but sometimes bronchial breathing is transmitted through the mass, es-
pecially in the interscapular region.
If the esophagus be compressed, the patient will complain of dysphagia
and localized pain. Examination with the esophageal bougie, or, better,
rontgenography with the aid of thick bismuth paste, will show the site and
extent of the esophageal stenosis. Esophagoscopy may also be resorted to.
When the nerves of the mediastinum are compressed, important
diagnostic signs also arise; thus, compression of the !N". vagus and espe-
cially of its branch, the K. recurrens, gives rise first to posticus paralysis
of the larynx. When the lesion is unilateral, there may be no hoarseness,
but laryngoscopy will reveal the paralysis. The irritable cough of bron-
chial-gland tuberculosis and the brassy cough of aortic aneurism are to be
regarded as pressure symptoms from mediastinal involvement of the N".
vagus. Other symptoms due to pressure on the N. vagus include brady-
cardia when the nerve is merely irritated, and tachycardia when it is
sufficiently compressed to be paralyzed. Nausea, vomiting, hyperacidity
and disturbance of intestinal function may also follow vagal injury in the
mediastinum.
Involvement of the "N. sympathicus may cause protrusio bulbi (uni-
lateral or bilateral), anisocoria, unilateral hyperhidrosis or anhidrosis,
sympathetic ptosis, etc.
Compression of the IN", phrenicus may cause hiccough or may give rise
to inequality of contraction of the two halves of the diaphragm (rontgen-
oscopy) ; one should make sure, however, that such inequality does not
depend upon unilateral bronchi ostenosis or upon phrenic involvement
through apical tuberculosis rather than upon mediastinal compression.
Pressure on the Nn. intercostales may cause severe intercostal neu-
ralgia.
Other physical signs of space-occupying processes in the mediastinum
include (1) dislocation of the heart and of the lungs, and (2) distortions
of the thoracic wall. These effects are recognizable by careful physical
examination of the thorax.
After determining the existence of symptoms pointing to a space-occupy-
ing process in the mediastinum, it is necessary to try to determine the
nature of that process. This part of the problem has been rendered much
DISEASES OF THE MEDIASTINUM 687
easier since the introduction of rb'ntgenographic methods in intrathoracic
diagnosis.
(a) Rontgenography of the Mediastinum
By means of x-rays we can determine the position and size of any
space-occupying mass or masses in the mediastinum. In general, rontgen-
ography is here more helpful than rontgenoscopy, but for the study of
pulsating masses (aneurisms, pulsating tumors, pulsating empyemas)
rontgenoscopy is essential.
In the diagnosis of large tumors of the mediastinum, several types
can be distinguished in x-ray pictures ; thus, if in the rontgenogram one
sees a shadow projecting like a mole-hill at the junction between the
cardiovascular stripe and the clear lung area, its surface being either
hemispherical, with the center of the sphere lying at the root of the lung,
or uneven, with jagged contours, one can be sure that he is dealing with
a hilus tumor. Such a mediastinal tumor at the hilus has to be distin-
guished from a tumor of the lung on the one hand and from an aortic
aneurism on the other.
In large tumors of the mediastinum due to Hodgkin's disease, one
sees a mass either to the right or to the left of the sternum, or on both
sides, usually feebly convex, and extending all the way from the clavicle
down to the heart. When the tumor projects to the left side, the differ-
ential diagnosis from aortic aneurism may be difficult, though the pulsa-
tion in aneurism, visible on rontgenoscopy, may help. Tumors of the
lung itself are usually easily distinguishable from mediastinal tumors
proper, though in some cases the rontgenogram leaves one uncertain. Thus,
a tumor arising in a lymph gland at the hilus of the lung, or in the
bronchial mucous membrane near the hilus, usually gives rise to a shadow
extending out into the lung but more or less separable from the cardiovas-
cular stripe; and when the shadow becomes confused with the cardiovas-
cular stripe, the predominant involvement of one lobe of a lung may give
one the clew to a pulmonary rather than a mediastinal origin of the mass
(v. Bergmann).
In judging of the nature of mediastinal tumors, one should pay atten-
tion not only to the appearance of the main shadow, but also to certain
additional points: (1) the presence or absence of a pleural effusion, (2)
the presence or absence of darkening of one whole lung area (bronchio-
stenosis), (3) the involvement or non-involvement of the arch of the aorta.
It is also important to make out, if possible, whether we are dealing with a
compact uniform mass or with a composite mass made up of several parts,
as in lymph-gland enlargement (bronchial-gland tuberculosis, Hodgkin's
disease). Examinations with the aid of the x-ray have proven so helpful
in the differential diagnosis of mediastinal growths that students and
physicians sometimes fail to apply thoroughly, in addition, the ordinary
688 DISEASES OF THE RESPIRATORY APPARATUS
physical methods of examination. This is a serious error, for the diag-
nostician who intelligently utilizes all the methods available in diagnosis
will make fewer mistakes than he who relies upon a more limited applica-
tion of diagnostic technic. When applying Rontgen rays to intrathoracic
diagnosis the rontgenographer should not be satisfied with rontgenoscopy
alone, nor with rontgenography alone ; he should use both methods, and in
some cases may find it necessary to make his observations not only in the
anteroposterior direction but also in the transverse and oblique diameters
of the chest. For wider reading on this subject, see Christian's article in
Osier and McCrae's "Modern Medicine," von Bergmann's article in Mohr
Fig. 182. — Large Vascular Sarcoma of Posterior Mediastinum. Clinically, a Pulsation
Was Visible Over a Dull Area in the Lower Back. The Shadow of the Tumor is Not to
be Confused with the Shadow Due to the Mammary Gland. (X-ray Dept., J. H. H.)
and Staehelin, Dieulafoy's paper, and the Atlases of Holtzknecht and of
Rieder and Rosenthal.
In the differential diagnosis between aneurism of the aorta and
malignant tumors of the mediastinum the following points are worthy
of emphasis: If the normal form and position of the arch of the aorta
can be seen undisturbed by the suspected mass, it is almost certain that
we deal with aneurism. On the other hand, a dislocated aorta does
not necessarily mean aneurism, since tumors can also cause displace-
ments. Expansile pulsation, when definitely recognizable, is helpful in
DISEASES OF THE MEDIASTINUM 689
the diagnosis of aneurism, but some aneurisms pulsate but little, and
some .mediastinal tumors show a propagated' pulsation which- may be
difficult to distinguish from aneurism. If the whole physical examina-
tion be carefully made, and the x-ray findings be thoroughly analyzed
and judged, the results of these, together with the general clinical con-
siderations of the case (Wassermann reaction!), will rarely leave one
in doubt.
Dislocation of the upper anterior weak spot of the mediastinum to
one side, visible on rontgenoscopy, is sometimes helpful in diagnosis. It
is to be remembered that in bronchiostenosis the bulging is toward the side
of the stenosis, as the weak spot of the mediastinum is drawn over to the
diseased side, while in pleural effusion and in pneumothorax exactly the
opposite occurs, in that the mediastinum is drawn over toward the healthy
side, owing to the greater negative pressure on inspiration on that side.
On rontgenography of the thorax we may discover changes in the
mediastinum that often have given rise to no symptoms and have therefore
been unsuspected (enlargement of mediastinal or of bronchial lymph
glands, beginning aneurism of the aorta, esophageal carcinoma, tumor in
the region of the sternoclavicular joint).
The frequency of mediastinitis in rontgenograms of the thorax is now
known to every clinician familiar with this technic. Occasionally, a
mediastinal emphysema or a mediastinal pneumothorax can be recognized
in a rontgenogram (v. Bergmann).
(6) Varieties of Mediastinal Tumors
Among the masses originating in the mediastinum itself, exclusive of
extramediastinal processes, intramediastinal suppurations, hemorrhages
and emphysema, and of enlargements of the esophagus, heart, pericardium
and great vessels, we may consider two groups: (1) small mediastinal
masses, and (2) large mediastinal masses. The smaller mediastinal
masses originate chiefly in the lymph glands; they include tuberculous
glands, especially the tuberculous bronchial glands of children, syphi-
litic lymph glands, the enlarged lymph glands in Hodgkin's disease and in
leukemia, as well as enlargements due to acute or chronic lymphadenitis
or to metastatic tumor-growth.
The large mediastinal tumors arise also chiefly from lymph glands or
from the thymus. Among the larger mediastinal tumors originating in
lymph glands may be included: (1) Hodgkin's disease, (2) lymphosar-
coma, (3) leukemic and aleukemic lymphadenosis, (4) metastatic sar-
comata or carcinomata. Those arising in the thymus usually take the
form of the so-called thymus-sarcoma, sometimes called thymus-carcinoma.
Certain benign tumors of the mediastinum (teratoma, dermoid cyst,
echinococcus cyst, intrathoracic goiter) may occasionally be met with.
In one tumor personally observed, the mass disappeared entirely, as
690 DISEASES OF THE EESPIKATOKY APPAKATUS
demonstrated by rontgenograms, after radium treatment by Drs. Kelly
and Burnam.
(c) Diagnosis of Mediastinal Tumors
If the symptomatology above described be thoroughly mastered, a
correct diagnosis should be arrived at in the majority of cases. Pressure
symptoms are usually the first to give a clew, though a mediastinal tumor
is sometimes treated for a considerable period as something else (angina
pectoris, pulmonary tuberculosis, chronic bronchitis, laryngitis, bronchial
asthma, whooping-cough), before the true nature of the process is recog-
nized. If on inspection and palpation there be no collateral circulation,
edema, abnormal pulsation, or bulging of the chest wall, on percussion no
abnormal dullness, and on x-ray examination in both the dorsoventral and
in the oblique diameter no shadow visible, certainly no large mediastinal
mass can be present.
It should be kept in mind that pressure symptoms involving the great
vessels (collateral circulation, edema) point rather to masses in the an-
terior mediastinum, whereas pressure upon the esophagus (dysphagia), or
upon the air passages (dyspnea, bronchiostenosis), points rather to the
posterior mediastinum.
Benign processes in the mediastinum are much rarer than the more
serious involvements. Malignant masses usually enlarge rapidly and
the general state of the patient quickly becomes impaired.
The general condition of the lymph glands is very important in differ-
ential diagnosis. If a mediastinal mass coexists with enlargement of the
lymph glands in the neck, one of the latter may be excised for histological
diagnosis. I have repeatedly been able by means of such gland excisions
to recognize the sarcomatous or malignant lymphomatous nature of a
mediastinal tumor. A thorough blood examination, including a careful
differential count of the white corpuscles, should always be made. A true
leukemia would then never be overlooked, and, if Bunting is right, the
diagnosis of Hodgkin's disease can, in many cases at least, be made early
from the blood picture.
References
Albert-Weil (E.}. La radiographie presque insfantanee des adenopathies tracheobron-
chiques. Bull. Soc. de pediat. de Paris, 1913, xv, 528-532. 1 pi.
D' Ambrosia (A.). Delia diagnosi dei neoplasmi primitivi del mediastino. Sludium,
Napoli, 1914, vii, 228, 275.
Beclere (H.). Radiographies montrant la rapidite devolution d'une tumeur du mediastin.
Bull, et mem. Soc. de radiol. med. de Paris, 1913, v, 268.
C. (/.). Radiographie des adenopathies bronchiques. Arch, de med. d. enf., Paris, 1914,
xvii, 907-912.
Camp (O. de la}. Die klinische Diagnose der Bronchialdrusentuberkulose. Ergebn. d.
inn. Med. u. Kinderh., Berlin, 1908, i, 556-574-
Cazzaniga (A.). Semeiologia dei tumori mediastinici. Riv. crit. di din. med., Firenze,
1914, xv, 359; 375; 406; 4%2.
DIAGNOSIS OF THE MEDIASTINUM 691
Cazzaniga (A.). Semeiologia de tumori mediastinici; considerazioni suite alterazioni anato-
miche e sulla genesi dei sintomi. Riv. crit. di din. med., Firenze, 1914,
xv, 744; 759; 775; 788; 808.
Clay (J. V. F.). A sarcoma of the mediastinum presenting early laryngeal symptoms. J.
Opth., Otol. &Laryngol, Lancaster, Pa., 1914, xx, 291-295.
Corica (A.}. II segno di Hochsinger nella diagnosi di adenopatia tracheobronchiale nel
lattante. Pediatria, Napoli, 1914, 2. s. xxii, 850-852.
Friedrich (P. L.)» Die dekompressive Thoraxsprengung durch longitudinale Sternotomie bei,
die Luftwege komprimierendem, Aneurysma und Tumor en des Mediasti-
nums. Beitr. z. klin. Chir., Tubingen, 1914, xciii, 312-325.
Haenisch (G. F.). Ein Fall von durch Rontgenbestrahlung gunstig beeinflusstem Mediastinal-
tumor. Strahlentherapie, Berlin u. Wien, 1913, Hi, 520-522.
Hoffmann (F. A.}. Atlas des Mediastinums im Roentgenbilde. Leipzig, 1909, W. Klink-
hardt.
Holzknecht (G.). Die roentgenologische Diagnostik der Erkrankungen der Brusteingeweide.
Hamburg, 1901, Grafe & Silleur. 229 p.
Howard (C. P.)« Diagnosis of tumors of the mediastinum. Med. Herald, St. Joseph, 1914,
n. s., xxxiii, 417-422.
Jehn (W.). Die operative Entfernung grosser intrathorakaler Strumen. Deutsche Ztschr. f.
Chir., Leipzig, 1915, cxxxiii, 25-57.
Kreuzfuchs (5.). Die intrathoracische Struma in klinischer und radiologischerBeleuchtung.
Abhandl. a. d. Gesamtgeb. d. prakt. Med., Wiirzburg, 1911-12, xii, 125-
150.
Lilienthal (/?•)• A case of mediastinal thyroid removed by transsternal mediastinotomy.
Surg.,Gynec. &0bst., Chicago, 1915, xx, 589-593.
Lindstedt (F.). Beitrag zur Kenntnis der mediastinalen Mischgeschwulste. Virchow's
Arch. f. path. Anat. [etc.] Berlin, 1915, ccxix, 299-308.
Mar fan (A. B.) & Mantoux (Dora}. Toux bitonale dans la tuberculose des ganglions
tracheo-bronchiques chez le nourrisson. Nourrisson, Paris, 1913, i, 325-
330.
d'Oelsnitz (M.) & Paschetta. Valeur de I'exploration radiologique du thorax pour le
diagnostic des affections respiratoires de I'enfance. Arch, d'electr. med.,
Bordeaux, 1914, xxiv, 8-13.
Rach (E.}. Zur Diagnostik der Bronchialdrusentuberkulose im Kindesalter. Beitr. z. Klin.
d. Tuberk., Wiirzburg, 1914, xxxii, 31-48. 1 pi.
Rieder (//.). Rbntgenuntersuchung des Mediastinum. In: Lehrbuch der Rontgenkunde
(Rieder & Rosenthal), Leipzig, 1913, i, .
Rist (E.}. The healing process of the infantile bronchial glands in tuberculosis. J. State
Med., London, 1915, xxiii, 7-12.
Rist (E.} & Ameuille (P.)- Le type adulte de I'adenopathie tracheo-bronchio^'-e tuberculeuse.
Bull, et mem. Soc. de med. d. hop. de Paris, 1914, 3. s., xxxvii, 651-658.
Ross (J. N. M. #.)• Some observations upon primary new growths of the mediastinum from
a study of sixty cases. Edinb. M. J., 1914, n. s., xiii, 444~454- 1 pi-
Sauerbruch (F.). Der gegenwdrtige Stand der intrathorakalen Chirurgie. Tr. Internal.
Cong. Med., 1913, London, 1914, Sect. VII, Surg., 301-318.
Speder (E.) & Dubourg (E.}. L'adenopathie tracheo-bronchique latente chez Venfant;
comparaison du radiodiagnostic et du diagnostic clinique. Arch, d'electr.
med., Bordeaux, 1914, xxiv, 529-547. 1 pi.
Stanley (D.). Inlrathoracic growths. Birmingh. M. Rev., 1915, Ixxvii, 1-5.
Stoll (H. F.) & Heublein (A. C.). Tuberculosis of the bronchial glands and lung hilus;
a clinical and radiographic study. Am. J. M. Sc., Philadelphia, 1914,
cxlviii, 369-386.
Thomas (G. F.). The Roentgen diagnosis of lesions in the region of the mediastinum. Am.
J. Roentgenol, Detroit, 1913-14, n. s., 132-145.
Tuffier (T.). 6tat actuel de la chirurgie intrathoracique. .Tr. Internal. Cong. Med., 1913,
London, 1914, Sect. VII, Surg., pt. 2, 249-326 ; [Discussion], 326-338.
Vallardi (C.). Sarcoma angiomatoso pleuro-polmonare a sindrome mediastinica. Atti d.
Soc. lomb. di sc. med. e biol, Milano, 1914-15, iv, 103-112.
Warnecke. Zur Diagnose der Bronchialdriisentuberkulose. Deutsche med. Wchnschr., Leip-
zig u. Berlin, 1914, xl, 126-128.
692 DISEASES OF THE KESPIKATORY APPARATUS
3. Diseases Involving the Lymph Spaces of the
Mediastinum
Here we consider the processes that develop in the mediastinal tis-
sues themselves. These may be the seat either of acute inflammatory
processes (mediastinitis acuta), or of chronic inflammation (mediastinitis
chronica) ; blood may be diffused through the mediastinal tissues (medi-
astinal hemorrhage), or these tissues may be infiltrated with air (medias-
tinal emphysema).
(a) Acute Mediastinitis and Mediastinal Abscess
Definition. — An acute inflammation, usually involving the anterior
mediastinum, more often diffuse than circumscribed, and in many cases
leading to suppuration with abscess formation.
Etiology. — In most cases the mediastinitis is due to an infection per con-
tiguitatem (neck, larynx, trachea, thyroid, sheath of the carotid artery or jugular
vein), most often as an extension from a retropharyngeal abscess following upon
suppuration of retropharyngeal lymph glands, tonsillar and peritonsillar abscesses,
or suppurative laryngeal perichondritis. Occasionally a mediastinal abscess
results from rupture of a pleural empyema, from an abscess of the lung, or a
suppurative osteomyelitis. Now and then rupture of the esophagus (carcinoma,
foreign body, passage of a bougie), of the trachea, of a pyopericardium, or of a
suppurating bronchial gland may be responsible.
Metastatic abscesses occasionally occur in pyemia, in typhoid fever, and in
erysipelas. Direct trauma is, in rare instances, an etiological factor.
Symptoms. — Fever and other signs of a severe infection (chills, sweats,
loss of weight) develop. The patient complains of pain behind or along-
side of the sternum, radiating to both sides. This pain may at first be
taken to be stenocardiac in nature. Pressure upon the sternum or upon
the chest wall near the sternum increases the pain. In the rare cases in
which the posterior mediastinum is involved, the pain may be referred to
the spine or to the shoulder blades, or there may be severe intercostal
neuralgias. Circumscribed edema of the skin may be present. Pressure
symptoms may occur but are less marked than in solid mediastinal tumors ;
among these, cyanosis, respiratory irregularity of the pulse, and paralysis
of the diaphragm are perhaps the most common. There is dullness behind
the sternum, and if an abscess be present its size and position may be
accurately determined by rontgenography. Sometimes an abscess from
which the mediastinal abscess has originated can be recognized. The ab-
scess may finally perforate the chest wall through one of the intercostal
spaces, or it may point in the jugulum, or in one of the supraclavicular
fossae. Unfortunately, mediastinal abscess more often perforates the
DISEASES OF THE MEDIASTINUM 693
trachea (death from asphyxia), the esophagus, the pericardium, or into
the pleural cavity.
(b) Chronic Mediastinitis
Definition. — A chronic productive inflammation of the mediastinal tis-
sues, leading to fibrous thickening1 of these tissues, usually arising by ex-
tension of a chronic pleurisy (pleuromediastinitis), or, more often still,
of a chronic pericarditis (mediastinopericarditis).
Etiology. — The disease may be of tuberculous, of rheumatic, or of unknown
origin. It is common in association with the different forms of polyserositis.
Symptoms. — In subacute cases there may be fever and pain, but in the
chronic cases these may be entirely absent.
As a result of the fibrosis there is often interference with respiration,
owing to the fact that the mediastinum cannot be stretched in the sagittal
direction during inspiration. Nerves, arteries and veins may become
compressed in the fibrous tissue. On rontgenography the hilus shadows
and the pericardial shadows may be markedly deepened.
One of the most important symptoms is the so-called pulsus paradoxus
(Griesinger), the pulse becoming smaller or intermitting during deep
inspiration ; there is at the same time an inspiratory swelling of the large
veins of the neck. According to Gaisboeck, the pulsus paradoxus in medi-
astinitis is to be looked upon as a vascular reflex due to excitation of the
vasomotor center from change in the distribution of the blood causing a
vasoconstriction at the periphery. Others maintain that the intermission
of the pulse is mechanical, due to narrowing of the aorta and other large
arteries by the scar tissue during inspiration.
(c) Mediastinal Hemorrhage
This is most often due to perforation of an aneurism of the aorta or of
one of its branches. The condition is rarely recognized during life.
»
(d) Mediastinal Emphysema
Since the artificial-pneumothorax therapy of pulmonary tuberculosis
has come into vogue, the subject of mediastinal emphysema has assumed a
new clinical importance. In connection with pneumothorax therapy it is
not uncommon to meet with a false mediastinal emphysema, properly
known as subfascial emphysema. If, for example, in the pneumothorax
therapy the cannula is inserted between the intrathoracal fascia lining the
intercostal muscles and the ribs on the one side and the costal pleura on
the other, the air becomes diffused between these two layers into the loose
connective tissue of the endothoracic fascia, causing pain. The air in this
694 DISEASES OF THE KESPIKATOKY APPAKATUS
case stays behind the ribs, while in subcutaneous emphysema and in, true
mediastinal emphysema it appears in the jugulum and spreads out into
the skin. In true mediastinal emphysema, the air gets into the medi-
astinal tissue from the larynx, trachea or bronchi, or it may reach the
mediastinum from the hilus of the lung, owing to-' tear of the lung tissue
or of one of the small bronchi, or to the perforation of a lung cavity, of a
lung abscess, or of a softened tumor.
One's attention may be first called to it by the appearance of subcu-
taneous emphysema in the neck. On examination the percussion note will
be found to be of high pitch and tympanitic over the mediastinum. The
heart dullness may be obliterated. On auscultation, crepitation synchro-
nous with the heart's action may be audible. The heart sounds are dis-
tant, or may be entirely inaudible. If the pressure be great the dyspnea
will be marked.
ISTot infrequently, owing to the cause of the mediastinal emphysema, a
phlegmonous mediastinitis secondarily develops.
References
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Berlin, 1913, xxvii, 430-445.
Corre (Gabriel). Contribution a I 'elude clinique des mediastinites syphilitiques et particu-
lierement des mediastinites avec obliteration de la veine cave superieure.
Paris, 1913, Jouve & Cie. 116 p. No. 198. 8°.
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Howard (C. P.}. The diagnosis of mediastinitis. Johns Hopkins IIosp. Bull., Baltimore.
1915, xxvi, 140-144.
Kusstnaul (A.). Ueber schwieliege Mediastino-pericardilis und paradoxen Puls. BerL
klin. Wchnschr., 1873, x, 433; 445; 461.
Renault (Charles). La mediastinite syphilitique. Paris, 1913. Jouve & Cie., 102 p.,
No. 140. 8°.
Riegel (F.). Ueber Pulsus paradoxus. Deutsche med. Wchnschr., Leipzig u. Berlin, 1903,
xxix, 345-347.
Za.rH (M.). Akutes mediastinales Zellgewebsemphysem und Hautemphysem bei einem
3 Monate alien Sdugling. Mitt. d. Gesellsch. f. inn. Med. u. Kinderh. in
Wien, 1914t xiii, 65-67.
Part VI
Diagnosis of Diseases of the
Circulatory Apparatus
(CLINICAL ANGIOLOGY)
SECTION I
METHODS OF DETEKMINING THE CONDITION OF THE
CIKCULATOEY SYSTEM
A. Introduction
The circulatory apparatus includes (1) the heart, made up of the
right atrium, the right ventricle, the left atrium and the left ventricle:
(2) the arteries, including the pulmonary artery, the aorta, and all their
branches; (3) the veins of both the pulmonary and the general circula-
tion; (4) the capillaries; and (5) the lymphatic system, including the
lymphatic vessels, the thoracic duct, the lymph glands, and the lymphatic
plexuses.
Before taking up the study of diseases of the circulatory system, the anatomy
and physiology of this system should be thoroughly mastered, and the physical
conditions of the organs in normal circumstances should be well known. A
student approaching the study of clinical angiology will, therefore, do well to
review the general topographical anatomy of the heart and great vessels, and the
form of the heart and its several chambers as seen in fresh specimens, at autopsy,
and in formalinized specimens. Anatomical and histological atlases and texts
should be consulted, and the study should include the microscopic anatomy and
histology of the heart muscle, the distribution of the coronary arteries and of the
cardiac nerves, the structure of the larger and smaller arteries, of the larger and
smaller veins, of the capillaries, and of the lymphatics.
The older and the newer physiology of the heart and of the circulation should
also be carefully reviewed. It is necessary to know how the heart does its work.
The general mechanics of the circulation should be well understood, including the
effects of contraction of the several chambers, the functions of the valves of the
heart, the phenomena accompanying systole and diastole, the systolic output,
695
696 DISEASES OF THE CIECULATOEY APPAEATUS
INTER JUQULAR £ML
OF 5l«US
SINOAURICULAR--
JUNCTION
SINUS PI--
Fig. 183. — Diagram of the Heart of
the Eel. (After McWilliam, Modi-
fled by Erlanger. "The Harvey
Lectures," published by J. B. Lip-
pincott Co., Philadelphia.)
the maintenance of a continuous flow, the significance of the pulse in the arteries
and veins, and the variations in blood supply corresponding to the varying needs
of the different organs of the body. Not only should the student have a good
grasp of the conditions of the general circulation and of the pulmonary circula-
tion in adult life, but he should familiarize himself with the conditions existing
during fetal life, since they throw light upon some of the pathological states met
with in adults.
JUCULAR VEINS
During the last
ten years a flood of
new light has been
thrown upon cardiac
pathology through
important discover-
ies that have been
made regarding the
origin and conduction
of stimuli within the
heart. To-day, there-
fore, in addition to the older anatomy and physi-
ology of the heart, we have to consider the newer
anatomy and physiology of a special irritable and
conducting system within the heart. This special
irritable and conducting system begins at the Keith-Flack node in the
sinus venosus at the iunc-
VENA CAW
SUPERIOR
tion of the superior cava
with the right atrium;
it includes (1) the walls
of the atria, (2) the
atrioventricular bundle
of His (with its inter-
calated Aschoff - Tawara
node) dividing into two
limbs: one going to the
right ventricle, the other
to the left ventricle, and
(3) a vast complex of
peculiar fibers known as
the Pur kin je system in
which the two limbs of
the His bundle termi-
nate, and through which
can be Conducted
BPOSCD
NDLES
(THOREl)
INK
-FUCK)
SINUS
CANALI5
AUKICULARIS
(A-VBUNDU)
Fig. 184.-Diagram of the Mammalian Heart for Comparison
with the Heart of the Eel ; the Probable Homologies of
the Hearts of Cold-blooded and Warm-blooded Animals almost Simultaneously to
are Schematically Represented. (After J. Erlanger. ft wbole series of TjOints
"The Harvey Lectures," published by J. B. Lippincott .
Co., Philadelphia.) in the ventricular walls.
INTRODUCTION 697
Under normal conditions, stimuli arise at the Keith-Flack node and are
conducted thence to the .atria, and, later, through the atrioventricular
bundle to the ventricles, so that the different parts of the heart, under
normal conditions, contract in regular sequence ; the different parts of the
organ thus have their activities coordinated in the way best suited to pro-
mote the functions that the heart subserves.
Normally, the stimuli originating at the Keith-Flack node furnish
the impulses dominant in the irritable system, and though the rest of
the system possesses autonomous irritability, this is kept in abeyance.
Since all the parts are subordinate, under normal conditions, to the activity
of the Keith-Flack node, this node is called the pacemaker of the heart.
Stimuli to contraction thus normally arising and normally conducted from
the Keith-Flack node through the heart are known as nomotopic stimuli
(from the Greek nomos, law, and topos, place). Under pathological condi-
tions the normal pacemaker may lose its dominance, and stimuli, arising
automatically elsewhere in the irritable system, and known as heterotopic
stimuli (Greek heteros, other, different), may escape control and give rise
to abnormal contractions of the heart. Those of us engaged in clinical
work owe a great debt to the experimental physiologists (Gaskell, Engel-
mann, Einthoven, Erlanger, Hi rschf elder, Thomas Lewis, Hering, Kahn,
Rothberger and Winterberg, Nicolai, Cohn, Fredericq, and others), who
have supplied us with this new knowledge. Its clinical applications will
become clear when the cardiac arhythmias are discussed. (See below.)
The automatic activities of the heart are continually being influenced
through the inhibitory and the accelerator nerves, or extrinsic nerves of
the heart. Of these, the N. vagus exerts, predominantly, an inhibitory
function and the N. sympathicus, predominantly, an accelerator function.
The newer studies of hemodynamics are also now being applied to a
very large extent in clinical work and the experimental studies of the phys-
iologists upon blood pressure, velocity of flow, and the conditions of the
vasomotor apparatus generally, have come to have a priceless value for the
clinician.
The student who approaches pathological angiology as a clinical career
could not do better than to spend a considerable period of apprenticeship
in anatomical, physiological, and experimental-pathological laboratories,
familiarizing himself with the knowledge concerning the circulation that
has already been gained by scientists of these departments, and attempt-
ing to make at least some extension of it, before engaging too busily in
the clinical work proper.
It is, of course, outside the province of this book to review the anatomy
and physiology of the circulation. It must be taken for granted that the
student has already acquired a knowledge of the anatomical and physio-
logical facts necessarily precedent to clinical study. In the accompanying
bibliography, however, references will be found, which, it is hoped, will
698 DISEASES OF THE CIRCULATORY APPARATUS
guide the reader to the anatomical and physiological sources should he
wish to consult them.
References
1. General Texts
Babcock (R. H.). Diseases of the heart and arterial system [etc.], 2. ed. New York &
London, 1905, D. Appleton & Co. 874 P- 8°.
Braun (Ludwig). Diagnose und Therapie der Herzkrankheiten. 2. Aufl. Berlin &
Wien, 1913, Urban & Schwarzenberg. 373 p. 8°.
Flint (A.}. A practical treatise on the diagnosis, pathology and treatment of diseases of the
heart. Philadelphia, Blanchard & Lea, 1859, xv, 16-473. 1 pi. 8°.
Futcher (Thomas Barnes). Outlines of physical diagnosis of the circulatory and respira-
tory systems. Prepared from his lectures by J. G. Murray, Jr., Baltimore,
1915, The Students' Book Store, 175 p.
Gallavardin (£•)• Precis des maladies du cceur et de Vaorte. Paris, 1908, 0. Doin.
876 p. 8°.
Gibson (G. A.). Diseases of the heart and aorta. Edinburgh & London, 1898, G. J. Pent-
land. 954 p. 8°.
Hirschfelder (A. D.). Diseases of the heart and aorta. 2. ed. Philadelphia & London
[1913], J. B. Lippincott Co. 738 p. 8°.
Huchard (//.)• Trait e clinique des maladies du coeur et de Vaorte. 3. ed., 3 v. Paris,
1899-1905, O. Doin. 8°.
Jagic (N. v.). Handbuch der allgemeinen Pathologic, Diagnostik und Therapie der Herz-
und Gefdsserkrankungen. Leipzig & Wien, 1913, Franz Deuticke.
von Jurgensen (Th.}, von Schrbtter (L.) & Krehl (L.). Diseases of the heart. Edited,
with additions, by George Dock. Authorized translation from the German
under the editorial supervision of Alfred Stengel. Philadelphia & Lon-
don, 1908, W. B. Saunders Co. 848 p. 8°. NothnageVs Encyclopedia
of Practical Medicine. Amer. ed.
Krehl (L.). Die Erkrankungen des Herzmuskels und die nervosen Herzkrankheiten. 2.
ed. Wien & Leipzig, 1913, A. Holder. 678 p.
Leclerq (A.). Les maladies du cccur et de Vaorte et leur traitement. Paris, 1914, 0. Doin
et fils. 551 p.
Mackenzie (J.}. Diseases of the heart. S.ed. London, 1913, H.Frowde [etc.]. 502 p. 8°.
Poynton (F. /.)• Heart disease and thoracic aneurysm. London, 1907, H. Frowde.
310 -p. 12°.
Roger (G. H.}, Gouget (A.} & Boinet (E.}. Maladies des Arteres et de I'Aorte. Paris,
1912, J. B. Bailliere & fils. 480 p. 8°. [Nouv. Traite de Med. de
Therap., xxiv.]
Romberg (E.). Lehrbuch der Krankheiten des Herzens und der Blutgefdsse. 2. Aufl.
Stuttgart, 1909, F. Enke. 600 p. 8°.
Sahli (Hermann}. Lehrbuch der klinischen Untersuchungsmethoden fur Studierende und
Aerzte. 6. Aufl. Bd. II, 1. Hdlfte. Leipzig & Wien, 1915, F. Deuticke.
8°.
Savill (Thomas Dixori). A system of clinical medicine, dealing with the diagnosis, prog-
nosis and treatment of disease. 4- ed. London, 1914, E. Arnold. 976 p.
8 .
Steell (G.). Textbook on diseases of the heart. With an appendix on the volume of blood in
relation to heart disease, by J. L. Smith, Phila., 1S06, P. Blakiston's Son
& Co. 402 p. 10 pi. 8°.
Stokes (W.}. The diseases of the. heart and the aorta. Dublin, 1854, Hodges & Smith.
$89 p. 8°.
INTRODUCTION 699
Vaquez (H.). Maladies du cceur. Paris, J. B. Bailliere & fils. 8°. [Nouv. Traite de Med.
de Therap., xxiii.]
2. Clinical Papers
Barker (L. F.}. On some of the clinical methods of investigating cardio-vascular conditions:
the Jerome Cochran lecture. Johns Hopkins Hosp. Bull., Baltimore,
1909, xx, 297-310.
Also: Gulf States J. M. & S. [etc.], Mobile, 1909, xv, 459-495.
France (J. /.)• Some observations on the nervous and mental symptoms of heart disease.
J. Am. M. Ass., Chicago, 1915, Ixiv, 652-654.
Gillespie (A. L.). An analysis of 2,368 cases admitted with cardiac lesions into the Royal
Infirmary, Edinburgh, during the five years 1891-1906. Edinburgh Hosp
Rep., 1898, v, 31-66.
Graham (Z>.). Massage, exercises and baths in the treatment of affections of the heart; their
relative value. Interstate M. J., St. Louis, 1915, xxii, 449-456.
Greene (C. L.). The diagnosis of heart disease considered in its relation to life-insurance
examinations. Med. Exam., New York, 1901, xi, 267-272.
Prognosis in chronic heart disease as adversely affected by certain medical
traditions. J. Am. M. Ass., Chicago, 1912, lix, 685-690.
Head (H.). Certain mental changes that accompany visceral disease. Brain, London,
1901, xxiv, 345-429.
Hirschfelder (A. D.). Methods of diagnosis in circulatory troubles. Tr. Internal. Cong.
Med., 1913, London, 1914, Sect. VI, Medicine, pt. 2, 271-273.
Hoover (C. F.). General considerations in cardiovascular disease. Mod. Med. (Osle','
& McCrae). 8°. Philadelphia & New York, 2. cd., 1915, iv, 17-40.
Ktilbs (F.). Erkrankungen dtr Zirkulationsorgane. In: Handb. d- inn. Med. (Mohr &
Staehelin), Berlin, 1914, ii, 811-1290.
Lewis (Thomas). Lectures on the heart. New York, 1915, P. B. Hoeber. 132 p. 8°.
Nicolai (G. F.). Kurze kritische Uebersicht uber den augenblicklichen* Stand der Herzdiag-
nostik, unter besonderer Berucksichtigung der objektiven Methoden. Ztschr.
f. arztl. Fortbild., Jena, 1915, xii, 193-239.
Putnam (Mary L.). Occupational provision for one type of the physically handicapped,
cardiac convalescents. Am. J. Care Cripples, New York, 1915, ii, 41-4$-
Sahli (H.). Textbook of clinical diagnosis. Eng. transl. by N. B. Potter. Philadelphia,
1914.
Staehelin (R.) & Ortner (N.). Diagnostik der Krankheiten des Zirkulalionsapparates.
In: Lehrb. d. klin. Diagnostik (P. Krause). 2. ed. Jena, 1913, G
Fischer, 159-224.
Vaquez (H.}. Semiologie cardiague; palpation; percussion. Clin. med. de la Charite.
Lecons et mem., Pans, 1894, 11-28.
Witt (W. H.}. Prognosis in heart disease from the point of view of etiology. J. Am. M
Ass., Chicago, 1915, Ixv, 478-482.
3. Physiological and Pathological Papers
Hasebroek (Karl). Ueber den extrakardialen Kreislauf des Blutes vom Standpunkt der
Physiologic, Pathologic und Therapie. Jena, 1914, G.Fischer. $57 p. 8°
Ueber exlrakardiale Kreislauftriebkrdfte und ihre Beziehung zum Adren-
alin. Zugleich eine Beantwortung der Einwande Prof. Hurthle's gegcn
meine Theorie vom extrakardialen Kreislauf. Berl. klin. Wchnschr.t 1915,
Hi, 236-241.
Hofbauer (L.)« Die Atmung als Hilfskraft des Kreislauf s. 1. Bedeutung der Atmung
als Auxiliarkraft des grossen Kreislaufs. Med. Klin., Berlin, 1913, ix
700 DISEASES OF THE CIKCULATOKY APPAEATUS
Huerthle (K.}. Beitrage zur Haemodynamik. Arch. f. d. ges. Physiol, Bonn, 1891,
xlix, 29-104.
Josue (O.). Les localisations cardiaques. Tr. Internal. Congress, 1913, London, 1914,
Sect. Ill, Gen. Path. & Path. Anat., 1-105.
Krehl (L.). Beitrage zur Kenntniss der Fullung und Entleerung des Herzens. Abhandl.
d. math.-phys. Cl. d. k. sdchs. Gesellsch. d. Wissensch., Leipzig, 1891,
xvii, 339-362.
Also: Pathologische Physiologic. 8. ed. Leipzig, 1914.
Krehl (L.) & Marchand (F.). Handbuch der allgemeinen Pathologic unter Milmrkung
von E. Albrecht [et al.]. Bd. II. 1. Abt.: Allgemeine Pathologic des Blut-
kreislaufs. Leipzig, 1912, S. Hirzel. 668 p., roy. 8°.
Lewis (T.). The mechanism of the heart beat. New York, 1914. P.B. Hoeber. 295 p.
Marey (E. /.). La circulation du sang d Vetat physiologique et dans les maladies. Paris,
1881,G.Masson. 748 p. 8°.
Sewall (//.). Factors in the clinical physiology of the heart. Internal. Clin., Philadelphia,
1913, s. 23, ii, 125-138.
Sherrington (C. S.}. Revised by J. Mackenzie. Physics of the circulation. In: Syst.
Med. (Allbutt & Rollcston). London, 1909, vi, 3-26. 8°.
Tigerstedt (R.). Lehrbuch der Physiologic des Kreislaufs, Achlzchn Vorlesungen fur
Studirende und Aerzte. Leipzig, 1893, Veil & Co. 584 P- 8°.
Wiggers (Carl John). Modern aspects of the circulation in health and disease. Phila-
delphia & New York, 1915, Lea & Febiger. 370 p. 8°.
Studies on the pathological physiology of the heart. Arch. Int. M., Chicago,
1915, xv, 132-148.
For other general references, see Special Diagnosis of Diseases of the Circulatory System.
B. Examination of the Position and Size of
the Heart and of its Several Chambers
1. Position and Size of the Normal Heart
The heart (cor), the wedge-shaped pump of the circulatory apparatus,
lies in the thorax, somewhat asymmetrically as regards the median plane,
more of it lying in the left than in the right half of the body. The base
of the heart, formed by the atria, is directed backward and somewhat to
the right. The apex, formed by the left ventricle only, projects forward
and to the left, coming into direct contact with the thoracic wall in the
•fifth intercostal space somewhat medial from the costocartilaginous junc-
tion. The apex is thus situated medial from the mammillary line and it
lies, usually, from eight to nine centimeters to the left of the median line.
The right margin of the heart, formed by the right atrium, lies from
3.5 to 4.5 cm. to the right of the median line (about a finger's breadth
beyond the right sternal margin). The upper margin of the heart, from
which the great vessels go off, lies in the second intercostal space or at the
upper margin of the third rib, behind the sternum* The left margin of
the heart passes somewhat obliquely downward and to the left to the
region of the apex.
EXAMINATION OF THE HEAKT
The markedly curved sternocosial surface of the heart, which looks
upward and forward and comes into direct contact with the anterior wall
of the thorax, is formed chiefly hy the right atrium and the right ventricle ;
'it lies just behind the sternum and behind the anterior extremities of the
third, fourth, fifth and sixth ribs, being in part overlapped by the margins
of the lungs. The diaphragmatic surface of the heart, posterior and in-
ferior, is almost flat and-lies upon the diaphragm. The left atrium lies at
the back of the heart and is directed toward the esophagus and spine; the
left ventricle lies behind and below, only a small portion of it projecting
forward to form the apex of the heart. The auricle of the left atrium is
in contact with the anterior wall of the chest close to the pulmonary artery.
The orifice of the pulmonary artery (ostium arteriosum dextrum) is sit-
uated at the sternal end of the third left intercostal space, while the orifice
of the aorta (ostium arteriosum sinistrum) lies just below the middle of
the left half of the sternum at the same level. The center of the mitral
orifice (ostium venosum sinistrum) lies behind the third left intercostal
space close to the sternum, and the center of the tricuspid orifice (ostium
venosum dextrum) lies behind the right half of the sternum at the level
of the sternal end of the fourth intercostal space.
References
Bertier (/.). Dextrocardie par attraction; pneumothorax therapeutique; contribution a
V elude du mecanisme des' dextrocardies acquises. Bull, med., Paris, 1913,
xxvii, 825-827.
Bond (C J.). On the influence of the position of the body on the position of the heart and on
iniracardiac pressure. Brit. M. J., London, 1885, ii, 1109-1112.
Butler (G. JR.). A note on the position of the lower border of the heart and the topographical
anatomy of the organ. Boston M. &S.J., 1898, cxxxix, 501.
Capitan. Les variations de la forme du cceur. Nature, Paris, 1898, xxvi, 38-382.
Determann. Die Beweglichkeit des Herzens bei Lageverdnderungen des Korpers.
Deutsche med. Wchnschr., Leipzig u. Berlin, 1900, xxvi, 242-245. [Dis-
cussion]. Ver.-BeiL, 59.
Also: Ztschr. f. Krankenpfl., Berlin, 1900, xxii, 417-423.
Dietlen (H.). Ueber Grosse und Lage des normalen Herzens und ihre Abhdngigkeit von
physiologischen Bedingungen. Deutsches Arch. f. klin. Med., Leipzig,
1907, Ixxxviii, 55-122.
Satterthwaite (T. E.). Mobility and malpositions of the heart. Internat. Clin., Phila-
delphia, 1911, 21. s., ii, 55-61.
2. Methods of Determining the Position and Size
of the Heart
Conclusions concerning the position and the size of the heart are drawn
from the data yielded by three principal methods of examination: (1)
the inspection and palpation of the apex beat of the heart; (2) the percus-
702 DISEASES OF THE CIKCULATOEY APPAKATUS
sion of the cardiac dullness; and (3) the delimitation of the margins of
the heart by means of Rontgen rays.
(a) The Determination of the Position of the Apex Beat
of the Heart
An elevation of the chest-wall, at regular intervals, at the times of the
systoles of the left ventricle can, in the healthy person, usually be seen and
felt in the fifth intercostal space of the left side, between the maimnillary
and the parasternal lines.
As the site of the apex beat we designate the most lateral and the
lowest part of the area of pulsation ; as a matter of fact, the "apex beat''
thus recorded does not actually correspond to the position of the heart's
apex, for x-ray examinations show that the latter always lies a .little lower.
Moreover, the point of maximal impulse (p. m. i.) is not always at the
site of the apex beat.
In early childhood the apex is in the 4th intercostal space nearer the nipple. The
position of the apex beat on standing is practically the same as in the recumbent
position. On deep inspiration, however, the apex beat may lie behind the 6th rib
or in the 6th intercostal space and be more feebly felt, while on deep expiration
it may rise as high as the 4th intercostal space and become more diffuse. The
position changes when the patient lies on his left side; it may then reach the
mammillary line, or, often, a point two centimeters to the left of it. (After rapid
emaciation this mobility may be greater; see "wandering heart.") When the patient
lies on his right side, the apex is very little displaced to the right, rarely passing
to the right of the left parasternal line.
The position of the apex beat varies somewhat with alterations in the
size and shape (long, short, or flattened) of the thorax, a fact that stu-
dents soon meet with in their clinical experience. Anything that lowers
the diaphragm also lowers the apex beat; anything that raises the level
of the diaphragm (meteorism, ascites, pregnancy, abdominal tumors) will
raise the position of the apex beat. Fluid or air in one pleural cavity will
displace the apex beat toward the opposite side ; retraction of a lung (fibroid
phthisis) will have an opposite effect. Enlargement of the left ventricle
alone displaces the apex downward and to the left; enlargement of the
right ventricle alone displaces the apex to the left but not downward. A
pericardial effusion may displace the apex beat upward to the 3d inter-
costal space.
Too much stress should not be laid upon slight abnormalities in the
position of the apex beat. Its determination, however, is the first step in
the attempt to ascertain the position and size of the heart, inasmuch as
the position of the apex indicates the situation of the left margin of the
heart.
Precordial Boss or Voussure. — This is the name given to a unilateral
EXAMINATION OF THE HEART 703
bulging occupying the precordial area, due to enlargement of the heart
or to pericardial effusion. The enlargement is oval in form, its long
diameter being vertical and extending from the third to the sixth rib near
the sternum. It can arise only in early life when the ribs are still flexible.
It should not be confused with the deformations, usually bilateral, due to
rickets or to emphysema.
References
Bard (L.). De V importance de la palpation du cceur; donnees cliniques et signes nouveaux
qu'elle fournit. Mem. et compt.-rend. Soc. d. sc. med. de Lyon (1896),
1897, xxxvi, 82-94.
Barr (/.). Report on the causes and mechanism of the cardiac impulse. Brit. M. J., London
1884, ii, 149-164.
Doll (K.). DieLehre vom doppelten Hcrzstoss. Berl. klin. Wchnschr., 1899, xxxvi, 877; 899-
Gerhardt (/>.). Ueber einige pathologische Formen des Spitzenstosses, nebst Bemerkungen
iiber Entstehung des gespaltenen erslen Herztones. Arch. f. exper. Path,
u. PharmakoL, Leipzig, 1894, xxxiv, 359-366, 1 diag.
Hibbert (P.). Ueber die Ursachen des normalen und des krankhaft verstdrkten Herzspitzen-
stosses. Ztschr. f. klin. Med., Berlin, 1893, xxii, 87-103.
Potain (C.). Du ntourement presystolique de la pointe du cceur. J. de physiol. et de path.
yen., Paris, 1900, ii, 101-124.
Vincent (#.)• Des de-placements physiologiques de la pointe du cceur. Bull. Soc. d'anat. et
physiol. de Bordeaux, 1886, vii, 261-268.
(b) Determination of the Areas of Cardiac Dullness by Percussion
We are able by percussion to outline upon the anterior surface of the
chest two areas, (1) that of the superficial, small or absolute cardiac dull-
ness, and (2) that of the deep, larger or relative cardiac dullness. The
•area of absolute dullness corresponds anatomically to the part of the sterno-
costal surface of the heart not covered by the lungs, while the area
of relative dullness corresponds anatomically to the whole heart in
orthogonal projection. The area of superficial dullness is outlined by very
feeble percussion along the margins of the right and left lungs where they
overlap the heart. ' Inside the boundary of this area the characteristic
resonant pulmonary note is entirely absent. The larger area of relative
dullness is outlined by percussing from the lungs toward the heart and
marking the points at which the percussion note becomes less resonant or
relatively dull. Though the heart is covered by the lungs at its periphery,
the change in the percussion sound elicited permits one to outline its
margins with reasonable accuracy. The determination of the superficial
dullness is a much easier procedure than that of determining the deep
dullness ; for the latter a degree of skill, obtainable only by considerable
practice, is required.
704 DISEASES OF THE CIKCULATOKY APPAKATUS
i. The Area of Absolute (or Superficial) Cardiac Dullness
At the level of the sternal end of the fourth costal cartilage on the
left side, the margins of the two lungs begin to diverge ; the area between
them below this level is that of the absolute (or superficial) cardiac dull-
ness. The margin of the left lung passes to the left along the lower
margin of the fourth costal cartilage and then forms a slight convex curve
lateralward and downward to the apex. The margin of the right lung
passes downward behind the sternum and a little to the right toward the
sternal end of the fifth and sixth costal cartilages of the right side. In
many textbooks the right margin of the superficial cardiac dullness is said
to correspond with the left sternal margin, but in many cases by very
careful feeble percussion it is possible, despite the pleximeter action of
the sternum, to outline the margin of the lung behind the left half of that
bone. It is seldom possible, however, exactly to delimit the margin of the
lingula of the left lung ; it is so very thin that it influences the percussion
note but little.
To outline the. superficial cardiac dullness one percusses very lightly
with the middle finger of the right hand, using either the index finger,
or the middle finger, of the left hand as a pleximeter. Some prefer to place
the tip of the flexed terminal phalanx of the pleximeter finger vertically
upon the surface of the thorax and to percuss proximal to the joint. One
may begin the percussion in the dull area and mark the points at which the
lung resonance appears, or one may pass in the opposite direction, marking
the points at which the lung resonance goes over into the so-called absolute
dullness. It is customary to determine first the right margin of the absolute
dullness, then the upper margin and finally the left margin. It is to be
borne in mind that the percussion sound is not always absolutely flat like
the sound over the thigh, for it may present a slightly tympanitic quality
owing to the proximity of the stomach.
Anything that influences the position of the edges of the lungs (e. g.,
respiration, changes in the position of the body, etc.) will also influence the
size of the area of absolute cardiac dullness.
The outline of this area tells us very little about increase in the size
of the heart as a whole, though it may be of value as a clew to enlargement
of one of the chambers of the heart or of the pulmonary artery. If the
edges of the lungs are not adherent, if there be no retraction nor distention
of the lungs, and further, if the heart itself be not dislocated, changes in
the area of absolute cardiac dullness may be helpful in diagnosis. Thus
enlargement of either ventricle will lead to displacement of the edges of
the lungs and will increase the area of absolute dullness. This holds espe-
cially when the right ventricle is enlarged, in which event the right margin
of the area as percussed out sometimes takes the form of a steplike line
(Kronig), instead of the straight vertical line obtained in normal condi-
EXAMINATION OF THE HEAET
705
Fig. 185. — Steplike Line of Kronig.
tions. An accumulation of fluid within the pericardial cavity also en-
larges the area of absolute dullness ;
the right margin of the area then
forms an obtuse angle with .the up-
per margin of absolute liver dull-
ness.
When the area of absolute dull-
ness extends upward along the left
margin of the sternum as far as
the second intercostal space (chimney-shaped dullness) we may suspect the
existence of either a dilatation of the left atrium (e. g., in mitral disease),
or a dilated pulmonary artery (e. g., along with a patent ductus Botalli).
ii. The Area of Relative (or Deep) Cardiac Dullness
Of far greater value for. the formation of a judgment as to the size of
the heart as a whole is the determination of the relative (or deep) cardiac
dullness.
To outline it, one does best to use the method of Moritz, who percusses
with moderate force as follows: (1) From the right mammillary line
toward the left until a diminution in resonance corresponding to the
right margin of the heart is reached. The pleximeter finger should be held
parallel to the long axis of the body, the patient being told to hold the
breath at the end of deep expiration since the right margin of the heart
is not dislocated during expiration (though the left is) and the lessened
volume of lung over the heart makes the delimitation of the right margin
much more easy. Normally this right margin is met with about a finger's
breadth to the right of the right sternal margin or about 3.5 to 4.5 cm.
to the right of the median line; the percussion note becomes shortened
there and of higher pitch. One percusses at different levels and outlines
the whole right margin of the heart and higher up the right margin of
the area occupied by the great vessels. (2) The lower part of the left
margin of the heart is best outlined by percussion with less force, the
patient making shallow respirations. Here, also, the pleximeter finger
is held parallel to the long axis of the body. (3) In percussing out the
upper part of the left margin of the heart, the pleximeter finger is held
transversely to the long axis of the body, beginning at the left margin of
the sternum and percussing from above downward, using considerable
force. Above the heart, one also determines the presence or absence of
dullness to the left of the sternal margin in order to ascertain whether or
not the great vessels extend further to the left than normal.
The upper limit of the relative cardiac dullness is usually situated
between the third and fourth ribs, the right margin about a finger's breadth
to the right of the right sternal border (3.5 to 4.5 cm. from the median
line), though in advanced life it is not uncommon to find no relative dull-
706 DISEASES OF THE CIKCULATOKY APPARATUS
ness to the right of the sternum. The left margin of the relative dullness
usually corresponds to the position of the apex beat (normally 8 to 9 cm.
lateral from the median line), but it may lie still further later alward if
the thorax be narrow or
if the heart be relative-
ly large.
One should make it a
point to examine patients
as far as possible in the
same position, inasmuch as
posture influences the area
of cardiac dullness. In
obesity and in emphysema,
the determination of the
relative dullness is very
difficult and the area ob-
tained is often much small-
er than that corresponding
to the true dimensions of
the heart. Much less stress
is, therefore, to be laid
upon diminution of the
area of relative dullness as
a sign of a small heart
than upon enlargement as
a sign of a large heart.
When the relative dullness
exceeds the normal limits, passing, for example, to the right as far as the right
parasternal line or farther, and upward as high as the second rib, while the left
margin of the heart is as far or farther to the left than normal, it is certain
that the heart is enlarged.
Several other methods of determining the area of relative (or deep)
cardiac dullness have been introduced besides the one recommended above.
Among them may be mentioned (1) the threshold-value percussion of
Ewald-Goldscheider and (2) the palpatory percussion of Ebstein. The
student will do best to begin with the method recommended above ; later
on, if he desire to do so,- he may familiarize himself with the special
methods mentioned. Above all, the student should avoid the very forcible
percussion formerly in vogue. When possible, one should control his tech-
nic of percussion by orthodiagraphy or telerontgenography until reliable
results are obtainable.
Fig. 186. — Normal Tcrcussio^ Areas of Liver
The Dotted Area Denotes Relative Dullness
Area Absolute Dullness.
Enlargement of the Area of Relative Dullness. — This may be due
either to (1) enlargement of the heart, or (2) pericardial exudate.
When due to enlargement of the heart itself, the size depends usually
upon dilatation, the changes resulting from hypertrophy alone rarely being
EXAMINATION OF THE HEART
707
Fig. 187. — Relative and Absolute Cardiac Dullness With En-
larged Right Ventricle and Auricle.
sufficient to cause any marked increase of the area of dullness. Dilatation
of the left ventricle
causes an expansion
of the area of relative
dullness toward the
left only, almost nev-
er toward the right.
Dilatation of the
right ventricle dis-
places the right mar-
gin of the area of
relative dullness to
the right. When
both relative and ab-
solute dullness are
increased to the right
of the sternal mar-
gin, we have to deal
usually either with a
dilatation of the
right atrium or with
a pericardial exudate.
When a pericardial exudate is present, the areas of cardiac dullness,
both relative and absolute, are increased in all directions ; they assume the
form of an equilat-
eral triangle, the
apex of which is sit-
u a t e d above, the
right lateral margin
extending to the
right as far as the
parasternal line or
farther, and the left
lateral margin ex-
tending to the left
beyond the region of
the apex beat. The
line of the right mar-
gin of dullness may
then form a very ob-
tuse angle with the
line delimiting the
lower margin of the
Fig. 188. — Absolute and Relative Cardiac Dullness With -1,1 / • •, i_
Enlarged Left Ventricle. right lung (*• «•> Wlth
708 DISEASES OF THE CIECULATOEY APPARATUS
the line delimiting the upper limit of the absolute hepatic dullness). The
angle is often referred to as the "cardiohepatic angle" or the "angle of
Eotch."
It must be borne in mind that the area of heart dullness (either absolute
or relative.) as outlined may be increased through the presence of tumors
in the neighborhood, of pleural effusions, or of infiltrations of the lung.
Similarly, a dislocation of a heart of normal size by a pleural effusion,
by a tumor, or by a pneumothorax may simulate an abnormal position of
one heart boundary due to enlargement.
Diminution of the Area of Relative Dullness. — This seldom indicates
diminution in the size of the heart; most often the diminution of the
area is due to emphysema.
Instead of cardiac dullness one may meet with a tympanitic or metallic
sound in cases of pneumopericardium ; this alters with the position of
the patient, in contrast with the persistently resonant, non-tympanitic per-
cussion note that replaces the cardiac dullness in cases of emphysema
of the mediastinum. In transposition of the viscera, the area of cardiac
dullness has a topography on the wall of the thorax corresponding to the
mirror-picture of that normally met with.
References
Cabot (R. C.)» Essentials and non-essentials of physical diagnosis. Bull. Rochester M.
Ass., 1915, i, 14-17.
Corvisart (/.). Essai sur les maladies et lesions organiques du coeur et des gros vaisseaux.
2. ed. Paris, 1811, Nicolle. 478 p. 8°.
Ebstein (W.)» Zur Lehre von der Herzperkussion. Berlin klin. Wchnschr., 1876, xiii,
601-503.
Die Tastpercussion. Ein Leitfaden fur den klinischen Unterricht und fur
die drztliche Praxis. Stuttgart, 1901, F. Enke. 63 p. 8°.
Goldscheider (A.). Ueber Herzperkussion. Deutsche med. Wchnschr., Leipzig u. Berlin,
1905, xxxi, 333; 382.
Moritz (F.). Einige Bemerkungen zur Frage der perkutorischen Darstellung der gesamten
Vorderflache des Herzens. Deutsches Arch. f. klin. Med., Leipzig, 1907,
Ixxxviii, 276-285.
Moritz (F.) & Rohl (W.). Experimentelles zur Lehre von der Perkussion der Brustorgane.
Deutsches Arch. f. klin. Med., Leipzig, 1909, xcv, 457-469.
Newton (R. C.). A sketch of the origin of auscultation and percussion and of the stale of
clinical medicine in the time of Auenbrugger and Laennec. Tr. Am.
Climat. & Clin. Ass., Philadelphia, 1914, xxx, 27-38.
Plesch (/.)• Einiges uber Perkussion. Deutsches Arch. f. klin. Med., Leipzig, 1908, xciii,
Smith (H. L.). The use of a no-sound stroke in percussing out the boundaries of superficial
dullness of airless bodies. J. Am. M. Ass., Chicago, 1914, Ixiii, 32(
Thayer (W. S.). On the importance of fundamental methods of physical examination in the
practice of medicine. South. M. Jn Nashville, 1914, vii, 933-942.
EXAMINATION OF THE HEART
709
(c) Determination of the Size and Position of the Heart by
Means of Rontgen Rays
The most accurate method of determining the size and position of the
heart is by means of transillumination of the thorax with Rontgen rays.
Either simple fluoroscopic examination (rontgenoscopy) may be employed
or actual photographs may be made (rontgenography).
Aorta ascendens
Vena cava superior
Art. pulmonalis
Left atrium
i. Simple Rontgenoscopy
The view of the patient obtained varies according to the direction of
transilhimination (sagittal, frontal or oblique).
Sagittal View. — When the rays are thrown in from behind at the level
of the fifth thoracic spine, and the fluorescent screen is placed in front
of the thorax, the transillumination is said to be sagittal and dorsoventral.
The heart and great vessels (together with the sternum and the spine)
appear as a large median shadow situated between the two pale triangular
rib-shaded lung areas, the whole picture being bounded below by the
shadows due to the rise and fall of the diaphragm. An examination of
the median shadow, known as the CARDIOVASCULAR STRIPE, shows that it
is narrower above than
below and that it pre-
sents characteristic boun-
dary lines. The right
margin is only slightly
curved but nevertheless
can be seen to consist of
two parts ; the upper part
above the third rib cor-
responds to the right
margin of the vena cava DiaPhr.*m
superior, whereas the low-
er part below the third rib
corresponds to the right
atrium. The left mar-
gin of the shadow pre-
sents three curves of which the upper one (I), extending between the first
and second ribs, is due to the edge of the aorta ; the middle one (II), some-
what flatter, extending between the second and third ribs, corresponds in
its upper part to the A. pulmonalis and in its lower part to the left atrium ;
whereas the lowest of the three curves (III), and much the longest, extend-
ing downward and lateralward from the third to the seventh rib, is due
to the left margin of the left ventricle.
When the thorax is looked through in the opposite direction (ventro-
Right lung area
Right atrium
Lett lung area
Left ventricle
Right ventricle
Fig. 189. — Normal Cardiovascular Stripe on Rontgenos-
copy. Schematic Representation of the Rontgen-
oscopic View of the Thorax on Dorsoventral Sagittal
Transillumination. (After T. Brugsch and A. Schit-
tenhelm.)
710 DISEASES OF THE CIKCULATORY APPARATUS
Left lung area
Right lung area
Fig. 190. — Cardiovascular Shadow as Seen on Vcntro-
dorsal Sagittal Transillumination, Schematic.
(After T. Brugsch and A. Schittenhelm.)
dorsal sagittal transillumination), the shadow becomes somewhat broader
owing to the greater proximity of the heart to the anti-cathode and the
consequent enlargement of the projection of the heart on account of the
diverging rays.
Frontal View. — On frontal transillumination, the patient holds his
arms above his head and the
tube is placed in one axillary
line while the fluorescent
screen is applied to the oppo-
site side; both tube and
screen are held parallel to the
median plane of the body.
A wholly different view is
now obtained. Two small
lighter areas appear; one of
these, lying ventralward, is
triangular in shape and is
known as the retrosternal area; the other lies dorsalward behind the heart
and above the diaphragm and is known as the retrocardial area. Between
these two light areas is the
shadow due to the heart.
The part of this shadow
that forms the posterior Retrocardial &™
inferior boundary of the Aorta descenden8
retrosternal area is due to
the right atrium, the conus
arteriosus of the right
ventricle and the ascend-
ing portion of the arch of
the aorta. Between the
retrocardial area and the spine lie the esophagus and the descending aorta.
Unfortunately, frontal transillumination can be satisfactorily employed only
in people that are not too large nor too obese. When one gets a good view,
Spine Clear middle area important Conclusions
can be drawn regarding
( 1 ) the ventrodorsal di-
ameter of the heart and
Left clear Inngr area (2) the presence Or al>
sence of aneurismal dil-
atations of the ascend-
i n g and descending
aorta.
Fig. 192. — Thorax in Oblique Transillumination, Lamp Be- ObllQUe VlGW. Ob'
hind the Left Shoulder, Screen in Front of Right Chest,
Schematic. (After T. Brugsch and A. Schittenhelm.) lique transillummation
Spine
Ketrosternal area
Diaphragm — _
Fig. 191. — Frontal Transillumination of Thorax, Sche-
matic. (After T. Brugsch and A. Schittenhelm.)
Right clear lung area
EXAMINATION OF THE HEABT 711
is also useful, though less for determining the size and position of the heart
than for examining the condition of the arch of the aorta (q. v.).
The simple rontgenoscopic examination is of most value for the study
of the movements of the heart (^7. v.) and for gaining information regard-
ing the general position of the heart and the size of its several chambers.
For exact measurements of the heart it is insufficient, and the modification
of fluoroscopy known as orthodiagraphy must be employed, or, better still
perhaps, Kohler's telerb'ntgenography (q. v.).
Among the abnormal forms of the cardiovascular stripe recognizable
by rontgenoscopy may be mentioned the following: (1) the so-called "drop
heart'7 (coeur de goutte of the French; Tropfenherz of the Germans),
(2) the senile heart, (3) the type of the enlarged left ventricle, (4) the
type of "mitral configuration," (5) the generally dilated heart, (6) the
dilated heart in mitral stenosis with tricuspid insufficiency, and (7) the
type of pericardial effusion.
In the DROP HEART it is the median position of the stripe, the narrow-
ness of the stripe, the small area in contact with the diaphragm, the
(a) (b) (c) (d)
Fig. 193. — Abnormal Forms of Cardiovascular Stripe on Rontgenoscopy, (a) the "Drop-heart"
on Dorsovontral Illumination, Schematic; (b) the Senile Heart on Ventrodorsal Illumina-
tion, Schematic; (c) Enlargement of Left Ventricle on Dorsoventral Illumination, Scho-
matic : (d) the Mitral Configuration of the Heart of Holzknecht, Dorsoventral Illumina-
tion, Schematic. (After T. Brugsch and A. Schittenhelm.)
lateral mobility of the stripe on change, of position, the high level of the
base of the heart and the exaggeration of the second left lateral curve
that are characteristic (Fig. 193 a).
In the SENILE HEART, due to the loss of elasticity and elongation of the
aorta, the heart is more transverse than normal (Fig. 193 b).
In the third type mentioned, due to HYPERTROPHY OF THE LEFT
VENTRICLE, the heart also lies more transversely. The lowest of the three
curves of the left border of the cardiovascular stripe forms a projection
that has been compared to a sheep's nose and the heart's apex is plump
and rounded (Fig. 193 c).
In the HEART OF "MITRAL CONFIGURATION" (Holzknecht) there is
marked exaggeration of the lower curve on the right due to enlargement
of the right ventricle and a characteristic bulging in the region of the
middle curve on the left due to enlargement of the left atrium and dilata-
tion of the pulmonary artery (Fig. 193 d). When there is aortic insuffi-
ciency the second curve on the left may be less marked than normal
(Baetjer).
712 DISEASES OF THE CIRCULATOBY APPAKATUS
In the UNIFORMLY DILATED HEART the cardiovascular stripe is broader
than normal and the widening of the vascular area is especially noticeable
owing to dilatation of the vena cava superior (Fig. 194 a).
The heart assumes a peculiar shape in MITRAL STENOSIS ACCOMPANIED
(a)
Fig. 194. — Abnormal Forms of the Cardiovascular Stripe (Continued), (a) the Generally
Dilated Heart, Dorsoventral Illumination: (b) Dilatation of the Heart in Mitral Stenosis
and Relative Tricuspid Insufficiency, Dorsoventral Illumination, Schematic; (c) the
Shadow in Pericardia! Effusion, Dorsoventral Illumination. (After T. Brugsch and
A. Schittenhelm.)
BY TRICUSPID INSUFFICIENCY. Here in addition to the. characters of the
heart of mitral configuration (vide supra) the effects of the great enlarge-
ment of the right ventricle and right atrium are visible and the cardio-
vascular shadow occupies a more median position in the thorax (Fig. 194 b).
When there is a PERICARDIAL EXUDATE, the normal curves delimiting
the cardiovascular stripe laterally are obliterated and one sees the straight
sides of a dark triangular shadow (Fig. 194 c).
Most important information is given by rontgenoscopy in the diagnosis
of DILATATION OF THE AORTA and of AORTIC ANEURISM.
A diffuse dilatation of the aorta, so common in people "past middle
life, especially when arterial hypertension has existed for some time (as
in arteriolar nephropathy) or where a chronic luetic aortitis has existed,
is easily visible through the fluoroscope.
In aneurism of the thoracic aorta there is usually a sharply circum-
scribed shadow undergoing active pulsation connected with the aortic
shadow. The pulsation is expansible in all directions. If an aneurismal
sac be partially or completely obliterated by lamellated clots, the pulsa-
tion may be slight or absent. For illustration see Aneurism (Special
Diagnosis).
To determine which part of the thoracic aorta has undergone aneuris-
mal dilatation, transillumination in oblique directions is desirable. There
is sometimes difficulty in distinguishing an aneurism from tumors or en-
larged glands lying upon the aorta and pulsating with it, but if a proper
diaphragm be used, the shadow due to aneurism can usually be seen to
go over more smoothly into the aortic shadow than does that thrown by
a tumor mass. Moreover, the margin of the sac in aneurism is usually
sharply circumscribed and the expansion during pulsation is equal in
all directions.
EXAMINATION OF THE HEAKT
713
In aneurism of the innominate artery, the shadow lies high to the
right and the trachea is usually displaced to the left. The aneurism some-
times appears as a sharp, noselike projection of the arch of the aorta
into the left lung area (Kiilhs).
In aneurism of the descending aorta, rontgenoscopy is rarely sufficient
for positive differentiation from tumors.
In aneurism of the pulmonary artery, the shadow is usually situated
in the second right intercostal space and can rarely be differentiated from
the shadow of the aorta itself.
In ARTERIOSCLEROSIS, lime deposits in the peripheral arteries can often
be demonstrated by rontgenography. In obscure neuralgias of the extrem-
ities and in intermittent claudication, rontgenography may be helpful in
diagnosis. In sclerosis of the coronary arteries there is rarely calcification
enough for recognition in x-ray plates. Calcification of the renal arteries
is sometimes demonstrable in the rontgenogram.
( Crayon
ii. Orthodiagraphy Screen
Another method of which much is
heard nowadays is the orthodiagraphic
s4udy of the heart. In it, the attempt is
made to ietermine very accurately the
size of the heart by obtaining by suc-
cessive orthogonal projections a number of
single points in the outline yielded by
x-rays falling perpendicularly upon the
fluorescent screen, all divergent rays being
cut off by a diaphragm. The lines join-
ing the points obtained form a figure called
the orthodiagram (Figs. 196 and 197). Certain distances on these ortho-
diagrams are measured and the results compared with normal values. The
method is valuable for research work ; the results exceed in accuracy those
of any other method yet invented, except telerontgenography, but for
practical clinical work we
can get along very well
without orthodiagraphy
provided we utilize the
other forms of rontgenos-
copy to the full, together
with accurate methods of
percussion. I think it
probable that orthodiagra-
phy will soon be entirely
displaced by telerontgen-
ography.
Table
Diaphragm
Fig. 195. — Schematic Representa-
tion of Orthodiagraph in Cross-
section.
Fig. 196. — Sagittal Orthodia-
gram. (After Moritz.)
Fig. 197. — Frontal
Orthodiagram. (Af-
ter Moritz.)
714 DISEASES OF THE CIKCULATOKY APPAEATUS
The size of the heart, and accordingly of the silhouette of the heart
obtained in the orthodia-
gram, varies within cer-
tain limits in healthy
people. The heavier the
body and the greater the
height of the person,
as a rule, the larger his
heart. In women, the
measurements are usual-
ly about half a centime-
ter smaller than in men
of the same size and
weight. In adolescence,
the measurements are
somewhat smaller than
in adult life ; in old peo-
ple, the measurements
are as a rule somewhat in-
creased.
In the following ta-
ble, Mr. = maximal dis-
tance from m e d i a n
line to right margin of
heart; Ml. = maximal
distance from median
line to left margin; Tr. = transversal diameter (or Mr. + M1.); L. =
length of heart shadow ; B. = breadth of heart shadow.
Fig. 198. — Orthodiagram of the Heart, Lung Area, and
Diaphragm of a Normal Man. Cl, Clavicle ; D,
Diaiphragm ; Mr, Distance of Right Border of Heart
from Median Line ; Ml, Distance of the Left Border
of Heart from Median Line ; Lt and Ut, Lower and
Upper Tartial Diameter of the Heart Drawn Per-
pendicular to Cardiac Axis, and Representing the
Width of the Heart.
TABLE
ORTHODIAGRAPHIC MEASUREMENTS IN HEALTHY MALE ADULTS (AFTER DIETLEN)
Height and Body
Weight
Mr.
cm.
Ml.
cm.
Tr.
cm.
L.
cm.
B.
cm.
Area in
Cm.2
Height 145-154 cm
I o IT
Body Weight, 47 kg
} 3'7
8.5
12.2
13.4
9.6
103
Height, 155-164 cm
\ A 0
Body Weight, 57 kg
/ 4'2
8.7
12.9
14.0
10.2
111
Height, 165-174 cm
\
Body Weight, 64 kg
} 4'3
8.8
13.1
14.2
10.3
117
Height, 175-187 cm
\
Body Weight, 71 kg
> 4.5
9.3
13.8
14.9
11.0
131
EXAMINATION OF THE HEART
715
According to Groedel, the following table represents the average values
for patients in the upright position :
Mr.
Ml.
Tr.
L.
Adult man
4.6
8.4
13.0
14 0
Adolescent males
4.1
7.8
11.9
12.7
Adult woman
3.9
8.0
11.9
12.9
Adolescent females
3.7
7.2
10.9
12.1
When the thorax is elastic and of normal shape and the heart of normal
size, careful percussion of the area of relative cardiac dullness will be found
to agree very accurately with the orthodiagraphic findings. Considerable
divergence in results, however, is found under certain circumstances,
especially when the heart is much enlarged to the left so as to be close
to the lateral wall of the thorax or when the thorax is very narrow. This
discrepancy is due to the
fact that in orthodiagra-
phy the outline of the
heart is a sagittal pro-
jection on a plane tan-
gential to the anterior
wall of the chest, while
in percussion we have to
follow the rounded sur-
face of the chest and
thus obtain a figure for
the relative dullness
the left margin of which
will be situated much far-
ther lateralward upon the
lateral wall of the tho-
rax. Obviously, in such
circumstances, there can
be no agreement be-
tween the orthodiagraph-
ic projection and the per-
cussion projection of the
heart limits, and in such cases the apex beat will lie to the left of the
lateral margin of the orthodiagram.
Fig. 199. — Orthodiagram of a Normal Heart. Dotted
Line, ID Recumbent Posture ; Black Line, in Upright
Posture. (After Moritz.)
716 DISEASES OF THE CIKCULATOKY APPAKATUS
iii. Telerontgenography
In my own diagnostic work, I now make use of telerontgenography in
place of orthodiagraphy. The method has been described in Part II. It
is accurate, expeditious, free from danger and not expensive. I advise
its use for the making of permanent records of the exact size and position
of the heart.
References
Adler (/.) & Krehbiel (O. F.}. Orthodiascopic observations concerning a certain type of
small heart and its relations to some general systemic affections. Arch.
Int. Med., Chicago, 1912, ix, 346-361.
Albers-Schbnberg (Heinrich Ernst). Die Rontgentechnik. 4- Aufl. Bearb. von Prof.
Dr. Walter, Prof. Dr. Albers-Schdnberg,Zahnarzt Hauptmeyer, Dr. Druner,
F.M.Groedel, Hamburg, 1913, L.Graf e&Sillem. 743 p. 17 pi. 4°.
Brugsch (T.) & Schittenhelm (A.). Die Beobachtung dcs Herzens im Rontgenbilde. In:
Lehrb. klin. Untersuchungsmethoden, Berlin & Wien, 1908, 231-250.
Dietlen (H.~). Orthodiagraphische Untersuchungen uber pathologische Herzformen und das
Verhalten des Herzens bei Emphysem und Asthma. Munchen. med.
Wchnschr., 1908, Iv, 1770-1774.
Orthodiagraphie und Teleroentgenographie als Methoden der Herzmessung.
Munch, med. Wchnschr., 1913, Ix, 1763-1766.
Franze (P. C.). Theorie, Technik und Methodik der Orthodiagraphie. Arch.f. phys. Med.
u. med. Techn., Leipzig, 1906, i, 248-268.
Groedel (F. M.). Zur Technik der Telerontgenographie. Ztschr. f. med. Elektrol. u. Ront-
genk., Leipzig, 1908 , x, 16S-172.
Die rdntgen-anatomische Situsuntersuchung des Herzens und der grossen
Gcfdsse. Zweck, Bedeutung und seitherige Leistungen dieses Verfahrens.
Deutsches Arch. f. klin. Med., Leipzig, 1913, cxi, 199-205.
Huismans (L.}. Der Telekardiograph, ein Ersatz des Orthodiagraphen. Munch, med.
Wchnschr., 1913, Ix, 2400-2404.
Kohler (A.}. Telerontgenographie des Herzens. Deutsche med. Wchnschr., Leipzig u.
Berlin, 1908, xxxiv, 186-190.
Moritz (F.). Eine Methode, um beim Rontgenverfahren aus dem Schattenbilde eines Gegen-
standes dessen wahre Grosse zu ermitteln (Orthodiagraphie} und die exakte
Bestimmung der Herzgrosse nach diesem Verfahren. Munchen. med.
Wchnschr., 1900, xlvii, 982-996
Ueber Tiefenbestimmungen mittels des Orthodiagraphen und deren Ver-
wendung, um etwaige Verkiirzungen bei der Orthodiagraphie des Herzens zu
ermitteln. Fortschr. a. d. Geb. d. Rontgenstrahlen, Hamburg, 1904, vii,
169-189.
Otten (M.). Die Bedeutung der Orthodiagraphie fiir die Erkrankung der beginnenden
Herzerweiterung. Deutsches Arch. f. klin. Med.. Leivzin, 1912, cv
370-439.
Williams (F. H.}. The importance of knowing the size of the heart; inaccuracy of percussion
in determining it, as shown by X-ray examinations. Med. Communicat.
Mass. M. Soc., Boston, 1899, xviii, 175-188. 6 pi.
Van Zwaluwenburg (J. G.) & Warren (L. F.). The diagnostic value of the orthodiagram
in heart disease. Arch. Int. Med.. Chicago, 1911, vii, 137-152.
SOUNDS OVEE THE HEAKT AND VESSELS 717
C. Cardiovascular Acoustics; Normal and
Abnormal Sounds Over the Heart and
Vessels
In health and in disease certain oscillations arise in the heart and
blood vessels that may cause audible sounds. These can be recognized
by listening (auscultation) with the naked ear or with the aid of the
stethoscope, or the oscillations that are the physical basis of the sounds
may be recorded mechanically (graphic registration).
1. The Heart Sounds
(a) Normal Heart Sounds
If the ear be placed over the chest in the cardiac region of a healthy
person, pairs of sounds are heard recurring at regular intervals. Each pair
of sounds consists of a first and a second sound, separated from one an-
other by a brief interval (the short pause). Each pair of sounds in turn
is separated from the next pair by a longer interval (the long pause).
On listening with the stethoscope the duration and accentuation of the
single sounds at the apex of the heart is found to be somewhat different
from that at the base; thus at the base and over the lower part of the
sternum the first sound is longer and more accentuated (rhythm of a
trochee -^-N-x, phonetically indicated as lubb-dup or td to), whereas at the
base the second sound is more accentuated, the rhythm becoming that of
an iambus v. _z_ (lubb-dup or ta td). The first sound of each pair occurs
during the first third of ventricular systole and is therefore synchronous
with the apex beat of the heart. The second sound occurs at the very
beginning of ventricular diastole. The short pause between the two sounds
of each pair is meso- and telesystolic in time, but the long pause sepa-
rating consecutive pairs is diastolic in time.
(b) Origin of the Normal Heart Sounds
The origin of the first sound of the heart is still in dispute. Physiolo-
gists believe it to be chiefly an intracardial-tension-tone due to oscillations
set up by vibrations of the walls of the ventricles (muscular, membranous
and valvular) ; the tension of the mitral and tricuspid valves is included
here. It is believed by some that the opening of the semilunar valves of
the aorta and pulmonary artery and the sudden tension of the walls of the
aorta and pulmonary artery also contribute to the sound. The intracardial-
tension-tone is probably much more important than the so-called arterial-
expulsion-tone.
718 DISEASES OF THE CIRCULATORY APPARATUS
Many have attempted to distinguish in the intracardial-tension-tone in turn
three sets of components: (1) the tension of the mitral and tricuspid valves;
(2) the tension of the semilunar valves of the aorta and pulmonary artery; and
(3) the tension of the muscular walls of the left and right ventricles. It seems
desirable, certainly, to keep in mind the fact that the normal first sound is due to
a combination of the sounds produced in the two ventricles, inasmuch as in dis-
ease the components due to either one of the ventricles may undergo alteration.
To a certain extent the sounds are analyzable as regards their components by
means of auscultation at different areas on the chest wall (vide infra}. Clinicians
are inclined, perhaps, to lay too much stress upon the portion of the first sound
due to valve tension to the neglect of that part of it due to tension of the rest of
the ventricular wall.
The second sound is coincident with and due to the closure and ten-
sion of the semilunar valves of the aorta and pulmonary artery at the
beginning of diastole; there is general agreement as to the origin of this
sound.
In children and young adults a third sound is in the majority of cases
audible and normal just after what has been described as the second sound.
Since it occurs very early in diastole it is designated a protodiastolic
sound. It is suggested that it may he due to the floating up of the atrio-
ventricular valves by the Wood that rushes into the ventricles before the
end of the first third of diastole (Hirschf elder). It is best heard at or
near the apex when the patient is somewhat turned to the left side
(Thayer). It corresponds to the A- wave on the phlebograin.
References
Blunter (G.). A note on the normal' peculiarities of the heart-sounds in the region of the
sternum. Arch. Int. Med., Chicago, 1914, xiv, 605-607.
Bramwell (If.) & Murray (R. M.). A method of graphically recording the exact time-
relations of cardiac sounds and murmurs. Lrit. M. J., London, 1888, i,
10-16.
Bridgman (E. W.}. Notes on a normal presystolic sound. Arch. Int. M., Chicago, 1914,
xiv, 475-480.
Observations on the third heart sound. Heart, London, 1914-15, vi,
41-50. 3 pi.
Geigel (JR.). Entstehung und Zahl der normalsn Herztone. Arch. f. path. Anat. [etc.],
Berlin, 1895, cxli, 1-28.
Lamed (C. W.). A practical method of imitating the normal and abnormal heart sounds
for teaching. Johns Hopkins Hosp. Bull., Baltimore, 1910, xxi, 4-5-47.
Lombard (W. P.} & Pillsbury (W. B.). Secondary rhythms of the normal human heart.
Am. J. Physiol., Boston, 1809, Hi, 201-228.
Morison (A.). A clinical study of the causes of the first sound of the heart. Lancet, London
1900, i, 1430-1433.
Quincke (//.). Beitrage zur Entstehung der Herztone und Herzgerdusche. Berl. klin.
Wchnschr., 1870, vii, 249-251, 263-265.
Thayer (W. 5.) On the early diastoUc heart sound (the so-called third heart sound). Eos-
ton M. &S.J., 1908, xlviii, 713-726.
Further observations on the third heart sound. Arch. Int. Med., Chicago,
1909, iv, 297-305.
SOUNDS OVER THE HEART AND VESSELS
719
(c) Auscultation Sites
Since the information yielded by auscultation is of greatest value in
determining the state of the various valves and orifices of the heart, the
sites that have been selected for auscultation are those at which clinical
study, controlled by postmortem examinations, shows the sounds due to the
vibration of particular valves to be best heard. These auscultation sites
for the several valves do not correspond as a rule to the surface overlying
the anatomical sites of the valves. The anatomical projections of the
valves are situated very close together on the chest wall (Fig. 200) ; the
Aortic-
Tricuspid
Pulmonary
Mitral
Fig. 200. — Diagram Showing Positions of the Valves of the Heart and the Auscultation Sites.
sites selected for auscultation are relatively widely removed from one
another.
Four principal auscultation sites are usually selected :
1. At the apex of the heart, where the muscle tone of the first sound
propagated through the whole left ventricle can be heard (mitral area) .
2. In the second left intercostal space close to the sternum where the
sounds produced by the pulmonary semilunar valves can be best heard
(pulmonary area). Here the auscultation site corresponds to the anatom-
ical projection site.
3. In the second right intercostal space close to the sternum (aortic
area). Hither the sounds produced at the aortic orifice are well propagated
and they can, here, be heard tolerably free from admixture with other
sounds.
720 DISEASES OF THE CIKCULATOKY APPABATUS
4. At the junction of the 5th rib with the sternum on both the right
and left sides (tricuspid area).
It will be noticed that only two of these sites correspond to anatomical
projections ; namely, the pulmonary and tricuspid. The auscultation site
for the aortic valves is not far removed from the anatomical projection
site, but the anatomical projection site of the mitral valve is entirely
unsuitable as an auscultation site for that valve since the whole right
ventricle intervenes between the mitral valve and the anterior chest wall.
References
Davies (//.)• On the four chief orifices of the heart. Lancet, London, 1872, ii, 109—111. '
Heitler (M.). Die Localisation des zweiten Aorten- und des zweiten Pulmonaltones. Wicn.
klin. Wchnschr., 1894, vii, 939-943.
Norris (G. W.} & Fetterolf (G.). The topography of the cardiac valves as revealed by the
x-rays. Am. J. M. Sc., Philadelphia & New York, 1913, cxlv, 225-233.
(d) Rhythm and Accentuation of the Heart Sounds
At each auscultation site, both sounds of the heart are audible, and
one must distinguish, at each site, the sound of autochthonous origin from
the propagated sound; the former is, under normal conditions, better
heard than the latter. Thus, over the pulmonary and aortic sites, the
second sounds are autochthonous and the first sounds are propagated, which
explains the iambic rhythm (^ -*-) heard there, while at the apex, and
in the tricuspid area, the first sounds are louder (autochthonous)1 and
the second feebler (propagated) ; hence the rhythm of a trochee (-*- ^).
(e) Identification of the Heart Sounds
There should be no trouble, over healthy hearts, in distinguishing the
first sound from the second sound ; first, by the accentuation, and, second,
I I I I i I I I I I I I I I I I I I I
0 0,5 1,0 1,5 2,0 Seconds.
Fig. 201. — Length of Pauses Between the Heart Sounds, in Seconds. (After P. Krause,
"Lehrb. d. klin. Untersuchungsmethoden," published by G. Fischer, Jena.)
by the length of the pause following each sound. In disease, the heart
beats may become very irregular (arhythmia) or the rate greatly acceler-
ated (tachycardia). In some instances, both the long pause and the first
sound become relatively shortened and the heart sounds then resemble the
ticking of a watch (pendulum rhythm) so that the ear may not be able to
1 At the apex both the first and second sounds are "propagated," but the source
of the first sound is nearer than that of the second.
SOUNDS OVEK THE HEAET AND VESSELS
721
distinguish which is the first or which the second sound. When this pendu-
lum rhythm occurs with a very rapid pulse, the heart sounds resemble
those heard in the fetus (embryocardia). If it be impossible by the accen-
tuation of the sounds, or by their relation to the pauses, to tell which is the
first and which the second sound, the examiner may help himself out by
palpating (simultaneously with auscultation) the apex beat "or the carotid
pulse. The first sound is synchronous with the apical impulse and pre-
cedes the carotid beat by about one-tenth of a second, thus occurring always
in the first half of systole. Beginners often make the mistake of trying
to time the sounds in all cases by palpation of apex or carotid; clinical
teachers should correct this tendency and encourage students to make their
decisions by paying attention rather to the accentuation of the sounds
and their relation to the pauses, resorting to palpation only in instances
where satisfactory timing is impossible otherwise.
References
Gillet (H.). Rythme foetal des bruits du cceur sans tachycardie ou embryocardie dissociee
(Grasset). Ann. de la Polidin. de Par., 1893, Hi, 81-95.
Huchard (H.}. Un nouveau syndrome cardiaque; V embryocardie ou rythme foetal des bruits
du cosur. Bull, et mem. Soc. med. d. hop. de Paris, 1889, 3. s., vi, 192-198.
Lemoine (G.). De V embryocardie. Gaz. med. de Paris, 1893, 8. s., ii, 133-137.
Pawinski (/.). Pendulum-like rhythm of the heart sounds. Deutsche med. Wchnschr., Leip-
zig u. Berlin, 1891, xvii, 143-145.
(f) Graphic Registration of the Heart Sounds
Physiologists and clinicians have devised several methods of registering
graphically the time and intensity of the heart sounds, but only two of the
more important methods will be here referred to. For full description,
the original sources should be consulted.
Einthoven and Geluk's Method. — The Dutch physiologists used a stethoscope
attached to a microphone, the current
from which was passed through a
capillary electrometer, the movements of
which were photographed. Later, a strong
galvanometer (q. v.) was used. Bond,
and also Bridgman, have found this satis-
factory in the heart station at the Johns
Hopkins Hospital.
Weiss's Method. — Weiss uses a "pho-
noscope," consisting of a closed chamber
containing a small funnel, which is covered
by a film of soap bubble. In the center
of the film are placed minute capillary
tubes, the movements of which are magni-
Fig. 202.— The First, Second and Third
Heart Sounds as Graphically Recorded by
the Method of Einthoven and Geluk.
(From A. D. Hirschfelder's "Diseases of
the Heart and Aorta," published by J. B,
Lippincott Co., Philadelphia.)
fied and projected upon a photographic recording apparatus,
membrane of collodion instead of the film of soap bubble.
Gerhartz uses a
722 DISEASES OF THE CIRCULATORY APPARATUS
Recently, Crehore's apparatus has been applied by Meara, for the registration
of sounds as well as of movements.
References
Austin (J. H.}. Some applications of the Crehore micrograph, with especial reference to
the recording of heart sounds. Am. J. M. Sc., Philadelphia & New York,
1912, cxliii, 193-198.
Brugsch (T.) & Wiedemann (G.). Registrierung der Bewegungs- und Schallerscheinungen
am Kreislauf system. In: Technik d. spez. klin. Untersuchungsmeth.
(Brugsch & Schittenhelm) , Berlin & Wien, 1914, 107-141.
Einthoven (W.) & Geluk (M. A. J.). Die Registrirung der Herztone. Arch. f. d. ges.
Physiol, Bonn, 1894, Ivii, 617-639.
Einthoven (W.}, Flohil (A.) & Battaerd (P. J. T. A.). Die Registrirung der mensch-
lichen Herztone. Arch. f. d. ges. Physiol., Bonn, 1907, cxvii, 461-472.
Frank (O.)« Die unmittelbare Registrierung der Herztone. Munch, med. Wchnschr.,
1904, li, 953-954.
Gerhartz (H.). Die Aufzeichnung von Schallerscheinungen insbesondere die des Herz-
schalles. Ztschr. f. exper. Path. u. Therap., Berlin, 1908, v, 105-130.
Herzschallstudien. Arch. f. d. ges. Physiol., Bonn, 1909-10, cxxxi,
509-567.
Joachim (G.) & Weiss (O.)« Registrierungen von Herztonen und Herzgerduschcn beim
Menschen. Deutsches Arch. f. klin. Med., Leipzig, 1910, xcviii, 513-539.
Lewis (T.}. Illustrations of heart-sound records. Quart. J. M., Oxford, 1913, vi, 441-4-51-
Weiss (O.) & Joachim (G.). Registrierung und Reproduction menschlicher Herztone
und Herzgerausche. Arch. f. d. ges. Physiol., Bonn, 1908, cxxiii, 341-386.
(g) Detection of Alterations in the Intensity of the Heart Sounds
The loudness of the sounds of the heart may be less or greater than
normal.
i. Enfeeblement of the First Sound
The first sound may be enfeebled when something exists that hinders
the transmission of the sound (obesity, pulmonary emphysema, large pleu-
ral or pericardial effusion). The first sound may also be enfeebled either
by defective contraction of the ventricles or by alterations of the atrioven-
tricular valves. A feeble contraction of the ventricle may occur in any of
the conditions that give rise to myocardial insufficiency. When vegeta-
tions appear upon the borders of the valves the first sound may be dimin-
ished or even disappear (e. g., in acute endocarditis).
ii. Accentuation of the First Sound
On the other hand, the first sound may be exaggerated in intensity by
causes operating in the direction opposite to those just mentioned. Thus
the transmission of the sound may be facilitated in emaciated patients
or when there are gas-containing cavities near the heart (pneumoperi-
cardium, dilated stomach) ; in the latter instance the quality of the heart
sound may be more metallic than normal. Again, abrupt ventricular con-
SOUNDS OVER THE HEART AND VESSELS 723
traction (e. g., in emotional excitement or on physical exercise) augments
the first sound, and certain alterations in the atrioventricular valves, such
as thickening or induration, may have the same effect. This explains
the loud first sound sometimes heard in chronic endocarditis (e. g., mitral
insufficiency) and in arteriosclerosis of a mitral cusp.
The accentuation of the individual heart sounds is often of great
practical diagnostic significance.
Thus marked accentuation of the first sound at the apex is often a
sign of the existence of mitral stenosis. The abrupt first sound heard at
the apex in this disease is believed to be due to the more powerful vibra-
tions set up by the sudden tension of the stiffened valve-cusps.
The lesion of mitral insufficiency tends to enfeeble the first sound while
that of mitral stenosis tends to exaggerate -it. When in the course of a
mitral insufficiency the first sound becomes louder and more abrupt, one
may infer that stenosis has been added to the insufficiency, and when in the
course of a mitral stenosis a mitral insufficiency develops, the first sound
may become somewhat feebler.
iii. Enfeeblement of the Second Sound
The second sounds of the heart may also be either enfeebled or ex-
aggerated. Though the pressure is much higher in the aorta than in the
pulmonary artery, the conditions of auscultation are such that the second
sounds, in normal adults, are approximately equal in intensity at the aortic
and pulmonary sites. In children, the pulmonic second may be normally
louder than the aortic second.
The second sounds may be feebler than normal owing to faulty trans-
mission to the stethoscope (in obesity, pulmonary emphysema, pericardia!
effusion), though in such cases the second sound is usually less enfeebled
than the first and if only one sound be audible it is usually the second
Aside from faulty transmission of the sounds, they may be feebler either
from alterations in the arterial valves themselves (e. g., endocarditis) or
from lowering of tension in the aorta or pulmonary artery (e. g.f myo-
cardial insufficiency, anemia, Addison's disease, tuberculosis, etc.).
iv. Accentuation of the Second Sound
The second sounds may be exaggerated (accentuated) whenever the
arterial tension is increased. Thus marked accentuation of the aortic
second sound usually indicates hypertension in the aorta ; it is frequently
met with in chronic nephritis and in some forms of arteriosclerosis.
When in addition to mere accentuation of the aortic second sound there
is alteration of the quality or timbre of the sound we may usually assume
the existence of sclerotic or other changes in the semilunar valves them-
selves, in which case the second sound besides being loud has a certain
724 DISEASES OF THE CIKCULATOKY APPAEATUS
tympanitic or ringing quality. Not only is the character of the sound
altered but it seems to be prolonged by a sort of echo or resonance which
follows it. In such cases one must take especial care to ascertain whether
or not the sound is followed by a diastolic murmur.
Some care must be taken in deciding whether it is the pulmonary
second or the aortic second sound that is accentuated in a given case.
When the accentuation is maximal to the right of the sternum it is
certainly aortic in origin, but when it is maximal to the left of the
sternum it is usually pulmonary though it is sometimes due to a sound
propagated from the aortic orifice, and other physical signs must be con-
sidered in making a decision.
When the pulmonary second sound is accentuated it is evidence of
increased pressure in the pulmonary artery and may be due to some
obstruction to the flow of blood in the lung (e. g., emphysema, fibroid
phthisis, pulmonary arteriosclerosis) or to faulty circulation in the left
heart (e. g._, mitral disease).
When a pulmonary second sound that has been accentuated becomes
enfeebled, it is often an indication of beginning insufficiency of the muscu-
lar wall of the right ventricle and is not infrequently coincident with the
advent of an insufficiency at the tricuspid orifice.
References
Creighton (Sarah R.}. The relative intensity of the second sounds at the base of the heart;
a study of one thousand cases. Med. Rec., New York, 1900, Mi, 45-47.
OJ Carroll (/.). On the accentuation of the second sound in the pulmonary area; Skoda' s sign.
Tr. Roy. Acad. M., Ireland, Dublin, 1899-1900, xviii, 31-37.
Vierordt (//.)• Die Messung der Intensitdt der Herztone. Centralbl. f. klin. Med.. Leipzig,
1885, vi, 17-20.
(h) Detection of Changes in the Number of the Heart Sounds
Instead of the first and second sounds of the heart above described,
there may be heard, either in healthy or in diseased hearts, three or four
or even more sounds (aside from the murmurs which are described later).
The additional sounds may be due (1) to failure of the components of the
first or second sounds to fuse to a single sound, especially when there is
a disturbance in the synchronism of events in the two ventricles, or (2)
to the formation of entirely new sounds.
i. Splittings and Doublings of the Heart Sounds (£ Rhythm)
The first sound or the second sound may be split, doubled, i. e., re-
duplicated, without any marked alteration in accentuation or in relation
to the short and long pauses of the cardiac cycle. When the first sound
is simply split, the fault in coincidence is slight (tra, to) ; when it is
SOUNDS OVEE THE HEAKT A1STD VESSELS 725
doubled, the fault in coincidence is greater (ta-ta to). Similarly the
second sound may be either split (ta tra), or doubled (ta ta-ta). Every
degree of transition from slight splitting to distinct doubling may be met
with. The origin of such splittings and doublings has been much dis-
cussed (Geigel, Sahli). These phenomena are frequently met with in
health at different phases of respiration; thus the first sound is often
split at the end of inspiration and the beginning of expiration, the second
sound (less often) at the end of expiration and the beginning of inspira-
tion. The doublings are more common in diseased conditions, and are then
audible in all respiratory phases. When the mitral valve is damaged, the
second sound is often split or reduplicated at the base, owing to increased
pressure in the pulmonary artery. The splitting of the second sound at
the apex (bruit de rappel of Bouillaud), so common in mitral stenosis, is
attributed by some to vibration of the rigid valve when the blood begins
to enter the ventricle from the atrium (claquement d'ouverture de la
mitrale}, this giving rise to a sound just after the normal second sound.
Many believe that this "cantering" sound is not a true reduplication of
the second sound heard at the apex beat, but is, in reality, a divided dias-
tolic murmur that points to mitral constriction.
References
Bard (L.}. De la multiplicite anormale des bruits du coeur. Semaine med., Paris, 1908,
xxviii, 3-5.
Dehio (K.). Die Enlschung und Bedeutung des gespaltenen zweiten Herztones. St. Petersb.
med. Wchnschr., 1891, n. /., viii, 279-285.
Gallavardin (L.). Pseudo-dedoublement du deuxieme bruit du cceur simulant le dedouble-
ment mitral par bruit extra-cardiaque telesystolique surajoute. Lyon med.,
1913, cxxi, 409-422.
Geigel (R.}. Der erste Herzton. Miinchen. med. Wchnschr., 1906, liii, 817-819.
Sahli (//".)• Spaltung und Vcrdoppelung der Herztone. In: Lehrb. d. klin. Untersuchungs-
methoden. 5. Aufl. Leipzig & Wien, 1909, 842-345.
ii. Triple or Gallop Rhythms (f Time)
The normal 2/4 rhythm of the heart is fairly well maintained in the
splittings and doublings above described. Sometimes the heart sounds,
however, appear, not in 2/4 rhythm, but as groups of three sounds, of
which the first and second and the second and third are separated by
approximately equal intervals, while the last member of each group is sepa-
rated from the first member of the next succeeding group by a somewhat
longer pause. In such cases a 3/4 rhythm arises, which, on account of its
resemblance to the sounds made by a galloping horse, has been designated
gallop rhythm. Sometimes the extra sound precedes the first sound of the
heart (presystolic gallop), sometimes it follows the second sound (proto-
diastolic gallop). In the presystolic type, the three sounds present the
726 DISEASES OF THE CIRCULATORY APPARATUS
rhythm of an amphibrachy (-— ' -*— ^-^), in which the middle one is long,
the first and last short ; in the protodiastolic type, the rhythm is that of a
dactyl (-«- ^ ^— '), the first sound being long, and the second and third
short. Gallop rhythms are usually most distinctly audible just medial
from the apex of the heart, though the rhythm can usually be heard over
the whole cardiac area.
The existence of gallop rhythm can be confirmed by palpation, inas-
much as the extra tone is accompanied by a distinct shock palpable at the
apex ; indeed the tactile features of the rhythm are often more conspicuous
than the acoustic. The waves on the mechanically-registered cardiogram
should be compared with the waves appearing upon the simultaneously-
registered phlebogram.
The significance of gallop rhythms has been much discussed. A proto-
diastolic gallop is common in bradycardia, in aortic insufficiency and in
mitral stenosis. It may be a normal phenomenon when a good normal
"third sound'7 is audible (Thayer). The presystolic gallop is most fre-
quently met with when a hypertrophied left ventricle is beginning to yield
to the strain (chronic nephropathy, coronary sclerosis, myocarditis).
Whether the so-called presystolic gallop is in reality presystolic and due
to sudden tension 01 the wall of the left ventricle from vigorous contrac-
tion of the atrium (Exchaquet, Johnson) or depends upon a dissociation
of the first sound of the heart, the shock due to contraction of the ventricu-
lar walls being separated from that due to valve closure (Bard) is still in
dispute, though a majority lean to the former view. A slight blowing
murmur between the first two sounds of this gallop may be met with when
the heart is weak (Lamacq).
The existence of a presystolic gallop rhythm is often more important
than that of a heart murmur for diagnosis and prognosis.
While the presystolic type of gallop rhythm most frequently met with
seems to be a phenomenon pertaining to the left ventricle, a certain number
of cases have been described in which a right-ventricle gallop existed
(pulmonary sclerosis). Here the rhythm is best heard in the region of
the xiphoid. It has been suggested (on the ground of electrocardiograms)
that gallop rhythm is a manifestation of injury to a branch of the His
bundle going to one or the other ventricle (Rothberger and Winterberg).
Diastolic Sound in Mediastinopericarditis. — In adherent pericardium
there sometimes arises a third sound just after the second sound. Fried-
reich thought this due to sudden diastolic expansion of the previously
indrawn thorax (diastolische Schleuderton) • the sound is heard, however,
after Brauer's operation of cardiolysis has been performed, so that this
explanation is inadequate. Since the sound is accompanied by a small
wave on the cardiogram, it is probably due to the inrush of blood from
the atrium into the ventricle in diastole and is the ordinary third sound.
SOUNDS OVER THE HEART AND VESSELS 727
References
Bard (L.). Du bruit de galop de Vhypertrophie du coeur gauche; son mecanisme et sa signifi-
cation clinique. Semaine med., Paris, 1906, xxvi, 229-231.
Handford (//.). The significance of the gallop-rhythm in cardiac disease. Quart. M. J.t
Sheffield, 1893-94, ii, 48-55.
Hoover (C. F.}. Gallop-rhythm and division of the pulmonic second tone. Phila. M. J .y
1898, ii, 424-428.
Kriege (H.) & Schmall (B.). Ueber den Galopprhythmus des Herzens. Ztschr. f. klin.
Med., Berlin, 1890-91, xviii, 261-272.
Midler (F.). Ueber Galopprhythmus des Herzens. Munchen. med. Wchnschr., 1906, liii,
785-791.
Offenbacher (R.). Experimented Beitrdge zur verstdrkten Vorhofstdtigkeit bei geschwachtem
Herzen, mit besonderer Benicksichtigung des Galopprhythmus. Arch. f.
exper. Path. u. Pharmakol., Leipzig, 1914, Ixxvi, 1—15.
Pezzi (C.) & Lutembacher (R.). Sur le mecanisme du rythme a trois temps de la stenose
mitrale. Arch. d. mal. du cceur [etc.], Paris, 1913, vi, 561-573.
Potain (C.). Les bruits de galop. Semaine med., Paris, 1900, xx, 175.
Robinson (G. C.). Gallop rhythm of the heart. Am. J. M. Sc., Philadelphia & New York,
1908, cxxxv, 670-687.
Sahli (H.}. Der Galopprhythmus. In: Lehrb. d. klin. Untersuchungsmethoden. 5. Aufl.
Leipzig u. Wien, 1909, 346-347.
Wiedemann (G.}. Zur Frage des mesosystolischen Galopprhythmus. Ztschr. f. d. ges. exper.
Med., 1914, ii, 297-304.
2. Heart Murmurs
(a) Introduction
From the standpoint of physics, the normal heart sounds, as well as
the abnormal sounds known as heart murmurs, are noises and never pure
tones ; they are all due to "aperiodic" vibrations. Some writers speak of
the heart sounds as "heart tones" and of the heart murmurs as "heart
noises," though as a matter of fact the vibrations of murmurs more often
approach the periodicity of clangs or tones than do the normal heart
sounds.
The chief difference between the sounds in the normal heart and the
heart murmurs met with in disease lies in the duration, and in the termina-
tion, of the noise. The normal sounds are briefer, and they die out more
quickly. Murmurs tend to be longer, and to fade away gradually. These
differences correspond to the origin of the sounds. The normal sounds
arise from a single sudden disturbance of the equilibrium of the sound-
producing body, while heart murmurs are due to a repeated disturbance
of this body ; in the normal sounds the duration depends upon the after-
vibration of the sounding body dependent upon its inertia, whereas in
murmurs the longer duration results from the repeated excitation to move-
ment that occurs (Sahli).
728 DISEASES OF THE CIKCULATOBY APPAEATUS
The character of the normal heart sounds is so different from that of
heart murmurs that the skilled observer can nearly always recognize the
sounds along with the murmurs and uses the former as a frame in which
he places the latter.
(6) Analysis of the Features Presented by Heart Murmurs
In studying heart murmurs, attention is paid to a whole series of
features. Of these, some are essential, others less important. Of the
essential features may be mentioned:
1. The time (or phase) in the cardiac revolution in which the murmur
occurs.
2. The site at which the murmur is best heard; and
3. The direction and propagation of the murmur.
Of the less important features may be mentioned:
4. The intensity of the murmur.
5. Its pitch ; and
6. Its quality or timbre.
i. The Timing of Heart Murmurs
The first point to attend to is the exact phase, or the phases, in the
cardiac revolution in which the murmur is audible. Clinically, all mur-
murs occurring between the moment at which the first sound of the heart
begins and the end of the short pause marked by the beginning of the
second sound are said to be systolic murmurs; while all murmurs audible
during the period extending from the moment at which the second sound
begins to the end of the long pause marked by the beginning of the first
sound are said to be diastolic murmurs. Obviously, therefore, the percep-
tion of the first and second sounds is of greatest importance in determining
the time of a murmur.
Systole and diastole (in this clinical sense) may be further subdivided
into three portions, a beginning, a middle and an end portion; for the
systole these times are known respectively as protosystolic, mesosystolic
and telesystolic, while for the diastole the corresponding terms protodias-
tolic, mesodiastolic and telediastolic are employed. Before these terms
came into use, murmurs occurring at the end of diastole, just before the
systole, were called presysiolic, and this designation is still in vogue ; thus
the terms presystolic and telediastolic may be regarded as identical. The
former term, however, is used to describe more particularly those murmurs
that run into the first sound.
The beginner should avoid the common mistake of thinking that a
murmur belongs to the phase of cardiac revolution represented by the
sound to which it stands nearest ; thus the second sound occupies only the
earliest part of diastole but a presystolfc murmur occurring just before
SOUNDS OVER THE HEART AND VESSELS
729
the first sound of systole is in reality a diastolic murmur, though it is
close to the normal systolic sound and far removed from the normal
diastolic sound.
When a murmur occupies the whole of systole, it is said to be holo-
INTRAVENTR1CULAR
PRESSURE
VOLUME OF
VENTRICLES
MITRAL 5YSTOUC
AORTIC SYSTOLIC
AORTIC DIASTOLIC
PRESYSTOLIC
Fig. 203. — Diagram Showing the Relation of the More Common Simple Murmurs to Events
of the Cardiac Cycle. Solid Black Bars Indicate the Heart Sounds. Vertical Parallel
Lines Reaching to the Base Indicate Blowing or Rough Murmur. Wavy Vertical Lines
not Reaching to the Base Indicate a Rumble. (After A. D. Herschf elder, "Diseases of
the Heart and Aorta," published by J. B. Lippincott Co., Philadelphia.)
systolic (Gr. holos, entire) ; if it occupies only a part of systole, it is
said to be merosystolic (Gr. meros, portion). Similarly, a murmur may
be Jiolodiastolic or merodiastolic.
When the heart sounds exist in fairly normal relation to the heart
pauses, there is but little difficulty in determining the phase of a cardiac
cycle to which a heart murmur belongs, even though the accentuation of
the sounds deviates from the normal. But in pendulum rhythm, and
more especially when one of the heart sounds ceases to be audible, con-
siderable difficulty may be experienced in timing a murmur. One has
to be guided in the auscultation then by simultaneous palpation, either
of the apex beat or of the carotid pulse.
ii. The Topography of Heart Murmurs
Since the more important cardiac murmurs are due to disease of the
valves of the heart, it is desirable to determine whether the location of
a murmur does or does not indicate an existing relation between it and
one of the orifices guarded by valves. The best auscultation sites for the
various valves have been described above in connection with the normal
heart sounds. Should a murmur be maximal at one of these sites, it will
he designated accordingly ; e. g., mitral systolic or mitral diastolic, aortic
730 DISEASES OF THE CIKCULATOEY APPAKATUS
systolic or aortic diastolic. One must be cautious, however, as sometimes
a murmur propagated to one of these areas may be mistaken for one of
local or autochthonous origin. Thus, a murmur in reality arising at the
mitral orifice is often maximal in the pulmonary area and the tyro might
Basilar zone
Mesocardiac
zone
Apical zone
Pig. 204. — Division of the Precordial Area into Zones and Regions. (After Potain ; from
L. Gallavardin, "Precis des maladies du coeur," published by O. Doin, Paris.)
easily think of a lesion of the pulmonary semilunar valves rather than of
the mitral valve.
In describing the exact position of the puncta maxima, it is sometimes
helpful to use the terminology introduced by Potain (Fig. 204). This
author divides the precordial area into three zones :
1. A basilar zone, subdivisible into
(a) A pre-aortic region, and
(b) A pre-infundibular region.
2. A mesocardiac zone, sudivisible into
(a) A sternal region,
(b) A xiphoid region, and
(c) A left preventricular region.
3. An apical zone, subdivisible into
(a) A supra-apical region,
(b) An apical region proper,
(c) An endo-apical region, and
(d) A para-apical region.
Murmurs occurring solely in the left preventricular region and in the
para-apical region are usually "accidental" murmurs, not indicating any
serious organic disease of the heart. Murmurs audible in the pre-infun-
dibular region sometimes indicate organic disease, though they, too, are
often merely functional in nature.
iii. The Direction and Propagation of Heart Murmurs
Since, as a rule, a murmur is best conducted in the direction of the
flow of the current that produces it, it is desirable to ascertain not only
SOUNDS OVEK THE HEAET AND VESSELS 731
the point at which a heart murmur is maximal but also the manner in
which the murmur is propagated in one or more directions from this point.
If, for example, a systolic murmur is produced by narrowing of the aortic
valves (aortic stenosis), the murmur will be maximal at the auscultation
site for that valve in the second intercostal space to the right of the
sternum and the murmur will be propagated upward toward the carotid
and the subclavian arteries since this is the direction in which the blood
flows from the narrowed spot at which the murmur arises.
If the aortic valves leak so that blood can pass back through them into
the left ventricle during diastole (aortic regurgitation) , the diastolic
Aortic Insufficiency
(*) Maximal Intensity
Aortic Roughening
£) Maximal Intensity
. Cardiac Dullness
Flint Murmur
»• • Mitral Insufficiency
Maximal Intensity
Fig. 205. — Distribution of Heart Murmurs in Man, Age 3G, With Aortic Insufficiency, Aortic
Roughening, Mitral Insufficiency and Aneurism of the Transverse Arch. (Med. Clinic,
J. H. H.)
murmur will be propagated downward and to the left along the left
margin of the sternum, corresponding to the direction of the regurgitant
flow.
In narrowing of the mitral valve (mitral stenosis), the blood is forced
through a narrow slit directly toward the apex of the heart and one hears,
during the period of the contraction of the atrium, a presystolic murmur
in the region of the apex. On the other hand, when the mitral valve
leaks and blood regurgitates through it during contraction of the ventricle.
732 DISEASES OF THE CIKCULATOKY APPAKATUS
(mitral regurgit&tion) , the murmur is propagated sometimes best toward
the apex of the heart, i. e., in a direction opposite to the regurgitation,
by transmission along the chordae tendineae and the papillary muscles (De
Sautelle and Grey), sometimes best toward the left atrium, and a systolic
murmur may be audible either at the apex, or in the pulmonary area where
the auricle of the left atrium comes nearest to the surface.
When multiple heart murmurs coexist, a determination of the maximal
Cardiac Dullness
—— • Mitral Insufficiency
XXXXMaximal Intensity
Mitral Stenosis
Aortic Insufficiency
Maximal Intensity
Fig. 206.— Distribution of Heart Murmurs in a Man, Age 33, with Mitral Stenosis, Mitral
Insufficiency, and Aortic Insufficiency. Intense Presystolic Murmur at Apex, Ending in
Snapping First Sound (Mitral Stenosis) ; Systolic Murmur at Apex, Widely Distributed
Over Chest, Maximal in Pulmonic Area (Mitral Insufficiency) ; Diastolic Murmur Widely
Distributed Over Chest and Axilla, Maximal Along the Sternum (Aortic Insufficiency).
(Med. Clinic, J. H. H.)
and minimal points for each murmur and of the direction in which it is
propagated is essential for exact diagnosis. One may, for example, hear
a systolic murmur in the aortic area and also in the mitral area at the
apex, in which event one has to decide whether the former murmur arises
at the aortic orifice, or is propagated to the aortic area after originating
at the mitral orifice. One may easily make either one of two mistakes ;
he may, in the first place, assume that a murmur is propagated when in
,re,ality both valves are diseased, or he may diagnosticate a defect in both
SOUNDS OVEE THE HEAKT AND VESSELS
733
valves, when, in reality, the murmur in one area is propagated from a
distant valve.
A difference in the character of the murmur at the two areas may help
to decide ; thus, if one be very rough and the other smooth, or if one be
musical and high-pitched while the other is soft and blowing, it is probable
Mitral Insufficiency
(a) Maximum Intensity
(b) Area of Transmission
Mitral Stenosis
Cardiac Dullness
Fig. 207. — Areas in Which Heart Murmurs Were Audible in a Patient Suffering from Acute
Rheumatic Fever with Mitral Insufficiency and Mitral Stenosis. Note the Limited Area
Just Medial from the Apex of the Heart in Which the Faint Rumbling Presystolic Murmur
Leading Up to the Accentuated First Sound Was Heard ; Also the Large Area Over Which
the Rough Systolic Murmur of Mitral Insufficiency Was Audible, Maximal in an Area of
Some Size Around the Apex But Transmitted to the Axilla and the Angle of the Left
Scapula. (Med. Clinic, J. H. H.)
that two different murmurs exist, though it has to be borne in mind that
a murmur during its propagation may not only be weakened but also, to a
certain extent, be modified in character.
In addition to noting differences in the quality of the murmur in the
two areas, the intensity should be carefully observed. When the murmur
is equally strong in both areas, it is probable that an autochthonous mur-
mur exists at each site, since a murmur propagated any distance is likely
to have its intensity lessened. When one murmur is more intense than
734 DISEASES OF THE CIKCULATOKY APPARATUS
the other, the view that the feebler murmur is propagated from the area
in which the stronger is heard is favored. If, on listening along a line
connecting one area with the other, the sound of the first murmur gradu-
ally lessens to a minimum and then increases to a second maximum in the
distant area, it is probable, that one has to deal with two autochthonous
murmurs.
When both systolic and diastolic murmurs are audible over the heart,
the diastolic murmur should first be carefully located and analyzed, to
the total neglect of the systolic; subsequently the systolic murmurs may
be analyzed for themselves.
Occasionally, murmurs are propagated far beyond the precordial
region. Thus they may be audible in almost any part of the body — along
the spine, in the flanks, in the head as far as the vertex, and even in the
limbs. Sometimes a patient may hear his own heart murmur or a person
several feet from him may hear it. Such great diffusion was once thought
to be characteristic of murmurs occurring in congenital malformation of
the heart, but it may accompany any orificial lesion that gives rise to an
intense, low-pitched, systolic blow.. As a general rule, aortic murmurs are
propagated toward the upper part of the body and mitral murmurs toward
the lower.
iv. The Intensity of Heart Murmurs
Though the intensity of heart murmurs is very variable, in diagnosis
too much stress should not be laid upon this fact. Diastolic murmurs are
usually less intense than systolic, though not always. The two factors con-
cerned in intensity are (1) the size of the opening, and (2) the force, or
velocity, of the flow. Care should be taken also not to over-estimate the
importance of intensity for prognosis. For a very loud murmur may ac-
company a slight lesion, whereas a very soft murmur may coexist with a
serious lesion of the heart. With a given murmur, a patient's condition
may be better when it is intense than when it is feeble, since the intensity
may, as we have seen, vary with the force of the cardiac contraction.
The intensity of a murmur is in part dependent upon the velocity of
flow through the narrow spot at which it is produced ; and since the flow
is usually quickest at the moment an orifice is opened, most murmurs are
more intense at the beginning and gradually fade away; in other words,
they manifest a decrescendo character. An important exception is the rate
of flow through a narrowed atrioventricular valve during ventricular dias-
tole. Here the flow is most rapid at the end of diastole, the presystolic
acceleration depending upon the atrial contraction. This murmur may
therefore approximate to a crescendo character.
The flow is probably maximal at the beginning of diastole under
normal conditions, but then wo have no murmur to point it out. In ad-
vanced mitral stenosis, where we have a presystolic murmur, the same con-
SOUNDS OVER THE HEART AND VESSELS 735
ditions that cause the murmur also slow the flow and then the greatest
flow is probably presystolic in time. Some divide mitral stenosis into
three grades:
1. Large opening = murmur protodiastolic.
2. Smaller opening = murmur f of way through diastole.
3. Small opening = greatest flow during atrial contraction and mur-
mur is presystolic.
In narrowing of the aortic orifice, the murmur produced may be at
first crescendo and later decrescendo.
The intensity of a murmur increases and diminishes with the changes
in blood pressure, due to the work done by the heart ; thus, when a heart
hypertrophies, murmurs in it become intensified, and when a heart weak-
ens, the murmurs may grow feebler.
The intensity of heart murmurs may also be influenced by body pos-
ture. Most murmurs are more intense in the recumbent position than on
standing ; the heart rate is less, and the ventricles contract more energeti-
cally. To accentuate the intensity of a heart murmur, one may take ad-
vantage of the suggestion of Azoulay, who makes the patient lie down with
the. head supported, the arms raised and resting gently on the head'of the
bed, and the lower extremities flexed so that the heels touch the buttocks.
In this attitude, the heart is still further slowe.d and the intensity of a
murmur is sometimes markedly increased.
The intensity of a murmur, other things being equal, depends largely
upon the size of the orifice at which the murmur is produced. If this be
too wide, or too narrow, sound vibrations do not occur ; thus, in stenosis of
the mitral valve, should the slit become very narrow, the presystolic mur-
mur, or rumble, may entirely disappear ; on the other hand, in leakage at
the mitral valve, a systolic murmur that has been loud may wholly dis-
appear should the left ventricle,- and with it the muscular ring at the mitral
orifice, become greatly dilated.
•Finally, the condition of the walls of a diseased orifice may affect the
intensity of the murmur produced there. Rigid, or calcified, valves may
emit loud sounds, whereas soft, fresh thickenings of the valves may give rise
only to feeble murmurs.
v. The Pitch, or Tonality, of Heart Murmurs
This depends largely upon the size of the orifice at which the murmur
is produced. If it be large, the murmur is likely to be low-pitched ; if
small, of higher pitch. Very low-pitched murmurs are "rumbling" sounds.
In contraction of the mitral orifice, a diastolic murmur may be a rumble
pf very low pitch, a presystolic blow of much higher pitch, or it may pre-
736 DISEASES OF THE CIKCULATOKY APPAKATUS
sent the characters of any one of several gradations between these two
extremes.
vi. The Quality, or Timbre, of Heart Murmurs
According to the peculiar quality that heart murmurs manifest, they
are designated as blowing, rasping, scratching, filing, musical, aspirative,
etc. Though these variations in quality must be due to the physical mech-
anisms upon which the murmurs depend, these differences are as yet too
poorly understood to permit us satisfactorily to value them.
Mitral systolic murmurs are most often blowing in character, aortic
diastolic most often aspirative. A musical murmur usually indicates the
existence of a vibrating cord in the course of the blood current (loose piece
of valve, thickened and retracted chordae tendineae).
(c) Physical Explanation of the Origin of Heart Murmurs
Various theories have been advanced but the most generally accepted is
that which attributes the origin of heart murmurs to the formation of a
"liquid vein," at a point where the blood passes through a narrow channel
connecting two cavities. Such a "liquid vein" is prone to be formed at the
point where the blood passes through the constriction into the larger cavity.
Under normal conditions the relations that exist among the cavities of
the heart, the valvular orifices, the velocity of flow and the composition of
the blood are such that no murmurs arise, but an abnormal condition of the
orifices, a change in the velocity of flow or in the composition of the blood
may give rise to a liquid vein, the particles of which vibrate so much that
they cause vibration of neighboring parts and give rise to murmurs. Much
experimental work has been done in this connection ; generally speaking,
the greater the velocity of flow, the greater the change in the size of an ori-
fice ; the thinner the blood and the rougher the surfaces over which the
blood passes, the more easily do murmurs arise and the louder they are.
Sometimes, a murmur arises when, through the mechanical conditions ex-
isting, one current of blood opposes or conflicts with another.
(d) - Significance of Heart Murmurs
A murmur audible over the heart may arise inside the heart (intracar-
diac murmur) or outside the heart (extracardiac or exocardial murmur).
A murmur may be produced by organic disease of the heart valves (organic
murmur), or it may be independent of -such disease (inorganic murmur).
Thus an inorganic murmur may be caused by a relative insufficiency of the
valves owing to the dilatation of the ring muscle surrounding the valve
orifice (functional heart murmur) or it may have its origin in conditions
not due to disease of the heart muscle or its valves (accidental murmur) , in
SOUNDS OVER THE HEART AOT3 VESSELS 737
which case it may depend upon an impoverished state of the blood (anemic
murmur) or upon increased rapidity of flow (velocity murmurs in fevers)
or upon causes that are as yet unknown to us.
i. Organic Intracardiac Murmurs
Pathological changes in the heart valves due to endocarditis or to
atherosclerosis may lead to imperfect closure of the orifice (valvular insuffi-
ciency), on the one hand, or to narrowing of the orifice (valvular stenosis)
on the other. Murmurs due to insufficiency of a valve will be produced in
those phases of the heart action during which the orifice is normally closed,
whereas murmurs due to stenosis will arise when the orifice is open and the
blood current is passing through it in the normal direction. The time rela-
tions of the murmurs arising at the four main orifices of the heart are rep-
resented in the following table :
TABLE OF ORGANIC MURMURS
Valves
Insufficiency
Stenosis
Aortic and pulmonary
Mitral and tricuspid
Diastolic
Systolic
Systolic
Diastolic
The special characters of these different murmurs will be more fully
discussed under the diagnosis of the several diseases. of the heart (vide
infra). As a rule, the murmur in stenosis is rougher and shorter and more
likely to be accompanied by a palpable thrill, than the murmur in insuffi-
ciency, which is softer and more prolonged. Ingenious methods for imi-
tating the heart sounds and murmurs have been devised by C. W. Lamed
and by H. L. Smith ; they are useful in didactic work.
ii. Inorganic Intracardiac Murmurs
Clinical experience has taught us that murmurs are frequently audible
over the heart during life, though at autopsy no changes in the valves
of the heart are demonstrable. Such murmurs, independent of anatom-
ical lesions of the valves, have been called inorganic murmurs. That
a certain number of these are due to imperfect contraction of the muscle
ring around the valve, leading to a functional or relative insufficiency of
the valvular closure, has already been pointed out. Relative insufficiencies
of this sort are common at the mitral and tricuspid orifices. They occur
occasionally at the aortic orifice (relaxation of Stewart's muscle ring) and
738 DISEASES OF THE CIKCULATOKY APPAKATUS
perhaps also, though still more rarely, at the pulmonic orifice (Graham-
Steell murmur "of high pressure in the pulmonary artery").
The term accidental murmurs is perhaps better reserved for the mur-
murs that are still less important as regards the condition of the heart
itself; namely, for those murmurs depending (1) upon slight abnormali-
ties in the course of the contraction of the heart muscle due to nervous or
other influences, (2) upon abnormal composition of the blood, or (3)
upon changes in the velocity of flow.
Accidental systolic murmurs at the apex, or in the pulmonary area, are
occasionally met with in healthy persons, especially in children between
the ages of 10 and 14.
In -all forms of anemia, but especially in chlorosis and in pernicious
anemia, accidental systolic murmurs may be heard over the whole heart;
occasionally an anemic diastolic murmur is audible. Perhaps some of the
accidental murmurs audible in cachexias may depend upon the accom-
panying anemia.
In conditions in which the action of the heart is excited (fevers, neu-
rasthenia, Graves's disease}, accidental systolic murmurs are often audible
in the pulmonary area and over the left ventricle. They appear to
depend in part upon increased velocity of flow and in part upon irregular
contraction of the heart muscle.
A certain number of murmurs resembling more or less closely those
above described have their origin in the lung during movements of the
heart (cardiorespiratory murmurs, q. v.). I mention them here because
they may closely simulate a murmur of intracardiac origin; they are,
however, extracardiac in origin. (See below.)
The criteria for differential diagnosis between these less important mur-
murs and the more important murmurs due to organic disease of the valves
or to relative insufficiency should be carefully studied. In general, it may
be said that the less important murmurs are systolic rather than diastolic
and that they are merosystolic rather than holosystolic. They are less
precisely localizable than the organic murmurs; some of them occur at sites
in which organic murmurs are often audible (apical and pulmonary areas),
but many of them are heard in areas at which organic murmurs are rarely
present (left preventricular and para-apical regions).
Accidental murmurs are rarely of very high or of very low pitch;
they are more commonly soft, aspirative and superficial, though, occasion-
ally, rough and even rasping, or musical, accidental murmurs may be
heard. Further, accidental murmurs are as a rule much more variable
in intensity than organic murmurs, especially under the influence of the
respiratory movements and of change in posture. Most important of all,
the accidental murmurs are not accompanied by those other changes in the
heart and circulation that follow upon organic diseases of the valves and
are demonstrable by other physical methods of examination.
SOUNDS OVER THE HEAET AND VESSELS 739
References
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Carrien (Af.) & Anglada (/.)• Contribution a la pathogenic du souffle deFlint. Insuffisance
aortique et retrecissement mitral relatif. Arch. d. malad. d. cceur, etc.,
Paris, 1913, vi, 253-265.
Cole (R. /.) & Cecil (A. B.}. The axillary diastolic murmur in aortic insufficiency. Johns
Hopkins Hosp. Bull, Baltimore, 1908, xix, 353-361.
Davison (J. T. R.}. The physics of cardiac sounds and murmurs. Lancet, London, 1895,
i, 1507-1574-
De Sautells (W. T.} & Grey (E. £.)• The relation of the papillary muscles to the mitral
regurgitant murmurs. Arch. Int. Med., Chicago, 1911, viii, 734-746.
Edwards (A. R.}. Cardiac murmurs; their differentiation and interpretation, with especial
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548-550.
Certain misconceptions regarding cardiac murmurs and their interpretation.
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Finlayson (/.)• On the occurrence of a diastolic murmur of aortic origin apart from aortic
incompetency or aneurism. Brit. M. J., London, 1885, i, 426-428.
Flint (A.}. On cardiac murmurs. Am. J. M. Sc., Philadelphia, 18S2, n. s., Ixiv, 29-54-
The mitral cardiac murmurs. Am. J. M. Sc., Philadelphia, 1886, n. s.,
xci, 27-40.
Gairdner (W. T.). A short account of cardiac murmurs. Edinb. M. J., 1861-62, vii, 438-
453.
Geigel (R.}. Ueber die Entstehung derGerdusche in Herz und Gefdssen. Sitzungsb. d. phys.-
med. Gesellsch. zu Wiirzburg, 1895, 12-16.
Gordon (W.). Posture and heart murmurs. Brit. M. J., London, 1902, i, 636-639.
Johnston (C. //.)• The differential diagnosis between functional and organic heart mur-
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M'Aldowie (A. A/.). Cardiac bruits audible at a distance from the chest. Edinb. M. J.,
1892-93, xxxviii, 619-622.
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Mitralinsufficienz am lautesten in der Gegend der Pulmonalklappe zu
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Systolisches Gerausch am Pulmonalostium bei Mitralinsufficienz. Berl.
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Oddo (C.). De la propagation lointaine des grands souffles cardiaques. Marseille med.,
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740 DISEASES OF THE CIKCULATOEY APPAEATUS
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3. Extracardiac (or Exocardial) Murmurs
Among the abnormal sounds audible over the heart, synchronous with
its action but arising outside its cavities, are:
(a) Pericardial friction.
(b) Pleuropericardial friction.
(c) Cardiorespiratory murmurs.
(d) Precordial crackling of mediastinal emphysema.
(e) Splashing and water-wheel sounds.
(a) Pericardial Friction Sounds
The sounds known as pericardial friction rubs are due to roughness of
the pericardium as a result of fibrinous deposits in acute pericarditis ; in
rare instances, cancerous nodules in the pericardium may be a cause. They
are usually scratching, interrupted and rough ; the sounds seem to be super-
ficial, close to the ear. Most often they resemble the sounds emitted when
one rubs a piece of silk or a new bank-note between the fingers. Occasion-
ally, the sound is like that of the creaking of a new saddle.
A portion of the sounds occurs cjuring systole and a portion of them
during diastole. They are therefore to and fro sounds, though the systolic
sounds nearly always predominate. Close attention shows, however, that
the sounds are rarely strictly related to the beginnings of systole and of
diastole ; they are more often mesosystolic and mesodiastolic. They may,
in rare cases, be limited to the systole, and, still more rarely, to diastole;
in the latter case, especially when soft, a pericardial rub may be mistaken
for the diastolic murmur of aortic insufficiency. Occasionally, the rub is
divided into three parts (locomotive murmur), yielding a f rhythm resem-
bling gallop rhythm, or the rub may even be divided into four parts, due
possibly to successive rubs during systole and diastole of both ventricles
and atria.
Pericardial friction is most often heard in the middle zone of the
precordial region at the level of the third left intercostal space, but it may
be met with at the base in either the aortic or pulmonary area, and,
occasionally, a rub is audible at the apex. The sounds are usually limited
to a rather small area though they are often more diffused ; in rare
instances, a rub may be widely propagated, even into the back, especially if
there be a coexisting pneumonia and the heart be beating powerfully.
It should be borne in mind that a pericardial friction rub may easily
be missed, owing to its feeble intensity, when the heart is weak. .
SOUNDS OVER THE HEART AND VESSELS 741
A friction rub is very easily influenced by alterations in the posture
of the patient, and by respiratory movements. The intensity is increased
with the pressure of the stethoscope. If the presence of a rub be sus-
pected, the patient should be examined in different postures, especially in
the sitting position with the trunk bent a little forward; in the right
lateral position, it is well to listen especially at the right margin of the
heart, and in the left lateral position at the left margin.
As fluid collects in the pericardial cavity and the heart floats on its
surface, the rub gradually disappears, remaining longest at the base.
References
Bruen (E. T.). The diagnosis by auscultation of pericardial friction murmurs. M. & S.
Reporter, Philadelphia, 1886, liv, 163-165.
Hinds (W.}. On pericarditis and pericardial murmurs. Birmingham, 1865. 12°.
Riesman (/>.)• Pericarditis; its symptoms and diagnosis. Tr. Coll. Phys., Philadelphia.
1904, xxvi, 138-207.
Shattuck (F. C.). Pericarditis; some points in its diagnosis and treatment. Tr. Ass. Am.
Physicians, Philadelphia, 1897, xii, 185-204.
Steell (G.). A clinical lecture on pericarditis. Brit. M. J., London, 1960, i, 181-183.
(b) Pleuropericardial Friction Sounds
A pulsatile friction sound, produced by rubbing of the outer surface
of the pericardium against the pleura, may be synchronous not only with
the heart's action but also with the respiratory movements. The portion
of the sound due to the latter will cease when the breath is held.
(c) Cardiorespiratory Murmurs
These sounds, known also as pulsatile pulmonary sounds (S. J. Gee),
arise in the lungs chiefly during the systoles accompanying inspiration.
Occasionally diastolic sounds are produced, and, sometimes, the sounds
are audible during expiration also. The heart becomes smaller during
systole and the ingress of air in the adjacent lung is increased, owing to
greater negative pressure in the lung. The sounds may be blowing like
those of vesicular breathing, or crackles and rales may be produced. The
systolic vesicular breathing may closely resemble a heart murmur. These
pulsatile pulmonary sounds usually cease, or are markedly modified, when
the breath is held. They are also much influenced by changes in posture.
When the lung is adherent in front of the vessels at the base of the
heart, a diastolic murmur sometimes becomes audible, the diastolic retrac-
tion of the aorta causing a localized aspiration into the adjacent pul-
inonary alveoli.
742 DISEASES OF THE CIECULATOKY APPAEATUS
References
Foshay (P. M.}. A case of cardiopulmonary murmur illustrating the importance of dif-
ferentiation. Cleveland J. M., 1901, vi, 236-238. .
Francois- Franck (A.}. Des bruits extra-cardiaques en general et en particulier des bruits
gastriques rhythmes avec le cceur; contribution au diagnostic de ^adherence
du pericarde. Gaz. hebd. de med., Paris, 1885, 2. s., xxii, 757-760.
Hall (C. JR.). On pulse-breath. M.-Chir. Tr., London, 1862, xlv, 167-175.
Harris (D. F.). The human cardiopneumatic movements. J. PhysioL, London, 1905, xxxiir
495-500.
Huchard (#.)• Les faux cardiaques (souffles cardiopulmonaires) . Bull, med., Paris, 1896,
x, 257-260.
Jones (T.). A study of heart murmurs, chiefly exocardial or cardiorespiratory ; their mechan-
ism and methods of investigation by posture, holding the breath, etc. North-
west. Lancet, St. Paul, 1896, xvi, 103-107.
Sanders (G.)« Cardiopulmonary murmurs. Edinb. M. J., 1896-97, xliii, 522-529.
(d) Precordial Crackling of Mediastinal Emphysema
If there be air in the mediastinal tissues (mediastinal emphysema), a
crepitant sound, synchronous with the heart's action, may be audible over
the heart and may closely resemble the sound emitted by pericardial
friction.
(e) Splashing and Water-wheel Sounds
If aij* and fluid occur together in the pericardial cavity, each beat
of the heart may give rise to a metallic, ringing splash. Similar sounds
are sometimes heard when there is a pulmonary cavity near the heart,
when a hydropneumothorax exists, or even when the stomach is much
distended with fluid and gas. Sometimes the sound resembles the clack-
ing, or chopping, noise made by the floats of a water-wheel (bruit de
moulin of Bricheteau). The character of this water-wheel sound varies
according to the predominance of the liquid or of the gas, or according
to their admixture. When the fluid predominates, the sound is crepitat-
ing, or resembles a metallic gurgle (Stokes). If the gas be large in
amount, the normal sounds of the heart, or any pericardial rubs present,
may possess a metallic consonance. The typical water-wheel sound arises
when the liquid and air are more or less mixed.
If the water-wheel sound have an extrapericardial origin, it will dis-
appear when the patient is sitting, to reappear when he lies down ; but if
it be intrapericardial in origin, the sound is heard in both positions (P.
Reynier).
References
Bricheteau (M.). Observation d'hydro-pneumo-pericarde, accompagnee d'un bruit de fluc-
tuation perceptible a I'oreille. Arch. gen. de med., Paris, 4- s., iv, 1844,
334-839.
Russell (W.) & Smith (J. C.). Case in which a loud, splashing sound was produced syn-
chronously with cardiac action. Edinb. M. J., 1885-86, xxxi, 518-521.
SOUNDS OVER THE HEART AND VESSELS 743
4. Auscultation of the Blood Vessels
When listening over the blood vessels, one must take care not to exert
pressure, unintentionally, with the stethoscope; otherwise, a narrowing
of the vessel will he produced, which will give rise to a murmur.
(a) Auscultation of the Arteries
One locates the vessel by palpation and sets the hell of the stethoscope
lightly upon it. Normally, two sounds are audible in the subclavian and
the carotid arteries, the first just after the beginning of ventricular sys-
tole (arteriodiastolic) , the second just after the beginning of ventricular
diastole (arteriosystolic) . If the artery be pressed upon now with the
stethoscope, a ventriculosystolic stenosis murmur will become audible; but
if the pressure be increased so as to close the vessel, a single tone is
heard (pressure tone). Occasionally, a single tone (arteriodiastolic) is
audible over the abdominal aorta, or over the femoral artery; but no
sounds are audible, normally, over the other arteries of the body.
Systolic murmurs due to narrowing at the aortic orifice are often
propagated into the carotid and the subclavian arteries. When the aortic
second sound is absent, as in some cases of aortic insufficiency, no arterio-
systolic tones are heard in the great vessels.
When a Corrigan pulse exists (see Pulsus celer), the pulse wave
rising quickly and sinking again very rapidly, an arteriodiastolic murmur
is often audible in the arteries of the neck, and an arteriodiastolic tone
over the femoral and the brachial and, sometimes, over the smaller arteries.
The phenomenon is most often met with in aortic insufficiency, but it
may also be encountered in Graves's disease, in fever, and even in nervous
palpitation. When a very loud sound is audible, it is spoken of as a
"pistol-shot sound."
Arterial murmurs are sometimes audible over the aorta and over the
carotid arteries in arteriosclerosis of the aorta ; these are supposed to be
due to the friction of the blood against the roughened intima.
In aortic insufficiency, on listening over the femoral artery, two tones,
quickly following one another, are sometimes to be heard (Traubes double
tone). On slight pressure with the stethoscope, these tones disappear and
one hears, first, a normal pressure murmur, and later, on stronger pressure,
a second murmur (Duroziez's double murmur). If the pressure be still
further increased, one hears only the normal pressure tone. The double
murmur of Duroziez may be heard also, sometimes, in chlorosis and in
Graves's disease.
Any compression of an artery may give rise to a stenosis murmur.
Use is made of this fact in the auscultatory method of determining maxi-
mal and minimal blood pressure (q. v.).
744 DISEASES OF THE CIKCULATOBY APPAKATUS
It is possible that some of the murmurs audible, at times, in the second
left intercostal space in pulmonary tuberculosis may be due to compression
of the pulmonary artery by the tuberculous changes in the lungs or by
enlarged bronchial glands. Similarly, the murmur sometimes audible
over the subclavian artery in apical tuberculosis may be due to com-
pression of the artery from pleural adhesions.
References
Bard (L.). De V appreciation des resistances peripheriques par V auscultation des souffles
arteriels. Arch. d. mal. du cceur [etc.], Paris, 1915, viii, 105-111.
Dehio (X.). Ueber das pulsatorische Tonen der Arterien. St. Petersb. med. Ztschr., 1913,
xxxviii, 259-268.
Duroziez (P.). Du double souffle intermittent crural, comme signe de I'insufflsance aortique.
Arch. gen. de med., Paris, 1861, 5. s., xvii, 417, 588.
Francois-Franck (A.). Essai sur le mode de production des souffles arleriels en general
et • du double souffle crural en particulier. Arch, de physiol. norm, et
path., Paris, 1889, 5. s., i, 659-666.
Heynsius (A.). Ueber die Ursachen der Tone und Gerdusche im Gefdsssystem. Leiden,
1878. 8°.
Schreiber (/.). Entstehung und Bedeulung der Doppeltdne im peripheren Gefdsssystem
(mil specieller Beriicksichligung derselben in der Cruralarterie) . Dcutsches
Arch. f. klin. Med., Leipzig, 1880-1, xxviii, 243-303.
Schultz (W.). Ueber Doppeltonbildung an den Cruralgcfdssen. Deutsche med. Wchnschr.,
Leipzig u. Berlin, 1905, xxxi, 1381-1383.
(b) Auscultation of the Right Jugular Vein
The stethoscope is placed over the sternal attachment of the right M.
sternocleidomastoideus, the patient sitting or standing (not lying) with
the head turned toward the left.
In the jugular vein certain sounds become audible under abnormal
conditions; they include (1) the venous hum, and (2) the venous tone.
Venous Hum. — In anemic patients, especially in chlorosis, and occa-
sionally in healthy people, a continuous blowing, singing or humming
murmur, with cardiosystolic accentuation, loudest during inspiration, is
audible (humming-top murmur, bruit de diable). It is due to the pro-
duction of a liquid vein in the blood flowing into the widened bulbus of
the Y. jugular is.
Less continuous, more intermittent, venous murmurs are unimportant.
Venous Tone. — This is sometimes audible, in the same situation, in
tricuspid insufficiency; it is due to sudden tension of the dilated vein
when the blood propelled by the contracting right ventricle rushes into it.
References
Carnac (C. N. B.}. A preliminary report on the venous hum in relation to the slate of the
blood. Med. News, New York, 1903, Ixxxii, 540-544.
Coombs (C.). The venous murmurs heard at the root of the neck in children. Brit. J. Child.
Dis., London, 1911, viii, 109-113.
MOVEMENTS OF HEAKT AND BLOOD VESSELS 745
Duckworth (/>.)• On the occurrence of venous murmur (bruit de diable} in anaemic males.
St. Earth. Hosp. Rep., London, 1875, 49-52.
Landis (H. R. Af.) & Kaufman (/.). The occurrence of venous hums in children. Arch
Pediat., New York, 1912, xxix, 88-93.
Langmead (F.). A case with Eustace Smith's bruit. Rep. Soc. Study Dis. Child.. London,
1907-08, viii, 829-331.
Ringer (S.) & Sainsbury (H.). Pulsations and murmurs in the great veins of the neck;
their physiological and clinical significance. Lancet. London. 1891. ii,
1212; 1268.
Also: 1892, i, 740; 790.
Verstraeten (C.). Contribution a I' elude des souffles veineux dits bruits de diable chez
I'homme. Ann. Soc. de med. de Gaud, 1894, Ixxiii, 887-398.
Ward (O.)« On the bruit de diable. Lond. Med. Gaz., 1837, 7.
D. Methods of Examining the Movements
of the Heart and Blood Vessels
The signs of tho activity of the heart include the heart sounds (q. v.),
and certain movements of the heart and blood vessels that are accessible
to clinical examination. These movements are visible and palpable as
pulsations in the heart and its neighborhood and in the arteries and veins
of the body. The movements can be most accurately analyzed by means
of instruments of precision yielding graphic records.
1. Inspection of the Movement of the Heart and
Blood Vessels
Every examination of the circulatory system should be begun by a
careful inspection of the naked parts in which movements of the heart
or vessels are visible in normal and abnormal states. The movements
include :
1. The apex beat, in which inspection is helpful chiefly in the locali-
zation of the area of palpation ;
2. Precordial movements, other than those of the apex beat, includ-
ing wavelike movements over the right ventricle, retractions at the base
and apex, and pulsations in the aortic and pulmonary areas ;
3. Movements in the left inferior thorax (Broadbent's sign) ;
4. Abdominal pulsation;
5. Visible pulsations in the peripheral arteries and veins; and
6. The capillary pulse.
The patient should be examined in at least two positions: (a) the
recumbent position, with the upper part of the body slightly elevated,
the patient being kept as quiet and free fronj emotional disturbance as
746 DISEASES OF THE CIKCULATOEY APPAKATUS
possible ; and (b) the sitting or standing position, in profile view, with
the eyes of the examiner on a level with the part inspected. On looking
for a capillary pulse, the patient's hand should be elevated, and the
quick of the finger nails observed for alternating flushing and pallor.
The data of inspection useful in detecting anomalies of the size and
position of the heart have already been referred to under that heading.
Here we have to deal with the data useful in the detection of anomalies
in the movements of the circulatory organs. Eor convenience, these will
be discussed together with the findings that are yielded by palpation and
by the application of instrumental methods.
2. Palpation of the Movements of the Heart and of
the Blood Vessels
With the hand, most of the movements mentioned under inspection
can be distinctly felt, and a number of movements that cannot be seen are
recognizable by palpation. Thus, for example, an apex beat that is invis-
ible may sometimes be felt; various invisible shocks and thrills are pal-
pable ; and, in addition, details of the movements of the blood vessels that
are not accessible to inspection can be made out on palpation.
In practicing palpation, the palm of the hand (the tips of fingers
for the pulse) is applied lightly and with varying degrees of pressure
upon the area to be examined. One should palpate not only the region
of the apex of the heart but also the whole precordial area, the axilla,
the vessels in the neck, the epigastric and hepatic regions and the more
superficial vessels in various parts of the body, including, of course, the
radial pulse.
3. Instruments for Mechanical Registration of Move-
ments of the Circulatory Apparatus
Thanks to the studies of physiologists, clinicians have been able to
apply very exact mechanical methods of registration to many of the
movements we are here considering. The movements of the walls of the
peripheral arteries and veins due to pressure changes within, can be
mechanically recorded as sphygmographic pulse-tracings (arterio grams,
phlebograms) , and the movements of the apex beat and of the right ven-
tricle in the precordium, by the same or a similar instrument, as car-
diosphygmograms. By registering the pulsations of a column of air in
a stomach tube, as an esophageal cardiogram,, we have a clew to the
contractions of the left atrium. Of the many instruments that have
been devised for these purposes, the two most commonly in use at the
MOVEMENTS OF HEAET AND BLOOD VESSELS 747
present time are the ink-polygraph of James Mackenzie and the cardio-
sphygmograph of Jaquet.
The movements of the heart and aorta can be observed and registered
in the form of rontgenograms and cinemato grams.
The electrocardiograph permits us to register graphically the elec-
trical action currents that arise in the heart muscle during the excitation
that precedes contraction, and we can, therefore, through the resulting
electrocardiograms, get information that indirectly informs us of the
cardiac movements that immediately follow such excitations.
The volume pulse can be mechanically recorded in the form of plethys-
mograms, and the velocity pulse in the form of tachograms.
(a) The Sphygmograph
Considerable practice is required in order to gain skill in the use of
the sphygmograph. The older instruments of Vierordt, Marey, and
Dudgeon have given way to the modifications devised by Jaquet and by
Mackenzie. The instruments now in use are polygraphic, recording
simultaneously the heart tracing (or cardiogram), the arterial pulse
tracing (or arteriogram), and the venous pulse tracing (or phlebogram).
i. James Mackenzie's Improved Ink-polygraph
This instrument resulted from the long study of the pulse by James Mackenzie
when he was a general practitioner in a small town in England. The apparatus
Fig. 208. — This Instrument Records Two Simultaneous Tracings Only, i. e., Radial Pulse, and
One Other, Such as Carotid, Jugular, Apex Beat, etc., and Writes With Ink on Glazed
Paper. The Clockwork Operates at Variable Speeds. fBv rom-tpsv of A H. Thorpi? Co.,
Philadelphia.)
748 DISEASES OE THE CIRCULATORY APPARATUS
is convenient and is satisfactory for clinical purposes. There are three receivers —
one for the heart, one for the vein, and one for the artery. "The levers bear ink
pens and write upon an endless roll of white paper."
ii. Jaquet's Cardiosphygmograph
The models now in use make three tracings, simultaneously, in addition to the
time-marker curve (£ sec.).
Fig. 209. — Jaquet Cardiosphygmograph, Two Tambour Type, With Arm Rest, in Position for
Recording Brachial Pulse and Showing Cardiograph Attached for Taking Apex Beat and
Receiving Tambour for Taking One Other Tracing Such as Jugular or Carotid Pulse.
Reproduced from Article by Dr. Geo. W. Norris, "Modern Instruments of Precision in the
Study of Cardiovascular Disease," in International Clinics, Vol. IV, Twenty-first Series.
(By courtesy of A. H. Thomas Co., Philadelphia.)
iii. Hirschf cider's Modification of the Erlanger Apparatus
This is an ingenious polygraph, "in which two small Marey tambours and a
time-marker are arranged to write above the lever of Erlanger's blood-pressure
apparatus." When the bag is inflated upon the arm, the brachial pulse is recorded
by the lever of the blood-pressure apparatus and this arteriogram is used as the
standard instead of a tracing from the radial or the carotid. Curves from the
jugular vein and from the precordial area are simultaneously recorded. In
UskofPs sphygmotonograph there is a similar arrangement for recording simul-
taneously the height of the blood-pressure curve and another tracing from apex,
vein, or artery. In Fig. 211? a new portable polygraph that is very satisfactory
is pictured.
MOVEMENTS OF HEAET AND BLOOD VESSELS 749
Fig. 210. — Erlanger Apparatus for Determining Maximal and Minimal Pressures, With Hirsch-
felder's Polygraph Attachment. (By courtesy of Schneider Bros., Jersey City.)
750 DISEASES OF THE CIECULATOEY APPARATUS
Fig. 211. — New Portable Polygraph. Three Recording Tambours. Sphygmomanometer for
Blood Pressure and Cuff for Recording Brachial Pulse Under Varying Pressure. Two
Receiving Tambours for Jugular, etc. Cardiograph for Taking Apex Tracing. Rolls of
Prepared Smoked Paper '20 Meters Long. (By courtesy of A. II. Thomas Co., Phila-
delphia.)
iv. Other Sphygmographs
The French instrument of Verdun is an excellent one, as is also A. G. Gibson's
upright polygraph.
The micrograph used by Crehore and Meara is an extremely delicate instrument.
One of the most complete instruments at present on the market is that of
Frank and Fetter. Recently, Frank has introduced a mirror-sphygmograph, in
which a mirror is attached to the receiving pelotte, and a light-ray thrown upon
this mirror is reflected upon a photographic registering apparatus.
References
Crehore (A. C.) & Meara (F. S.). The micrograph: a preliminary report. J. Am. M.
Ass., Chicago, 1911, Ivi, 1549-1552.
Frank (O.)« Die Registrierung des Pulses durch einen Spiegelsphygmographen. Munch,
med. Wchnschr., 1903, I, 1809-1810.
Frank (O.) & Fetter (J.}. Ein neuer Sphygmograph. Zlschr. f. Biol., Miinchen & Berlin,
1907, xxxi, 70-76.
Hirschfelder (A. />.)• Graphic methods in the study of cardiac diseases. Am. J. M. Sc.,
Philadelphia & New York, 1906, cxxxii, 378-393.
Jaquet (A.). Der Kardiosphygmograph. Verhandl. d. Kongr. f. innere Med., Wiesbaden,
1901, xix, 579-583.
Mackenzie (James). The study of the pulse and the movements of the heart. New York,
1902, Macmillan Company. 321 p.
MOVEMENTS OF HEAET AND BLOOD VESSELS 751
Nor r is (G. W.}. Modern instruments of precision in the study of cardio-vascular disease.
Internal. Clin., Philadelphia, 1911, 21. s., iv, 60-71. 7 pi.
Fetter (/.). Die Leistungen des Sphygmographen. I. Abhandlung. Theorie des Sphyg-
mographen. II. Spezielle Kritik der Sphygmographie. Ztschr. f. BioL,
Munchen u. Berlin, 1908, U, 335-384.
Vaschide (N.) & Lahy (J. M.}. La technique sphygmographique. Rev. de med., Paris,
1904, xxiv, 165; 220.
(b) The Plethysmograph; Volume Pulse
This is used but little clinically. The periodic dilatation of the
arteries causes a rhythmical variation in the volume of the arm. With
the plethysmograph, this variation is recorded in the form of a curve,
called a plethysmogram.
The apparatus consists of a cylinder for receiving one upper extrem-
ity. The space in the cylinder between it and the arm is filled with
water or air and the pulsations due to changes in volume are transmitted
by means of a tambour and lever to a revolving drum. The tracing
gives us information regarding the volume of the pulse and the readings
are absolute when the apparatus is so calibrated that 1 mm. of ordinate
in the tracing corresponds to a definite number of cubic millimeters (or
centimeters) of increase in volume.
Morawitz (1907) applied it to determine the amount of blood present in the
arm included in the instrument, and tried to draw deductions therefrom as to the
total amount of blood in the body. Weber has used the plethysmograph to study
the volume-changes accompanying psychic processes.
References
von Basch (S.). Die Deutung der plethysmographischen Curve. Arch. f. Physiol, Leipzig,
1881, 446-454-
Brodmann (K.}. Plethysmographische Studien am Menschen. J . f. Psychol. u. Neurol.,
Leipzig, 1902, i, 10-71. 8 diag.
M tiller (O.). Experimentelle und kritische Beitrage zur modernen Kreislaufdiagnostik und
ihr weiterer Ausbau durch Einfiihrung des dbsoluten Plethysmogrammes.
Verhandl. d. Kong. f. innere Med., Wiesbaden, 1907, xxiv, 384-392.
Weber (E.). Der Einfluss psychischer Vorgange auf den Korper, insbesondere auf die
Blutverteilung . Berlin, 1910, J . Springer. 4%6 P-
(c) The Tachograph; Velocity Pulse
The speed with which the volume of an arm changes can be roughly measured
by a tachograph (v. Kries; Frank). A little illuminating gas is allowed to pass
through a chamber surrounding an arm and is lighted. As the arm increases in
volume, the flame rises; as it decreases in volume, the flame falls. The alterations
in the height of the flame are greater when the volume-change is rapid. By photo-
graphic registration of the flame on bromide paper, a curve known as a tachogram
is obtained, which represents the rhythmical alterations of the velocity of the blood
flow in the arteries (assuming that the current velocity in the veins is constant).
752 DISEASES OF THE CIKCULATOKY APPARATUS
By registering simultaneously changes in current velocity and blood pressure,
conclusions can be drawn as to alterations in the force of the heart. If the changes
in pressure and in velocity are in opposite directions the cause is to be sought in
changes in the peripheral resistance; the plethysmogram may then be used as a
control.
T. G. Brodie has used a special method for estimating the blood flow in an
organ. He suddenly occludes its efferent vein and measures the change of volume
of the organ by an oncometer. The arterial blood enters without diminished speed
at first, but the flow is soon retarded, owing to the rise of pressure in the veins
and capillaries ; thus the organ swells rapidly at first, and afterwards progressively
more slowly. The early portion of the curve is said to represent the rate at which
the blood enters under normal conditions. Hewlett and Van Zwaluwenburg have
applied Brodie's principle to determine the rate of flow in the arm of man.
They apply a distensible cuff similar to that used for determining arterial pressure
and then try to adjust the pressure in the cuff so that the veins shall be occluded
while the arteries are left open. They record the resultant changes in the volume
of the arm by means of a plethysmograph and a Brodie volume-recorder.
Stewart (1911) has worked out a method that permits the quantity of blood
passing through a part like the hand to be easily determined WK!I approximate
accuracy. The method is based upon the fact that the amount of heat produced by
a part like the hand during rest is negligible in comparison with the heat conveyed
to it by the arterial blood. The amount of heat given off by the hand to a calo-
rimeter in a given time is determined and also the temperature of the incoming
(arterial) and of the outgoing (venous) blood. From the data thus secured the
amount of blood that must have passed through the hand to give off this amount
of heat can le calculated.
The method for the measurement of the flow in the hands has also been modified
by Stewart to apply to the feet, thus making it possible to secure observations on
persons too ill to sit in a chair for hand-flow measurements.
Stewart has made careful studies of the blood flow in several forms of anemia,
in fever, in diseases of the heart, in arteriosclerosis and thoracic aneurism, in
peripheral neuritis, in hemiplegia, in certain pulmonary diseases, and in Graves's
disease. The results are summarized in his lecture before the Harvey Society of
New York (1912).
References
Hewlett (A. W.) & Van Zwaluwenburg (J. G.). The rate of blood-flow in the arm.
Heart, London, 1909-10, i, 87-97.
Method of estimating the blood-flow in the arm. Arch. Int. Med., Chicago,
1909, Hi, 254-256.
von Kries (/.)• Ueber ein neues Verfahren zur Beobachlung der Wellenbewegung des
Blutes. Arch. f. Physiol, Leipzig, 1887, 254-284.
MacWilllam (J. A.}, Kesson (J. E.) & Melvin (G. £.)• The conduction of the pulse-
wave and its relation to the estimation of systolic blood-pressure. Heart,
London, 1913, iv, 393-408.
Stewart (G. N.). Measurement of the rate of flow of the blood in man. Cleveland M. J.,
1911, x, 385-400. 1 pi.
• Studies on the circulation in man. V. Effect on the blood flow in the hand
of applying different pressures to the Mpper arm: a contribution to the
clinical measurement of blood-pressure. Arch. Int. Med., Chicago, 1912,
ix, 706-735.
Studies on the circulation in man. The Harvey Lectures, Philadelphia.
& Lond., 1912-13, 86-149, J. B, Lippincott Co,
MOVEMENTS OF HEAKT AND BLOOD VESSELS 753
(d) Rontgenoscopy and Cinematography of the Movements of
the Heart and the Aorta
Besides the important information afforded concerning the form and
position of the cardiovascular shadow, rontgenoscopy also yields us inter-
esting data regarding the movements and pulsations of the great vessels
and the several heart chambers. With each systole of the normal heart
one can see a shrinking in the region of the lower left lateral curve (con-
traction of the left ventricle) and often a bulging of the upper left lateral
curve (expansion of the aorta). Occasionally, systolic expansion of the
middle curve on the left can be made out (pulmonary artery in patent
ductus Botalli and occasionally in mitral disease). In tricuspid insuffi-
ciency it is sometimes possible to see a systolic expansion of the lower
right curve due to reflux of blood into the right atrium on ventricular
systole. Ventricular extrasystoles can also be observed fluoroscopically.
The beginner should practice on bradycardiac patients, as the longer inter-
val between systoles makes the observation easier.
Great practical importance in diagnosis accrues to rb'ntgenoscopic
examination of the movements of the walls of the aorta in aneurism (q. v.).
Cinematographic rontgenograms of the heart movements have been
made but as yet have not attained to clinical importance.
References
v. Elischer (/.). Ueber Moment- Rontgenbilder des gesunden und kranken Herzens in
verschiedenen Phasen seiner Tdtigkeit. Ztschr. f. klin. Med., Berlin,
1912, Ixxv, 45-52.
Gott (T.). & Rosenthal (/.). Ueber ein Verfahren zur Darstellung der Herzbewegung
mitlels Rontgenstfahlen (Rontgenkymographie}. Munchen. med. Wchnschr.,
Groedel (F. M.). The present state of Roentgen cinematography and its results as to the
study of the movements of the inner organs of the human body. Interstate
M. J., St. Louis, 1915, xxii, 281-290. <
Groedel (T.) & Groedel (F.}. Kombinierte rontgenkinema-
tographische und elektrokardiographische
Herzuntersuchung. Deutsch. Arch. f. klin.
Med., Leipzig, 1913, cix, 52-72.
(e) The Electrocardiograph
As has long been known, the excited part of
a strip of muscle behaves electronegatively toward
the unexcited part. If an excitation extends along
a muscle from one end to the other, each part be-
comes successively electronegative as the wave of
excitation passes over it. Thus, if a beating heart
be connected with a galvanometer, and the deflec-
tions of the needle be photographed, a curve known
as an electrocardiogram is obtained. Waller the surface of the
showed that the action currents could be led off w^ifer.) (A"er A* D*
754 DISEASES OF THE CIRCULATORY APPARATUS
from the human heart by applying electrodes to the extremities, those aris-
ing at the base of the heart being led off from the right arm, those from
the apex from the
arm or the left
Waller used the
M
Fig. 213. — Small Electrocardiograph, Edelmann Model. New
Simplified Electrocardiographic Outfit, Complete with
L Arc Lamp, G Einthoven String Galvanometer with
Permanent Magnet, M Projection Microscope, S1 S2 S3
and S4 Electric Devices for Determining the Sensibility
of the Galvanometer and for Compensation of Skin
Currents, Photographic Register, Electrodes and Stand.
This Outfit is One of the Latest and Lowest Priced
Complete Installations for the Taking of Electrocardio-
grams. (By courtesy of A. II. Thomas Co., Philadel-
phia.)
' left
leg.
rather sluggish capil-
lary electrometer. A
-. great step forward
was made when Ein-
thoven devised his
delicate string gal-
vanometer. The
early heart stations
v/ere equipped with
Edelmann's construc-
tion of the Eintho-
ven apparatus. Re-
cently, the conven-
ient Cambridge
electrocardiograph
has come into vogue.
Dr. H. B. Williams
of New York has re-
cently designed an in-
strument similar in
character to the origi-
nal Einthoven instru-
ment, but the outfit as
a whole is less expen-
sive. It is accurate,
convenient of manipu-
lation, and is provided
with all necessary ad-
justments, including fo-
cusing fine adjustments
and accurate centering
devices for both micro-
scopes, micrometer cen-
tering arrangements for
the upper and lower
ends of the string and
a very fine micrometer
for adjusting the ten-
sion of the string.
The string can be eas-
ily adjusted so that it can be tightened and loosened over the entire working range
without material change of focus or zero. The deflections are proportional to the
strength of current for 8 cm. either side of zero at the usual magnification of 900
MOVEMENTS OF HEAKT AKD BLOOD VESSELS 755
diameters. The lenses are made by the Spencer Lens Company of Buffalo, the
projection lens being a 4 mm. apochromatic. The entire instrument is so rigid
as to be but little affected by external vibrations and for clinical purposes it can
Fig. 214. — Large Electrocardiograph, Cambridge Model. (A) The Einthoven String Gal-
vanometer Consists of a Fine Silvered Glass Fiber, Suspended Between the Poles of a
Powerful Electromagnet. This Fiber or "String" Moves in Response to the Minute Cur-
rents Generated by the Action of the Heart; (B) the Camera Photographically Records
the Magnified Movements of the Fiber; (C) the Automatic Arc Lamp Produces the
Shadow (which is Photographed) of the Fiber ; (D) the Control Board Facilitates the
Making of the Necessary Tests and Connections; (E) the Time-marker Automatically
Marks the Time Intervals on the Record; (F) the Electrodes by which the Patient is
Connected to the Instrument; the Switchboard (G) Carries all Power Switches and
Connections. (By courtesy of Taylor Instrument Co., Rochester, N. Y.)
be placed upon a solid wooden table in any reasonably substantial building. The
weight of the apparatus is about 180 pounds. It is made by the mechanician,
C. F. Kindle of Elmhurst, N. Y.
The resistance box arrangements for use with the instrument are made by
Leeds and Northrup of Philadelphia after suggestions made by Dr. Williams.
The whole outfit will be described in detail in the American Journal of Physiol-
ogy. I am indebted to Dr. H. B. Williams for advance information regarding it.
It is gratifying that a really satisfactory apparatus is now made in this country.
In these instruments, the movements of the string are magnified and;
projected through a slit upon a moving photographic film or plate. The,
electrocardiogram thus obtained is remarkably constant in health. In
diseased conditions, striking deviations from the normal curve may be
obtained, and they have proved to be valuable for diagnosis.
The technic, though complicated, can easily he learned in a properly
equipped heart station. For the details, my paper on electrocardiography
and electrophonography may he consulted.
756 DISEASES OF THE CIKCULATOKY APPAKATUS
Fig. 215. — The Williams-Hindle Electrocardiographic Outfit.
(By courtesy of Dr. H. B. Williams.)
Several modes of leading off the current are used. For clinical pur-
poses, three leads suffice. These are known as :
Lead (or Derivation) I — Right arm and left arm.
Lead (or Derivation) II = Right arm and left leg.
Lead (or Derivation) III = Left arm and left leg.
Fig. 215a. — The Williams-Hindle Electrocardiographic Outfit
(By courtesy of Dr. H. B. Williams.)
MOVEMENTS OF HEAKT AND BLOOD VESSELS 757
Since the form of the electrocardiogram is to some extent affected by
the posture of the body, it is desirable to examine patients always in one
m
Fig. 215b. — The Williams-Hindle Electrocardiograph^ Outfit.
(By courtesy of Dr. H. B. Williams.)
position, say the recumbent posture. A description of the normal and of
pathological electrocardiograms will be given farther on.
References
Barker (L. F.). Electrocardiography and phonocardiography; a collective review. Johns
Hopkins Hosp. Bull., Baltimore, 1910, xxi, 358-389.
Edelmann (M.), Jr. Ueber ein kompletes Instrumentarium zur Aufnahme von mensch-
lichen Elektrokardiogrammen. Miinchen, 1908.
Einthoven (W.")* Ein neues Galvanometer. Ann. d. Phys. u. Chem., Leipzig, 1903, xii,
1059.
Ueber einige Anwendungen des Saitengalvanometers. Ann. d. Phys. u.
Chem., Leipzig, 1904, xiv, 182.
Waller (A. D.). A demonstration on man of electromotive changes accompanying the heart's
beat. J. Physiol, Cambridge, 1887, viii, 229-234.
Wei$S (G.). Le galvanometre a corde el V electrocardiographie. Presse med., Paris, 1909 ,
xvii, 289-291.
758 DISEASES OF THE CIKCULATOEY APPAEATUS
E. Analysis of the Movements of the Heart
and Vessels as Studied Clinically
We may now pass to an analysis of the several movements the study
of which may be helpful in clinical diagnosis.
1. The Apex Beat of the Heart
The determination' of the position of this has already been discussed.
The features of the apex beat that we are concerned with here include :
(a) The extent of the beat; (b) its strength; (c) its resistance to com-
pression; (d) its exact form and the relations of the details of this to
happenings within the heart and vessels ; and (e) its rhythm.
References
Braun (Z/.). Der Ausdruck der Herzbewegungen an der Thoraxwand. Wien. med.
Wchnschr., 1896, xlvi, 2121; 2177.
Chauveau (A.}. La pulsation cardiaque exterieure et ses rapports avec les autres phenomenes
du mecanisme du coeur. J. de physiol. et de path. g£n., Paris, 1899, i,
785-805.
(a) The Extent of the Apex Beat
In extent, the area of the apex beat varies greatly both in health and
in disease. In some instances no apex beat is visible or palpable. Usually,
in health, it occupies an area 10 to 15 mm. in diameter, but anything
that excites the heart (emotion, sudden change of posture, exertion)
will give rise to a more diffuse pulsation.
Temporary changes in extent of the apex beat are of but little clinical
significance, but a permanent enlargement of the area indicates hyper-
trophy or dilatation of the left or of the right ventricle or of both.
When the left ventricle alone is enlarged, as in some cases of aortic
insufficiency, the apex beat may be tolerably well circumscribed, pre-
senting a rounded elevation resembling a segment of a small sphere (choc
en dome). When this domelike impulse coexists with enlargement of
the heart, as revealed by percussion, and with throbbing arteries (pulsus
celer), it is pathognomonic of aortic insufficiency, even in the absence of a
diastolic murmur (Bard).
A more diffuse shock is met with when both ventricles are hypertro-
phied and dilated (renal heart, chronic alcoholism, arteriosclerosis, some
forms of valvular disease). The area is larger and the elevation is some-
what elongated, resembling the curve of an upturned, boat, or of an arch of
a cathedral (choc qlobuleux of Bard).
MOVEMENTS OF HEART AND BLOOD VESSELS 759
Reference
Bard (L.). De I 'importance de la palpation du occur; donnees cliniques et signes nouveaux
quelle fournit. Mem. et compt. rend. Soc. d. sc. med. de Lyon (1896),
1897, xxxvi, 82-94.
(b) The Strength of the Apex Beat
The strength of the apex beat, as felt by the palpating hand, also
varies within wide limits. An enfeebled apex beat does not always indi-
cate disease of the heart ; it may depend upon pulmonary emphysema, or
upon obesity. Only when in the course of observation an apex beat that
has been strong is noticed to grow weaker, is it an indication of enfeeble-
ment of the heart muscle accompanying dilatation. Thus, in acute in-
fectious diseases, particularly in acute rheumatism, such a change should
make one suspect the development of a cardiac complication.
The apex beat may be feeble, even when the heart is hypertrophied
and the blood pressure high, as in some cases of contracted kidney and
arteriosclerosis. In this case, the feeble heart may point to a failing heart-
muscle.
The energy of the apex beat is often apparently increased in fevers
when the contractions of the heart are really less vigorous than normal.
This apparent increase in energy is probably due to the abruptness and
brevity of the weakened ventricular systoles. Contractions of the heart
that give rise to what seem to be violent apex beats have often little effect
upon the blood pressure, as one can readily observe in paroxysmal tachy-
cardia.
(c) The Resistance of the Apex Beat to Compression
The resistance of the apex beat to compression is a better guide to the
vigor of the contracting heart than is the apparent energy of the beat
itself. The hypertrophied left ventricle in aortic insufficiency gives rise
to an apex beat (choc en dome), mentioned above, which is markedly
resistant to the pressure of the palpating hand. The determination of
the resistance of the apex beat to compression is therefore of considerable
diagnostic importance.
Reference
Ebstein (W.). UebeY die Bestimmung der Herzresistenz beim Menschen. Berl. Idin.
Wchnschr., 1894, xxxi, 595; 627.
(d) The Exact Form of the Apex Beat as Revealed in the Cardiogram
The exact form of the elevation known as the apex beat and the rela-
tions of the details of this to the happenings within the heart itself can
be studied best with the aid of graphic records.
760 DISEASES OF THE CIRCULATORY APPARATUS
Graphic curves of the apex beat, cardiograms, can be secured by the
use of Jaquet's cardiosphygmograph or of Mackenzie's polygraph. A
cardiogram represents partly a pressure curve and partly a volume curve,
for changes in volume as well as changes in pressure of the heart during
systole will modify the curve. Of all sphygmographic curves, the car-
diogram is the most difficult satisfactorily to interpret. Clinicians have
accordingly made but relatively little use of it.
The ordinary form of curve obtained is a trapeze. Often there is a
small wave (due to atrial contraction) just preceding the main elevation.
Sometimes this is fused with the ascending limb of the main elevation, in
which event the curve rises almost perpendicularly to its height, then
falls a little, after which a plateau is formed, followed by an almost per-
pendicular fall of the descending limb.
A second form of cardiogram, by no means uncommon, is the jerking,
or quickly rebounding, type, in which the ascending and descending limbs
of the curve form the two sides of a triangle.
In making a cardiogram of the apex beat, care should be taken to
distinguish between the true apex formed by the left ventricle and eleva-
tions medial therefrom due to the right ventricle. A comparison of the
cardiogram with a simultaneous arteriogram of the carotid artery makes
analysis much easier. The ascending limb of the cardiogram corresponds
Fig. 216. — Cardiogram, Phlebogram and Arteriogram in a Person Presenting a Third Heart
Sound (Protodiastolic Gallop). Normal Heart. The Upper Tracing is from the Jugular
Vein ; the Middle Tracing is the Apex-cardiogram ; the Lowest Tracing is from the
Brachial Artery. The Time Registers Tenths of Seconds. The Third Heart Sound
Occurs at the Point Marked "2" in the Tracings ; this Corresponds to the Foot of the
h Wave in the Phlebogram and to the Protodiastolic Wavelet P in the Cardiogram.
(After W. S. Thayer, Arch. Int. Med.).
MOVEMENTS OF HEAET AND BLOOD VESSELS 761
to the closure-time or tension-time, that is, to the 'period in which all the
heart valves are closed (first phase of systole). The beginning of the expul-
sion-time of systole is indicated in the carotid arteriogram by its ascend-
ing limb, while in the cardiogram the expulsion-time of systole corresponds
to the plateau and to a part of the descending limb of the curve. The
second sound of the heart, corresponding to the end of systole, occurs dur-
ing the descending limb of the cardiogram; thereafter the curve falls
rapidly to the abscissa. Sometimes, during diastole, the curve falls belo\v
the abscissa, corresponding to slight diastolic retraction in the apex region.
Systolic retraction of the apex is shown as a negative cardiogram, that
is to say, the curve is reversed, falling below the abscissa instead of form-
ing an elevation above it. Thus in mediastinopericarditis the systolic
retraction yields a cardiogram in which the curve during the whole of
systole lies below the abscissa. A similar curve can, in normal cases, be
obtained over pulsations of the chest wall caused by the right ventricle.
References
Bard (L.). L' inter systole physiologique et ks chevauchements pathologiques des systoks.
Lyon med., 1900, xciv, 73; 109. [Discussion], 90.
Chauveau (A.) & Marey (E. /.). Determination graphique des rapports du choc du coeur
avec ks mouvements des oreilkttes et des ventricuks; experience faite A
Vaide d'un o.ppareil enregistreur (sphyymographe) . Compt. rend. Acad. d.
Sc., Paris, 1861, liii, 622; 1862, liv, 32-35.
Etienne (Gf.). IS intersy stole chez I'homme, demonstration clinique de son existence chez
I'homme et du mecanisme de la fermeture des valvuks auriculoventriculaires.
Arch. d. malad. d. cceur, etc., Paris, 1913, vi, 161-174-
Fredericq (L.). Sur k trace cardiographique et la nature de la systole ventriculaire. Bull.
Acad. roy. d. sc. deBelg.,Bruxelks, 1887, 3. s., xiii, 711-772.
von Frey (M.). Einige Bemerkungen uber den Herzstoss. MiLnchen. med. Wchnschr., 1893,
xl, 865-868.
Garrod (A. H.)* On cardiograph tracings from the human chest wall. J. Anat. & PhysioL,
London, 1870-71, v, 17-27.
Gerhardt (D.}. Ueber einige pathologische Formen des Spitzenstosses, nebst Bemerkungen
iiber Entstehung des gespaltenen ersten Herztones. Arch. f. exper. Path,
u. Pharmakol, Leipzig, 1894, xxxiv, 359-366.
Hiirthle (K.). Ueber die Erkldrung des Cardiogramms mil Hiilfe der Herztonmarkirung
und uber eine Methode zur mechanischen Registrirung der Tone. Deutsche
med. Wchnschr., Leipzig u. Berlin, 1893, xix, 77-81.
MacDonnell (#.)• Cardiograms from the human heart. Practitioner, London, 1890, xliv,
178-184.
Martins (F.}. Ueber normale und pathologische Herzstossformen. Deutsche med. Wchnschr. ,
Leipzig u. Berlin, 1888, xiv, 241-245.
Graphische Untersuchungen uber die Herzbeioegung. Ztschr. f. klin.
Med., Berlin, 1888, xiii, 327; 453; 558.
Weitere Untersuchungen zur Lehre von der Herzbewegung. Ztschr. f. klin.
Med., Berlin, 1888-89, xv, 536-560.
Cardiogramm und Herzstossproblem. Deutsche med. Wchnschr., Leipzig
u. Berlin, 1893, xix, 685-688.
Robinson (G. C.) & Draper (Geo.). A study of the presphygmic period of the heart.
Arch. Int. Med., Chicago, 1910, v, 168-216.
762 DISEASES OF THE CIKCULATOKY APPARATUS
Swann (A. W.} & Janvrin (E. R. P.}. A study of the ventricular systole-subclavian in-
terval, with a discussion of the presphygmic period. Arch. Int. Med.,
Chicago, 1913, xii, 117-136.
von Ziemssen (H.) & von Maximowitsch (/.)• Ueber Form, Dauer und Deutung der
einzelnen Herzphasen und die Stellung der Herztone im Cardiogramm,
Arb. a. d. med.-klin. Inst. d. k. Ludwig-Maximilians Univ. zu Munchen,
Leipzig, 1890, ii, 387-404-
Esophageal Cardiogram (Fredericq, Minkowski). — The graduated
stomach tube is covered at its end by a fine rubber balloon 4 cm. long. The
tube is introduced into the stomach, after which the balloon is distended
by blowing air into it. It is then withdrawn through the cardiac end
of the stomach into the esophagus. The outer end of the tube is connected
by a T-shaped tube with a Marey tambour and with an inflating bulb.
By slowly withdrawing the tube, the site will be found where pulsations
of the left atrium are maximal (7-9 cm. above the cardiac orifice of the
stomach). The patient holds his breath, and the curve is recorded, the
pressure within the tube being kept low (30 mm. water). It is well to
record simultaneously a phlebogram of the jugular vein, and an arterio-
gram of the carotid artery.
The esophageal cardiogram permits one to recognize paralysis of the
left atrium and allows of a study of the behavior of the left atrium in the
cardiac arhythmias.
References
Benjamins (C. E.). Ueber die Untersuchung des Herzens von der Speiserohre aus. Das
Oesophagogramm, die oesophageale Auscultation und die Regisirierung der
oesophageaten Herztone. Arch. f. d. ges. PhysioL, Bonn, 1914, clviii,
125-154.
Fredericq (//.)• Historisch-kritische Bemerkungen iiber die von klinischer Seite neuerdings
anerkannte Identitat der Venen- und Oesophaguspulsbilder mil den Vorkam-
merdruckkurven. Zeniralbl. f. PhysioL, Leipzig u. Wien, 1908, xxii,
297-305.
Janowski (W.). Das Ocsophagokardiogramm, seine Erkldrung und Bedeutung. Ztschr. f.
klin. Med., Berlin, 1910, Ixx, 211-234.
Minkowski (O.). Die Registrierung der Herzbeivegungen am linken Vorhof. Deutsche
med. Wchnschr., Leipzig u. Berlin, 1906, xxxii, 1248-1250.
Rautenberg (E.). Die Vorhof pulsation beim Menschen, ihre Registrierung und die bisheri-
gen Resultale ihrer Erforschung. Samml. klin. Vortr., Leipzig, 1909,
n. F. No. 557-558. (Inn. Med., No. 171-172, 91-140.)
Young (C. /.) & Hewlett (A. W.}. The normal pulsations within the esophagus. J.
Med. Research, Boston, 1907, xvi, 427-434.
(e) The Rate and Rhythm of the Apex Beat
The palpation of the apex beat further reveals the variations in rate
and rhythm to which the contractions of the left ventricle are subject.
The palpating hand can recognize the existence of rapid action of the
heart (tachycardia), of slowed action (bradycardia), of many of the forms
of disturbed rhythm (arhythmia), and sometimes of gallop rhythm.
MOVEMENTS OF HEART AND BLOOD VESSELS 763
Most of these disturbances of rhythm are better studied, however, by
means of the analysis that arteriograms, phlebograms and electrocardio-
grams permit.
References
Cohn (A. /?.). Auricular tachycardia, with a consideration of certain differences between
the two vagi. J. Exper. M., Lancaster, Pa., 1912, xv, 49-61.
Dehio (K.). Ueber die Brady cardie der Reconvalescenten. Deutsches Arch. f. klin. Med.,
Leipzig, 1894, Hi, 74-96.
Gibson (G. A.). Bradycardia. Edinb. M. J., 1905, n. s., xviii, 9-25.
Lewis (T.). Exceptional types of slow heart action. Quart. J. M., Oxford, 1913, vi, 221-233.
Loeper (M.). La brady cardie dans les affections intestinales. Pr ogres med., Paris, 1913,
xliv, 337-340.
Neusser (E.). [Bradycardia and Tachycardia.] Ausgewdhlte Kapitel der klinischen
Syw.ptomatologie und Diagnostik. Hft. 1. Wien, 1904, H. Braumuller.
49 p. 8°.
Roger (H.}. Les bradycardies dans les maladies infectieuses. Semaine med., Paris, 1913,
xxxiii, 289-294.
Snyder (C. /).). A study of the causes of heart rate. Am. J. PhysioL, Baltimore, 1915,
xxxvii, 104-117.
2. Precordial Movements Other than the Apex Beat
Besides the apex beat, certain other pulsations over and near the heart
should be looked for. On inspection in pathological states one may see :
(a) wavelike movements over the right ventricle: (b) retractions at the
base or apex; or (c) pulsations over the aorta or pulmonary artery. On
palpation, these various movements may be felt, and in addition the pal-
pating hand may perceive (d) certain shocks due to closure of valves, (e)
certain thrills, the palpatory equivalent of some kinds of murmurs, or
(f) friction fremitus, the palpatory equivalent of the pericardial friction
rub heard on auscultation.
(a) Wavelike Movements in the Precordium
In young, thin people and even in adults, during excitement, or on
exertion, slight visible movements can often be made out in the third,
fourth and fifth intercostal spaces to the left of the sternum. When
marked, and especially in the adult, they often indicate either hypertrophy
of the right ventricle or an adherent pericardium. They are also some-
times seen when the heart is not diseased, owing to retraction of the
lung and consequent approximation of a larger surface of the heart to
the chest wall. A marked palpable pulsation over the lower part of the
sternum or to either side of it is usually due to a hypertrophied right
ventricle.
764 DISEASES OF THE CIKCULATOKY APPAKATUS
(b) Retractions at the Base and Apex
In young, thin people with cardiac hypertrophy one can often make
out a systolic retraction at the base of the heart at the level of the third
and fourth interspaces. It is most marked in cases where there has been
retraction of the borders of the lungs. It is of no special diagnostic
significance.
More important is a systolic retraction visible and palpable at the apex.
At the moment when the palpating hand feels the hardening of the apex
one can see a depression synchronous with the systole, and the cardio-
graphic tracing reveals this still more distinctly (see above). The re-
traction may be limited to one or may involve several intercostal spaces.
Two conditions must be considered:
1. Adherent pericardium (mediastinopericarditis) with enlargement
of the heart, and
2. Enlargement of the right ventricle so that the apex of the heart
is formed by this rather than by the left ventricle. A cardiogram taken
over the right ventricle always shows systolic depression, that over the
normal apex beat (left ventricle) shows systolic elevation (see above).
The meaning of the sign can be decided only with the aid of other
methods of examination.
References
Braun (L.). Ueber die systolischen Einziehungen in dzr Herzgegend. Wien. klin. Wchnschr.,
1898, xi, 255-260.
Erben (F.). Ueber Bedeuiung der systolischen Einziehungen in der Herzgegend. Prag.
med. Wchnschr., 1908, xxxiii, 559-561.
Ortner (N.). Zur Genese und Bedeutung echter systolischer Spitzenstosseinziehungen und
eines abnormen Hochstandes des Aortenbogens in der Incisura sterni.
Deutsche med. Wchnschr., Leipzig u. Berlin, 1908, xxxiv, 630-634-
(c) Pulsations Over the Aorta and the Pulmonary Artery
The aortic and pulmonary areas should always be carefully inspected.
A pulsation in either region usually indicates a dilatation of the under-
lying artery. Such a dilatation may be dynamic or it may be due to
aneurism. Aneurism of the ascending and transverse portion of the arch
of the aorta often causes a pulsation in the second and third intercostal
spaces on the right side, or the whole upper part of the sternum may be
elevated. The pulsations are almost synchronous with the apex beat.
Many an aortic aneurism is missed because the examiner has failed to
undress his patient and to view the chest carefully in profile. When
the aneurism is large an actual pulsating tumor may be seen, and the
hand feels not only an elevation but also a characteristic expansion in
the mass.
MOVEMENTS OF HEART AND BLOOD VESSELS 765
Not infrequently there is visible pulsation in the pulmonic area (second
intercostal space on the left, close to the sternum). This may be of no
significance, though sometimes it indicates a dilatation of the pulmonary
artery and is occasionally associated with pulmonary stenosis. Now and
then the pulsation seen here may be due to marked activity in the auricular
appendix of the left atrium. A faint systolic pulsation at the sternal ends
of the second, third and fourth left interspaces that is due to the expansion
of the internal mammary artery, which underlies the thoracic wall in this
situation, is not infrequently seen.
(d) Shocks Due to Valve Closure
If one palpate over the areas designated as "auscultation sites" for
the four main orifices of the heart, the hand will sometimes feel a vibratory
shock, the tactile equivalent of the valvular component of the heart sounds,
due to the tension of the valves. In normal hearts, these shocks are
scarcely perceptible, but in certain diseased states they may become pro-
nounced and be valuable aids in diagnosis ; the local conditions most often
responsible are abrupt closure of valves, sudden tension, or thickened
valves.
An exaggerated mitral valve shock is best felt over the apex. It is
most marked in mitral stenosis as an abrupt shock immediately succeeding
the presystolic thrill (durete cldturale of L. Bard). This sign may
suffice for the making of a diagnosis of mitral stenosis when the arhythmia
or tachycardia are so great as to interfere with the- production, or the
perception, of the characteristic audible signs of mitral stenosis.
An exaggerated vibratory shock, transmitted from the semilunar valves
of the aorta, is sometimes felt in the second or third intercostal space to
the right of the sternum in arterial hypertension, especially when associ-
ated with arteriosclerotic thickening of the valves.
An exaggerated tricuspid valve shock, palpable over the xiphoid, is
rarely felt, as tricuspid stenosis is an uncommon affection.
Exaggerated shock over the pulmonary area is a very common palpatory
phenomenon met with in the various conditions that increase the pressure
in the pulmonary artery (mitral disease, emphysema, pulmonary arte-
riosclerosis, fibroid phthisis).
Corresponding to the doubling of the second sound, audible when the
pulmonary and aortic valves do not close simultaneously, a double vibratory
shock can sometimes be felt.
Reference
Bard (L.). De la palpation large du coeur et des vibrations de fermeture des valimles auriculo-
ventriculaires. Lyon med., 1897, Ixxxiv, 145-155; Also: Mem. et compt.-
rend. Soc. d. sc. med. de Lyon (1897), 1898, xxxvii, 3-14.
766 DISEASES OF THE CIRCULATORY APPARATUS
(e) Certain Thrills, the Palpatory Equivalent of Some
Kinds of Murmurs
The liquid veins that give rise to vibrations that, on auscultation,
are recognizable as murmurs or rumbles, can sometimes be felt, on palpa-
tion, as thrills. The sensation perceived by the hand reminded Laennec
of that obtained on stroking a purring cat.
The liquid veins that cause slow vibrations yielding low-pitched
murmurs are the ones that favor the formation of thrills, whereas those
that yield rapid vibrations producing high-pitched murmurs may not
give rise to palpable thrills. This explains why a thrill may sometimes
be felt when a murmur is not audible or is a very indistinct rumble and
why the loudest and most distinct blowing murmurs may be unaccompanied
by thrills. Palpation and auscultation here supplement one another ad-
vantageously in diagnosis.
Thrills are best felt during expiration and when the heart rate is
somewhat accelerated. The most distinctive thrill is that which accom-
panies mitral stenosis. Like the murmur due to this lesion, it may be
perceptible only in the presystole, or it may occupy a longer period of
diastole. It is usually maximal a little above and just medial from the
apex beat, in the exact situation in which mitral stenotic murmurs are
usually best heard. It is important to time this thrill exactly in order
not to confuse it with the systolic thrill that accompanies mitral in-
sufficiency. The purring thrill of mitral stenosis terminates abruptly
with the exaggerated mitral valve shock at the beginning of the first
sound; the systolic thrill of mitral insufficiency begins only with this
shock and follows it into systole.
A systolic thrill, maximal in the aortic area and propagated upward,
is more important than a systolic murmur in the same area for the
diagnosis of aortic stenosis. A thrill in the same area is sometimes palpable
over the expansile pulsation of an aortic aneurism. Diastolic aortic thrills
are occasionally met with, but are rare. When present they are felt along
the left margin of the sternum.
In tricuspid stenosis, a diastolic, or a presystolic, thrill may be felt
over the tricuspid auscultation site.
A systolic thrill in the pulmonary area, propagated toward the left
clavicle, often accompanies stenosis of the pulmonary orifice. A systolic
thrill in the same region or a little lower down, propagated, however, in
a transverse rather than in an upward direction, is met with in perforate
interventricular septum.
From what has been said it is obvious that the palpatory thrills are
more commonly met with and more helpful in the diagnosis of stenoses
of the mitral and aortic orifices than in other conditions; they occur only
rarelv in association with valvular insufficiencies. The student will do
MOVEMENTS OF HEAKT AND BLOOD VESSELS 767
well to practice the appreciation of thrills at every opportunity that
offers, as nowhere else in diagnosis is the tacius eruditus more helpful.
(/) Pericardial Friction Fremitus
This is the palpatory equivalent of the friction rub audible on ausculta-
tion and due to dry pericarditis. To the hand, it feels very superficial
and differs from pleuritic friction (1) in its rhythm and (2) in the fact
that it can be felt when the patient holds his breath. Occasionally, peri-
cardial friction fremitus is very easily perceptible, but the rubs are often
too delicate to yield tactile sensation and auscultation is, therefore, more
helpful than palpation in the diagnosis of pericarditis.
3. Broadbent's Sign and Other Pulsations in the Back
In cardiac cases, the back and sides, as well as the front, of the thorax,
should be inspected. In adherent pericardium, there may often be ob-
served a systolic retraction of one or more ribs in an area a little below
and lateral from the angle of the scapula on the left side, persisting when
the patient holds his breath (Broadbent' s sign).
While inspecting the back, one should also ascertain the presence or
absence of pulsation in the left interscapular space, as occasionally an
aneurism of the thoracic aorta presents here. In one instance, I observed
a pulsating angiosarcoma presenting in this region.
References
Broadbent (John F. H.}. Adherent pericardium. London, 1895,Bailliere, Tindall & Cox.
126 p. 12°.
Also: New York, 1896, W. Wood & Co.
Camac (C. N. #.). Broadbent's sign. Johns Hopkins Hosp. Bull., Baltimore, 1898, ix,
271-272.
Ortner (N.}. Ueber ein falsches Broadbentsche Zeichen. Berl. klin. Wchnschr., 1915, Hi, 758.
Tallant (Alice W.). Some observations on the occurrence of Broadbent' s sign. Boston M.
& S. J., 1904, cli, 457-461.
4. Abdominal Pulsations
The abdomen should be carefully examined for the presence of epigas-
tric, abdominal or hepatic pulsations.
(a) Epigastric Pulsation
By this is meant pulsation in the epigastric fossa, in the neighborhood
of the xiphoid process between the two costal margins, due directly or.
768 DISEASES OF THE CIKCULATOKY APPAKATUS
indirectly to the heart. It may depend upon (a) the abdominal aorta,
or (h) the right ventricle.
The most common aortic form is that met with in neurasthenics and
emaciated dyspeptics with thin, loose abdominal walls ("dynamics aorta").
This pulsation is slightly to the left of the middle line and extends for a
variable distance downward, below the xiphoid process. The pulsation is
perpendicular from behind forward, has only a slight breadth and is some-
what later than the apex beat. One tone, or a systolic murmur, may be
audible on auscultation. The pulsation is increased by anything that
excites the heart's activity. The tyro is only too prone to think of the
existence of aortic aneurism in his earlier experiences with this compara-
tively insignificant form of epigastric pulsation. In many cases in which
this form of aortic pulsation is present the aorta can be grasped in the
palpating hand, which then becomes aware of marked lateral expansion-
with each pulsation. In such cases, however, the aorta can be palpated
lower down and the same condition found to be present there; there is
never a localized expansile tumor such as is present in aneurism of the
abdominal aorta.
In aneurism of the abdominal aorta the pulsation is more powerful and
a definite tumor is distinctly expansile in all directions, a fact that helps
to distinguish aneurism from propagated aortic pulsations due to inter-
vening fecal masses or neoplasms. Abdominal aneurism is usually accom-
panied by severe pain.
Epigastric pulsations due to the right ventricle itself may be either
systolic elevations or systolic retractions. Systolic elevations are usually
due to a lowered and enlarged right ventricle (pulmonary emphysema,
dilated right heart, cardioptosis).
Systolic retractions in the epigastrium, due to the right ventricle, are
rather diffuse, wavelike movements depending upon elevation of the
diaphragm by the contracting right ventricle; they are of no clinical
significance.
(6) Hepatic Pulsation
This is best made out by palpation. When the right heart begins to
fail, the liver usually enlarges from chronic passive congestion and its
lower edge can be made out on palpation. Sometimes this enlarged liver
can be felt to pulsate, though the details of the pulsation can only be
discerned by graphic registration. The curve shows a systolic pulsation
approximately synchronous with that of the apex beat; it is due, in
tricuspid insufficiency, to a wave propagated through the vena cava inferior
from the right heart. A presystolic wave on the hepatic pulse, synchronous
with the atrial contraction, is occasionally met with in tricuspid stenosis
(J. Mackenzie)..
MOVEMENTS OF HEAKT AND BLOOD VESSELS 769
5. Pulse in Arteries, Veins and Capillaries
The pulsations due to aneurisms of the aorta have already been referred
to. Aneurisms may occasionally be seen and felt in other arteries of
the body.
On inspecting the thorax for pulsations and anomalies, a superficial
internal mammary artery is occasionally met with pulsating in the second
and third intercostal space, but is easily recognized. When many dilated,
tortuous arteries are seen pulsating over the thorax without apparent
cause one should think of a narrowing of the arch of the aorta.
Markedly throbbing carotids are highly characteristic of aortic insuffi-
ciency, though one occasionally sees similar throbbing in Graves's disease
and other states. fc
Pulsation in the jugular fossa from below upward may indicate either
a high position of the arch of the aorta or dilatation thereof.
Pulsations in the veins of the neclc may be visible in health, though
they are much more often seen in disease. A normal venous pulse when
visible presents two waves recognizable by the eye, one diastolic, the other
presystolic in time. In tricuspid insufficiency a single large wave is
visible, systolic in time. For the finer details of the venous pulse, graphic
registration is essential. Palpation is of little value in the study of the
venous pulse.
In heart block, inspection of the jugular pulse combined with ausculta-
tion or palpation at the apex will often suffice to show that the atria (or
auricles) are contracting at a more rapid rate than the ventricles.
Visible pulsation of the peripheral arteries occurs also in aortic in-
sufficiency. For the characters of the arterial pulse, however, we rely
mainly upon palpation and upon graphic registration.
A visible capillary pulse is met with in conditions associated with
hypertrophy of the left ventricle, especially in aortic insufficiency. If
one scratches a line with the finger nail on the forehead or skin of the
trunk, or presses slightly upon the end of the patient's finger nail in
order to make a pale spot in the nail bed, the borders of which may be
closely watched, one can see alternately blush and pallor if a capillary
pulse exists. A very good way to look for a capillary pulse is to press
gently with a glass slide on the lips. Sometimes a blush of the cheek can
be seen with each systole of the heart.
Reference
Lazarus-Barlow (W. S.). Capillary pulsation and its diagnostic value in diseases of the
heart. Practitioner, London, 1889, xlii, 174-187.
(a) Value of Studies of the Pulse
The movements of the blood wave in the arteries and veins permit us
to draw conclusions regarding the activities of the muscular walls of the
770 DISEASES OF THE CIKCULATOKY APPAKATUS
left ventricle and of those of the right atrium respectively. The activity
of the left atrium can be registered, as has been seen, by means of a
tube introduced into the esophagus. We get some clews to the movements
of the right ventricle by registering the movements in the third and fourth
intercostal space on the left side and by a study of the venous pulse, since
some of the movements of this ventricle are transmitted to the blood
in the veins.
(6) Arterial Pulse
The arterial pulse is studied clinically (1) by palpation, and (2) by
sphygmography.
i. Palpation of the Arterial Pulse
In ordinary clinical work the radial artery is felt with the tips of
the second, third and fourth fingers applied to the wrist, where the vessel
can be easily pressed against the underlying radius. By pulse one means
the pressure wave of enlargement of the artery that occurs at each systole
of the heart and which takes a perceptible time to travel from the heart
to the periphery. One pays attention to seven qualities: (1) the fre-
quency; (2) the rhythm; (3) the volume; (4) the quickness or celerity;
(5) the tension; (6) the fullness; and (7) the equality on the two sides
of the body.
The thickness of the vessel, which is usually attended to at the same
time, is not a pulse phenomenon, but has to do with the condition of the
arterial wall itself.
1. Frequency of the Pulse (Pulsus frequens et rarus). — This varies
in healthy adults between 60 and 80 beats per minute (average 72) ; in
children 90 to 140; in old age 70 to 90. The pulse is faster in women
than in men. On sitting or on lying, the pulse is slower than on standing
or on exercising.
Acceleration of the pulse rate is known as pulsus frequens; it is due
to heart hurry or TACHYCAEDIA. It is met with normally on exertion, dur-
ing emotion, and after taking food. In fever, for each degree centigrade
the temperature is raised above 37° C., there is ordinarily an increase
in the pulse frequency of about eight beats per minute; exceptions to
this rule, are, however, met with in typhoid fever, where the acceleration
is much less, and in scarlet fever and diphtheria, where it may be much
greater.
In vagus paralysis, in Graves's disease, and in some neurasthenic
states, tachycardia is common. A frequent pulse is often an important sign
of cardiac weakness or collapse. In paroxysmal tachycardia, attacks of
great frequency of rate having a sudden onset, and ceasing suddenly, are
met with, alternating with periods of normal frequency. The attacks may
MOVEMENTS OF HEAKT AND BLOOD VESSELS 771
last from a few minutes to several days, the pulse beats often numbering
between 140 and 280 per minute.
A tachycardia, with regular pulse, that persists for months and is not
due to Graves's disease, the arterial pulse rate remaining above 120, espe-
cially if it occurs in an elderly person, is most often due to atrial (or
auricular) flutter. The venous pulse then usually has a rate double that
of the arterial pulse. This condition will be described further on.
Slowing of the pulse rate is known as pulsus rams or BKADYCARDIA.
It is met with in convalescence from many infectious diseases, especially
typhoid and pneumonia, in disturbances of digestion, in conditions in
which the vagus centers are stimulated (brain tumors, hydrocephalus,
beginning meningitis), in icterus and in various diseases that affect
the heart itself (aortic stenosis, coronary sclerosis, myocarditis). In
Stokes-Adams syndrome, where the stimulus from the sinus and auricles
is prevented from reaching the ventricles, the latter contract in their own
independent rhythm; in these cases the arterial pulse rate may fall below
thirty.
A bradycardia arising in the heart itself, either as a result of di-
minished stimulus-formation, or of slowed or interrupted stimulus-conduc-
tion, can be distinguished from one due to vagus stimulation by the
subcutaneous injection of 0.001 gram of atropin. Vagal bradycardias
disappear under atropin since this drug paralyzes the terminations of the
nerve and so removes its inhibitory effect.
2. Rhythm of the Pulse (Pulsus regularis et irregularis) . — Nor-
mally, the single pulse waves follow one another regularly (pulsus regu-
laris), but in pathological conditions the rhythm may become irregular
(pulsus irregularis). The irregular pulse is due to cardiac arhythmia.
Under this heading we shall have to study (1) respiratory irregularities,
(2) extrasystolic irregularities, (3) heart block, (4) perpetual arhythmia,
and (5) the alternating pulse. The subject will be dealt with more fully
further on.
3. Volume of the Pulse (Pulsus magnus et parvus). — What clinicians
speak of as the volume of the pulse is dependent chiefly upon the differ-
ence between the increase in pressure during arterial diastole (ventricular
systole) and the decrease in pressure during arterial systole (ventricular
diastole). The size of the pulse waves depends chiefly upon (1) the
volume of the systolic output of the left ventricle; and (2) the ease with
which blood flows out of the arteries through the capillaries. The volume
of the pulse is, therefore, the palpatory equivalent in the radial artery
of what is known as the pulse pressure (difference between maximal sys-
tolic and minimal diastolic pressure). The latter can now be very accu-
rately measured (q. v.*).
When the volume of the pulse is large it is spoken of as a pulsus magnus
(aortic insufficiency, renal cardiopathy) ; when the volume is small we
772 DISEASES OF THE CIKCULATOEY APPAKATUS
speak of a pulsus parvus (aortic stenosis, some cases of myocardial insuffi-
ciency, syncope).
4. Quickness, or Celerity, of the Pulse (Pulsus celer and Pulsus tar-
dus.)— By celerity is meant the time taken for the widening and subse-
quent contraction of the arterial tube. If the pulse wave rises very quickly
and falls rapidly, it is spoken of as a pulsus celer (Corrigan pulse). If,
on the other hand, the artery expands slowly and also collapses slowly, we
speak of a pulsus tardus. The greater the systolic output and the lower
the minimal blood pressure depending on lowered peripheral resistance,
the greater, as a rule, the celerity of the pulse. The most outspoken pulsus
celer is met with in aortic insufficiency, whereas the pulse in aortic stenosis
is a good example of pulsus tardus. The pulsus celer is sometimes spoken
of as the awater-hammer pulse."
5. Tension of the Pulse (Pulsus durus and Pulsus mollis). — This
refers to the degree of tension (not thickening nor hardening) of the wall
of the artery; on palpation it is judged by the force required to obliterate
the pulse when the fingers press upon it. Three fingers are placed upon
the radial ; one presses with the most distal of these hard enough to pre-
vent a recurrent pulse wave through the palmar arch; pressure is then
made with the most proximal finger until the pulse ceases to be perceptible
to the finger in the middle. If difficult to compress, the pulse is said to
be of high tension (P. durus) ; when easily compressible it is of low ten-
sion (P. mollis). Even skilled observers are sometimes wrong in their
judgment as to the tension of the arterial wall, and it is better to rely
upon objective measurements with the blood-pressure apparatus. What
one attempts to measure here by palpation is the maximal systolic blood
pressure.
A marked degree of hypertension is met with in contracted kidney,
in lead colic, in the gastric crises of tabes, in pseudo-anginas, in other
arterial crises, in some cases of arteriosclerosis, and in polycythaemia
hypertonica. Marked hypotension is seen in Addisoii's disease, in fevers,
in anaemias, in tuberculosis, and in some cases of failing heart.
One must distinguish between the tension of the pulse here described
and thickening or sclerosis of the arterial wall. In the latter, if one
obliterate the pulse with one finger and palpate the artery distal from the
point of compression, the thickened vessel can be rolled between the finger
and the bone. Instead of being smooth, straight and scarcely perceptible
like a normal radial artery, it may feel thickened like a whip-cord under
the finger, elongated and tortuous. If the thickening be irregular, and
especially if the artery be calcified, a string of nodules will be felt (goose-
neck artery).
6. Fullness of the Pulse (Pulsus plenus et inanis). — While the volume
of the pulse above described depends upon variations of the pressure in
the artery, the fullness of the pulse is a special conception, referring to
MOVEMENTS OF HEAET AND BLOOD VESSELS 773
the mean state of filling of the artery. Either with constant pressure or
with pressure-variations, the artery may in one case be large and full (P.
plenus) and in another seem small and empty (P. inanis). To judge of
the "mean filling" the observer must pay attention to the volume of the
collapsed artery between two pulses, as well as to the size of the pulse
wave. It is only the more marked deviations from the normal filling
which can be recognized.
A full pulse is met with in healthy, strong men during and after mus-
cular exertion, and often at the beginning of febrile diseases, whereas an
empty pulse is encountered in anaemia, in cachexias, in chronic febrile
diseases and in cardiac weakness. In aortic insufficiency the pulse feels
full at the height of the wave but empty between two waves. The fullness
of the pulse is, as a rule, but little regarded by clinicians, and, in my
opinion, with right.
7. Equality of the pulse in the two radials as regards both time and
altitude should be examined by palpation. The pulse at one wrist may
appear slightly before the other, or the pulse wave may be higher in
one radial than in the other. In either case we have to deal with a
PULSUS DIFFERENS (quoad tempus aut altitudinem) due to the narrow-
ing of the lumen of one of the arm arteries (congenital difference, tumors,
aneurisms, etc.).
The most common cause of differences in the pulse in the two radials
is the presence of an abnormally small radial artery on one side. This is
a common anomaly in the arterial system of the forearm. As a result, the
pulses vary chiefly in absolute volume : they are equal in time. In aneu-
rism of the arch of the aorta, or of one of the arterial trunks supplying the
arms, differences in the time as well as in the volume and tension of the
two pulses are prominent.
ii. Graphic Registration of the Arterial Pulse (Sphygmography)
Curves or tracings of the arterial pulse (arteriograms) are obtained
either with the polygraph of Mackenzie or the sphygmograph of Jaquet,
referred to above. The
tracing of each pulse beat
presents an ascending limb
and a descending limb.
The ascending limb rises
abruptly and corresponds
to a very brief period ; the
descending limb falls slow- Flg 217_Carotla Arterlogram (Lower Traclng) wlth
ly, Covering a longer peri- Cardiogram (Upper Tracing) for Comparison, (c)
or! nf tirnp SWondarv Time of BeSinning of Anacrotic Limb of Arterio-
QG- ^ gram, (d) Time of Dicrotic Notch. (Personal Ob-
waves occur normally on serration^ j. H. H. Bun.)
774 DISEASES OF THE CIECULATOKY APPAEATUS
the descending limb (catacrotic waves) ; in abnormal conditions, secondary
waves may appear on the ascending limb (anacrotic waves).
In the normal radial pulse the descending limb shows usually a small
wave near the apex (predicrotic or systolic accessory wave). Opinions
differ as to its origin; some regard it as due to the heart, others as a
reflection from the periphery. Formerly, it was called an "elasticity
elevation," being then thought to be due to vibrations of the elastic wall
of the artery. This systolic accessory wave is most marked in hypertension
and sometimes is as high, or even higher, than the first crest of the pulse
wave; in hypotension, the. wave is less pronounced and may be entirely
absent.
The most important secondary wave on the descending limb is the
second one, due to the impulse given the blood in the aorta by closure
of the semilunar valves. It is called
the DICROTIC WAVE. When the blood
pressure is low, this wave is large
and easily perceptible by the finger.
When very pronounced, it gives the
sensation of a double pulse (dicrotic
pulse). It is important to remember
that the time elapsing between tho
beginning of the ascending limb of
the arteriogram and the beginning
of the dicrotic wave corresponds to
the time during which the semilunar
valves of the aorta are open (expul-
sion time of the left ventricle).
Arteriograms are of no value in
estimating the volume of the pulse
since the height of the curve is large-
ly dependent upon the mode of appli-
cation of the instrument, the thick-
ness of the soft parts, and other exter-
nal influences.
The celerity of the pulse can
be very well studied in the arterio-
gram, provided one pays attention
only to the rapidity of the rise
and fall and not to the length of the ordinates of the curve.
Arteriograms are also valuable in following the dicrotism of the pulse.
Dicrotism occurs chiefly in fever; as the temperature rises and the blood
pressure falls, the pulse becomes at first infradicrotic (the dicrotic wave
still lying distinctly in the descending limb, interrupting its course, the
abscissa of the curve being reached subsequently). As the frequency of
Pig. 218. — Diagram Showing Various
Forms of Arterial Pulse Curve En-
countered Clinically. Systolic Por-
tion of the Curves Underlined.
(From A. D. Hirschfelder, "Diseases
of the Heart and Aorta," published
by J. B. Lippincott Co., Phila.)
MOVEMENTS OF HEAET AND BLOOD VESSELS 775
the pulse increases, the depression preceding the dicrotic wave reaches a
point as low as the beginning of the ascending limb (complete dicrotic
pulse). When the pulse is very frequent, it may become supradicrotic, the
depression preceding the dicrotic wave, then falling to a lower level than
the beginning of the ascending limb preceding. In rare instances, the
dicrotism is so extreme that the dicrotic wave becomes swallowed up in
the ascending limb of the main wave (monocrotic pulse).
The arteriogram is of but little help in judging of blood pressure,
though, where the mean blood pressure is high, a secondary anacrotic wave
may appear before the apex of the main wave, and the dicrotic wave
may become insignificant or may disappear.
The arteriogram is of greatest value in the analysis of cardiac irreg-
ularities and yields data indispensable for forming judgments regarding
the activities of the left ventricle and their time relations. The arterio-
gram of the carotid pulse is much more helpful for these purposes than
is that of the radial pulse ; indeed, if one have good carotid arteriograms to
compare with simultaneously recorded phlebograms and cardiograms, he
may very well dispense with radial arteriograms.
References
Berkeley (W. N.). An informal consideration of the clinical value of graphic methods in the
study of heart disease. Internal. Clin., Philadelphia, 1915, 25. s., i, 18-
32. 7 pi.
v. Frey (A/.). Die Untersuchung des Pulses und ihre Ergebnisse in gesunden und kranken
Zustdnden. Berlin, 1892, J. Springer. 260 p. 8°.
Hay (/.)• Graphic methods in heart disease. London, 1909, H. Frowde. 184 P- 12°.
Hewlett (A. W.). The pulse flow in the brachial artery. IV. Reflections of the primary
wave in dicrotic and monodicrotic pulse-forms. Arch. Int. M., Chicago,
1914, xiv, 609-619.
Lewis (T.). The interpretation of sphygmograph tracings and of tracings produced by com-
pressing the brachial artery, the factors which are involved in the production
of anacrotism. Practitioner, London, 1907, Ixxviii, 207-240.
Mackenzie (/.)• The study of the pulse, arterial, venous and hepatic, and of the movements
of the heart. Edinburgh & London, 1902, Y. T. Pentland. 325 p. 8°.
Meara (F. S.), Coffen (T. H.) & Crehore (A. C.). A comparison of simultaneous poly-
graph and micrograph tracings. J. Exper. M., Lancaster, Pa., 1912,
xvi, 280-290.
Ohm (R.). Herzdiagnostik aus den gleichzeitig registrierten Bewegungsvorgangen des Arte-
rienpulses, Venenpulses und Herzschalles mit eigenen hochempfindlichen
Methoden. Tr. Internal. Cong. Med., 1913, London, 1914, Sect. VI,
Medicine, pt. 2, 259-265.
Parkinson (/.). The effect of the inhalation of oxygen on the rate of the pulse in health.
J. Physiol, London, 1912-13, xliv, 54-58.
Parsons-Smith (B.). A lecture on the value of the clinical polygraph in certain cardiac
disorders. Lancet, London, 1913, ii, 1599-1606.
Richter (G.). The technique of the sphygmogram, with remarks on the use of instruments of
precision in the study of cardiovascular disease. Med. Fortnightly, St.
Louis, 1913, xliv, 461-466.
776 DISEASES OF THE CIRCULATOEY APPAEATUS
Rihl (/.)• Die graphische Aufnahme des Arterien- und Venenpulses, des Herzstosses und
der Atmung auf der propddentischen Klinik. Prog. med. Wchnschr.,
1913, xxxviii, 579-583.
Roy (C. S.) & Adami (J. G.)» Heart-beat and pulse-wave. Practitioner, London, 1890,
xliv, 81; 161; 241; 347; 412: xlv, 20.
Sahli (H.). Ueber die Volummessung des menschlichen Tladialpulses, die Volumbolometrie,
zugleich eine neue Art der Arbeilsmessung des Pulses. Deuisches Arch. f.
klin. Med., Leipzig, 1914, cxv, 124-145.
Smith (J. G.). The use of the sphygmograph in the physical examination of gymnastic
workers and others. Proc. Am. Ass. Adv. Phys. Educat., 1888, New
Haven, 1889, iv, 36-46.
Tiger stedt (#.)• Der Arterienpuls. Ergebn. d. Physiol., Wiesbaden, 1909, viii, 593-656.
Urban (F. M.)» L 'analyse des sphygmogrammes. J. de physiol. et de path, gen., Paris,
1906, viii, 398-412.
Van Santvoord (#.). The clinical uses of the sphygmograph. Med. Rec., New York, 1900,
Mi, 313-320.
Vierordt (J5T.-)» Die Lehre vom Arterienpuls in gesundcn und kranken Zustdnden. Gegriindet
auf eine neue Methode der bildlichen Darstellung des menschlichen Pulses.
Braunschweig, 1855, F. Vieweg u. Sohn. 271 p. 8°.
Wiggers (C. J.)« The contour of the normal arterial pulse. J. Am. M. Ass., Chicago, 1915,
Ixiv, 1380-1382.
(c) Venous Pulse
The venous pulse is studied clinically (1) by inspection and palpation;
and (2) by sphygmography.
i. Inspection and Palpation of the Venous Pulse
To inspect the venous pulse, the patient should be in a reclining posi-
tion, the head and neck supported by a single pillow. If venous stasis
be marked, the upright or sitting position may be better. A wave becomes
visible when the intravenous exceeds the atmospheric pressure ; a collapse
becomes visible when the intravenous pressure is less than the atmospheric.
If the intravenous pressure be continuously negative, or continuously posi-
tive, no venous pulse will be seen.
A pulse in the veins of the neck can be seen in a majority of healthy
persons. This pulse is diffuse and wavy ; as a rule, it cannot be felt by a
palpating finger. An interesting feature of it lies in the fact that, on
inspection, the collapse of the vessel is usually a more marked phenomenon
than the positive impulse.
Under normal conditions, two pulsations occur in the vein for one
in the artery; the collapse of the vein after the first pulsation is syn-
chronous with the arterial pulse, L e., it corresponds in time to the ventric-
ular systole. This normal venous pulse is often referred to as the ''physio-
logical," "negative" or "double" venous pulse in contradistinction to
the "positive" or "single" venous pulse met with in tricuspid insufficiency.
After one has studied graphic tracings (see below), he can make out
much more from simple inspection. Thus, if a normal venous pulse be
MOVEMENTS OF HEAET AND BLOOD VESSELS 777
present, he can make out for each palpated pulsation of the carotid, two
positive, waves in the vein (a* and i;-waves) and two collapses (x- and y-
depressions).
Volhard has devised a simple instrument for determining the char-
acter of a venous pulse by inspection. For this he makes use of two
U-shaped glass tubes, in each of which there is a colored fluid. To the
open end of each tube is attached some rubber tubing and a small re-
ceiving funnel. One funnel is placed on the carotid and the other on
the jugular bulb; the fluids are set into pulsation. If the two pulsa-
tions are in the same direction, the venous pulse is systolic or positive;
if in the opposite direction, the venous pulse is presystolic or negative.
I would suggest that the student first familiarize himself with the graphic
records as described below and, afterwards, take up the study of simple inspection
and palpation of the veins of the neck.
ii. Graphic Registration of the Venous Pulse
The receiver of the registering apparatus is placed above the clavicle
over the bulb of the jugular vein, preferably between the two heads of
the sternocleidomastoid muscle. The patient should assume the position
in which the venous pulse is best marked. As a rule, a reclining position
with the head slightly elevated and turned to the left side is best, though
various positions may have to be assumed before the optimal one is
found. Occasionally, a better
tracing can be secured by pla-
cing the receiver over the exter-
nal jugular vein than over the
internal jugular.
Tracings of ike venous pulse,
or phlebograms, are of but little
value except in association with
simultaneously recorded arterio-
grams and cardiograms, for
only with these is it possible,
in many cases, to refer the
waves of the venous pulse to
particular phases of the cardiac
revolution.
The waves of the venous
pulse are due to alterations in
the blood pressure existing in
the jugular vein and in the Flg 219_The ghadea port]on o( the Card|ac
right atrium ; the latter, in turn, Cycle Corresponds to Ventricular Systole.
are in part dependent upon the T(TFro^ A; ?• Hifschfeider "Diseases of the
" Heart and Aorta," published by J. B. Lippin-
functions of the tricuspid valve cott Co., Philadelphia.)
778 DISEASES OF THE CIRCULATOKY APPAKATUS
and the activities of the right ventricle. Important conclusions can there-
fore be drawn from the venous pulse regarding the functions and activities
of the whole right side of the heart. In Fig. 219 the pressure changes in
the atrium, ventricle and aorta during one heart beat are schematically
represented.
(1) Physiological Venous Pulse (Normal PUlebogram)
The tracing of the physiological venous pulse (Fig. 220) presents
ordinarily three positive waves, designated respectively, a, c and v. Of
Fig. 220. — Simultaneous Tracings of the Carotid and Venous Pulses, etc. (From W. II.
Howell, "Textbook of Physiology," published by W. B. Saunders Co.)
these, the a- and t;-waves are the more constant, the c-wave sometimes being
almost, or wholly, imperceptible. The two main depressions on the wave
are designated by the letters x and y.
The a-wave, usually the highest elevation, is simultaneous with atrial
systole, and due to it; it is therefore known as the atrial wave (or auricular
wave).
The c-wave is approximately synchronous with the main wave of the
carotid pulse. For a time it was supposed to be due to a transmitted im-
pulse from the artery and was therefore called the carotid wave. It has
been definitely shown, however, to be due to the transmission, to the blood
in the right atrium and the jugular vein, of the shock imparted to the
atrioventricular septum by the contraction of the, right ventricle. The
flow of blood from the coronary veins into the atrium occurs also at this
moment and may be a contributing factor. The wave may still be desig-
nated the c-wave, though it is independent of the carotid pulse.
Eegarding the origin of the i>-wave, there has been, considerable dif-
ference of opinion, some authors believing it to be due to stagnation of
blood with gradual rise of pressure in the atrium, subsequent to closure
of the tricuspid valves, during ventricular systole (ventricular-stasis theory
of Hering), others looking upon it as a wave, occurring during the diastole
MOVEMENTS OF HEAET AND BLOOD VESSELS 779
of the ventricle, due to a dislocation upward of the base of the heart at
the moment when the systole of the ventricle ceases and its diastole begins.
Both factors, in all probability, play a part. In the majority of in-
stances, the crest of the f-wave is protodiastolic in time, though the earlier
portion of the ascent is telesystolic in time ; an encroachment of the crest
of this wave upon systole indicates an impending (or already existing) tri-
cuspid insufficiency.
The main depression, x, corresponds to the collapse of the vein that
occurs immediately after the atrial systole at the beginning of atrial
diastole. Since this moment coincides with the early part of ventricular
systole, the veins on inspection are seen to undergo a systolic collapse.
For this reason, the physiological venous pulse is often spoken of as a
negative venous pulse; but since the positive waves on the physiological
venous pulse are presystolic (a-wave) and diastolic (v-wave) in time, this
pulse is also sometimes referred to as the diastolic-presystolic venous pulse.
It is these two .positive waves and the collapse of the vein after each
of them that give rise to the "double venous pulse" seen on inspection
in conditions of slight venous stasis and in some healthy persons during
each cardiac revolution.
The lesser depression on the phlebogram, designated as ?/, lies between
the v-wave and the a-wave; it is therefore a diastolic collapse, and is due
to the flow of blood out of the right atrium into the ventricle just before
the atrium contracts.
When the heart is beating slowly, additional waves may sometimes be
seen upon the venous pulse, even in health. One of these wavelets, known
as the A-wave (Hirschf elder), follows the v-wave by a definite interval
and is believed to be due to the snapping together of the atrioventricular
cusps at the end of ventricular filling in mid-diastole. It corresponds in
time to (1) the third heart sound, (2) the onset of Henderson's period
of diastasis, and (3) the minute p-wave sometimes seen on the cardiogram.
(2) Abnormal Forms of Venous Pulse
A whole series of abnormalities of the venous pulse have been de-
scribed. To avoid confusion it is best to familiarize oneself first with
two or three characteristic deviations from the normal and, later, as one's
knowledge grows, to undertake the study of less common abnormalities.
Only the common types will therefore be referred to here; namely: (1)
the venous pulse of atrial paralysis (or atrial fibrillation) ; (2) the venous
pulse of outspoken tricuspid insufficiency (typical ventricular venous
pulse).
The Venous Pulse of Atrial Paralysis (or Atrial Fibrillation). — When
the right atrium is paralyzed (or is shown by the electrocardiogram to be
780 DISEASES OF THE CIRCULATORY APPARATUS
fibrillating) , the a-wave disappears from the venous pulse and only the
c- and 'i?-waves are recognizable. The ^'-depression becomes less markepl.
This form of phlebogram is most often met with when the arteriogram
reveals a pulsus irregular is perpetuus. In the electrocardiogram, simul-
taneously recorded, the nor-
mal P-wave has disappeared ;
in its place one sometimes
sees a number of small eleva-
tions due to the electrical
variations that accompany
atrial fibrillation (q. v.).
Fig. 221. — Phlebogram from a Patient Suffering from VeilOUS Pulse Of Ollt-
Paralysis of the Right Atrium. Drum Moving , _ . . , _ ffi
Rapidly. Disappearance of o-wave. Arteriogram
for Comparison. (Personal Observation, J. H. H. ciency (Ventricular VeilOUS
Pulse). — In marked tricus-
pid insufficiency, all threo positive waves of the normal venous pulse dis-
appear and each systole of the heart is accompanied by a single huge
broad wave on the venous pulse. This single large wave is due to the
direct propulsion of blood by the contracting right ventricle into the right
atrium and jugular vein through the insufficient tricuspid valve. This
is the typical ventricular type
of venous pulse. Since the
dilatation of the vein is syn-
chronous with ventricular sys-
tole, this pulse is often spoken
of as a positive venous pulse, in
contrast with the negative ve-
nous pulse (or systolic collapse)
seen under normal conditions.
This type of venOUS pulse, when Fig> 222.— Phlebogram in a Case of Tricuspid
Outspoken, is easily reCOglriz- Insufficiency with Cardiogram for Comparl-
i-, *, ,, ' , , . D/<IX son. (Personal Observation, J. H. II. Bull.)
able by the naked eye, since (1)
it is single instead of double, and (2) the positive wave is systolic in
time (synchronous with the apex beat and carotid pulse). Occasionally,
before the atrium is paralyzed, the ventricular wave is preceded by an
a-wave.
References
Bachmann (<?.). The interpretation of the venous pulse. Proc. Path. Soc., Philadelphia,
1908, n. s., xi, 251-266.
Bailey (H. C.). Pulsations in the peripheral veins. Am. J. M. Sc.t Philadelphia & New
York, 1911, cxli, 709-715.
Bard (L.). De Venregistrement graphique du pouls veineux des jugulaires chez Vhomme.
J. de physiol. et de path, gen., Paris, 1906, viii, 454~459.
MOVEMENTS OF HEAKT AND BLOOD VESSELS 781
Bard (!/.)• Des divers details du pouls veineux des jugulaires chez I'homme. J. de
physiol. et de path, gen., Paris, 1906, viii, 466-479.
De Vorigine et de la signification de Vonde protosystolique du pouls veineux
des jugulaires. Arch. d. mal. du cceur [etc.], Paris, 1908, i, 337-358.
Les caracteres du pouls veineux jugulaire dans Vasystolie du cceur gauche,
Semaine med., Paris, 1910, xxx, 181-185.
Broadbent (W.}. Pulsation in the neck. Practitioner, London, 1911, Ixxxvii, 227-235.
Ewing (E. Af.)« The venous pulse. Am. J. Physiol., Boston, 1914, xxxiii, 158-185.
Eyster (J. A. E.]. The time relations of the venous pulse and the heart sounds. J. Exper. M.t
Lancaster, Pa., & New York, 1911, xiv, 594-605. 1 tab. 1 pi.
Gerhardt (/>.)• Klinische Untersuchungen uber Venenpulsalionen. Arch. f. exper. Path.
u. Pharmakol., Leipzig, 1894, xxxiv, 402—445. 1 diag.
Her ing (H. E.). Ueber die vorhofdiastolische Welle aa, eine neue Welle des Venenpulses.
Arch. f. d. ges. Physiol., Bonn, 1913, cxlix, 594-600.
Hewlett (A. W.}. The interpretation of the positive venous pulse. J. Med. Research,
Boston, 1907-08, xvii, 119-136.
Hirschf elder (A. />.)• Inspection of the jugular vein; its value and its limitations in func-
tional diagnosis. J. Am. M. Ass., Chicago, 1907, xlviii, 1105-1108.
Hun (H.) & Hawn (C. B.}. Clinical studies of Ihz circulation with the polygraph, especially
in regard to the venous pulse. Albany M. Ann., 1914, xxxv, 1—19. 10 pi.
Keith (A.). An account of the structures concerned in the production of the jugular pulse.
J. Anal. & Physiol., London, 1907-08, xlii, 1-25.
Lian (C.)« Du pouls veineux jugulaire dit <fphysiologique." Presse med., Paris, 1912, xxt
694-696.
Lombard (W. P.). A diagram of the heart cycle, picturing the changes of form of the auri-
cles, ventricles, cardiogram, and venous and carotid pulse curves. Tr. Clin.
Soc. Univ. Mich., Ann Arbor, 1914, v, 81-86.
Ohm (#.)• Die diastolischen Schwankungen des Venenpulses; ihre Entstehung und ihr Ver-
halten unter normalen und pathologischenBedingungen. Zentralbl.f. Herz-
krankh. [etc.], Wien u. Leipzig, 1913, v, 153-156. 1 pi.
Quincke (H.}. Beobachtungsn uber Kapillar- und Venenpuls. Berl. klin. Wchnschr.f
1868, v, 357.
Ueber Capillarpuls und centripetalen Venenpuls. Berl. klin. Wchnschr.,
1890, xxvii, 265-267.
Rihl (/.)• Ueber das Verhalten des Venenpulses unter normalen und pathologischen Beding-
ungen. Ztschr. f. exper. Path. u. Therap., Berlin, 1909, vi, 619-688. 3 pi.
Roth (O.)« Ueber den Venenpuls beim diastolischen Vorschleudern der Herzspitze. Zen-
tralbl. f. Herzkrankh. [etc.], Wien u. Dresden, 1314, vi, 8-12. .
Samways (D. W.}. On the genesis of the venous pulse. Brit. M. J., London, 1912, i, 835;
1425.
Veiel (E.} & Kapff (W.). Studien uber den Venenpuls. I. Deutsches Arch. f. klin. Med.t
Leipzig, 191i, cxiii, 494-522.
Volhard, Ueber Venenpuls. Verhandl. d. Cong. f. innere Med., Wiesbaden, 1902, xx,
394-403.
Wiggers (C. J.). The supraclavicular venous pulse in man. J. Am. M. Ass., Chicago, 1915,
Ixio, 1485-1487.
Zielinski (Michel}. Le pouls jugulaire dans Vinsuffisance tricuspidie+ne. Paris, 1913,
J.B.Bailliere. 124 p. No. 248. 8°.
782 DISEASES OF THE CIKCULATOKY APPAKATUS
F. Electrocardiograms
Our chief object in graphic registration is to determine the actual sequence of
events in the cardiac cycle. It is obvious that the fewer sources of error there are
in the method, the more accurate will be our knowledge of the heart's action. In
phlebograms, cardiograms, and arteriograms, we record the heart's action only
indirectly in the form of secondary changes produced in the blood stream. These,
in turn, we must mentally transpose to those phases of the contraction of the
heart that probably produce the different waves in the vessels. These pulsations
are easily subject to modification from causes entirely outside of the heart, such
as engorgement of, or pressure upon, the vessels, or even by the method used to
record the pulsation.
We have, however, a method that seems to eliminate most of these difficulties,
and that gives us an accurate means by which we can determine the actual form
of the cardiac contraction. This is electrocardiography, a description of which
has already been given. The cardiac electrical variations that are recorded by
this method have been shown to be the same whether they are led off from the
heart itself, or from distant parts of the body. Therefore, secondary modifications
do not have to be considered in interpreting the waves obtained in their relations
to the various phases of the heart's action.
These electrical currents are given off from the muscle at a time about 1/100
of a second prior to the actual mechanical contraction. They are products of the
stage of readjustment within the muscle between the times of stimulation and
contraction, or what is known as the period of excitability. Since, however, con-
traction always follows the course of excitation, for all diagnostic purposes this
time relation can be disregarded and the electrical waves are often referred to as
indicating the path of "contraction."
The curve obtained by electrocardiography (see p. 783) is known as
an electrocardiogram. The summation of action currents in the heart
muscle thus recorded gives us clews to the origin and course of excita-
tions in the heart muscle, and thus, indirectly, also, as to the course of the
contraction wave as it passes over the heart.
1. The Electrocardiogram of a Normal Heart
For the excitations belonging to one cardiac cycle, we find in an
electrocardiogram of a normal heart — known as a normal or typical EK —
a rather complicated curve. First, there is a small upward wave, P.
This is followed by a pause, after which we see a small downward wave,
Q, 'then a high upward wave, R, followed by a second small downward
wave, S, then a medium-sized upward wave, T, and, finally, a long pause
at the end of the cycle, which ends with the appearance of the P-wave of
the next cardiac cycle.1
In all three leads (or derivations), the three main waves, P, P, and T,
1 Often, after the T-wave there is still another small upward wave called the
27-wave (see Lewis and Gilder).
ELECTEOCAEDIOGEAMS
783
are visible, though the height of the waves may vary somewhat for the
different leads.
The 72-wave is always the largest wave, and normally the T-wave is
* * * 4 4 -*—4-"~4 *-••* * i * *- 4 A
I. Right Arm and Left Arm.
II. Right Arm and Left Leg.
III. Left Arm and Left Leg.
Fig. 223.— Normal Electrocardiograms Obtained by Photographing the Movements of a
Sensitive Galvanometer. Waves with the Apex Upward Indicate that the Base of the
Heart (or the Right Ventricle) is Negative to the Apex (or Left Ventricle). Waves
with the Apex Downward have the Opposite Significance. Wave P is Due to the Con-
traction of the Auricle. Waves Q, R, B, and T Occur During the Systole of the Ventricle.
The Curve Seems to Show that the Contraction in the Ventricles Begins First Toward
the Apex (or in the Left Ventricle), Since the Negativity First Appears Toward that
Side (Wave 9),
784 DISEASES OF THE CIKCULATOKY APPARATUS
taller and broader than the P-wave. The P-wave corresponds to the ex-
citation of the atria ; the Q, R, 8, T complex corresponds to the excitation
of the ventricles.1
It is believed by Einthoven that the P-R interval corresponds to the period of
conduction of the excitation from the atria to the ventricles along the atrio-
ventricular bundle of His. Arriving in the Purkinje system, the excitation reaches
a large number of spots in the walls of the ventricles almost simultaneously.
Should the excitation of the ventricle occur first near the heart's apex, there is a
well-marked ^-depression, but should some other portion of the ventricle be first
excited the ^-depression does not appear. The .R-wave is evidence of the pre-
dominance of the excitations, at the moment, in the wall of the right ventricle and
at the base of the heart, while the subsequent /^-depression points to a temporary
predominance of excitation in the left ventricle and in the apical region. The
interval between (Q, R, S) and T and the T-wave itself correspond to a period in
which the whole musculature of both ventricles is excited. Should the excitation
cease in the left ventricle before it does in the right, the T-wave becomes negative
instead of positive; should the base of the heart remain excited longer than the
apex, the T-wave in Lead III is directed upward, while if the apex remains
longer excited than the base, the T-wave in Lead III is directed downward.
According to Kraus and Nicolai, the .R-wave depends upon excitation of the papil-
lary muscles, the R-T interval corresponds to the period of excitation of the main
muscle-bundles of the ventricles, and the T-wave is due to excitation at the base
of the heart.
Other observers deny a relationship of the form of the EK to the complicated
course followed by the excitation through the heart muscle. Thus Fredericq
believes that the form is due to a peculiarity of the heart muscle and that it may
be obtained by registering the currents from an isolated strip of heart muscle;
his view is not unlike that of Eyster, who got R- and T-waves from isolated strips
of terrapin ventricle. Straub and Hoffmann suggest that the EK is not the
result of the excitation process alone but depends also upon the contraction process
and upon metabolic changes.
Florence Buchanan believes that the R-wave is due to a slight asynchronism
between the two ventricles.
As a matter of fact, the real explanation of the waves of the ventricular com-
plex must still be awaited.
One must always bear in mind that the heart's contraction is not a single
muscular action, but a coordinate movement of many parts, and the electrical
1 Nicolai has introduced another terminology, in which he has attempted to
signify the cause of each wave by the letter applied to it. The first or atrial wave
he calls A (= P-wave of Einthoven). The ventricular contraction being repre-
sented by two main waves, the first is lettered / for initial contraction (== .R-wave
of Einthoven) and the second F for final contraction (= T-wave of Einthoven).
Depressions below the base line are lettered a and p according to the relation they
bear to the three main waves. For example, the Q- and £-waves of Einthoven
are in this nomenclature called la and Ip. The space between A and I is called
"ft," as it represents the time taken for the stimulus to pass over the bundle of His.
That between I and F is termed "t" for during this time the ventricular circular
muscle or "Triebwerk" contracts. That between F and A is known as "p" because
it represents the diastolic pause. Most writers have adhered to the original letter^
ing of Einthovem,
ELECTEOCAEDIOGKAMS 785
curve obtained is the resultant of a large number of component electrical poten-
tials. Any change in the position or relative strength of contraction of any
portion of the heart will disturb this equilibrium and modify the form of the
electrocardiogram. This is particularly striking in the interaction of the muscu-
lature to the right and left of the heart's axis. Waller has applied to this the
principle and arithmetical formula of the mechanical balance, and calculates, from
the electrocardiographic curves, the angle of inclination of the heart's axis in
relation to the midline of the thorax.
It seems fairly certain, however, that the action currents begin during excita-
tion of a part and before its actual contraction. According to Einthoven, the first
electrical deviation in the ventricular complex of the EK occurs about 0.03 sec.
before the first sound of the heart occurs as shown by mechanical registration,
and about 0.06 sec. before the main oscillations of the first sound occur. Again,
the EK precedes the contraction of the anterior wall of the ventricle by 0.03 sec.,
and the .R-wave has been finished for 0.65 sec. before there is a rise in the intra-
ventricular pressure. The end of the T-wave coincides approximately with the end
of the expulsion-time of the ventricle.
2. Clinical Value of Electrocardiography
Electrocardiography has not only made us acquainted with a whole
series of new facts regarding the origin and conduction of excitations
within the heart, but it has greatly simplified the diagnosis of the several
forms of cardiac arhythmia. While these arhytlimias could, it is true, be
analyzed before the advent of electrocardiography by means of the arterio-
grams and phlebograms obtained by sphymography, still the securing of
electrocardiograms and their analysis are relatively simple compared with
the difficulties, the tedium, and the circumstantiality of securing the
sphygmographic data. As a matter of fact, when a heart station, equipped
with a modern electrocardiograph, is available, sphygmography can, for the
majority of clinical purposes, be entirely dispensed with. The informa-
tion desired can be more quickly, more easily, and more certainly gained
by electrocardiography. Indeed, if we except the usefulness of venous
pulse-tracings for the diagnosis of tricuspid insufficiency and of pulsus
alternans, electrocardiography has relegated sphygmography to a place of
scarcely more than historical interest.
3. Physiological Variations of the Electrocardiogram
P-Wave. — Usually a single wave, it may be double, even normally,
especially in Lead III. In dextrocardia, the P-wave is negative. But a
normally situated and functioning heart may occasionally yield a negative
P-wave in any one or in all three of the leads.
Q-Wave. — This is not always present, or if present, may be very
indistinct. Not infrequently, it is better marked in Lead III than in
.Leads I and II,
786 DISEASES OF THE CIKCULATOKY APPARATUS
/?-Wave. — Always the highest wave, it is, however, subject to great
variations in height. It is smaller in Lead III than in Leads I and II.
In hypertrophied hearts, the 72-wave may be very high.
S-Wave. — This is usually best marked in Lead III, and most indis-
tinct in Lead I. It seems to be exaggerated when the heart tends to be
more horizontally placed in the thorax than normal. It was, formerly,
believed to be especially pronounced in neurasthenic states and was even
dubbed the "neurasthenic wave," but this idea no longer prevails.
7*-Wave. — This wave is extraordinarily variable, not only in height
but also in breadth. Usually positive, it is sometimes negative normally,
and may even be diphasic. As age advances, the T-wave becomes less pro-
nounced (Nicolai). By some it is thought that a flattening of the T-wave
is an early sign of myocardial insufficiency, but this view is strongly com-
bated by others.
P-Q Interval. — This interval, now called the "alpha interval," aver-
ages-0.1 sec. in normal duration. In tachycardia, it is much briefer. In
cases of delayed conduction, this interval may be greatly lengthened.
Thus Hoffmann describes cases in which the interval was 0.23 sec., and
my colleague, Prof. W. S. Thayer, has studied a pathological case in
which the alpha interval had the astonishing length of 0.6 sec. In one
of my own patients, now under observation, the conduction time is length-
ened for some beats; in an EK made for me by Dr. Bridgman the P-R
interval was, for a single cycle, no less than 1.03 second ! The duration
varied considerably in other cycles.
5-T'Interval. — This interval, now called the "beta interval," may also
vary considerably under normal conditions, depending mainly upon the
rate of the heart. It is usually horizontal in course above the abscissa, but
it may rest upon the base line and is sometimes slightly curved.
T-P Interval. — This interval, now called the "gamma interval," also
varies in length. In it, as was mentioned above, we sometimes meet with
a Z7-wave. Thus, in one report, a £7-wave was present in 44 out of 49
persons in Lead II.
Age Differences. — The EK, in childhood, has been studied especially
by Nicolai and Funaro ; in old age, by A. Hoffmann and by Nicolai. In
sucklings, the $-wave is large and the T-wave small. In the senile heart,
the ^-wave may be negative in Lead III and the T-wave is negative in the
same lead.
According to Mcolai, the general rules hold: (1) that, as life advances,
the 72-wave gets larger and the T-wave smaller; (2) that with increasing
blood pressure the .K-wave gets larger and the T-wave is first larger and
later smaller; and (3) that as the heart increases in size the J?-wave be-
comes larger and the T-wave gradually smaller,
ELECTROCARDIOGRAMS
787
4. The Electrocardiogram in Pathological States
It must be emphasized at the beginning that one must not expect the
EK to yield information that it is incapable of giving. Above all, it
should be recognized that the EK is not a measure of the functional ca-
pacity of the heart in the ordinary sense of that term. For a man with
outspoken myocardial insufficiency (dyspepsia, cyanosis, anasarca, dilated
heart), may still have an electrocardiogram exhibiting waves indistinguish-
able from those obtained from a normal person. Moreover, when com-
pensation is reestablished by rest, 'diet and strophanthin, the curve may be
the same as in the stage of decompensation.
Certair conclusions regarding (1) the size of the heart chambers, (2)
the position of the heart, and (3) above all, the disturbances of rhythm
of the heart, can, however, be drawn from the EK.
Size of the Heart Chambers. — A careful study of the height of the
waves in different valvular lesions has been made by Steriopulo. The
results are shown in the following table in which the highest ^-wave (in
aortic insufficiency) was taken as 100 and the height of the other waves
were compared with it :
Wave
Mitral Stenosis
Mitral Insufficiency
Aortic Insufficiency
P
20 6
9
12
R
34 6
42
100
T . . .
21.3
16
10
The high P-wave in mitral stenosis is a striking feature, due probably
to atrial hypertrophy. The very high 72-wave in aortic insufficiency
may depend upon the hypertrophy of the left ventricle. The marked 8-
wave in mitral insufficiency is also interesting.
Position of the Heart. — In true dextrocardia, in wrhich the heart is on
che right side with its long axis extending from the left above to the right^
and downward, we get a mirror picture of the normal electrocardiogram,
in that the waves P, R and T are all directed downward. In false dextro-
cardia, in which the heart is merely displaced to the right by a pleural
effusion or by retraction of the thorax, this reversal of the curves does not
occur. In congenital heart disease, the P- and T-waves are positive while
the R-WSLVG is negative.
Disturbances of Cardiac Rhythm. — Here the EK gives us informa-
tion of the greatest clinical value. To-day, in the heart station of our
larger clinics, an EK is made as a routine measure in patients exhibiting
788 DISEASES OF THE CIECULATOKY APPAEATUS
tachycardia, bradycardia, respiratory arhythmia, extrasystolic arhythmia,
perpetual arhythmia, or conduction disturbances causing partial or com-
plete heart block.
The electrocardiographic findings in these various states are described
further on. (See Clinical Disorders of the Heart Beat.)
5. The Electrocardiogram in Experimental Physiology
One great advantage derivable from electrocardiography is the possibility of
subjecting ideas, arrived at by the clinical study of patients suffering from cardiac
disease, to experimental test. If, for example, a patient yields an atypical EK
and we think this might be accounted for by a given lesion in the heart, or by
the origin of an excitation at some abnormal site, we may go into the laboratory
and produce this hypothetical lesion in an animal or stimulate the animal's heart at
the unusual site postulated, and make an EK to see if it agrees in form with the
one obtained from the patient.
This imitation of clinical disorders by laboratory experiment is proving to be
exceptionally useful in the study of disturbances of the heart beat. Our concep-
tions of cardiac disease are being rapidly altered by the thorough application of
graphic and of experimental methods. If one compare the chapter on diseases of
the circulation in an up-to-date text with the chapter on the same subject in a
text o"f ten years ago, he will easily confirm his conviction regarding the evolution
of ideas that has been taking place. In America, Cohn, James, Williams, Hirsch-
felder, Bond, Bridgman, Eyster, Meakins, the Oppenheimers, White, Carter,
Rothschild and others have been engaged in this work. In England, aside from
the pioneer work of Waller, Bayliss and Starling, brilliant experimental work has
been carried on by Thomas Lewis and his associates in London, and by Gotch and
Florence Buchanan at Oxford. Those interested should read the "Lectures on
the Heart" recently delivered in this country by T. Lewis.
References
1. General; Clinical
Barker (L. F.). Electrocardiography and phonocardiography. Johns Hopkins Hosp.
Bull, Baltimore, 1910, xxi, 358-389.
Barker (L. F.}, Hirschfelder (A. Z>.) & Bond (G. S.). The electrocardiogram in clin-
ical diagnosis. J. Am. M. Ass., Chicago, 1910, Iv, 1350-1352.
Brugsch (T.) & Nicolai (G.). Elektrokardiographik. In: Technik d. spez. klin. Unter-
suchungsmeth. (Brugsch & Schittenhelm) , Berlin u. Wien, 1914, i, 80-106.
Dally (J. F. H.}. Electrocardiography and its clinical application. West Lond. M. J.,
London, 1914, xix, 266-276.
Einthoven (W.}. Die galvanometrische Registrirung des menschlichen Elektrokardio-
gramms, zugleich eine Beurtheilung der Anwendung des Capillar-Elek-
trometers in der Physiologie. Arch. f. d. ges. PhysioL, Bonn, 1903, cxix,
472-480.
Galeotti (G.) & Di Jorio (E.). Suite modifizioni degli elettrocardiogrammi per azione delV
alcool. Arch, difisiol., Firenze, 1913-14, xii, 401-414.
Goddard (C. H.). Changes in the wave of the human electrocardiogram. Arch. Int. Med.,
Chicago, 1915, xvi, 633-643.
Goodall (J. S.) & Richards (H. N.}. Some instrumental variations in the human electro-
cardiogram. Middlesex Hosp. J., London, 1915, xix$ 19-26.
ELECTROCARDIOGRAMS 789
Groedel (T.) & Meyer -Lierheim. Vergleich des Saitengalvanometer und des Oscillo-
graphen-Elektrocardiogramms. Berl. klin. Wchnschr., 1911, xlviii, 1082—
1085.
Bering (H. E.). Ueber die klinische Bedeutung des Elektrokardiogramms. Deutsche
med. Wchnschr., Leipzig u. Berlin, 1909, xxxv, 7-9.
Zur klinischen Diagnose aus dem Elekcrokardiogramm. Zentralbl. /.
Herz- u. Gefasskrankh., 1913, v, 105-110.
Hoffmann (A.). Die Ehktrokardiographie als Untersuchungsmethode des Herzens und
ihre Ergebnisse. Wiesbaden, 1914, J. F. Bergmann. 848 p. 3 pi. 8°.
James (W. B.) & Williams (H. B.). The electrocardiogram in clinical medicine. Med.
& Surg. Rep., Presbyterian Hosp., New York, 1012, ix, 17-59. 12 pi.
The electrocardiogram in clinical medicine. II. The electrocardiogram in
some familiar diseases of the heart. Am. J. M. Sc., Philadelphia & New
York, 1910, cxl, 644-669.
Jolly (W. A.}. On the electrocardiogram. Quart. J.Exper. PhysioL, London, 1915-16, ix,
9-43.
Kahn(R.H.). Das Elektrokardiogramm. In:Ergebn. d. Physiol. (Asher u.Spiro). Wies-
baden, 1914, xiv, 1-252.
Kraus (F.) & Nicolai (<?.)• Das Elektrokardiogramm des gesunden und kranken Menschen.
Leipzig, 1910, Veil & Co. 322 p. 8°.
Richards (E. T. F.) & Morris (R. E.). The value of the electrocardiograph in the study of
the heart. St. Paul M. J., 1915, xvii, 539-552.
Robinson (G. C.). A study with the electrocardiograph of the mode of death of the human
heart. J. Exper. M., Lancaster, Pa., 1912, xvi, 291-302.
Talley (J. E.). The electrocardiograph as a clinical instrument. Am. J. M. Sc., Phila-
delphia & New York, 1914, cxlvii, 692-698.
Watson-Wemyss (H. L.) & Gunn (J. D.}. Simultaneous electro- and phono-cardio-
grams. Edinb. M. J., 1913, xi, 124-127.
, 2. Physiological
Bittorf (A.). Ueber das Elektroangiogramm bei Menschen und Tieren. Zentralbl. f. inn.
Med., 1913, xxxiv, 82-83.
Boruttau (H.}. Beitrdge zur Erkldrung der Endzacken im Elektrokardiogramm. Arch. /.
Anat. u. Physiol. (physiol. Abtheil), Leipzig, 1913, 519-540.
Buchanan (F.). Note on the electrocardiogram, frequency of heart-beat and respiratory
exchange in reptiles. J. Physiol., London, 1909—10, xxxix, 25—27.
Dale (D.) & Mines (G. R.). The influence of nerve stimulation on the electrocardiogram.
J. Physiol., Cambridge, 1913, xlvi, 319-336.
Einthoven (W.), Fahr (G.) & de Waart (A.). Ueber die Richtung und die manifeste
Grosse der Potentialschwankungen im menschlichen Herzen und uber den
Einfluss der Herzlage auf die Form des Elektrokardiogramms. Arch. /.
d. ges. Physiol., Bonn, 1913, cl, 275-315.
Eppinger (II.) & Rothberger (C. /.)• Zitr Analyse des Elektrokardiogramms. Wien.
klin. Wchnschr., 1909, xxii, 1091-1098.
Eyster (J. A. E.} & Meek (W. J.). The interpretation of the normal electrocardiogram.
A critical and experimental study. Arch. Int. Med., Chicago, 1913, xi,
204-247.
Gotch (F.). The succession of events in the contracting ventricle as shown by electrometer
records (tortoise and rabbit}. Heart, London, 1909-10, i, 235-261.
Bering (H. E.). Erklarungsversuch der U-Zacke des Elektrokardiogramms als Elektro-
angiogramm. Arch. f. d. ges. Physiol., Bonn, 1913, cli, 111-114-
Hirschfelder (A, D.). Recent studies upon the electrocardiogram and upon the changes in
the volume of the heart. Interstate M. J., St. Louis, 1911, xviii, 557-600.
790 DISEASES OF THE CIKCULATOEY APPAKATUS
Kraus (F.)t Nicolai (G. F.) & Meyer (F.). Prinzipielles und Experimentelles nber das
Elektrokardiogramm. Arch. f. d. ges. Physiol., Bonn, 1913, civ, 97-167.
Nicolai (G. F.) & Vogelmann (S.). Die Beziehungen der Form der Initialgruppe desElek-
trocardiogramms zu den beiden Herzventrikeln. Ztschr. f. exper. Path. u.
Therap., Berlin, 1914, xvii, 1-10.
Tigerstedt (C.)« Vermutliche Aktionsstrome bei den Arterien. Skand. Arch. f. Physiol. ,
Stockholm, 1913, xxviii, 433-441.
Vogelmann (5.). Der Einfluss des Lebensalters auf die relative Grosse der J- und Jp-Zacke.
Ztschr. f. exper. Path. u. Therap., Berlin, 1914, xvii, 11-15.
Waller (A. />.)• A demonstration on man of electromotive changes accompanying the heart's
beat. J. Physiol., Cambridge, 1887, viii, 229-234.
Introductory address on the electromotive properties of the human heart.
Brit. M. J., London, 1888, U, 751-754.
On the electromotive changes connected with the beat of the mammalian
heart, and of the human heart in particular. Phil. Tr., 1889, London,
1890, clxxx, B, 169-194.
The electrical action of the human'heart in 1887 and in 1915. St. Mary's
Hosp. Gaz., London, 1915, xxi, 35-37.
Weitz (W.). Exper imentelle Untersuchungen uber die Verdnderungen des Elektrokardio-
gramms bei Aenderung der Herzarbeit. Deutsches Arch. f. klin. Med.t
Leipzig, 1913, cxi, 530-565.
Wertheim-Salomonson (J. K. A.}. Das Elektrokardiogramm von Huhnerembryonen.
Pfliiger's Arch. f. d. ges. Physiol., Bonn, 1913, cliii, 553-573.
G. Measurements of Blood Pressure
(Sphygmomanometry, or Tonometry, of the Blood Vessels)
1. Introduction
Methods of determining, clinically, the maximal (systolic) and minimal
(diastolic) pressure in the arterial system, and of measuring the pressure
in the superficial veins, have been worked out and are of value for
diagnosis. By blood pressure is meant the pressure exerted by the blood
at any selected point in the circulation at a given moment, either on the
blood current lying in front of it (end pressure) or on the vessel wall
(lateral pressure). The pressure on the wall of the vessel is a little less
than that on the column of blood in front, since the latter includes not only
the pressure proper but also the force in the stream itself. The pressure
varies at different points (intra ventricular, aortic, brachial, radial, capil-
lary, venous, intra-atrial). Clinically, we measure the arterial pressure in
the brachial artery and the venous pressure in the veins of the hand or in
the median vein at the elbow.
In physiological experiments, cannulae can be introduced into open ves-
sels for measuring the blood pressure, but in clinical work we use bloodless
methods of determination.
Definitions. — By MAXIMAL ARTERIAL BLOOD PRESSURE or SYSTOLIC
PRESSURE is meant the highest point reached by the blood pressure in the
MEASUREMENTS OF BLOOD PRESSURE 791
artery during the ventricular systole (pulsatory blood pressure maximum).
By MINIMAL ARTERIAL BLOOD PRESSURE Or DIASTOLIC PRESSURE is meant
the lowest point reached by the blood pressure within the artery during
ventricular diastole (pulsatory blood-pressure minimum).
If we subtract the minimal from the maximal blood pressure, we ob-
tain what is known as the PULSE PRESSURE or pulse-pressure amplitude.
For example, if the systolic pressure be 124 and the diastolic pressure 84,
the pulse pressure is 40. The term MEAN PRESSURE is used to designate
the average pressure during a certain period, not the arithmetic mean
between the maximal and minimal pressures.
References
1. General
Cornwall (E. E.). Clinical significance of variations in the systolic and diastolic blood-
pressure and the pulse-pressure. Internal. Clin., Philadelphia, 1915, 25 s..
i, 151-168.
Faught (F. A.). Blood pressure from the clinical standpoint. Philadelphia & London,
1913, W. B. Saunders Co. 280 p. 8°.
The relationship and value of the- systolic, diastolic and pulse pressure.
N. York M. J. [etc.], 1915, ci, 396-399.
Geisbock (F.) , Die Bedeutung der Blutdruckmessung fur die Praxis. Deutsches Arch. f.
klin. Med., Leipzig, 1905, Ixxxiii, 363-409.
Hasebroek (K.). Die Bluldrucksteigerung vom aetiologischen und therapeutischen Stand-
punkt. Wiesbaden, 1910, J. F. Bergmann. 163 p. 8°.
Homer (Arthur). Der Blutdruck des Menschen; Ergebnisse der Tonometrie. Mil einem
Vorworl von J. Pal. Wien & Leipzig, 1913, M. Perles. 204 P- 8°.
Janeway (T. C.). The clinical study of blood pressure [etc.]. New York, 1904, D. Apple-
' ton & Co. 313 p. 8°.
Important contributions to clinical medicine during the past thirty years
from the study of human blood pressure. (Illustrated.) Johns Hopkins
Hosp. Bull, Baltimore, 1915, xxvi, 341-350.
Jones (F. A.). The present status of blood pressure. J. Tenn. M. Ass., Nashville, 1914-15,
vii, 231-236.
MacWilliam (J. A.) & Melvin (G. 5.). Some observations on the significance of blood-
pressure readings in man. Brit. M. J., London, 1914, ii, 777-781.
Middleton (W. S.}. The influence of athletic training on blood-pressure. Am. J. M. Sc.,
Philadelphia, 1915, cl, 426-430.
Nicholson (P.). Blood pressure in general practice. 2. ed. Philadelphia & London
[1914], J. B. Lippincolt Co. 183 p. 8°.
Norris (G. W.}. Blood pressure: its clinical applications. Philadelphia & New York,
1914, Lea & Febiger. 397 p.
Norris (G. W.) & Davies (J. R.). Blood-pressure studies, with especial reference to the
t(energy index" and the ''cardiac load." Tr. Am. Climat. & Clin. Ass.,
Philadelphia, 1914, xxx, 222-232.
Potain (P.-C. E.). La pression arterielle de Vhomme a Vetat normal et pathologique. Paris,
1902, Masson et Cie. 191 p. 8°.
Rubino (C.). La sfigmomanometria e la sfigmografia in clinica. Roma, 1914. 242 p. 8°.
Snyder (C. />.). The inversion of respiratory waves in sphygmomanometer records. Am.
J. Physiol, Baltimore, 1914-15, xxxvi, 430-439. 1 pi.
792 DISEASES OF THE CIKCULATOKY APPARATUS
2. Maximal (Systolic) Pressure
Bachmann (G.). The measurement of arterial pressure in man. New York M. J. [etc.],
1911, xciii, 212-215.
Dally (J. F. H.). A clinical lecture on maximal and minimal blood-pressures and their
significance. Brit. M. J., London, 1913, 899-901.
Flack (M.), Hill (L.) & McQueen (/.)• The measuring of the arterial pressure in man.
I. The auditory method. Proc. Roy. Soc., London, 1915, Ixxxviii, 508-
516.
The measuring of the arterial pressure in man. II. A schematic investiga-
tion. Proc. Roy. Soc., London, 1915, Ixxxviii, 516-536.
Hill (L.). The measurement of systolic blood pressure in man. Heart, London, 1909-10,
i, 73-82.
Hill (L.), McQueen (J.) & Flack (M.). The conduction of the pulse-wave and the measure-
ment of arterial pressure. Proc. Roy. Soc., London, 1914, Ixxxvii, 344~
354.
Jump (H. />.)• The value of blood pressure estimation in internal medicine. Intemat.
Clin., Philadelphia, 1911, 21. s., i, 49-54.
Kraus (F.). Die Methoden zur Bestimmung des Blutdrucks beim Lebenden und ihre Bedeu-
tung fur die Praxis. Deutsche med. Wchnschr., Leipzig u. Berlin, 1909,
xxxv, 235-239.
Kulbs (F.). Beitrdge zur Pathologie des Blutdruckes. Deutsches Arch. f. klin. Med.y
Leipzig, 1907, Ixxxix, 457-484-
MacWilliam (J. A.}, Kesson (J. E.) & Melvin (G. £.)• The conduction of the pulse-
wave and its relation to the estimation of systolic blood -pressure. Heart,
London, 1913, iv, 393-408.
Miiller (O.)- Der arterielle Blutdruck und seine Messung beim Menschen. Ergebn. d.
inn. Med. u. Kinderh., Berlin, 1908, ii, 367-417.
Die unblutige Blutdruckmessung und ihre Bedeulung fur die praktische
Medizin. Med. Klin., Berlin, 1908, iv, 47, 83, 121.
3. Minimal (Diastolic) Pressure
Erlanger (J.) & Hooker (D. /?.). An experimental study of blood-pressure and of pulse-
pressure in man. Johns Hopkins Hosp. Rep., Baltimore, 1904, xii,
145-378.
MacWilliam (J. A.} & Melvin (G. S.). The estimation of diastolic blood-pressure in man.
Heart, London, 1913-14, v, 153-196.
Musser (J. H., Jr.). The relation of high systolic to diastolic pressure. Arch. Diagnosis,
New York, 1914, vii, 229-233.
Nicholson (P.). The clinical significance of diastolic and pulse pressure. Am. J. M. Sc.,
Philadelphia & New York, 1914, cxltii, 514-523.
Stone (W. J.). The clinical significance of diastolic pressure-variations, with special refer-
ence to hypertension and cardiac overload. Lancet-Clinic, Cincinnati.
1914, cxi, 247-254.
Warfield (L. M.). Further observations on diastolic and pulse-pressure. Am. J. M. Sc.
Philadelphia, 1914, cxlviii, 880-885.
2. Instruments for Determination of Arterial Blood
Pressure
The earlier instruments employed for clinical use were (1) the sphyg-
momanometer of von Basch, (2) that of Riva Rocci, and (3) the tonome-
ter of Gartner. There are now a number of modifications of these instru-
ments and it is unnecessary to describe all of them.
MEASUREMENTS OF BLOOD PKESSUKE 793
The principles underlying all these instruments for bloodless blood-
pressure determinations are the same: (1) the arterial pulse is obliterated
by compression from without by means of a cuff; and (2) the pressure
necessary for this is measured by some form of manometer. By the older
methods, only the systolic pressure could be measured ; the newer instru-
ments permit of accurate determinations of both systolic and diastolic
pressure.
(a) The Cuff for Compressing the Arm
The arm is encircled by an elastic cuff or arm band, which, when in-
flated by pumping air into it, obliterates the arterial pulse below the cuff
as soon as the pressure within has been sufficiently raised. It is best
quickly to increase the pressure to some point above that necessary to
obliterate the radial artery, and then to allow the air smoothly to escape
until the pulse just reappears in the radial artery. This point corresponds
to the maximal systolic pressure; that is, an external pressure has been
supplied just sufficient in amount to overcome the internal resistance,
which includes, in addition to the blood pressure, the force of the stream,
the arterial wall, and the surrounding soft tissues. Comparative observa-
tions on animals show that readings thus obtained differ by only a few
millimeters from direct blood-pressure readings obtained by the insertion
of a cannula into the artery.
The width of the cuff is very important. In the original Riva-Rocci
instrument the cuff used was only 5 to 6 cm. broad and the readings ob-
tained were 40 per cent too high, owing to the fact that a part of the
pressure in the cuff was used up in dislocating the soft parts of the arm.
The error was especially great in stout people. If, as suggested by v.
Recklinghausen, a cuff 12 to 15 cm. broad be used, the error is much
smaller, amounting to only about 10 per cent, as has been proven by ex-
periments on human beings in which a cannula has actually been inserted
into the open artery for control (amputations).
In children, a cuff 7 cm. in width is sufficient.
It is customary to apply the cuff over the upper arm, a little above the
elbow. The sleeve of a thin shirt, or of a thin blouse, between the arm and
the cuff is not objectionable. The error when the cuff is thus applied is
less than when a tight sleeve is rolled up above a cuff in order to apply
the latter directly to the skin. The reasons for choosing the brachial
artery in blood-pressure determinations are, according to Janeway, as
follows: "It gives us the systolic lateral pressure within the subclavian,
since brachial and axillary are continuous in direction, and therefore a
near approximation to systolic lateral pressure in the aorta. This, com-
bined with estimation of diastolic lateral pressure in the brachial, which
is practically the same as aortic diastolic pressure, gives the best insight
ilito actual variations of systemic blood-pressure.. " It must be remem-
794 DISEASES OF THE CIKCULATOKY APPARATUS
bered, however, that though the brachial pressure is generally equal to
that in the aorta, it is not always so. There are observations that indi-
cate that the pressure in the brachial arteries of the two sides may, in the
same person, vary as much as 20 mm. (Bing).
(6) Manometers for Measuring the Pressure Within the Cuff
Several varieties of manometer are in use. They include (1) mercury
manometers, (2) compressed-air manometers, (3) aneroid manometers,
and (4) spring manometers.
Mercury Manometers. — Two main types of these have been intro-
duced : ( 1 ) the reservoir type,, and ( 2 ) the U-shaped type.
RESERVOIR TYPE OF MERCURY MANOMETER. — The Riva Rocci is the
typical example of the reservoir type.
The Riva-Rocci Instrument. — Many modifications of the Riva-Rocci
instrument are on the market, including (1) the new Nicholson (probably
the best), (2) .the Cook, (3) the Staunton, and (4) the Hill instru-
ment. Othor similar instruments are the Kercher, the Gartner and
the Westenrijk.
The new Nicholson-Prince sphygmomanometer comes
in a neat case and is easily portable. It yields reliable
readings, and has a stopcock that can be closed if one
wishes to maintain the pressure for any length of time.
U-SHAPED MERCURY MANOMETERS. — The two best in-
struments of this type are (1) Janeway's sphygmoma-
nometer, and (2) Faught's mercury sphygmomanometer.
Other instruments of similar type are those introduced by
Martin, by Linnell, by Mercer, and by Fellner.
Ths J anew ay instrument is very popular among Amer-
ican physicians. The manufacturers now supply it with a
little metal-valve pump instead of the
rubber bulb formerly used.
Another instrument, popular in this
country, is that of F aught. It is com-
pact, makes use of a metal pump, and
of a special expansion tubing for the
inflator.
Compressed- Air Manometers. — Ma-
nometers of this type are also conven-
ient. A little colored liquid, or a little
mercury, is placed in the bulbous end of
a glass tube. On raising the pressure, a
drop of this fluid is forced up into the
deiphia.) tube and is an index from which
224.— The New Nicholson Sphygmo-
manometer. When Closed, the In-
strumont Fits into a Morocco Pocket-
case, which Contains also the Bulb
MEASUREMENTS OF BLOOD PRESSURE
795
the height of the pressure can be read. The Oliver mercurial com-
pressed-air manometer is perhaps the best known instrument of this type.
Bendick's air-water
sphygmomanometer and
Hertz's sphygmomanometer
are other examples.
Aneroid Manometers. —
These are very convenient
for bedside use, being small
and easily portable. They
may require, however, to be
adjusted, at intervals, on com-
parison with a mercury ma-
nometer. Many physicians
prefer a mercury manometer
for office work and use an
aneroid manometer for house-
to-house visits. Of the several
aneroids on the market, the
best known are (1) the Rog-
ers-Tycos, (2) the Faught
aneroid, and (3) Pachon's Fig' 225--Tne Janeway Sphygmomanometer.
. (By courtesy of Dressier-Beard Mfg Co.)
sphygmometnc oscillomeler.
I have myself used the Rogers-Tycos instrument for a number of years
Fig. 226. — The New Oliver (Compressed Air) Sphygmomanometer.
(By courtesy of Dressier-Beard Mfg. Co.)
with satisfaction. Bachman praises highly Pachon's instrument. It is
said, however, that the latter yields systolic readings 20 to 40 mm. Hg.
796 DISEASES OF THE CIKCULATOKY APPAKATUS
higher than does the Staunton apparatus,
though its diastolic readings show less dis-
crepancy.
Other types of aneroid manometers on
the market are (1) Brunton's, and (2) Jac-
quet's.
Spring Manometers. — An instrument
much in use in Germany is von Reckling-
hausens tonometer. I have used this in-
strument and find it very clumsy. It is far
less satisfactory than the instruments in
general use in this country.
(c) Instruments for Graphic Registration
of Blood Pressure
For the most careful studies, graphic
tracings of the radial pulse may be taken
while the pressure in the cuff is falling from
a level ahove that of the systolic pressure to
Fig. 227.— Tycos Sphygmomanom- a level below that of the diastolic pres-
sure. For ordinary clinical purposes this
is entirely unnecessary, but when original
research is being carried out, it may be
desirable to employ this method. Of the
instruments in use for this purpose the
most convenient is Erlanger's sphygmo-
manometer. Other instruments much used
in this way are A. G. Gibson's record-
ing sphygmomanometer, C. Singer's instru-
ment, Uskoff's sphygmotonograph, Silver-
EXACT
SIZE}
eter. Method of Use': Pointer
on Dial Operated by an Ane-
roid Chamber of Corrugated
Metal — Not a Spring. (By
courtesy of Taylor Instru-
ment Co., Rochester, N. Y.)
^^^•^^•^^^^
Fig. 228. — Faught's Blood-pressure Apparatus. Aneroid Type.
<(By courtesy of G. P. Pilling & Son, Philadelphia.)
I
MEASUREMENTS OF BLOOD PRESSURE
797
mann's tonograph, Muenzer's sphygmoturgograph, Brugsch's sphygmo-
tonograph, Fleischer's turgograph, and Bussenius' sphygmotonograph.
Fig. 229. — Uskoff's Blood-pressure Apparatus.
(By courtesy of A. H. Thomas Co., Philadelphia.)
(d) Oscillatory Instruments
In addition to those already described, mention should be made of
certain instruments fitted with oscillating devices, intended to magnify
(indirectly) the fluctuations of the mercurial column or of the pulsations
in the cuff. They have been especially useful in the study of diastolic
pressure. Among these may be mentioned, Bing's sphygmomanometer,
Pal's sphygmoscope, Fedde's oscillometer, Widmer's oscillomanometer, and
Vaquez's sphygmosignal.
(e) Selection of an Instrument for Measuring Blood Pressure
For ordinary clinical work, I would advise either a small aneroid
manometer (Rogers-Tycos or Faught) or a simple mercury manometer of
the Riva-Rocci type (new Nicholson, Janeway or Faught). I advise using
the palpatory method for the determination of the systolic pressure, and
the auscultatory method for the determination of the diastolic pressure.
References
1. Instruments
von Basch (5>.). Der Sphygmomanometer und seine Verwerlhung in der Praxis. Berl.
klin. Wchnschr., 1887, xxiv, 179; 206; 225; 244.
798 DISEASES OF THE CIKCULATOKY APPAKATUS
Er longer (/.)• A new instrument for determining the minimum and maximum blood-
pressures in man. Johns Hopkins Hosp. Rep., Baltimore, 1904, ' xii,
52-110.
Faught (F. A.). The development of the sphygmomanometer and the method of its use.
Internal. Clin., Philadelphia, 1911, 21. s., i, 35-48. 4 pi.
Pachon (F.). Sur la methode des oscillations et les conditions correctes de son emploi en
sphygmomanometrie clinique. Comp. rend. Soc. de biol., Paris, 1909,
Ixvi, 733-735.
v. Reckling hausen (//.)• Unblulige Blutdruckmessung. Arch. f. exper. Path. u. Phar-
makol., Leipzig, 1906, Iv, 375-504.
Also: Neue Apparate zur Messung des arteriellen Blutdrucks beim Men-
schen. Munch, med. Wchnschr., 1913, Ix, 817; 869.
Riva-Rocci (S.). Un nuovo sfigmomanometro. Gazz. med. di Torino, 1896, xlvii, 981;
1001.
Uskoff (L. J.}. Der Sphygmotonograph. Ztschr. f. klin. Med., Berlin, 1908, Ixvi, 90-105.
Weber (/?.). %ur fortlaufenden Registrierung der Schwankungen des menschlichen Blut-
drucks. Die Aenderung des Blutdrucks durch Bewegungsvorstellung.
Arch. f. Anal. u. Physiol, physiol. Ablh., Leipzig, 1913, 205-224-
2. Critical
Hoover (C. F.). A criticism of the blood-pressure apparatus. J. Am. M. Ass., Chicago,
1910, Iv, 815-819.
Howell (W. //.) & Brush (C. E.~). Critical note upon clinical methods of measuring blood
pressure. Boston M. & S. J., 1901, cxlv, 146-151.
J oneway (T.). A modification of the Riva-Rocci method for determining the blood pressure
in the dog. Proc. Soc. Exper. Biol. & Med., New York, 1908-9, vi, 108,
Norris (G. W.}. Modern instruments of precision in the study of cardiovascular disease.
Internal. Clin., Philadelphia, 1911, 21. s., iv, 60-71. 9 pi.
3. Determination of the Maximal (Systolic)
Arterial Pressure
(a) The Palpatory Method
This is probably the best method for clinical determinations of maxi-
mal pressure. The cuff, 12 cm. in width, is applied on the arm and
inflated until the radial pulse disappears. Air is then allowed cautiously
to escape until the radial pulse suddenly reappears. The exact moment is
easy to determine. On watching for the return of the radial pulse the
artery should be palpated with the ball, rather than with the tip, of the
finger.
The patient should be examined in the sitting or recumbent position.
A first reading may be quickly made to prove to the patient that the pro-
cedure is harmless and not painful. This reading may be discarded and a
subsequent reading accurately made. If the patient be excited or anxious,
this should be noted and a later reading made. The arm should riot be kept
compressed long and the pressure should be allowed to fall to zero between
MEASUREMENTS OF BLOOD PKESSUKE 799
observations, sufficient time between readings being permitted for the
venous pressure to fall to the normal level.
Sometimes, a few beats will go through to the wrist at a much higher
pressure than the majority of beats; if so, this fact should be noted.
(6) Oscillatory and Auscultatory Methods
These methods can be used also for the determination of the maximal
systolic pressure, but are less satisfactory than the palpatory method above
described. For the details of these methods, the reader may consult the
treatise of Norris or that of Janeway.
4. Determination of the Minimal (Diastolic)
Arterial Pressure
One may use the palpatory, the oscillatory or the auscultatory method.
For very exact determinations by the oscillatory method, the Erlanger
instrument is perhaps best; but for all ordinary clinical work, the aus-
cultatory method of Korotkow is strongly recommended.
(a) Palpatory Method (Janeway)
By this method the amount of external pressure, just sufficient to make
the pulse, peripheral to the site of compression, begin to become smaller, is
regarded as the "palpatory minimal arterial pressure." If, for example,
the maximal blood pressure in the brachial artery amounts to 115 mm. of
mercury and the minimal pressure to 65 mm., the pressure in the radial
artery will vary by about 50 mm. with every pulse beat. If one now blow
up the cuff on the arm so that the manometer indicates; a pressure of 70
mm., the artery is closed until, with the rise of the pulse wave, the internal
pressure reaches 70 mm. ; a little less blood will therefore pass through
and the pulse must become smaller. This diminution of the pulse can be
felt on palpation, though it is best registered as a radial sphygmographic
curve; while the pressure in the cuff over the brachial is gradually in-
creased, every five millimeters of pressure-increase is noted on the radial
arteriogram. Jacquet's sphygmotonograph or Uskow's instrument will be
found convenient, permitting the recording of blood pressure in milli-
meters of mercury simultaneously and on the same strip with other
tracings. The method yields results that are 25 to 30 per cent higher
than the figures obtained when the open artery is used for control (Miiller
and Blauel). The palpatory method has given place to the auscultatory
method.
800 DISEASES OF THE CIRCULATORY APPARATUS
(6) Oscillatory Method (von Reckling hausen; Erlanger)
If one observe the slightly oscillating level of the mercury meniscus in
the manometer, or the very small excursions of the needle of a spring
tonometer or of an oscillometer, when a pressure somewhat below the
minimal pressure is determined by method (a), he will note that when
the pressure is gradual-
ly increased a point will
be reached where larger
excursions suddenly ap-
pear. The pressure then
existing is called the
"oscillatory minimal ar-
terial pressure" (Erlan-
ger). As long as the
Fig. 230. — Determination of Maximal and Minimal Pressure • • -, ,1
by Erlanger's Apparatus; Maximal Pressure at About pressure inside the ar-
145, Minimal at About 95; Brachial Arteriogram tprv ia ^^f nnrnr^onea+orl
Beneath. (Personal Observation, J. H. H.) "V ll
for by an equal external
pressure, the arterial wall makes only slight excursions, but as soon as the
external compression corresponds to the inner pressure, the arterial wall
can float freely and will communicate large excursions to the air in the cuff,
^s soon then as the pressure in the cuff has just exceeded the minimal
Fig. 231. — The Auscultatory Method of Determining Minimal Blood Pressure. (From G. W.
Norris, "Blood Pressure : Its Clinical Applications," published by Lea & Febiger, Phila-
delphia.)
MEASUREMENTS OF BLOOD PRESSURE 801
blood pressure (for a part of the pulse wave), the oscillations of the
mercury or of the tonometer needle become larger.
(c) Auscultatory Method (Korotkoiv)
This is the simplest and, in my opinion, the best clinical method for
determining the minimal pressure. It has been carefully controlled in my
wards and can be warmly recommended.
A cuff is applied over the brachial artery and the pressure in it raised
until the radial pulse disappears. The bell of the stethoscope is then
placed over the ulnar artery close to the cuff. If the pressure in the cuff
be now allowed to sink gradually one will hear a slight tone, usually at
the moment the first pulse wave is felt at the wrist or a little earlier (maxi-
mal auscultatory arterial pressure). As the pressure is allowed to sink
further, the tones accompanying the pulse beats grow louder and are some-
times accompanied by blowing murmurs. Soon after these become
maximal, a point is reached when, on further lowering of the pressure, the
sounds suddenly become feebler and soon vanish entirely. The sudden
enfeeblement of the sounds corresponds exactly to the junction of larger
and smaller oscillations in the preceding method and indicates the level of
the "auscultatory minimal blood pressure." It is customary now to speak
of FIVE DISTINCT PHASES as the sound varies during the fall of the pres-
sure in the cuff.
First Phase. — When the pressure falls to the level of the maximal
systolic pressure, an arterial tone is heard, not unlike the first sound of the
llliiii
in n i
Fig. 232. — Gallavardin's Diagrammatic Representation of the Auscultatory Phases. I, Arterial
Tone (Muffled) ; II, Tone and Murmur; III, Arterial Tone (Loud and Unaccompanied
. by Murmur ; IV, Sudden Diminution and Muffling of Sound. The Beginning of IV
Indicates the Diastolic Minimal Pressure. (From G. W. Norris, "Blood Pressure: Its
Clinical Applications," published by Lea & Febiger, Philadelphia.)
heart. It is due to the return of the pulse wave in the artery, the vibra-
tions being supplemented by the resonance of the air within the cuff.
Second Phase. — As the pressure in the cuff falls further, the sound
of the first phase is accompanied by a hissing murmur, due to the forma-
tion of a "liquid vein" as the blood flows through the constriction into the
wider artery below.
Third Phase. — As the minimal diastolic pressure is approached, the
murmur of the second phase disappears, and a tone, usually much louder
than that of the first phase becomes audible. The murmur disappears
because the lessening of the constriction of the artery leads to a disappear-
802 DISEASES OF THE CIRCULATOKY APPARATUS
ance of the "liquid vein." This third phase corresponds to the period of
large oscillations in the curve obtainable by Erlanger's apparatus; it is
the period of maximal arterial filling and collapse. The external pressure
is now causing a partial flattening of the artery (MacWilliam & Melvin).
Fig. 233. — Gallavardin's Diagram Illustrating the Relationship Between the Oscillatory and
the Auscultatory Phenomena. The End of the Third Auscultatory Phase Corresponds
to the Last Large Oscillation. (From G. W. Norris, "Blood Pressure : Its Clinical
Applications," published by Lea & Febiger, Philadelphia.)
Fourth Phase. — At the end of the third phase, if the sound be atten-
tively listened to, it will be found to become diminished suddenly and
markedly and to assume a muffled character (Ettinger, 1907). The onset
of this fourth phase indicates the exact moment in which the pressure
within the cuff corresponds to the minimal (diastolic) pressure in the
brachial artery.
Fifth Phase. — The fourth phase is very short; at the end of it, the
sound disappears entirely (fifth phase). These phases and their relations
to the oscillations of the mercury column have been diagrammatically
represented by Gallavardin. Careful studies of the duration of the differ-
ent phases have been made by Goodman and Ho well (1911).
For listening to the sounds in the radial artery on using the auscultatory
method, Filling's bracelet stethoscope is convenient. It may be used with any
form of sphygmomanometer. After the arm band has been applied in the ordi-
nary way above the elbow, the bracelet is adjusted over the radial artery just below
the bifurcation. The sounds can then be observed very accurately.
The auscultatory method has one limitation; it is somewhat unsatis-
factory when tones are audible in the peripheral arteries before the cuff is
applied (e. g., in aortic insufficiency) ; it can be used, however, by paying
close attention to the beginning of the 4th phase ; the 5th phase is absent.
In recording minimal pressure in clinical histories, the mode of deter-
mination (palpatory, oscillatory or auscultatory) should always be men-
tioned. While the auscultatory and oscillatory values are identical when
accurately determined, the palpatory value is higher and corresponds to a
somewhat different point on the blood pressure curve. The true minimal
MEASUREMENTS OF BLOOD PKESSUKE
803
diastolic pressure within the artery is not quite identical with any of the
clinically determined "minimal pressures" ; the "maximal* systolic pres-
G.P.PILLING & SON CO. PHILK
Fig. 234. — A Bracelet Stethoscope, Convenient for Observations on Blood Pressure by the
Ausculiatory Method. (By courtesy of G. P. Pilling & Son Co., Philadelphia.)
sure" as determined clinically undoubtedly approaches much more closely
to the true systolic intra-arterial pressure.
References
Et linger (W.}. Auskultatorische Methode der Blutdruckbestimmung und ihr praktischer
Wert. Wien. klin. Wchnschr., 1907, xx, 992-996.
Gittings (J. C.). Auscultatory blood-pressure determinations. A preliminary report.
Arch. Int. Med., Chicago, 1910, vi, 196-204.
Korotkow. Bcr. d. Kais. Militarztl. Akad., Si. .Petersb., 1905, xii.
Melvin (G. 5.) & Murray (J. /?.)• Blood-pressure estimations in disease by the oscillatory
and auditory methods. Quart. J. M., Oxford, 1914, vii, 419-426.
Swan (J. M.). The auscultatory method of blood-pressure determination: a clinical study.
Internal. Clin., Philadelphia, 1914, 24th s., iv, 130-190.
Tornai (J.). Ueber den diagnostischen Wert der auskultatorischen Blutdruckmessung,
insbesondere vom Standpunkte der Funktionsprufung des Herzens. Ztschr.
f. physikal. u. didtet. Therap., Leipzig, 1909, xiii, 504-512.
Weysse (A. W.} & Lutz (B. /?.). -A- comparison of the auscultatory blood pressure phe-
nomenon in man with the tracing of the Erlanger sphygmomanometer.
Am. J. Physiol., Boston, 1913, xxxii, 427-487.
5. The Arterial Blood Pressure Under Normal
Conditions
In young adults, between 20 and 25 years of age, the blood pressure,
measured when the individual is reclining, averages 110 mm. maximal
(systolic), 65 mm. minimal (diastolic), and 30-45 mm. pulse pressure
(J. Erlanger).
804 DISEASES OF THE CIRCULATOKY APPARATUS
In 1,000 presumably healthy individuals reported by Woley, the aver-
age maximal (systolic) blood pressure, determined with the Tycos instru-
ment was as follows : —
Age 15 to 30 .................... 122
" 31 to 40 .................... 127
" 41 to 50 .................... 130
" 51 to 60 .................... 132
As the upper unit of normal, Woley regards 140 mm. at the period
between 15 and 30, and 155 at 60. In women, the blood pressure normally
averages 8-10 mm. below that of men of the same age.
In infancy, the maximal pressure is about 80 mm. (Trumpp). Up to
the tenth year it rarely exceeds 90 mm. ; at or near puberty it ranges be-
tween 90 and 110 mm.
(a) Variations Under Physiological Conditions
Gravity has a distinct effect as shown by change in posture; on standing, after
lying recumbent, the minimal (diastolic) pressure rises, the pulse pressure
decreases, and the heart rate is accelerated (Erlanger and Hooker).
The eating of food increases the maximal (systolic) pressure, the pulse pressure,
and the heart rate.
The effect of muscular exercise is, at first, similar to that of eating, but on
fatigue the blood pressure falls and the heart is slowed (Schott, Cabot).
It has been shown that mental effort, like stimulation of a sensory nerve, causes
vasoconstriction, rise of blood pressure (especially of the minimal pressure), and
acceleration of the heart rate. During sleep, there is a slight fall in maximal
blood pressure and a marked fall in the minimal blood pressure.
References
Abel (J. J.) & Macht (D. /.)• Two crystalline pharmacological agents obtained from the
tropical toad (Bufo agua). J. Pharm. & Exper. Therap., Baltimore, 1911-
12, Hi, 319-377.
Auer (J.) & Meltzer (J. J.}. Der afferente Splanchnicus als Depressor. Zentralbl. f.
l., 1913, xxvi, 1316-1318.
Barach (J. H.) & Marks (W. /,.)• Effect of change of posture — without active muscular
exertion — on the arterial and venous pressures. Arch. Int. Med., Chicago,
1913, xi, 485-494.
Bruce (J. W.}, Miller (J. R.} & Hooker (D. R.}. The effect of smoking upon the blood-
pressures and upon the volume of the hand. Am. J. PhysioL, Boston,
1909, xxiv, 104-116.
Brush (C. E.} & Fayerweather (R.). Observations on the changes in blood-pressure dur-
ing normal sleep. Am. J. PhysioL, Boston, 1901, v, 199-210.
Cabot (R. C.). Measurements of blood-pressure in fevers before, during and after the ad-
ministration of strychnin. Am. Med., Philadelphia, 1904, viii, 31.
Cathcart (E. P.] & Clark (G. H.}. The mode of action of carbon dioxide on the blood-
pressure. J. PhysioL, London, 1915, xlix, 801-309.
Clough (F. E.). Blood-pressure variations as influenced by rapid changes in altitude. A
study of 100 normal men. Arch. Int. Med., Chicago, 1913, xi, 590-592.
MEASUREMENTS OF BLOOD PEESSUEE 805
Gushing (H. W.). The blood-pressure reaction of acute cerebral compression, illustrated
by cases of intracranial haemorrhage. Am. J. M. Sc., Philadelphia &
New York, 1903, cxxv, 1017-1044.
Dawson (P. M.). The lateral blood " pressures " at different points of the arterial tree.
Am. J. Physiol, Boston, 1905-06 , xv. 244-256.
Donaldson (M.}. Some observations of blood pressures in cases of normal and abnormal
pregnancies and labors. J. Obst. & Gynaccol. Brit. Emp., 1913, xxiv.
133-144-
Erlanger (/.) & Festerling (E. G.}. Respiratory waves of blood pressure, with an in-
vestigation of a method for making continuous blood pressure records in
man. J. Exper. M., Lancaster., Pa., 1912, xv, 370-387.
Eyster (J. A. E.} & Wilde (A.). The action of urea and of hypertonic solutions on the heart
and circulation. J. Pharmacol. & Exper. Therap., Baltimore, 1909-10. i,
303-403.
Groedel (F. M.). Wird der Blutdruck durch Roentgenbestrahlung der Nebennieren beein-
flusst? Strahlentherap., 1913, ii, 224-226.
Hare (H. A.}. The difference between systolic pressure in the arm and in theJeg in aortic
regurgitation. Therap. Gaz. [etc.], Detroit, 1910, xxxiv, 457-460.
Hawley (M. C.). Studies of blood-pressure in states of excitement and depression. Arch.
Int. Med., Chicago, 1913, xii, 526-538.
Hoskins (R. G.} & McPeek (C.). The effects of adrenal massage on blood-pressure. J.
Am. M. Ass., Chicago, 1913, Ix, 1777-1779.
Janeway (T. C.)« The influence of the soft tissues of the arm on clinical blood-pressure de-
terminations. Arch. Int. Med., Chicago, 1909, Hi, 474~475.
Janeway (T. C.) & Park (E. A.}. An experimental study of the resistance to compression
of the arterial wall. Arch. Int. Med., Chicago, 1910, vi, 586-613.
The question of epinephrin in the circulation and its relation to blood
pressure. J. Exper. M., Lancaster, Pa., 1912, xvi, 541—557.
Lee (W. E.). The action of tobacco smoke, with special reference to arterial pressure and de-
generation. Quart. J. Exper. Physiol., London, 1908, i, 335-358. 1 pi.
McCurdy (J. H.}. Effect of maximum muscular effort on blood-pressure. Am. J. Physiol.,
Boston, 1901, v, 95-103.
MacWilliam (J. A.) & Kesson (J. E.}. The estimation of systolic blood-pressure in man,
with special reference to the influence of the arterial wall. Heart, London.
1913, iv, 273-318.
Moritz (F.). Anomalien derFaktoren, welche die Hohe des Blutdrucks bestimmen. Handb.
d. allg. Pathol. (Krehl & Marchand), Leipzig, 1913, ii, 2, 42-60.
Retzlaff (Karl}. Beeinflussung des Blutdruckes durch hypertonische Losungen. Ztschr. f.
Exper. Pathol. u. Therap., Berlin, 1915, xvii, 192-199.
Schneider (E. C.) & Sisco (D. L.\. The circulation of the blood in man at high altitudes.
1 . The pulse rate, arterial, capillary, and venous pressures. 2. The rate of
blood flow and the influence of oxygen on the pulse rate and blood flow.
Am. J. Physiol., Boston, 1914, xxxiv, 1-47.
Stephens (O. Z.). Blood-pressure and pulse-rale as influenced by different positions oj
the body. J. Am. M. Ass., Chicago, 1904, xliii, 955-962.
Trumpp (J.). Blutdruckmessungen an gesunden und kranken Sduglingen. Jahrb. f.
Kinderh., Berlin, 1906, Ixiii, 43-59.
Voegtlin (C.) & Macht (D. T.). Isolation of a new vasoconstrictor substance from the
blood and the adrenal cortex. Presence of the substance in the blood and
its action on the cardiovascular apparatus. J. Am. M. Ass., Chicago,
1913, Ixi, 2136-2138.
Weysse (A. W.} & Lutz (B. R.). Diurnal variations in arterial blood pressure. Am. J.
Physiol., Baltimore, 1915-16, xxxvii, 330-337.
806 DISEASES OF THE CIKCULATOKY APPAKATUS
Williamson (C. S.). The effects of exercise on the normal and pathological heart; based upon
the study of one hundred cases. Am. J. M. Sc., Philadelphia, 1915, cxlix,
492-503.
Woley (H. P.). The normal variation of the systolic blood-pressure. A study of one thousand
cases. J. Am. M. Ass., Chicago, 1910, Iv, 121-123.
6. The Blood Pressure in Pathological States
(a) Chronic Arterial Hypertension
Among the pathological states in which the blood pressure may con-
tinue to be much higher than normal over a long period, may be men-
tioned: (1) increased intracranial tension, (2) chronic nephropathies,
especially contracted kidneys, (3) aortic insufficiency, (4) certain forms of
arteriosclerosis, (5) chronic polycythemia, (6) certain cases of Graves's
disease, and (7) chronic cyanosis, especially that due to failing myocar-
dium.
When there is an increase of intracranial tension, due to meningitis, brain
tumor or other cause, the maximal blood pressure may become very high (300-400
mm. of Hg), the minimal blood pressure may rise to 160, and there is bradycardia.
Whenever the intracranial pressure rises above the blood pressure, general vaso-
constriction due to stimulation of the vasomotor center results; the blood pressure
rises in a series of stages ( Traube-Hering waves) until the mean blood pressure
exceeds the intracranial pressure (Gushing). Nitrites do harm in such cases,
though lumbar puncture or cerebral decompression may be beneficial by lowering
intracranial pressure.
In chronic diffuse renal diseases, especially those in which the kidneys are
contracted, high blood pressures (150 to 300 mm.) are common, though in some
cases, not well understood as yet, the blood pressure may not be elevated. The
cause of the arterial hypertension in chronic renal disease has been much discussed.
Some have attributed it to narrowing of the renal arterioles and consequent defec-
tive elimination of urinary solids, especially of the non-coagulable nitrogenous sub-
stances of the blood. Experimental researches indicate that reduction of the
amount of kidney substance in the body will lead to arterial hypertension and to
hypertrophy of the heart. As endocrinology has advanced, theories that the hyper-
tension is of hormonic origin have been advanced; thus some have held an internal
secretion of the kidney (renin) responsible, others a hypersecretion of epinephrin
(Vaquez, Neusser) with resulting epinephrinemia ; neither theory has had, as yet,
sufficient support.
According to Janeway, hypertension of renal origin may be due: (1) to a
purely quantitative reduction of renal tissue with resulting hypertonus due to
retained poisons, (2) to the poisons which intoxicate the nervous system giving
rise to the symptoms which we call "uremic," (3) to a superimposition of a renal
factor upon a hypertension due primarily to an irritability of the vasoconstricting
mechanism and which leads to general sclerosis of the small arterioles, including
those of the kidneys.
Recently, Voegtlin and Macht have discovered a crystalline pressor substance,
not epinephrin, which stimulates the heart and causes pronounced vasoconstriction ;
they believe it to be a derivative of cholesterin, and think that it may originate
in the adrenal cortex. N. B. Foster, in 1915, reported the isolation of a crystalline
MEASUREMENTS OF BLOOD PEESSUKE 807
substance from the blood of uremic patients, which may prove to be of great
importance.
In nephropathic hypertension the maximal pressure is as a rule more increased
than the minimal ; there is, accordingly, a large pulse pressure. It has been shown
that the minute-volume of the heart and the systolic output are normal or a little
subnormal (Bergmann and Plesch) and the rate of flow is not increased (Stewart).
Apoplexy, uremia, myocardial insufficiency, paroxysmal dyspnea, Cheyne-
Stokes breathing, and edema of the lungs are among the complications not infre-
quently encountered in cases of chronic hypertension.
In aortic insufficiency, the large pulse pressure depends upon (1) increase of
maximal pressure (180-200 mm.) and (2) reflex decrease of minimal pressure
(30-60 mm.). The main fall of pressure is systolic in time and is due to increased
capillary flow, not to regurgitation into the heart in diastole (H. A. Stewart).
In aortic insufficiency, there may be a large difference (as much as 150 mm.)
between the maximal blood pressure in the arm and that in the leg, when both
are measured when the patient is in the recumbent posture. Under normal condi-
tions, these pressures are equal.
Among the forms of arteriosclerosis accompanied by arterial hypertension,
that in which the small arterioles are principally involved (arteriocapillary
fibrosis, arteriolar sclerosis) is the most important. Even then, it may be the
involvement of the renal arterioles that counts most. The larger arteries, like the
brachial and radial, may be extensively sclerosed without causing hypertension.
The high blood pressure due to vasoconstriction before arteriosclerosis has set
in is called hyperpiesis (Allbutt).. Patients suffering from arteriosclerosis are
more prone than normal individuals to suffer from crises of vasoconstriction — the
so-called "vascular crises" (Collier; Pal). Such crises are common also in tabes,
in lead poisoning, in pregnancy, and in the nephropathies. Here belong angina
pectoris, angina abdominis, crises of constriction of the cerebral arteries, and
intermittent claudication. In these vascular crises, the maximal pressure may rise
40-80 mm. of Hg. A patient with angina pectoris may have a low blood pressure
ordinarily and high pressure during his attacks.
In one form of chronic polycythemia, sometimes designated "polycythemia
hypertonica" (Geisbock), arterial hypertension is present. The cause of the
hypertension is not known.
In Graves's disease, the blood pressure may be normal or low, but in some
cases, outspoken arterial hypertension is present. When the blood pressure is
high in exophthalmic goiter, the cause is to be sought, not in the thyreointoxication
directly, but rather in the secondary processes in the heart, blood vessels or kidneys.
In chronic cyanosis, due to a failing heart, the arterial hypertension may
be marked, due to overloading of the blood with C02 and stimulation of the vaso-
constrictors as in experimental asphyxia. This form of high blood pressure asso-
ciated with venous stasis has been carefully studied by Sahli, who calls it "high
pressure stasis." Cardiotonic therapy will often reduce the blood pressure in these
cases by overcoming the myocardial insufficiency so that the blood is better aerated.
References
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808 DISEASES OF THE CIRCULATORY APPARATUS
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794.
Williams (T. A.). The antecedents of high blood pressure and nervousness. West Virginia
M. J., Wheeling, 1914-15, ix, 363-366.
Willson (R. N.~). The decomposition food products as cardiovascular poisons. J. Am. M.
Ass., Chicago, 1915, Ixv, 1077-1088.
(6) Acute and Chronic Arterial Hypotension
A persistently low blood pressure is more often due to loss of arterial
tonus than to failure of the heart. Hypotension is common in (1) acute
infections, (2) pulmonary tuberculosis, (3) surgical shock, and (4)
chronic wasting diseases of various sorts.
In acute infections, the toxins may injure or paralyze the vasomotor center,
so that the peripheral arterioles dilate markedly. Thus in typhoid fever, the
maximal blood pressure may fall below 70, though in most cases it ranges between
110 and 90 (minimal between 85 and GO). In acute peritonitis similar low
pressures are met with. Indeed, in most acute infections there is hypotension at
the height of the fever. In lobar pneumonia, the course may be run with normal
blood pressures, but not infrequently collapse is associated with marked hypo-
tension from vasomotor paralysis. In meningitis, there is often high blood pres-
sure, owing to the increased intracranial tension.
In pulmonary tuberculosis, the maximal blood pressure is usually abnormally
low, say from 20 to 40 mm. lower than in healthy people of the same age. Hypo-
MEASUREMENTS OF BLOOD PKESSURE 809
tension is not constantly present, however, and the pressure may vary considerably
at different times in the same individual. According to Haven Emerson, the causes
are (1) a toxic action on the vasomotor center and (2) a progressive atrophy of
the cardiac muscle.
It should be remembered that pleural effusion tends to increase blood pressure,
and the blood pressure falls when the fluid is drawn off. The fall amounts ordi-
narily to 20 mm. of Hg (Capps).
In surgical shock, there is a fall of blood pressure. Some believe this to be
due to exhaustion of the vasomotor center or of the brain cells, the result of
violent sensory stimuli or "noci" impulses (G. W. Crile) ; others maintain that
shock is the result of lack of fluid in the circulation, the total volume of blood
being decreased through transudation of fluid into the tissues, this in turn depend-
ing upon diminished hemic osmotic tension due to loss of C02 from the blood or
acapnia (Yandell Henderson). Whatever the explanation of the fall of blood
pressure, certain it is that observation of this fall, associated with increase of the
heart rate, is the best method of recognizing beginning shock during or after
operations. The prevention of acapnia during anesthesia is favored by regulating
the amount of C02 inspired (Gatch).
In the cachexias, in which there is anemia and brown atrophy of the heart,
tachycardia and arterial hypotension are nearly always observable.
References
Bloodgood (J. {?.)• Traumatic shock and blood pressure. Int. J. &urg., New York,
1913, xxvi, 303-310.
Crile (G. W.}. The blood pressure in surgery. An experimental and clinical research.
Philadelphia & London, 1903, J. B. Lippincott Co. 422 p. 8°.
The kinetic theory of shock and Us prevention through anoci-association
(shockless operation}. Lancet, London, 1913, i, 7-16.
The kinetic theory of surgical shock and anoci-associaiion. Interstate M. J.,
St. Louis, 1913, xx, 499-506.
A successful method of performing shockless operations, based on a clinical
experience of 3,000 cases. South. M. J., Nashville, 1913, vi, 575-579.
Goodman (E. H.}. Some cases of hypotension associated with a definite symptomatology.
Am. J. M. Sc., Philadelphia & New York, 1914, cxlvii, 603-514.
Henderson (Y.}. Acapnia and shock. II. A principle underlying the normal variations*
in the volume of the blood stream and the deviation from the principle in
shock. Am. J. Physiol, Boston, 1909, xxiii, 345-373.
Henderson (Y.) & Underhill (F. P.}. Acapnia and glycosuria. Am. J. Physiol.,
Boston, 1911, xxviii, 275-289.
Janeway (H. H.) & Ewing (E. M.}. The relation of acapnia to shock, and a consideration
of the mechanical (ffects of artificial hyperrespiration upon the circulation.
Biochem. Bull., New York, 1913, ii, 403-406.
Pearce (R. M.) & Eisenbrey (A. B.). A study of experimental conditions of low blood-
pressure of non-traumatic origin. Arch. Int. Med., Chicago, 1910, vi,
218-230.
7. The Absolute Sphyjjmogram (Sahli)
The ordinary sphygmogram of an artery (or arteriogram), which is a
blood pressure curve in which the heights of the ordinates are indefinite,
can be transformed into an absolute sphygmogram by introducing the pulse
810 DISEASES OF THE CIRCULATOEY APPARATUS
curve into a system of ordinates in which the minimal blood pressure is
used as the base, or lowest point, of the pulse curve, and the maximal blood
mm Hg
" A -?
/ \ ^C-T
tffQ
\ WO
1*0
\? 18O
" J \ »!>
03 i "
% /v I
l\ a ' rjX
tS I AC /\
"f'^f, I \S. I \
00 " V / \ -
S-T V / ^
/ XC «
-0 J < ^
a f ^
Fig. 235. — Course of the Blood Pressure in the Radial Artery. Blood Pressure Apparatus
on Upper Arm; Sphygmograph on Wrist, (a-b) Ascending Portion; (b) Top of the First
Systolic Wave; (c) End of Second Systolic Wave; (c-d) Post Systolic Fall: (d) Begin-
ning of the Dicrotic Wave; (e) Top of Dicrotic Wave; (d-f) Diastolic Portion of the
Curve. (After Seifert and Mailer, "Taschenbuch d. Medizin — Klin. Diagnostik," pub.
lished by J. F. Bergmann, Wiesbaden.)
Fig. 236. — Absolute Sphygmograms and Pulse Tracings from Two Persons, One with
Normal Blood Pressure, One with Nephropathic Hypertension. (After Gallavardin, from
G. W. Norris' "Blood Pressure: Its Clinical Applications," published by Lea & Febiger,
Philadelphia.)
MEASUREMENTS OF BLOOD PKESSUKE
811
pressure as its highest point ; in such a curve, the ordinates now represent
the pressures in millimeters of Hg and the abscissae the time in fractions
of a second, the whole curve corresponding to the course of the pressure in
the artery (Sahli). ~No attention need be paid to the secondary elevations
of the arteriogram, since it is only the rapidity of the ascent and descent
of the pulse waves that need be here regarded.
In the absolute sphygmogram, the pulse pressure can be read off di-
rectly, since it is the difference between the maximal and the minimal
blood pressures. Our best measure of the tension of the pulse is the mini-
mal blood pressure.
Reference
Sahli (H.). Uber das absolute Sphygmogramm und seine klinische Bedeutung, nebst krit-
ischen Bemerkungen iiber einige neuere spygmomanometrische Arbeilen.
Deutsches Arch. f. klin. Med., Leipzig, 1904, Ixxxi, 493-542.
8. Determination of Venous Blood Pressure
Many methods have been devised for determining the blood pressure
in the veins. Only three of these will be described.
(a) Method of Hooker and Eyster (1908)
Applying a principle utilized by v. Basch and,
later, by v. Recklinghausen, Hooker and Eyster
place a pressure- chamber over a vein on the front
of the wrist and blow in air until the vein "col-
lapses," reading off the pressure at that moment
on a water-manometer (see Fig. 237).
(6) Method of Moritz and v. Tabora (1909-10)
A hollow needle, connected with a buret of
normal salt-solution is introduced into the vein
at the bend of the elbow (asepsis!), the patient
recumbent. The fluid is allowed to run in, its
level in the buret gradually falling until flow
ceases. The level of the saline above the level of
the heart (say a point on the fourth rib, 5 cm. be-
low the level of the surface of the chest) is then
read off; the result is the venous pressure at the
heart in cm. of normal saline. The calculation in centimeters of H2O may
easily be made, since 10 cm. normal saline equals 10.07 cm. H2O. The
method is believed to be accurate.
Fig. 237.— Apparatus of
Hooker and Eyster for
Determining the Ve-
nous Pressure. (J. H.
H. Bull.)
812 DISEASES OF THE CIRCULATORY APPARATUS
(c) Method of A. A. Howell (1912)
Two cuffs are used, each being attached to a water manometer. One is
applied to the upper arm, the other to the forearm. The latter is inflated
so as to fit snugly but without exerting over 3 cm. (H2O) pressure. The
cuff on the upper arm is then cautiously inflated until the water in the
forearm manometer begins to rise. The pressure in the upper-arm cuff is
equal to the venous pressure.
In a similar instrument, devised by Frank and Reh (1912), the read-
ings may be graphically registered.
9. The Normal Blood Pressure in the Veins
At the level of the heart, the venous pressure varies normally between
1 and 13 cm. of H2O=0.7-9.5 mm. Hg.
The figures in the bibliography vary a good deal, as will be seen from the fol-
lowing table:
NORMAL VENOUS PRESSURE AT LEVEL OF HEART
Observer
Cm. H.O
Mm. Hg
Hooker and Eyster
3-10 cm.
Average 8 cm.
2.2-7.3 mm.
Average 5.9 mm.
Moritz and Tabora
1.1-8.7 cm.
Average 5.2 cm.
0.8-6.4 mm.
Average 3.8 mm.
Howell
4-13 cm.
2.9-9.5 mm.
Average 7.6 cm.
Average 5.6 mm.
Physiological Variations of Venous Pressure. — The most important factor
influencing venous pressure is the position of a part with relation to the heart.
The pressure in the veins in parts in various positions has been carefully studied
and recorded by v. Recklinghausen. The venous pressure rises slightly on exercise,
and on sudden changes in temperature. The venous pressure is but little affected
by changes in arterial blood pressure. The changes in venous pressure during the
phases of respiration have been examined by Burton-Opitz, who finds that, during
expiration, the pressure in the jugular vein rises; it begins to fall in the pause
following expiration and continues to fall in the early part of inspiration.
10. The Venous Blood Pressure in Pathological
States
As the myocardium begins to fail, blood begins to accumulate in the
systemic circulation and the venous blood pressure is an index of this. A
high venous pressure is associated with a dilatation of the heart, while a
FUNCTIONAL CAPACITY OF THE HEART 813
low venous pressure is associated with insufficient filling of the heart and,
accordingly, a decrease in the size of the heart.
In cardiac decompensation, the venous blood pressure may be as high
as 25 cm. H2O in the veins of the arm at the level of the heart (A. A.
Howell). After intravenous injections, the venous pressure rises more
proportionately than does the arterial pressure (Bayliss and Starling).
A very low venous pressure may be found in neurasthenia and in post-
operative asthenia. Cody, working with Hirschfelder in my wards, meas-
ured venous pressures in such states as low as -2 to -7 cm. H2O, though
the arterial pressures were not markedly altered, varying as they did be-
tween 104 and 125 mm. Hg.
References
Clark (A. H.). A study of the diagnostic and prognostic significance of venous pressure
observations in cardiac disease. Arch. Int. Med., Chicago, 1915, xvi, 587-
604-
Hooker (D. R.). Observations of the venous blood pressure in man. Am. J. Physiol., Boston,
1914, xxxv, 73-86.
Hooker (D. R.) & Eyster (J. A. E.). An instrument for the determination of venous
pressure in man. Johns Hopkins Uosp. Bull.. Baltimore, 1908, xix,
274-277.
Howell (A. A.}. A new method of determining venous blood-pressure. Arch. Int. Med.,
Chicago, 1912, ix, 148-155.
Henderson (T.) & Barringer (T. B.}. The relation of venous pressure to cardiac effi-
ciency. Am. J. Physiol., Boston, 1913, xxxi, 352-369.
Marchand (F.). Die Storungen der Blutverteilung . Handb. d. allg. Pathol. (Krehl &
Marchand), Leipzig, 1912, ii, 1, 218-280.
H. Determination of the Functional Capac-
ity of the Heart
Laudable efforts have been made to test the functional power of the
heart or to estimate the work done by the heart, clinically, but the results
have been notoriously unsatisfactory. The methods in use try to establish
the absolute power of the heart. To calculate the work of the left ventricle,
we should have to know (1) the systolic output and (2) the mean pres-
sure in the aorta. But, clinically, these factors cannot be determined
accurately, and, moreover, as Kiilbs emphasizes, if it were possible in
some way or another to measure the power of the heart at a given moment,
the result obtained, to be of any use, would have to be related to many other
coexistent factors. For the absolute power of the heart is less important
than the response of the heart to different somatic and psychic needs and
814 DISEASES OF THE CIRCULATORY APPARATUS
this response is not only different for different persons but varies extra-
ordinarily in the same person from day to day and from hour to hour.
The multiple factors concerned in this variation are still inaccessible to us
clinically; probably they are largely neural. It is well for the student to
be familiar, however, with the attempts now being made to measure the
functional capacity of the heart, for out of them, sooner or later, some-
thing of distinctly practical value may emerge.
References
Cabot (R. C. & Bruce (R. /?.)• The estimation of the functional power of the cardio-
vascular apparatus. Am. J. M. Sc., Philadelphia & New York, 1907,
cxxxiv, 491-500.
Janowski (W.). Die' funktionelle Herzdiagnostik. Berlin, 1910, A. Hirschwald. 166
p. 8°.
Kiilbs (F.). Diefunktionspriifungdes Herzens. Handb. d. inn. Med. (Mohr & Staehelin) .
Berlin, 1914, ii, 932-937.
Norris (G. W.}. The functional capacity of the heart. Internal. Clin., Philadelphia,
1907, 17. s., i, 66-87.
Swan (J. M.). How shall we tell whether or not the myocardium is competent? Arch.
Int. Med., Chicago, 1915, xv, 269-285.
Weiss (G.). Le travail du coeur. J. de physiol. et de path, gen., Paris, 1913, xv, 999-1013.
Williams (C. S.). An experimental study in the functional diagnosis of the heart. Louis-
ville Month. J. M. & S., 1914-15, xxi, 299-304.
Williamson (C. S.}. An experimental study in the functional diagnosis of the heart.
Lancet-Clinic, Cincinnati, 1915, cxiii, 208-210.
As has long been known, the pulse rate increases when work is done by the
muscles. The accompanying blood pressure changes during work have recently
been systematically studied.
Graupner's Test for Functional Capacity.— This author made certain muscle
groups perform a definite amount of work and studied the blood pressure while
the work was being done. He believed he could draw conclusions regarding the
power of the heart and the peripheral resistance.
The work consisted in the turning of a wheel provided with a brake, and per-
mitting of a measurement of the work done. He concluded that (1) if the blood
pressure remained constant, the heart was sufficient for the work; (2) if the
blood pressure fell, the heart was insufficient for the work; (3) if the blood
pressure rose at first, and then returned to normal, the heart possessed "com-
pensatory capacity"; and (4) if the blood pressure rose, fell rapidly, and did not
again tend to rise, the heart was fatigued.
Graupner's method has been controlled by F. Klemperer and by A. Hoffmann
and found unreliable.
References
Graupner (S. C.). Die Messung der Herzkraft und deren Bedeutung fur die Diagnose
und Behandlung der chronischen Herzkrankheiten. Munchen, 1905
Otto Gmelin. 23 p. 8°.
FUNCTIONAL CAPACITY OF THE HEART 815
Strasburger's Method of Estimating Functional Capacity. — When the work
of the heart increases there is an increase not only of the maximal pressure in the
arterial system but also of the pulse pressure and of what Strasburger calls the
pulse pressure quotient (pulse pressure divided by mean pressure), commensurate
with the increased systolic output ; when the work of the heart is lessened, all these
factors are smaller. In hypertony of the peripheral arteries the maximal pressure
rises, but the pulse pressure (and pulse-pressure quotient) falls. In dilatation of
the peripheral vessels the pulse pressure rises but the maximal pressure falls.
Thus, when maximal pressure and pulse-pressure quotient are altered in the same
direction it is the central component of the blood pressure (systolic output) that
is the important factor; when maximal pressure and pulse-pressure quotient alter
in an opposite direction, it is the peripheral component of the blood pressure
(peripheral resistance) that is responsible. Strasburger goes further and tries
to estimate the amount of the work done by the heart from the number of beats,
the pulse pressure and the mean pressure. He regards the. quotient, pulse pres-
sure divided by maximal (systolic) pressure, as a fair measure of the size of the
systolic output on the ground that the relation of the pulse pressure to the blood
pressure must show itself. If the pulse pressure were to rise until it equalled the
maximal pressure, then this quotient would become 1 and the diastolic pressure
would equal 0. These would be, hypothetically, the best conditions for the out-
flow of blood in the artery, the vascular resistance being very small. In the oppo-
site case, where the above-mentioned quotient is smaller, the outflow of blood
would be more difficult, owing to greater resistance in the periphery.
According to Strasburger, the following conclusions may, accordingly, be drawn :
1. When the systolic pressure is altered, the blood-pressure quotient remaining
unchanged, the cause is a change in the work of the heart ; a rise indicates increased
heart work; a fall indicates diminished work.
2. Change in the systolic pressure and in the quotient about equally marked,
but in opposite directions, indicates change in the vascular tonicity; rise of systolic
pressure and fall of quotient indicate increased vascular tonus; the reverse,
depressed tonus.
3. When the systolic pressure and the quotient move in the same or in oppo-
site direction but in unequal degree, there is an alteration both of the vascular
tonus arid of the work of the heart.
Strasburger's method is unreliable since (1) it ignores the enormous importance
of nervous influences, and (2) it tries to draw "dynamic" conclusions from
"static" data.
Reference
Strasburger (/.)• Ueber den Einfluss der Aortenelasiizitdt auf das Verhdltnis zwischen
Pulsdruck und Schlagvolumen des Herzens. Deutsche med. Wchnschr..
Leipzig u. Berlin, 1907, xxxiii, 1033-1036.
Also: Deutsches Arch. f. klin. Med., Leipzig, 1907, xci, 378-427.
Erlanger's and Hooker's Method for Estimating Heart Work. — These investi-
gators, working in Howell's laboratory in Baltimore, draw conclusions regarding
changes in the work of the heart and of the peripheral resistance from clinical
determinations of (1) the maximal blood pressure and (2) the product of pulse
pressure multiplied by pulse rate.
816 DISEASES OF THE CIKCULATOEY APPAEATUS
TABLF
CHANGES
CAUSE
Maximal Blood
Pressure
Pulse Pressure
X
Pulse Rate
Work of Heart
Resistance
Unchanged
/Greater
i^Less
[Unchanged
\ Greater
[Less
[Unchanged
] Greater
[Less
f Increased
\Decreased
[Increased
•j Increased
[Unchanged
{Decreased
Unchanged
Decreased
(Decreased
\Increased
[Increased
j Unchanged
[increased
[Decreased
j Decreased
[Unchanged
Rise
Fall ...
This method is subject to the same criticism as has been made of Strasburger's
method.
'ic out-
References
Dawson (P. M.) & Gorham (L. W.). The pulse-pressure as an index of the
put. J. Exper. Med., Lancaster, Pa., 1908, x, 484-489.
Erlanger (/.) & Hooker (D. R.). An experimental study of blood-pressure and of pulse-
pressure in man. Johns Hopkins Hosp. Rep., Baltimore. 1904, xiL
145-378.
Evans (C. L.) & Ogawa (5.). The effect of alterations of the blood viscosity of the circulating
blood on the cardiac output in the heart-lung preparation. J. Physiol.,
London, 1915, xlix, 9-11.
Gasser (H. 5.) & Meek (W. /.)• A study of the mechanisms by which muscular exercise
produces acceleration of the heart. Am. J. Physiol., Boston. 1914, xxxiv,
48-71.
Henderson (F.) & Prince (A. L.). The relative systolic discharges of the right and left
ventricles and their bearing on pulmonary congestion and depletion. Heart,
London, 1914, v, 217-226.
Miiller (O.) & Vochting (K.). Zur Frage des Herzschlagvolumens. Deutsche Arch. f.
klin. Med., Leipzig, 1913, ex, 389-410.
Katzenstein's Method of Estimating the Functional Capacity of the Heart
from the Behavior of the Blood Pressure on Exclusion of Certain Arterial
Domains. — The patient is placed in the recumbent posture, and the iliac arteries
are compressed for a period of 21/^-5 minutes, care being taken to avoid mental
excitement and pain. The work of the heart is increased by this narrowing of
the arterial bed. Katzenstein found that:
(1) If the heart be normal and sufficient, there is an increase of 5-15 mm. Hg
in the blood pressure, the pulse rate remaining unchanged or being slowed;
(2) If the heart be hypertrophied and sufficient, the blood pressure rises 15 to
40 mm. Hg, the pulse rate remaining stationary or becoming slowed;
(3) If the heart be slightly insufficient, the blood pressure remains unchanged,
the pulse rate unchanged or plus; and
FUNCTIONAL CAPACITY OF THE HEABT 817
(4) If the heart be markedly insufficient, the blood pressure falls and the
pulse rate is accelerated.
Here, again, it is almost impossible to exclude the psychic factors that influ-
ence the heart and the arteries ; and the results obtainable are of doubtful clinical
value.
Reference
Katzenstein (M.). Ueber erne neue Funktionsprufung des Herzens. Deutsche med.
Wchnschr., Leipzig u. Berlin, 1904, xxx, 807; 845.
Ueber eine neue Funktionsprufung des Herzens. Deutsche med. Wchnschr.,
Leipzig u. Berlin, 1905, xxxi, 695-696.
Ueber Funktionsprufung des Herzens nach einer zehnjahrigen klinischen
Erfahrung. Deutsche med. Wchnschr., Leipzig u. Berlin, 1915, xli, 457—
460.
Zuntz and Plesch's Method of Estimating the Functional Capacity of the
Heart, Based upon Calculations of the Systolic Output. — The systolic output is
calculated from the difference in the oxygen in the arterial and the venous blood
and from the oxygen-intake during respiration. First, the oxygen-content of the
blood taken from an artery is determined by the colorimetric method of Plesch
(q. v.). The oxygen-content of the blood in the right ventricle is judged by the
02-tension in the residual air of the lungs, since the two stand in equilibrium.
Plesch determines the 02-tension by allowing the patient after a deep inspiration
to exhale and inhale several times, using a balloon containing a definite amount of
nitrogen. Subsequently, he determines the oxygen used per minute with the Zuntz-
Goeppert respiration apparatus. The minute-volume contains the amount of
oxygen that is taken up on respiration; it is equal to the difference in total
oxygen-content of the arterial blood and of the venous blood that flows through
the lungs during one minute. Now if the minute-volume of the heart be divided
by the pulse rate per minute, we get the "systolic output."
References
Brugsch (T.) & Plesch (/.)• Hamodynamik. In: Technik d. spez. klin. Untersuchungs-
meth. (Brugsch & Schittenhelm) , Berlin u. Wien, 1914, i, 1-79.
Lindhard (/.)• Ueber das Minutenvolum des Herzens bei Ruhe und die Muskelarbeit.
Arch. f. d. ges. Physiol., Bonn, 1915, clxi, 233-383.
Moritz (F.). Anomalien der Dynamik des Herzens und der Gefdsse. Handb. d. allg. Pathol.
(Krehl & Marchand), Leipzig, 1913, U, 2, 2-41.
M tiller (F.). Die Stickoxydul-Methode zur Bestimmung des Herzschlagvolumens beim
Menschen. In: Technik d. spez. klin. Untersuchungsmethoden (Brugsch
& Schittenhelm), Berlin u. Wien, 1914, i, 75-79.
Plesch (/.)• Hdmodynamische Studien. Ztschr. f. exper. Path. u. Ther., Berlin, 1909,
vi, 880-618. 2 tab.
Bestimmung des Herzschlagvolumens. Deutsche med. Wchnschr., Leipzig
u. Berlin, 1909, xxxv, 239-242.
Sahli's Sphygmobolometry. — Sahli attempts to get at the functional power of
the heart indirectly by estimating the energy of the single pulse waves. For
this purpose, he has devised a special instrument, the sphygmobolometer. This
instrument is not difficult to use, and the necessary observations can be made in
a few minutes.
The normal amount of energy of the brachial pulse wave is usually between
40 and 60 g/cm. In pathological states, these values may be doubled. For the
technic, Sahli's descriptions should be consulted.
818 DISEASES OF THE CIRCULATORY APPARATUS
References
Hartmann (C.). Untersuchungen mil dem neuen Sphygmobolometer nach Sahli. Deulsches
Arch. /. klin. Med., Leipzig, 1915, cxvii, 86-110.
Sahli (H.}. Weitere Beitrdge zur Kritik der Sphygmobolometrie und zur Verbesserung ihrer
Methodik. Ztschr. /. klin. Med., Berlin, 1912, Ixxiv, 230-269.
Die Sphygmobolometrie, eine neue Untersuchungsmethode der Zirkulation.
Deutsche med. Wchnschr., Leipzig u. Berlin, 1907, xxxiii, 628-672.
The latest form of the pneumatic sphygmobolometer. Tr. Internal. Ccng.
Med.,1913, London, 1914, Sect. VI, Medicine, pt. ,
Christen's Energometry. — The energometer of Christen consists of a cuff,
which is applied to the calf of the leg or the upper arm, a special manometer, a
pump, and a syringe with piston — all connected with one another. By means of
the pump, a definite pressure is produced within the cuff, after which the pump
is clamped off and the excursions of the tonometer needle noted. Enough air is
now injected into the cuff with the syringe to displace the oscillations -of the
tonometer needle by about their own amplitude, that is, so that the needle at every
pulse beat oscillates between two limits, of which the lower had been (before the
air was injected) the higher limit of the oscillation. The volume of air used for
this purpose is read off on the scale of the syringe; it is equal to the systolic
increase of volume of the arteries under the inflated cuff. By multiplying this
volume by the mean pressure within the cuff, one obtains the "work" in gram-
centimeters performed by the pulse wave. Such a measurement can be made for
a series of different pressures within the cuff; in each instance, the energy (E) is
equal to the pressure (P) multiplied by the volume (V) ; that is, E = PV.
By plotting these pressures and their corresponding volumes in one curve, and
the pressures and their corresponding energies in another curve, we get two curves
known as "dynamic diagrams," which represent the volumes and the energies as
functions of the pressure. In drawing the curves, the pressures are plotted as
abscissae, and the volumes and energies as ordinates.
The dynamic curves may be characteristic in certain pathological states, espe-
cially in aortic insufficiency, in arteriosclerosis, and in cachectic states.
References
Christen (T. F.}. Dynamic diagrams of the pulse. Internal. Clin., Philadelphia, 1911,
21. s., Hi, 92-99.
Christen (Theodor). Die dynamische Pulsuntersuchung. Leipzig, 1914, F. C. W. Vogel.
172 p. 8°.
Christen (T.). Die neuen Methoden der dynamischen Pulsdiagnostik. Ztschr. f. klin.
Med., Berlin, 1911, Ixxiii, 55-102.
Neue Experimente zur dynamischen Pulsdiagnostik. Deutsches Arch. f.
klin. Med., Leipzig, 1913, ex, 382-888.
Die dynamische Pulsuntersuchung. Uebersichtsartikel. Zentralbl. f.
Herz- u. Gefasskrankh., 1914, 225-230.
Die Fiillung des Pulses und das Pulsvolumen. Deutsches Areh. f. klin.
Med., Leipzig, 1915, cxvii, 111-126. [Entgegnung von H. Sahli], 155-174.
The method of Sahli and that of Christen are of considerable promise
for research work. It is too early, as yet, however, to say how valuable
they will prove to he in practical clinical work.
Attempts such as the ahove to determine changes in the work of the
FUNCTIONAL CAPACITY OF THE HEART 819
heart and the peripheral resistance are laudable; but we deal here with
such complicated relations that too much stress should not be laid, as yet,
upon the results that they yield. The time may come when we shall be
able to attain more nearly than we can at present to the ideal toward which
this work tends. In atherosclerosis and in valvular diseases of the heart,
especially, efforts at determination of the work of the heart based upon
blood-pressure measurements are liable to error.
SECTION II
DIAGNOSIS OF THE SPECIAL DISEASES OF THE HEAET
AND BLOOD VESSELS
The circulatory system, like the other systems of the body, is suscep-
tible to a variety of diseases. Those, involving the heart include :
(1) Disturbances of development (congenital heart disease).
(2) Retrogressive disturbances of nutrition (atrophies and degenera-
tions).
(3) Circulatory disturbances (infarctions, thromboses, diseases of the
coronary arteries, aneurism of the heart).
(4) Inflammations of the heart as a whole (carditis), of the lining
membrane of the heart (endocarditis), of the heart muscle (myocarditis)
or of the pericardium (pericarditis). These inflammations give rise to
acute inflammatory cardiopathies and, later on, to chronic inflammatory
cardiopathies.
(5) Reparative and adaptive processes in the heart (hypertrophy,
dilatation).
(6) Alterations in the position and shape of the heart.
(7) Foreign bodies and parasites in the heart.
(8) Tumors of the heart.
Only the more important of these can be considered here. For the
others, special monographs should be consulted.
Before proceeding to the more systematic study of the diseases of the
heart, certain gross disturbances of cardiovascular function must be dis-
cussed, namely, (1) Certain Clinical Disorders of the Heart Beat and (2)
Acute and Chronic Circulatory Insufficiency.
A. Clinical Disorders of the Heart Beat
1. Introduction
Among the commonest of clinical phenomena met with by practitioners
are derangements of the rate, sequence, and force of the pulse and of the
heart beat. They include the tachycardias, the bradycardias, the cardiac
arhythmias, and the alternating heart. The analysis of these disturbances
&2O
CLINICAL DISOEDEES OF THE HEAET BEAT 821
lias made great progress since 1870. We owe the progress partly to ad-
vances in experimental physiology, partly to careful clinical studies, espe-
cially those involving the use of graphic methods (sphygmography, electro-
car diography).
The functions of the cardiac musculature include (1) the power of ini-
tiating primary stimuli at regular intervals (automatic rhythmicity), (2)
the power of responding to stimuli (excitability), (3) the power of con-
ducting stimuli (conduction capacity), (4) the power of contractility.
Influences, neural or other, that affect these several functions, have been
given special names. Thus, influences affecting the automatic rhythmicity
are known as chronotropic ; those affecting the excitability, as bathmo-
tropic ; those affecting the conductivity, as dromotropic ; and, finally,
those affecting the contractility, as inotropic.
Methods of graphic registration are of great importance in the un-
ravelling of the mysteries of cardiac irregularities. They further afford
us a means of checking, and consequently of improving, our ordinary
methods of physical diagnosis in these types of cases. Working with Drs.
Hirschfelder, Bond, and Bridgman, I have had manifold opportunity
during the past ten years to convince, myself of the great clinical value of
these methods. Arteriograms and phlebograms should always be taken
simultaneously for comparative study, in analyzing any form of irregu-
larity, though, when electrocardiograms are available, the sphygmographic
tracings may usually be dispensed with. Most of the beautiful electro-
cardiograms that illustrate this section of the book were taken by Dr.
George S. Bond in the Heart Station at the Johns Hopkins Hospital; a
few of them were taken by Dr. Bridgman.
For analysis of the curves obtained, the various forms of cardiac
arhythmia may be grouped under different headings, depending upon the
causal factors that produce each one.
2. Classification of the Cardiac Arhythmias
The following classification serves as a good working basis :
I. Sinus irregularities.
(a) Phasic variations in rate.
1. Associated with respiration.
2. Not associated with respiration.
(b) Dropped beats.
II. Abnormal impulses arising in the heart.
(a) Extrasystoles.
1. Ventricular.
822 DISEASES OF THE CIKCULATOKY APPAKATUS
2. Atrial (or auricular).
3. Nodal.
(b) The paroxysmal tachycardias.
(c) Atrial (or auricular) fibrillation.
(d) Atrial (or auricular) flutter.
III. Changes in contractile force.
(a) Pulsus alternans.
IV. Disturbances in the conduction system in the heart (heart block) .
(a) Disturbances of the atrioventricular conduction-path.
1. Slowed conduction.
2. Partial block.
3. Complete block.
(b) Disturbances of the intraventricular conduction-path.
References
1. Anatomical
Albrecht (E.). Der Herzmuskel und seine Bedeulung fiir Physiologic, Pathologic und
Klinik des Herzens [etc.]. Berlin, 1903, J. Springer. 607 p. 8°.
Cohn (A. #.). On the auriculo-nodal junction. Heart, London, 1909-10, i, 167-176.
Observations on injection specimens of the conduction system in ox hearts.
Heart, London, 1913 ', iv, 225-228.
Cullis (W.) & Tribe (E. M.). Distribution of nerves in the heart. J. PhysioL, Cam-
bridge, 1913, xlvi, 141-150.
Flack (M.) . An investigation of the. sino-auricular node of the mammalian heart. J. Physiol.,
London, 1910, xli, 64~77.
Keith (A.). On the evolution and action of certain muscular structures of the heart. Lancet*
London, 1904, i, 555; 629; 703.
Keith (A.) & Flack (M. W.). The auriculoventricular bundle cf the human heart. Lancet,
London, 1906, ii, 859-364.
The form and nature of the muscular connections between the primary
divisions of the vertebrate heart. J. Anal. & PhysioL, London, 1906-7,
xli, 172-189.
Kent (A. F.). A neuro-muscular mechanism in the heart. [Discussion]. Tr. Internal.
Cong. Med., 1813, London, 1914, Sect. I, Anat. & Embryol., pt. 2, 16-22.
Kent (A. F. S.). Observations on the auriculoventricular junction of the mammalian heart.
Quart. J. Exper. PhysioL, London, 1913, vii, 193-195.
Ktilbs (F.). Das Reizleitungssystem im Herzen. Berlin, 1913, J. Springer. 28 p.
MacCallum (J. B.). On the muscular architecture and growth of the ventricles of the heart.
Contrib. Sc. Med. Pupils of W. H. Welch, Baltimore, 1900, 307-385.
McFarland (J.) & Anders (A.). The morbid histology of the cardiac nervous ganglia. J.
M. Research, Boston, 1913, xxvii, 425-435.
Mall (F. P.). On the muscular architecture of the ventricles of the human heart. Am. J.
Anat., Philadelphia, 1911, xi, 211-266.
Mathewson (G. /).). Lesions of the branches of the auriculoventricular bundle. Heart,
London, 1913, iv, 385-390.
Meiklejohn (J.). On the innervation of the nodal tissue of the mammalian heart. J. Anat.
& Physiol., Lond., 1913, xlviii, 1-18.
CLINICAL DISORDERS OF THE HEART BEAT 823
Morison G4.). The auriculoventricular node in a malformed heart, with remarks on its
nature, connections and distribution. J. Anat. & PhysioL, Lond;, 1913,
xlvii, 459-478.
Renon (L.) & Geraudel (E.). Comment examiner lefaisceau de His? Tr. Internal. Cong.,
1913, London, 1914, Sect. Ill, Gen. Path. & Path. Anat., pt. 2, 113-118.
Retzer (JR.). Some results of recent investigations on the mammalian heart. [Abstr.] Anat.
Record, Baltimore, 1908-9, ii, 149-155.
Tawara (<S>.). Ueber die sogenannten abnormen Sehnenfdden des Herzens; ein Beitrag zur
Pathologie des Reizleitungssystems des Herzens. Beitr. z. path. Anat. u.
z. allg. Path., Jena, 1906, xxxix, 563-584.
Das Reizleitungssystem des Sdugetierherzens. Eine anatomisch-histol-
ogische Studie liber das Arterioventricularbundel und die Purkinjeschen
Fdden. Mil einem Vorwort von L. Aschoff. Jena, 1906, G. Fischer.
209 p. 8°.
Thorel (C.). Pathologie der Kreislauforgane des Menschen. In: Ergebn. d. allg. Path,
u. path. Anat. [etc.] (Lubarsch & Ostertag), Wiesbaden, 1911, xiv, Abt. ii.
133-711.
Wilson (J. G.). The nerves of the atrio-ventricular bundle. Proc. Roy. Soc., London, 1909 9
s. B., Ixxxi, 151-154.
2. Physiological
Auer (J.). Anaphylactic alterations of the heart. [Abstr.] Proc. Path. Soc., Philadelphia
1914, xvi, 34-36.
Bond (G. S.). The relation of the auriculo-ventricular region to the sequence of contraction
of the heart. Heart, London, 1912-13, iv, 1-3.
Boothby (W. M.). A determination of the circulation rate in man at rest and at work. The
regulation of the circulation. Am. J. PhysioL, Baltimore, 1915-16, xxxvii,
383-417.
Carlson (A. /.). Vergleichende Physiologic der Herznerven und der Herzganglien bei den
Wirbellosen. In: Ergebn. d. PhysioL (Asher & Spiro), Wiesbaden, 1909,
viii, 371-462.
Cohn (A. E.}. On the differences in the effects of stimulation of the two vagus nerves on rate
and conduction of the dog's heart. J. Exper. M., Lancaster, Pa., & New
York, 1912, xvi, 732-757. 8 pi.
The effect of morphine on the mechanism of the dog's heart after removal of
one vagus nene. J. Exper. M., Lancaster, Pa., 1913, xviii, 715-738. 5 pi.
Observations on injection specimens of the conduction system in ox hearts.
Heart, London, 1912-13, iv, 225-228. 1 pi.
The production of reversed cardiac mechanism in the dog.- Proc. Soc. Exper.
Diol. & Med., New York, 1912-13, x, 36.
Cohn (A. E.} & Kessel (Leo). The function of the sino-auricular node. Arch. Int. Med.,
Chicago, 1911, vii, 226-229.
Cushny (A. R.). On periodic variations in the contractions of the mammalian heart. J.
PhysioL, London, 1899-1900, xxv, 49-62.
Erlanger (Joseph). The localization of impulse initiation and conduction in heart. Arch.
Int. Med., Chicago, 1913, xi, 334-364,
Eyster (J. E.) & Meek (W. J.). The path of conduction between the sino-auricular and
auriculo-ventricular nodes. Am. J. PhysioL, Baltimore, 1914-15, xxxvit
367.
Fahr (G.) & Weber (A.}. Ueber die Ortsbeslimmung derErregung im menschlichen Herzen
mil Hilfe der Elektrokardiographie. Deutsches Arch. f. klin. Med., Leip-
zig, 1915, cxvii, 361-396.
824 DISEASES OF THE CIECULATOEY APPAKATUS
Fredericq (H.). Les f auctions des nerfs accelerateurs du coeur et les modifications qu'elles
eprouvent sous ^influence de divers agents therapeutiques. Arch, internal,
d. physiol, 1913, xiii, 115-125.
Qu'est-ce que la contraction cardiaque? fjtude de physiologic humaine et
de physiologie comparee. Biologica, Paris, 1913, Hi, 298-308.
Ganter (G.) & Zahn (A.). Ueber die Beziehungen der Nerti vagi zu Sinusknoten und
Atrioventrikularknoten. 'Arch. f. d. ges. Physiol., Bonn, 1913, cliv, 492-
514.
Zur Lokalisation der automatischen Kammerzentren. Zentralbl. f. Physiol.,
Leipz. u. Wien, 1913, xxvii, 211-213.
Gaskell (W. H.}. The contraction of cardiac muscle. Text-book of Physiol. (Schdfer),
Edinburgh & London, 1900, ii, 169-227.
Hering (H. E.). Zur experimentellen Analyse des unregelmdssigkeiten des Herzschlages.
Arch. f. d. ges. Physiol., Bonn, 1900, Ixxxii, 1-33.
Howell (W. H.). The cause of the heart beat. J. Am. M. Ass., Chicago, 1906, xlvi, 1665;
1749.
On the relation of the blood to the automaticity and sequence of the heart-
beat. Am. J. Physiol., Boston, 1898-99, ii, 47-81.
Kiilbs (F.}. The excitatory and connecting muscular system of the heart; das Reizleitungs-
system des Herzens. Tr. Internal. Cong., 1913, London, 1914, Sect. I,
Anat. & Embryol., pt. 2, 1-26.
Lewis (T.}. Galvanometer curves yielded by cardiac beats generated in various areas of the
auricular musculature. The pace-maker of the heart. Heart, London,
1910-11, ii, 23-40.
The mechanism of the heart beat. New York, 1914, P. B. Hoeber. 295 p.
The pacemaker of the mammalian heart. Tr. Internal. Cong., 1913,
London, 1914, Sect. I, Anat. & Embryol., pt. 2, 105-119.
A method of measuring the rate of transmission of the contraction wave in
the dog's auricle. Heart, London, 1913-14, v, 21-24-
Lewis (T.}, Meakins (J.) & White (P. />.)• The excitatory process in the dog's heart.
Phil. Trans. Roy. Soc., London, 1914, ccv, 375-420.
Lewis (T.}, Oppenheimer (B. S.) & Oppenheimer (Adele). The site of origin of the
mammalian heart-beat; the pace-maker in the dog. Heart, London,
1910-11, ii, 147-169.
Loeb (J.) & Ewald (W. F.). Die Frequenz der Herztdtigkeit als eindeutige Funktion der
Temperatur. Biochem.Ztschr., Berlin, 1913, Iviii, 177-185.
Loevenhart (A. ' S.) & Eyster (J. A. E.). The effect of certain oxidizing substances and
of acids and alkalies on the isolated mammalian heart. J. Pharmacol. &
Exper. Therap., Baltimore, 1913, v, 21-55.
Mackenzie (J.). The excitatory and connective muscular system of the heart. (A study in
comparative anatomy.) Tr. Internal. Cong., 1913, London, 1914, Sect. I,
Anat. & Embryol., 121-150. 10 pi.
Martin (E. G.). On the relation of the blood salts to cardiac contraction. Am. J. Physiol.,
Boston, 1913, xxxii, 165-183.
Mines (G. R.}. On dynamic equilibrium in the heart. J. Physiol., Cambridge, 1913,
xlvi, 349-383.
Moorhouse (V. II. K.). The action of various influences upon the rhythmicity of the nodal,
sinus, and auricular musculature of the mammalian heart. Am. J.
Physiol., Boston, 1913, xxxi, 421-438.
Robinson (G. C.) & Auer («/.)• Disturbances of the heart-beat in th<>, dog caused by serum
anaphylaxis. Tr. Ass. Am. Phys., Philadelphia, 1913, xxviii, 545-571.
Rothberger (C. J.) & Winterberg (H.). Ueber den Einfluss von Strophanthin auf die
Reizbildungsfdhigkeit der automatischen Zenlren des Herzens. Arch. /.
d. ges. Physiol., Bonn, 1913, cl, 217-261.
CLINICAL DISORDERS OF THE HEART BEAT 825
Schlomovitz (B. H.), Eyster (J. A. E.) & Meek (W. /.)• Experiments on the origin and
conduction of the cardiac impulse. V. The relation of the nodal tissue to
the chronotropic influence of the inhibitory cardiac nerves. Am. J. Physiol.,
Baltimore, 1915-16, xxvii, 177-302 .
Stewart (G. N.). Einfluss der Herztemperatur auf die Tatigkeit der Hemmungsnerven des
Herzens. Ztschr. f. Biol., Miinchen, 1913, lix, 531-560.
von Tabor a (D.). Anomalien der Schlagfolge und Schlagfrequenz des Herzens. Handb. d.
allg. Pathol. (Krehl & Marchand) , Leipzig, 1913, ii, 2, 112-129.
Tiger stedt (/?.)• Die chemischen Bedingungen fur die Entstehung des Herzschlages. In:
Ergebn. d. Physiol. (Asher & Spiro), Wiesbaden, 1912, xii, 269-314.
Zahn (A.). Experimentelle Untersuchungen ueber Reizbildung und Reizleitung im Atrio-
ventrikularknoten. Arch. f. d. ges. Physiol., Bonn, 1913, cli, 247-278.
Zwaardemaker (H.). DieEnergetik der autochthon periodischenLebenserscheinungen. In:
Ergebn. d. Physiol. (Asher & Spiro), Wiesbaden, 1908, vii, 1-26.
3. General Clinical
Allbutt (Sir C.). Functional disorders of the heart. In: Syst. Med. (Allbutt & Rolleston).
8°. London, 1909, vi, 493-546.
Barton (W. M.}. Non-technical differentiation of cardiac arhythmias. South. M. J.t
Nashville, 1915, viii, 20-23.
Cabot (R. C.). The diagnosis of cardiac disease. Long Island M. J., Brooklyn, 1913, vii,
379-387.
The four common types of heart disease; an analysis of six hundred cases.
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Kinderh., Berlin, 1908, ii, 418-441-
Gibson (G. A.). The nervous affections of the heart. Edinburgh & London, 1904 , Y. J.
Pentland. 108 p. 8°.
Hart (T« S.). The diagnosis of abnormalities of myocardial function. Arch. Diagn., New
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Hewlett (A. 17.). The common cardiac arrhythmias and their clinical significance. In-
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Handb. d. allg. Pathol. (Krehl & Marchand), Leipzig, 1913, ii, 2, 1-129.
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826 DISEASES OF THE CIECULATOKY APPARATUS
Wenckebach (Karl Friedrich). Die unregelmassige Herztdtigkeit und ihre klinische
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i, 65-84.
Die Arhythmie als Ausdruck bestimmter Functionsstorungen des Herzens.
Leipzig, 1903, W. Engelmann. 193 p. 7 pi.
3. Common Examples of Cardiac Arhythmia
A rough idea of the majority of these disturbances can be quickly
arrived at by any general practitioner who will appeal to his personal
experience in palpating the pulse of patients. Thus, (1) he will recall that
on feeling the pulse of young persons, he has often noticed a difference in
the pulse rate in the two phases of respiration; this is an example of a
sinus arhythmia. He will remember (2) instances in which the pulse
occasionally interrpits, and on listening over the heart ho will have noticed
that such an intermittence is associated with a cardiac contraction occur-
ring before a regular beat is due and that this early contraction is followed
by a pause longer than the ordinary pause between two beats ; this is an
example of a premature beat, or so-called extrasystolic irregularity.
Again, he may recall (3) instances in which the pulse of a patient has
suddenly doubled its rate; the rapid pulsation has continued for a time,
and has then abruptly ceased. The patient complains that such attacks of
rapid heart recur from time to time; this is an example of paroxysmal
tachycardia.
Occasionally, he may encounter (4) an elderly person in whom the
pulse rate is continuously accelerated (120-160 per minute) though there
is no exophthalmic goiter, and the pulse is not irregular; such a tachy-
cardia is usually due to atrial (or auricular) flutter.
More often, he will have noticed (5) in patients who have long suf-
fered from disease of the mitral valve, the onset of a "perpetually irregular
pulse/' an "utterly disordered heart action," in which the pulse rate is '
accelerated, but there is no regularity of sequence of the beats whatever,
and the patient shows signs of cardiac decompensation; this clinical pic-
ture is characteristic of atrial (or auricular) fibrillation.
In some patients, especially in those with high blood pressure, he may
have noticed (6) that the pulse beats at the wrist, though rhythmical, vary
in force, the beats being alternately strong and weak; this is an example
of pulsus alternans.
Finally, he may have seen (7) one or more patients in whom the pulse
at the wrist is regular but only 30 or 35 per minute, though on looking at
the jugular vein in the neck, three or four small regular pulsations are seen
to occur between two carotid pulses ; this is an example of complete heart-
block.
Such typical disturbances are recognizable without the use of graphic
methods, hut, in clinical work, we often have to unravel phenomena that
CLINICAL DISOKDEES OF THE HEAET BEAT 827
are far less differentiate, and then we must resort to sphygmography,
to electrocardiography, or to both, to arrive at a satisfactory diagnosis.
The simple examples given above may serve as paradigms for the classes
of disturbances now to be considered.
4. Sinus Irregularities
(a) Phasic Variations in Rate
The small portion of tissue at the junction of the superior vena cava
with the. right atrium (the so-called "sinus region") is the point at which
the cardiac rhythm normally originates, and this sino-auricular node
(Keith and Flack) has been termed "the pacemaker of the heart" (T.
Lewis. ) The rapidity at which
the stimulus to cardiac contrac-
tion is initiated at this point is
subject to the controlling influ-
ence of the vagUS and the Sym- Fig. 238. — Phlebogram and Arteriogram in the
pathetic nerves. In normal MackeSie TJP<H °H B^f)1""7' ^"^ J'
adults, the balance between the
inhibiting or slowing influence of the vagi and the accelerating influence
of the sympathetic is well preserved, and the heart rate remains constantly
about 72 when a person is at rest. In children, however, or in adults whose
nervous systems are unstable from any cause (infections, toxemias, etc.),
the heart rate will fluctuate with every change of vagal tone. This is most
often associated with the phases of respiration, but, occasionally, the
change in rate may have no relation to respiration as in the youthful irreg-
ularity (Mackenzie).
The arteriograms, phlebograms and electrocardiograms in this form of
irregularity all present characteristic features. (Fig. 238). This form
of arhythmia is easily recog-
nized by the periodic variation
in the rate of the heart when a
rather long stretch of a sphyg-
mographic or an electrocardio-
graphic curve is examined.
There is first a series of beats
in which diastole becomes long-
er and longer, and this is fol-
lowed by a series of quickened
beats with shortened diastole.
When the arhythmia is associ-
ated with the phases of respiration (pulsus irregularis respiratorius) the
longer intervals between beats usually occur during expiration and the
shorter ones during inspiration. Most irregularities of the heart in chil-
Expiration
Retplralory arrbyttmla.
Fig. 239. — Phlebogram and Arteriogram in Pulsus
irregularis respiratorius. (After A. W. Hew-
lett, J. II. II. Bull.)
828 DISEASES OF THE CIKCULATOKY APPAEATUS
dren before puberty are sinus arhythmias. These arbythmias disappear if
the heart rate be accelerated by exercise, by fever, or by the administration
of drugs, like atropine, that paralyze the vagus.
Fig. 240. — Electrocardiogram in Sinus Arhythmia. Respiratory Form. Note the Marked
Variation in Rate with the Phases of Respiration. There is no Change in the Form of
Contraction of the Heart, as is Shown by the Normal Type of Electrocardiographic Curve.
(&) Dropped Beats
This is another form of sinus arhythmia, occasionally met with. It
may also be due to vagus inhibition, or it may result from an actual change
in the sinus region itself. It is characterized by a complete absence of
Fig. 241. — Electrocardiogram of Dropped Beats. As Shown in this Electrocardiogram, a
Complete Cardiac Contraction is Missing in a Rhythm, Otherwise Normal. This may
be Due to a Sino-auricular Block, or to Lack of Stimulation in the Sinus Itself.
contraction of the whole heart (standstill) for a period lasting through one
or more cardiac revolutions. All forms of graphic registration point out
that the entire heart is quiescent during this pause (Fig. 241).
References
Cohn (A. £".). Experiments dealing with the relation of the sinus node to the effects of stimu-
lation of the vagus nerves. Proc. Soc. Exper. Biol. & Med., New York,
1913-14, xi, 108.
Vaquez (£T.). Arhythmie respiratoire et ses formes diniques. Bull, et mem. Soc. med. d.
hCp.de Paris, 1909, 3. s., xxviii, 732-737.
(F. N.}. Three cases showing changes in the location of the cardiac pacemaker asso-
ciated with respiration. Arch. Inter. M., Chicago, 1915, xv, 86-97,
CLINICAL DISOKDEKS OF THE HEAET BEAT 829
5. Arhythmias Dependent upon Abnormal, Premature
Impulses Arising in the Heart
(a) Extrasystolic Arhythmias
Normally when an impulse originates in the "pacemaker," it passes,
thence, in regular sequence, through the other cardiac chambers. This
regular order is due to the fact that each succeeding portion of the heart
muscle traversed by the impulse has an independent rhythmicity, which is
slower than that of the preceding one, and, consequently, it receives a
stimulus conducted from above and responds to it before it can initiate its
own automatic impulse and contraction. However, when the irritability
of any part of the heart is increased, it may release a spontaneous contrac-
tion, itself, before it receives a regular stimulus from the superior part.
This phenomenon has been termed aheterogenetic beat/7 a "premature
contraction/' or "an extrasystole." Such new and isolated impulses may
originate in any portion of the cardiac musculature — in the atria, in the
ventricles, or in any part of the conducting system between the atria and
the ventricles. They are classified, according to their point of origin, as
(1) atrial, (2) ventricular, and (3) nodal extr asystoles. Such extrasys-
tolic contractions of the heart, occurring before the regular, normal time,
disturb markedly the normal order of the mechanism of the heart.
TO
Fig. 242. — Diagram of Disturbance Produced by a Ven-
tricular Extrasystole (/>). Note that the Atrium
Beats Regularly Throughout. The Ventricle Re-
sponds to Six Atrial Impulses, but the Impulse of
the Atrial Systole in the Center of the Diagram is
Lost, for it Falls while the Ventricle is in Prema-
ture Systole. The Break in the Center of the Ven-
tricular Boat Indicates its Abnormal Origin. Note
that the Lengths of Periods (a) and (b) are Equal,
while Period (c) is the "Compensatory Pause."
(From T. Lewis, "Clinical Disorders of the Heart
Beat," published by P. B. Hoeber, New York.)
is not disturbed by the
ventricular action, and atrial systole occurs during, or just after, the
premature systole of the ventricles. In consequence of the latter, the
ventricle is unable to respond to the impulse conducted from the atrium
i. Ventricular Extrasystoles
The term "ventric-
ular extrasystole" is
applied to a premature
beat when it arises in
the wall of one of the
ventricles. The con-
nection, however, be-
tween the two ventri-
cles is so intimate that,
regardless of where this
abnormal stimulus may
originate, both ventri-
cles take part in the
premature contraction.
Usually, the regular
rate of the atrial rhythm
830 DISEASES OF THE CIECULATOEY APPAKATUS
until the succeeding atrial contraction, and there thus results a delay
in the ventricular rhythm following the premature beat. It is known
as the compensatory pause, because the time occupied by (1) the beat
preceding the premature beat, (2) the premature beat itself and (3)
the pause following it, just equals the time of two regular cardiac cycles.
If the extrasystole occurs very early and the atrial rate is slow, the ventri-
cle may be able to respond to the first regular atrial stimulus succeeding it.
In that event, the extrasystole is a true extra beat in the ventricular
rhythm, and is known as an interpolated extrasystole.
zo zo
Fig. 243. — Ventricular Extrasystoles. (After K. 31. Wenckebach, "Arch, dos Maladies du
cceur," published by Bailliere et Fils, Paris.)
Pulse Tracings Illustrating Ventricular Extrasystoles (Fig. 243).—
The premature ventricular contraction, as well as the lengthened diastolic
pause that follows it, are easily recognizable on the cardiogram of the
apex beat.
In the arteriogram of the carotid or of the radial pulse, the premature
contraction may or may not be represented by a wave, depending upon the
strength of the extra-contraction and the amount of blood it has forced into
the aorta. Thus, there may be only a long pause of two cardiac revolu-
tions, or the extrasystole may be marked by a small arterial wave, occui*-
ring early and followed by the compensatory pause.
The phlebogram or jugular tracing shows a single wave coincident with
Fig. 244. — Ventricular Extrasystoles. Extrasystole Shown at E, No a-Wave Precedes.
(Tracing by Dr. A. D. Hirschf elder, J. H. H. Bull.)
the extrasystole, and not preceded by an atrial a-wave. When the regu-
lar atrial systole occurs simultaneously with the ventricular extrasystole,
the single wave on the phlebogram is very large ; it represents a com-
bined venous impulse from both the atrium and the ventricle, and, in it,
the atrial element is magnified, because the atrium has contracted against
CLINICAL DISOEDERS OF THE HEAET BEAT 831
a closed ventricle. Such sphygmographic evidence is sufficient for the
decision that an extrasystole has originated in the ventricles, but the elec-
trocardiogram permits of still further analysis and differentiation.
Electrocardiograms of Ventricular Extrasystoles (Fig. 245). — This
electrical method of registration also points to the features observable by
the other methods just described. Thus, one sees a wave representing the
early ventricular systole. It is not preceded by an atvial wave (P), but
it is followed by a compensatory pause. Furthermore, the wave due to the
premature contraction itself does not assume the usual ventricular type
(Q-R-S-T complex) but is of an anomalous form. In explaining this dif-
ference, one must remember that, in the normal heart beats, all parts of the
ventricular system contract nearly simultaneously, while in the ventricular
extrasystole, the abnormal stimulus arises at some point in either the right
or the left ventricle, and is thence propagated to the remaining parts as a
wave of stimulation and contraction. This extrasystolic type of ventricular
ii
Fig. 245. — Electrocardiograms of Ventricular Extrasystoles. The Ventricular Extrasystole is
Shown by an Electrical Curve that is Entirely Different from that Produced by a Normal
Cardiac Contraction. The Wave is a Single, Large, Diphasic Form, which Indicates
that it is Probably More Like a Wave of Contraction, than Like a Single Contraction of
All Parts of the Muscle Simultaneously.
The Direction that the First Part of the Extrasystole Curve Takes, Indicates the Ventricle
in which it Originated. 'Thus :
I. The Electrical Curve Goes Up First, and Means that the Contraction Started in the Right
Ventricle.
II. This Curve Goes Downward First, and Means that It Originated in the Left Ventricle.
832 DISEASES OF THE CIRCULATORY APPARATUS
contraction, therefore, produces electrical variations in the form of a large
diphasic wave, which consumes about the same period of time in the elec-
trocardiogram as the normal ventricular complex. The initial direction of
this atypical wave is an indication of the portion of the ventricles first
contracting, and permits us to differentiate between extrasystoles begin-
ning in the right from those beginning in the left ventricle. If the
diphasic wave be first upward and then downward, it denotes that the
extrasystole originated in the right ventricle; while if the wave be first
downward and then upward, it originated in the left ventricle.
Patients who suffer from extrasystolic irregularity of this type may
complain of "palpitation," of a feeling "as though the heart turned over in
the chest," or they may notice the long pause following the premature beat
and be uneasy about it. The prognostic importance of ventricular extrasys-
toles depends upon the conditions with which they are associated; these
may be either benign or grave, and, in each case, the condition of the heart
and other organs should be carefully studied before prognostications are
made.
ii. Atrial (or Auricular) Extrasystoles
This term should, strictly speaking, be applied only to those instances
in which there is an early
|P atrial systole and no as-
A sociated ventricular con-
traction following it,
\ \ \ \ \ \ \ However, the term is
^H L» HB HM « ^H M used most frequently in
v another sense, namely, to
H || IH SB IB • | designate what is in real-
* ' """ 5 — ^ ity an atrioventricular
Fig. 246.— Diagrammatic Representation of an Atrial extrasystole. b 6 C a 11 S 6
Extrasystole. The Atrial Rhythm is Disturbed by , / , -, T
the Abnormal and Premature Atrial Beat (p) ; the tnOUgn the abnormal
Disturbance in the Ventricular Rhythm is Parallel, impulse arises in the
for Each Atrial Systole Yields a Ventricular Re- . ...
sponse. The Rhythm of the Whole Heart is Dislo- atrium it IS also COU-
cated, the Period a being Longer than the Period 6. ducted to the Ventricle
(From T. Lewis, "Clinical Disorders of the Heart , . ,
Beat," published by P. B. Hoeber, New York.) wniCil as a rule re-
sponds to it by a con-
traction that succeeds the atrial contraction (Fig. 247).
Pulse Tracings Illustrating Atrial Extrasystoles (Pig. 248). — In
patients manifesting atrial (or auricular) extrasystoles, the cardiograms
and arteriograms show a disturbance of rhythm, due to the premature ven-
tricular contraction that is a part of the extrasystole. This early sys-
tole may be followed by a long pause, but the whole period of the dis-
turbance is not equivalent, as in the case of ventricular extrasystoles, to
two full cycles of normal cardiac rhythm.
CLINICAL DISORDEES OF THE HEART BEAT 833
Z.O
SO 20 3 20 ZO
Fig. 248. — Atrial Extrasystoles. (Tracing by A. D. Hirsch-
f elder, J. H. H. Bull.)
Fig. 247.— (a) Extrasystole Arising in the Atrium or Auricle; (6) Extrasystole Arising in
the Sinus. (After K. F. Wenckebach, "Arch, des Maladies du coeur," published by
Bailliere et Fils, Paris.)
Simultaneous tracings of the venous pulse and of the arterial pulse
easily differentiate t":is
form of extrasystole.
The phlebogram associ-
ated with the prema-
ture beat consists of the
normal double pulsa-
tion made up of the a-,
c-, and t>-waves, but the
distinguishing feature
is the presence, in the extrasystole, of the atrial (a-) wave that indicates its
origin.
Electrocardiograms of Atrial Extrasystoles (Fig. 249). — In an elec-
trocardiogram, the atrial extrasystole is revealed simply by the occurrence,
prematurely, of a cycle of the normal form, all of the waves P, R, and T,
being present in ordinary sequence. In the premature beat, the atrial wave
(P) is subject to variations in form, depending upon the part of the atrium
in which the abnormal stimulus originates. If the extrasystole arise at or
near the sinus region, the P-wave will be of the same type as the atrial
waves of the remaining regular contractions. Should it originate, how-
ever, at any other point in the atrial tissue, the P-wave will be modified in
form. This change is now utilized, clinically, more accurately to localize
the site of origin of atrial extrasystoles.
iii. Nodal Extrasystoles
By nodal extrasystoles are meant premature beats that have their
point of origin in the conduction system between the atria and the muscular
wall of the ventricles, that is, especially in the node of Tawara in the
atrioventricular bundle of His. From this point, the stimulus spreads in
both directions, retrograde to the atria or auricles and downward to the
ventricles, so that atria and ventricles contract almost simultaneously.
834 DISEASES OF THE CIKCULATOKY APPAEATUS
ii
Fig. 249. — Electrocardiogram of Atrial or Auricular Extrasystoles. I. Arising At or Near
the Point of Origin of the Normal Stimulus. This is Shown by the Fact that the
P-Wave that Starts Each Extrasystole is of the Same Form as the Normal P-Wave. In
this Case it is Superimposed upon the T-Wave of the Preceding Contraction, and Increases
the Height of that Wave. II. Arising at Some Other Point in the Auricles than the
Normal Point. The P-Wave of the Extrasystole is Inverted, which Means that the
Contraction of the Auricle was Different in Form from that of the Normal Beats in
the Same Tracing.
Often, however, there is no evidence of an atrial contraction on the curves,
in which event it is impossible to rule out an extrasystole originating
rather high up in the conducting system below the node.
Pulse Tracings of Nodal Extrasystoles (Fig. 250). — In cardiograms,
arteriograms and phlebograms the picture is like that of a ventricular
Fig. 250. — Shows Two Nodal Extrasystoles (a'), the Auricular Waves a' appearing prematurely
and at the same time as the extrasystole in the radial. (After James Mackenzie,
"Diseases of the Heart," published by Oxford Press, London.)
CLINICAL DISOEDEES OF THE HEAET BEAT 835
extr asystole, though, in the jugular tracing, the atrial a'-wave may be dis-
tinguished as a premature wave synchronous with the extrasystole in the
radial pulse.
Electrocardiograms of Nodal Extrasystoles (Fig. 251). — The elec-
trocardiographic method affords the best means of differentiating this
nodal type of extrasystole from that of ventricular origin. In place of the
Fig. 251. — Electrocardiogram of Extrasystole Arising at a Point Somewhere Between the
Auricles and Ventricles (Nodal Extrasystole). The Extrasystole Shown is Not of the
Auricular Type, for it is Not Preceded by a P-Wave. (The T-Wave of the Contraction
Before it is Not Different from those of the Other Normal Beats, and for this Reason
is Probably Not a Combination of P and T.) Neither is it of the Form Usually Seen
in Ventricular Extrasystoles. In Form it is Much Like the Normal Ventricular Complex,
which Indicates that a Large Portion of the Internal Conduction-Mechanism Entered
into its Production. This Means that the Abnormal Stimulus Must have Begun High Up
in the Bundle and was Transmitted to the Ventricle in the Normal Manner.
large diphasic wave of the ventricular extrasystole, the premature beat of
nodal origin gives electrical variations that are more of the form of the
normal ventricular complex. This would indicate that a large portion of
the. internal ventricular musculature must have been included in the abnor-
mal contraction, and, therefore, the stimulus must have originated very
high in the atrioventricular conduction-system. The determination of the
presence of a P-wave on the curve is often quite uncertain, so that it is not
always possible to say that retrograde stimulation (and contraction) of the
atrium has occurred.
ZO
ZO
Fig. 252. — Pulus bigeminus; Each Normal Systole is Followed by an Extrasystole, which
Follows the First at an Interval that is Constant. These are Nodal Extrasystoles.
(After K. F. Wenckebach, "Arch, des maladies du coeur," published by Bailliere et Fils,
Paris.)
836 DISEASES OF THE CIRCULATORY APPARATUS
In all types of extrasystolic irregularity the occurrence of the prema-
ture contractions may follow a regular sequence in relation to the normal
rhythm. Thus, an extrasystole may succeed each regular systole, giving
rise to a "coupled beat" or apulsus bigeminus" of extrasystolic origin. Or
two extrasystoles may follow each regular beat, in which case we speak of a
"triple beating" or "pulsus trigeminus." It should not be forgotten that
"coupled beats" and "triple beating" are not always extrasystolic in origin ;
they may also be met with in heart block (q. v.).
References
Dresbach (M.) & Munford (S. A.}. Interpolated extrasystoles, in an apparently normal
human heart, illustrated by electrocardiograms and polygrams. Heart,
London, 1914, v, 197-216.
Gallavardin (L.). De la realite des extrasystoles ventriculaires retrogrades et de leur asso-
ciation avec des^extrasystoles interpolees au cours d'une bradycardie Male.
Arch. d. malad. d. cceur, etc., Paris, 1913, vi, 625-632.
Her ing (H. E.} & Rihl (/.). Ueber atrio-ventriculare Extrasy stolen. Ztschr. f. exper.
Path. u. Therap., Berlin, 1995-6, ii, 510-524.
Hirschfelder (A. D.) & Eyster (J. A. E.). Extrasystolcs in the mammalian heart. Am.
J. Physiol., Boston, 1907, xviii, 222-249.
Laslett (E. E.). Observations on auricular and nodal (?) extrasystoles. Quart. J. M.t
Oxford, 1913, vi, 209-220.
Mackenzie (/.)• The extra-systole: a contribution to the functional pathology of the primi-
tive cardiac tissue. Quart. J. Med., Oxford, 1907-08, i, 131-149.
Abnormal inception of the cardiac rhythm. Quart. J. Med., Oxford,
1907-08, i, 39-48.
Rihl (/.)• Klinische Beobachtungen ueber Verldngerung der postextrasystole folgenden
Vorhofperioden bei supraventrikularen Extrasystolen, nebst kritischen
Bemerkungen uber die Genese der frequenzhemmenden Wirkung der Extra-
systole auf automatisch tatige Herzabschmitte. Ztschr. f. Exper. Pathol.
u. Therap., Berlin, 1913, 1-19.
Supraventriculdre Extrasystolen mil Ausfall der nachfolgenden Kammer-
extrasy stolen. Ztschr. f. exper. Path. u. Therap., Berlin, 1913, xiv, 480-
495. 2 pi.
Rothberger (C. J.} & Winterberg (H.}. Studien ueber die Bestimmung des Ausgangs-
punktes ventrikuldrer Extrasystolen mil Hilfe des Elektrokardiogramms.
Arch. f. d. ges. Physiol., Bonn, 1913, cliv, 571-598.
Wilson (F. N.). Report of a case showing premature beats arising in the junctional tissues.
Heart, London, 1914-15, vi, 17-22. 2 pi.
(b) The Paroxysmal Tachycardias
These peculiar forms of cardiac activity also indicate abnormal impulse-
formation in some part of the heart. Just as the atria and the ventricles
are capable of producing, when in a state of hyper-irritability, a single
premature contraction in spite of the predominating rhythm, so also they
can initiate a prolonged series of abnormal beats and give rise to a tachy-
cardia. In such forms of tachycardia, the onset, as well as the cessation, of
the attack is very abrupt, and this accounts for the designation "aproxys-
mal" ; this feature distinguishes them from other tachycardias, e. g., those
of Graves's disease, of atrial flutter and of atrial fibrillation. The simple
^ CLINICAL DISOEDEKS OF THE HEAET BEAT 837
paroxysmal tachycardias may be divided, according to the place of origin
of the abnormal rhythm, into atrial, ventricular, and nodal tachycardias.
The heart rate varies between 110 and 200; usually the rate is some-
where between 140 and 190 per minute. One should not rely on the pulse
count at the wrist, but should count the heart rate with the aid of a stetho-
scope. An attack may last from a few seconds to several days ; I knew one
young man whose attacks lasted for two weeks at a time. It may occur at
any age. One of my patients, now over 80 years old, has had attacks since
early childhood.
An interesting point in diagnosis is that the heart rate does not change
when the patient passes from the standing to the recumbent position.
Pulse Tracings and Electrocardiograms in Paroxysmal Tachycardia
(Figs. 253, 254, 255, 256). — If the reader will remember that this condi-
tion represents merely a series of atrial, ventricular or nodal extrasystoles
that follow one another in rapid, regular sequence, and that these impulses
arise in a single focus at some distance from the normal pacemaker, it will
be unnecessary further to discuss the form of the curves obtained by
graphic methods. The atrial form of paroxysmal tachycardia is the com-
monest type ; it shows a rapid repetition of the features that characterize
the individual atrial extrasystole. In the same manner, the ventricular
form of paroxysmal tachycardia is characterized by the rapid recurrence
of ventricular extrasystoles, and the nodal by the rapid recurrence of nodal
extrasystoles.
References
Bouveret (L.). De la tachycardie essentielle paroxystique. Rev. de med., Paris, 1889, ix,
753; 837.
Butterfield (H. G.) & Hunt (G. //".)• Observations on paroxysmal tachycardia. Quart.
J. Med., Oxford, 1914, vii, 209-220.
Cohn (A. E.) & traser (F. R.}. Paroxysmal tachycardia and the effect of stimulation of
the vagus nerves by pressure. Heart, London, 1913-14, v, 93-104. 2 pi.
Groedel (T.)* Ueber paroxysmale Tachycardie insbesondere ueber das Verhalten der Herz-
grosse wdhrend des tachycardischen Anfalles. Ztschr. f. exper. Path. u.
Therap., Berlin, 1909, vi, 796-805.
Hamilton (W. F.). Paroxysmal tachycardia: with a review of four cases. Canad. Med.
Ass. J., Toronto, 1914, iv, 865-870.
Hay (/.)• Paroxysmal tachycardia. Edinb. M. J., 1907, xxi, 40-58.
Herringham (W. P.). Paroxysmal tachycardia in a child. Lancet, London, 1914, i, 785.
Hirschfelder (A. /).)• The functional disturbances in paroxysmal tachycardia. Arch.
Int. Med., Chicago, 1910, vi, 380-387.
Hoffmann (A.}. Die paroxysmale Tachycardie (Anfalle von Her zjagen). Wiesbaden, 1900,
J. F. Bergmann. 215 p. 8°.
Hutchison (JR.) & Parkinson (/.)• Paroxysmal tachycardia in a child aged 2% years.
Brit. J. Child. Dis., London, 1914, xi, 241-246.
Lewis (T.). The experimental production of paroxysmal tachycardia and the effects of liga-
tion of the coronary arteries. Heart, London, 1909-10, i, 98-137.
Paroxysmal tachycardia, the result of ectopic impulse-formation. Hearty
London, 1909-10,1, 262-282.
838 DISEASES OF THE CIKCULATORY APPARATUS
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Fig. 255. — Electrocardiogram in Paroxysmal Tachycardia. Atrial or Auricular Type. Rate
170 per Minute. The Rapid Rate is Shown by the Shortened Diastole, the Auricular
Wave Falling upon the Final Wave of the Preceding Contraction. There is an Inverted
P-Wave, Beginning Each Ton traction of the Heart. This Indicates that the Tachycardia
Arises in the Atria ( Auricles), but at Some Part Other than at the Normal Point of
Origin.
Fig. 25G. — Electrocardiogram in Paroxysmal Tachycardia. Ventricular Type. Rate 230 per
Minute. This Form Consists of a Series of Ventricular Extrasystoles Following Each
Other in Rapid Succession. There is no Sign of any Atrial or Auricular (P) Waves to
be Seen. The First Part of the Wave of Ventricular Contraction is Downward, which
Indicates that the Left Ventricle Contracts First.
Lewis (!T.) & Silberberg (M. />.)• Paroxysmal tachycardia accompanied by the ventricular
form of venous pulse. Quart. J. M., Oxford, 1911-12, v, 5-9.
Parsons-Smith (/?.)• Some types of paroxysmal tachycardia, with special reference to
that of auricular fibrillation. Practitioner, London, 1915, xciv, 533-550.
Peabody (F. IF.). A note on the venous pulse in paroxysmal tachycardia. Arch. Int.
Med., Chicago, 1909, iv, 432-439.
Robinson (G. C.)« Paroxysmal auricular fibrillation. Arch. Int. Med., Chicago, 1914,
xiii, 298-313.
Schmoll (E.). Paroxysmal tachycardia. Am. J. M. Sc., Philadelphia, 1907, cxxxiv,
662-675.
(c) Atrial (or Auricular) Fibrillation
One of the most common forms of cardiac irregularity met with clin-
ically is that in which the ventricular action shows a gross disturbance of
its rhythm. The ventricular contractions follow one another in dis-
orderly fashion and show marked differences in the amount of force
expended. To this form of disturbance of rhythm have been given the
840 DISEASES OF THE CIKCULATOKY APPARATUS
Fig. 257. — Diagram of Atrial (or Auricular) Fibrillation. The
Fibers of the Atria do not Contract Coovdinately or To-
gether. There are Multiple Foci in which Stimuli Orig-
inate. Occasionally, at Very Irregular Intervals, Impulses
Leave the Atria and Stimulate the Ventricles ; Hence
the Rapid and Absolutely Irregular Pulse. (After T. Lewis,
"Clinical Disorders of the Heart Beat," published by
P. Hoeber, New York.)
names: absolute arhythmia, perpetual arhythmia, and pulsus irregularis
perpetuus. Clinically, the disorder is characterized by phenomena depend-
ent upon (1) virtual paralysis of the atria, and (2) persistent irregularity
of the ventricles. It
i ^ »- jfT-fr'i--"'* ^ ~-_-~ ^ - --_ -~~- _r -^r_--_---_ *s on^y in recent
A ^^^^^f^^^^-^^^?^^ ^-^^'i years that it has
5- =^fr^~^f^f^ V-^ ^-^-^r^r--^ ^r=z-£-x z* been demonstrated
that this condition is
associated with an
abnormal form of
contraction of the
atria, known as
atrial (or auricular)
fibrillation. The
muscle of the atria,
after a long period
of stress, may cease
to contract as a co-
ordinate unit and the individual muscle-bundies then begin to contract
independently of one another. These independent contractions originate
at multiple foci in the atria, and some are ocurring throughout the entire
cardiac cycle. The stimuli, arising at all these points in the atria, are con-
ducted in a "rapid and haphazard" way to the ventricles, and, thus, the
ventricles are continuously bombarded with stimuli of varying strength ;
to these they respond at irregular intervals. The times of the ventricular
contractions depend upon the relations between the strength of stimuli
received and the time interval after preceding ventricular contractions.
Pulse Tracings in Atrial Fibrillation (Fig. 258). — Arteriograms and
cardiograms show that the ventricular contractions are of increased fre-
quency, and are very irregular in force and in rhythm.
The venous pulse as studied in phlebograms is found, usually, to exhibit
a single, broad wave co-
incident with each ven-
tricular systole; it is
the so-called "ventricu-
lar" or "positive" ve-
nous pulse (q. v.). The
absence of the normal
atrial contraction is
shown by the absence
of the a-wave, and, in
a few instances, the fact
that the atria are fibrillating is evidenced by small undulations in the
diastolic pauses.
Fig. 258. — Phlebogram and Arteriogram in Pulsus irregu-
laris perpetuus with Atrial Paralysis. (Personal Ob-
servation, J. H. H. Bull.)
CLINICAL DISOEDEKS OF THE HEAET BEAT 841
Electrocardiograms in Atrial Fibrillation (Fig. 259). — Theelectro
cardiographic method of registration yields a very striking and character-
istic picture in this condition. A ventricular complex (R- and T-wave)
marks each ventricular contraction, and the unequal spacing of the ven-
tricular complexes certifies to the irregularity of the ventricular rhythm.
The ventricular complex often shows variations in form in successive beats,
an indication that the ventricles do not alwavs contract in the same man-
.'-'-'— UW--'
Fig. 259. — Electrocardiograms in Atrial (or Auricular) Fibrillation and Flutter. In Auricu-
lar Fibrillation and Flutter the Main Features are, Complete Absence of the P-Wave,
Marked Irregularity of the Ventricle (Shown by the .R-Wave), and an Almost Constant
Vibration of the String, Caused by the Fibrillating Auricle. A, Fine Type. Here the
Waves are Small and Very Rapid. B, Coarse Type. The Waves in this Form are Much
Larger and Slower. The Fibrillation Waves Vary Greatly In Size and Form, as well as
in Time. C, Auricular Flutter. In this we See a Distinct Regularity in Size, Form,
and Time of the Auricular Oscillations.
842 DISEASES OF THE CIKCULATOKY APPAEATUS
ner. The atrial wave (P), seen in the electrocardiogram of the normal
heart, is here absent because there is no distinct coordinated atrial contrac-
tion. It is replaced by many small oscillations that continue throughout
both systole and diastole, and which are caused by the fibrillary contrac-
tions of the atria. These fibrillary waves have been divided into three
classes: (1) fine fibrillation, where the waves are extremely rapid and
minute; (2) coarse fibrillation, in which the oscillations are larger, though
quite irregular in form and size and (3) atrial flutter, characterized by
rather large uniform undulations and a regular rhythm. This last form
deserves separate consideration (See below). The pulse rate in patients
with atrial fibrillation varies usually between 80 and 150.
The condition may occur at any age, and is much more common in
males than in females. It is always associated with serious lesions of the
myocardium. It is very often associated with valvular lesions, and when
it occurs in women, it is most often associated with mitral stenosis; as
Thomas Lewis puts it, "mitral stenosis and auricular fibrillation are bosom
companions." In about half the cases, a history of rheumatic fever is
obtainable. Of the non-rheumatic cases, other infections, especially lues
and influenza, are common antecedents ; but atrial fibrillation may develop
in any one of several different forms of myocardial degeneration ; I have
met with several instances in the thyreotoxic heart.
Patients with atrial fibrillation nearly always show signs, and complain
of the symptoms, of cardiac decompensation with chronic circulatory in-
sufficiency (q. v.).
The occurrence of atrial fibrillation in mitral lesions is often the cause
of diagnostic blunders. As T. Lewis has pointed out, a murmur of mitral
stenosis that originally extends through the whole diastole of the shorter
cycles, "is replaced, as the heart slows, by an early diastolic murmur that
is maximal in the region of the apex. It is the last murmur that so fre-
quently misleads the physician and suggests to him an insufficiency of the
aortic valves." When mitral stenosis and atrial fibrillation aare present in
the same patient and the heart rate is slow, an early diastolic murmur most
clearly audible at the apex but often spreading beyond it, is an expected
sign. A diagnosis of aortic reflux is never justifiable when the heart is
grossly irregular and slow, unless unequivocal signs of it are present apart
from such a murmur."
It is in cases of atrial fibrillation that drugs of the digitalis group yield
their most brilliant benefits. A heart rate above 100 in atrial fibrillation
is an indication for digitalis, or strophanthin, in amounts sufficient to slow
the rate to 80 or lower. Patients with atrial fibrillation and outspoken
tachycardia who do not respond to rest and to digitalis properly adminis-
tered are in grave danger.
When the atria once begin to fibrillate, the condition is, as a rule, per-
manent (perpetual arhythmia). But cases of paroxysmal fibrillation are
CLINICAL DISOKDEKS OF THE HEAET BEAT 843
known and are often confused with simple paroxysmal tachycardia. The
electrocardiogram quickly differentiates between the two conditions.
References
Allen (H. W.). Auricular fibrillation. Calif. State J. M., San Francisco, 1913, xi, 496-
499.
Arndt (/.). Perpetuierliches Vorhofflimmern bei permanenter Kammer automatic. Eine
klinische Beobachtung auf dem Grenzgebiete des kompletten Herzblocks und
der Arhythmia perpetua. Ztschr. f. klin. Med., Berlin. 1913. Ixxviii, 526-
542.
Berger (F.). Anatomische Untersuchungen des Herzens bei Pulsus irregularis perpetuus.
Deutsches Arch. f. klin. Med., Leipzig, 1913, cxii, 287-301.
Clarac (G.)« L'arythmie complete. Paris, 1913. J. B. Balliere. 234 P- 8°.
Cohn (A. E.} & Heard (J. D.). A case of auricular fibrillation with a post-mortem examina-
tion. Arch. Int. Med., Chicago, 1913, xi, 630-640.
Cushny (A. /2.) & Edmunds (C. W.). Paroxysmal irregularity of the heart and auricular
fibrillation. Am. J. M. Sc., Philadelphia & New York, 1907, cxxxiii,
66-77.
Carrey (W. E.). The nature of fibrillary contraction of the heart. Its relation to tissue mass
and form. Am. J. Physiol, Boston, 1914, xxxiii, 397-414.
Gossage (A. M.) & Hicks (J. A. B.). On auricular fibrillation. Quart. J. M., Oxford,
1913, vi, 435-440.
Heitz (/.). La forme paroxystique de Varythmie complete. Caracteres cliniques — evolution.
Ann. de med., Paris, 1914, i, 483-524.
Hering (H. E.). Ueber den Pulsus irregularis perpetuus. Deutsches Arch. f. klin. Med.,
Leipzig, 1908, xciv, 185-204.
Hertz (J.) & Clarac (G.). La mort subite dans Varythmie complete. Arch. d. malad. d.
ccsur, etc., Paris, 1913, vi, 175-190.
Hewlett (A. W.} & Wilson (F. N.). Coarse auricular fibrillation in man. Arch. Int.
Med., Chicago, 1915, xv, 786-792.
Hirschfelder (A. D.). Contributions to the study of the auricular fibrillation, paroxysmal
tachycardia, and the so-called auriculo-(atrio)ventricular extrasy stoles.
Johns Hopkins Hosp. Bull, Baltimore, 1908, xix, 322-326.
James (W. B.) & Hart (T. 5.). Auricular fibrillation: clinical observations on pulse
deficit, digitalis and. blood pressure. Am. J. M. Sc., Philadelphia &
New York, 1914, n. s. cxlvii, 63-71.
Jores (/£.)• Vorubergehender Pulsus irregularis perpetuus (absolutus) aufGrund einer thy-
reotoxischen Storung. Zentralbl. f. Herzkrankh. [etc.], Dresden u. Wien,
1915, vii, 77-84. 1 pi.
Koch (W.) & Jarisch (A.). Pathologisch-anatomische Befunde bei Pulsus irregularis per-
petuus. Tr. Internal. Cong. Med., 1893, London, 1914, Sect. Ill, Gen.
Path. & Path. Anat., pt. 2, 123-129.
Lewis (T.)« Auricular fibrillation: a common clinical condition. Brit. M. J., London,
1909, ii, 1528.
Auricular fibrillation and its relationship to clinical irregularity of the
heart. Heart, London, 1909-10, i, 306-372.
Fibrillation of the auricles: its effects upon the circulation. J. Exper. M.t
Lancaster, Pa., 1912, xvi, 395-420.
Pardee (H. E. B.}. The prognosis of auricular fibrillation. J. Am. M. Ass., Chicago,
1915, Ixiv, 2057-2060.
Robinson (G. C.). The relation of the auricular activity following faradization of the dog's
auricle to abnormal auricular activity in man. J. Exper. Med., Lancaster,
Pa., 1913, xviii, 704-714.
844 DISEASES OF THE CIRCULATORY APPARATUS
Rothberger (C. J.) & Winterberg (#.). Vorhofflimmern und Arhythmia perpetua.
Wien. klin. Wchnschr., 1909, xxii, 839-844.
Ueber die Entstehung und die Ursache des Herzflimmerns. Zentralbl. f.
Herzkrankh. [etc.], Dresden u. Leipzig, 1914, vi, 453; 465.
Ueber Vorhofflimmern und Vorhofflattern. Arch. f. d. ges. PhysioL, Bonn,
1914 tclx, 42-91. 3 pi.
Schoonmaker (//.). The clinical significance of auricular fibrillation. Med. Rec., New
York, 1915, Ixxxvii, 505-507.
Sutherland (G. A.) & Coombs (C. F.~). A case of acute rheumatic carditis and auricular
fibrillation in a child. Heart, London, 1913, v, 15-20.
Wiggers (C. /.)• Studies on the pathological physiology of the heart. I. Theintra-auricular,
intra-ventricular and aortic pressure curves in auricular fibrillations-
Arch. Int. Med., Chicago, 1915, xv, 77-91
(d) Atrial (or Auricular) Flutter
In this condition, the normal beats of the heart disappear and are re-
placed by heart beats originating in the atria as a result of automatic,
regular, recurring pathological impulses, which vary in rate from 200 to
350 per minute.
The condition differs from simple paroxysmal tachycardia (1) in that
the atrial rate exceeds 200 per minute, ordinarily being from 2 G 0-3 20 per
minute, and (2) in that the ventricular rate is usually from 130-160 per
minute, or exactly half the atrial rate, owing to the existence of a 2:1 heart
block. Occasionally, the ventricular rate is much less, owing to the exist-
ence of a 3 : 1 or a 4 : 1 heart
I I 1 1 1 1 1 1 block, or there may even be
A ventricular bradycardia with
a pulse rate of 30-38 per min-
ute, owing to complete heart-
block.
It is believed that, in atrial
flutter, the pathological stim-
Fig. 260. — Diagram of Atrial and Ventricular uK arise at a Single foCUS in
Beats in Atrial (or Auricular) Flutter. The , i , • n ,• "* i ,1 - 1 •
Abnormal Atrial Beats are Broken in their "16 atrial tlSSUC, and that this
Centers. The Atrial Rate is Very Rapid. foCUS lies at Some distance
The Ventricular Rate, though Rapid, is only , -• /. .-•
Half the Atrial, since a 2:1 Heart Block at least f™m the pacemaker
Exists. (After T. Lewis, "Clinical Disorders of the heart and is
ef the Heart Beat," published by P. Hoeber, -, -, ,, ,. . , ., .
New York.) enied by the cardio-mhibitory
nerves.
Flutter is most common in advanced life (age 50-80), but it may occur
as early as the third decade. Males are much more often, attacked than
females.
It is not always easy to recognize the condition clinically without elec-
trocardiographic studies, though sometimes it is possible. It may be sus-
pected in elderly patients who have a regular pulse and persistent tachy-
CLINICAL DISORDERS OF THE HEART BEAT 845
cardia of from 130-160 per minute, especially if there be no change of rate
on change, of posture, on rest, or on exercise. If electrocardiograms be
taken in such patients, the atrial rate will usually be found to be just twice
the ventricular rate ; in other words, the condition is, as a rule, associated
with 2:1 heart block.
But, in some patients with atrial flutter, the ventricular responses may
be irregular, though, on exercise, the ventricular action becomes accelerated
and perfect regularity of the pulse may then follow (T. Lewis). When
flutter exists with a heart rate within normal limits, and with a regular
pulse at the wrist, it is almost sure to be overlooked unless an electrocardio-
gram be made. Fortunately, in such cases, failure to detect the flutter is
relatively unimportant ; moreover, such cases are rare.
Many patients have short paroxysms of atrial flutter, resembling par-
oxysms of simple paroxysmal tachycardia ; they may occur off and on for
a considerable period before persistent flutter sets in.
It is remarkable how little subjective disturbance, atrial flutter may
cause. The patients complain, it is true, of fatigability and of a feeling
of exhaustion, but otherwise they may be completely free from subjective
disturbances. Now and then, the heart block, usually present in flutter,
passes off; the ventricular rate then becomes immediately doubled so as to
assume the full atrial rate of say 300 per minute. In such an attack, the
patient often becomes unconscious, and, unless the heart block returns, he
may soon die. Thomas Lewis has known flutter to last for four years in
one patient whose ventricle beat unceasingly at the rate of 160 per minute.
He states that of 17 patients manifesting flutter observed by him, only one
has died and he as a result of operation.
It is interesting that the ventricular rate in flutter can be reduced by
full doses of digitalis or of strophanthin. Sometimes the flutter ceases
under such medication to be replaced by atrial fibrillation, after which, if
the treatment with digitalis be stopped, the fibrillation may vanish and a
normal rhythm be resumed !
References
Levine (S. A.} & Frothingham (C.). A study of a case of auricular flutter. Arch. Int.
Med., Chicago, 1915, xvi, 818-831.
Parkinson (J.) & Mathias (H. H.}. Tachycardia of auricular origin and flutter with
phasic variation in auricular rate and in conduction. Heart, London,
1914-15, vi, 57-59.
Ritchie (William Thomas). Auricular flutter. Edinburgh & London, 1914, W. Green
& Co. 156 p.
Auricular flutter. New York, 1914, P.B. Hoiber. 144 P-
Roth (O.). Ueber isolierte linksseilige Vorhofstachy systolic (linkseitiges Vorhofsflattern) .
Ztschr. f. klin. Med., Berlin, 1914, Ixxx, 351-859.
Sutherland (G. A.}. Auricular flutter in acute rheumatic carditis. Proc. Roy. Soc. Med.,
London, 1913-14, vii, Sect. Stud. Dis. Child., 133-141.
846 DISEASES OF THE CIRCULATORY APPARATUS
White (P. />.)• A study of atrioventricular rhythm following auricular flutter. Arch. Int.
Med., Chicago, 1915, xvi, 517-535.
Wilkinson (K. D.} & Butter field (H. G.}. Paroxysmal heart-block with paroxysmal
auricular fibrillation. Heart, London, 1914-15, vi, 3-9. 1 pi.
6. Changes in the Contractile Force of the Heart
(a) Pulsus alternans
The contractile force of the ventricular muscle may be diminished
either from weakening of the muscle itself, or from the fact that the heart
rate may be so rapid (e. g.f in some cases of paroxysmal tachycardia) that
Fig. 261. — Pulsus alternans Due to Disturbance of Cardiac Contractility. (After K. F.
Wenckebach, "Arch des maladies du coeur," published by BailliSre et Fils, Paris.)
there is not sufficient time in diastole for its recuperation. This is often
evidenced by a rhythmic variation in the strength of alternate contractions
of the ventricle. The heart beats regularly, but larger and smaller quan-
tities of blood are expelled at alternate contractions.
Pulse Tracings ( Fig. 262). — It is best seen in arteriograms from either
the carotid or the radial arteries. The alternating large and small pulse
waves indicate the variation in the forces of the ventricular contraction.
Fig. 262. — Jugular Phlebograin and Braohial Arteriogram in Paroxysmal Tachycardia with
Ventricular Venous Pulse. (After A. D. Hirschfelder, J. H. H. Bull.)
In arteriograms of pulsus alternan? the beats, though unequal in size,
are seen to occur at approximately equal intervals ; whereas, in the coupled
beats resulting from regularly recurring premature contractions (pulsus
bigeminus), the pause following the premature contraction is distinctly
lengthened.
Electrocardiogram. — This, in many instances, is unchanged ; but occa-
sionally a similar variation in the height of the waves may be seen. But,
in the cases reported, a peculiar feature is that the larger electrical varia-
CLINICAL DISOKDEKS OF THE HEAET BEAT 847
tions correspond to the beats that produce the smaller arterial pulsations ;
in other words, excitation may be greater when contraction is less !
Significance. — Alternation of the pulse is a sign either that a fairly
healthy heart is overloaded, or that a diseased or intoxicated heart muscle
is making the effort to do more work than it is equal to.
In some instances, the alternation of the pulse is distinctly perceptible
to the palpating finger ; but, in the majority, graphic methods of registra-
tion are necessary for its recognition. It should be tested for by sphyg-
mography in cases of angina pectoris and in all cases of high blood pressure
(cardiac disease, arteriolar nephropathy), especially in elderly people.
When extrasystoles are present, alternation should be looked for in the
beats that immediately succeed them. Persistent pulsus alternans is a
sign of bad omen and demands careful protection of the heart.
References
Bard (L.). De la recherche par V auscultation des arteres des degres legers du pouls alternant.
Arch. d. mal. du cceur [etc.], Paris, 1915, viii, 112-114-
Esmein (C.). Note sur le pouls alternant transitoire et sa valeur pronostique. Arch. d.
rfialad. d. cceur, etc., Paris, 1913, vi, 385-389
Gordinier (II. C.). Pulsus alternans. Am. J. M. Sc., Philadelphia, 1915, cxlix, 174-182.
Gravier (Laurent}. L'altcrnance du cceur; etude critique et clinique. Lyon, 1914 , A. Rey.
433 p. No. 121. 8\
Hering (H. /?.). Ueber die alternierende Mitralinsufflzienz und das Wesen des Herzal-
ternans. Munchen. med. Wchnschr., 1909, Ivi, 565-566.
Zur Erkldrung des Herzalternans. (Zugleich eine Kritik der einschldgigen
Arbeiten von Leon und Henri Fredcricq.) Ztschr. /. exper. Pathd. u.
Therap., Berlin, 1913, xii, 325-327.
Kahn (R. H.} & Slarkenstein (E.). Die Storungen der Herztatigkeit durch Glyoxylsdure
(Pulsus alternans) im Elektrokardiogramm. Arch. f. d. ges. Physiol.,
Bonn, 1910, cxxxiii, 579-596. 3 pi.
McGill (C.). The determination of pulsus alternans by the sphygmomanometer. J. Am. M.
Ass., Chicago, 1915, Ixiv, 2061-2062.
Muskens (L. J. J.). Genesis of the alternating pulse. J. Physiol., London, 1907-08,
xxxvi, 104-112.
White (P. D.}. Alternation of the pulse; a common clinical condition. Am. J. M. Sc.,
Philadelphia^ 1915, cl, 82-97.
Windle (/» D.). The incidence and prognostic value of the pulsus allernans in myocardial
and arterial disease. Quart. J. M., Oxford, 1913, vi, 453-462.
7. Disturbances in Conduction in the Heart
(Heart Block)
The different chambers of the heart are connected, as we have seen,
through a distinct, specialized structure, by means of which the stimulus is
passed from one to the other. This is the atrioventricular bundle of His,
which begins in the atria and from them passes down to the ventricular sep-
tum, where it divides, in a Y-shaped manner, into two limbs, one going to
848 DISEASES OF THE CIECULATOEY APPAKATUS
the muscular wall of the right, the other to the muscular wall of the left,
ventricle. Each limb of the bundle is distributed by means of the Purkinje
system of fibers in the ventricular wall. Functional or organic changes
in the bundle may delay, or prevent, the transmission of the stimulus to the
succeeding portion of the heart. When this defect does occur, it gives
rise to a disturbance of the cardiac cycle, characterized by a partial, or
a complete, dissociation of the contractions of the two parts of the heart
separated by the lesion. To this condition of dissociation, the term heart
block has been applied. The most common form is that in which block
develops between the atria and the ventricles ; and this is the type that is
sometimes accompanied by the clinical picture of the Adams-Stokes syn-
drome. The obstruction may, however, affect other points in the conducting
system. Recently, it has been shown that one branch of the bundle} after
its division may, alone, be affected, giving rise to an intraventricular
block. Heart block is divided into classes primarily according to the
location of the lesion,, but these groups may be again subdivided, according
to the degree of the disturbance produced. We meet with different grades
of severity, which have been termed: (1) delayed conduction, (2) partial
heart block; (3) complete heart block. In each of these forms, again,
slightly different pictures may be encountered, both clinically and in the
curves obtained by graphic registration.
(a) Atrioventricular Block
i. Delayed Conduction
When conduction is slightly impaired at the atrioventricular junction,
the stimulus from the atria reaches the ventricles, it is true, but more time
is required for its transmission than in normal conditions. This is spoken
of as delayed conduc-
tion, and is usually
the first stage of a be-
ginning block. It is
manifested in the
y heart by the increase
in the time between
the atrial systole and
Fig. 263.— Delayed Conduction. Increase of As-Vs Interval. ^6 Ventricular^ SyS-
(A) A Diagram Representing the Action of the Normal tole (As-Vs inter-
Heart. The Auricle Contracts First and Transmits an vol^
Impulse (the Oblique Line) to the Ventricle. The Ven-
tricle Responds and Commences to Contract Immediately In the pulse tra-
at the Cessation of Auricular Systole ; (B) A Diagram . .
Illustrating the Earliest Stage of Heart Block. There is CingS and in electro-
Delay in the Transmission of the Impulse from Auricle to r»arrli no-ram Q tliia rip
Ventricle (Indicated by the Obliquity of the Line that lOgraniS, I
Joins the Rectangles in the Diagram). (After T. Lewis, lav is evidenced hv
"Clinical Disorders of the Heart Beat," published by P. B. , J . .
Hoeber, New York,) the Widening of the
CLINICAL DISOKDERS OF THE HEAET BEAT 849
space separating the atrial from the ventricular waves, that is, in the
lengthening of the As-Vs interval. In the venous tracing, this is the a-c
interval, while in the electrocardiogram it is the P-R (or P-Q) interval,
i. e., what is now called the "alpha interval." This interval in normal
hearts ranges from 0.1 to 0.2 of a second in duration, but in delayed con-
duction it may be increased to as much as 0.6 of a second. The longest
Fig. 204. — Remarkable Delay in Conduction Time with Beginning Heart Block. Personal
Observation. Note that the P-P Interval Varies Between .97 and 1.01 Second. The P-R
Interval for the First Cycle is .31, for the Second Cycle .38, for the Third Cycle the
Extraordinary Length of 1.01 Second, so that the Ventricular Complex is Practically
Coincident with the P-Wave of the Next Cycle. This Last P-Wave is Not Followed by
a Ventricular Complex. The Final P-Wave in the Tracing is Followed by a Ventricular
Complex After Leaving an Interval of .27 Second. The Rhythm Here is Thus 5 :4, Since
One Ventricular Complex Falls Out. (Electrocardiogram by Dr. E. W. Bridgman.)
interval recorded hitherto occurred in a case reported by my colleague,
Professor W. S. Thayer. A still longer delay in conduction-time is ob-
servable in a patient now under my observation, referred to me for study
through the kindness of Dr. McCurdy of Frederick, Md. The P-R interval
in one cardiac cycle reached the great length of 1.03 second, as was shown
by the electrocardiogram made for me by Dr. Bridgman. In the accom-
panying figure, an alpha interval of 1.01 second is shown.
ii. Partial Block
When the lesion is more advanced, conduction may be so impaired that
the stimulus from the atria is occasionally prevented from reaching the
ventricles ; this is known as partial block. In the heart itself, it is mani-
fested by failure of the ventricles to
contract after certain contractions of
the atria or auricles ; in other words,
certain beats are "dropped." There
may be only an occasional dropping
of a beat, or the atrial rhythm may
have a definite ratio to that of the
ventricles. Thus we speak of a 2 : 1,
a 3 : 1, and a 4 : 1 block, these figures
indicating the ratio between the num-
bers of the atrial and the ventricu-
lar contractions. Very often, 'as a
Fig. 265.— A Diagram of 2:1 Heart
Block in which Alternate Ventricu-
lar Beats are "Dropped," though
the Atrial Beats are Regular.
(After T. Lewis, "Clinical Disor-
ders of the Heart Beat," published
by P. B. Hoeber, New York.*
850 DISEASES OF THE CIECULATOEY APPARATUS
"dropped beat" is approached, its proximity is heralded by a progressive
increase in length of the preceding As-Vs intervals.
In arteriograms and phlebograms, simultaneously recorded, this condi-
tion of partial block is easily recognized. On the arterial pulse curve are
seen the pulsations corresponding to the ventricular systoles ; there is some
variation in the intervals between the beats both before and after a beat
is dropped. Coincident with each arterial pulse wave there is, on the
jugular tracing or phlebogram, a complete cardiac cycle of a-, c-f v-waves,
Tig. 266. — Beginning Heart Block. The Ventricle only Responds to Every Alternate Auricular
Systole — Ventricular Rate 48, Auricular Rate 96. This is a 2 :1 Rhythm. (After James
Mackenzie, "Diseases of the Heart," published by Oxford Press, London.)
in which the distance between a and c may be lengthened, as an indication
of the delayed conduction. Also, in the long ventricular diastoles, may
be seen one or more small, regularly-spaced waves, which are produced by
the atrial systoles that are not followed by ventricular systoles.
In the electrocardiogram, the same features can be much more easily
observed. The atrial contractions, recorded by the P-waves, exhibit a
regular rhythm, but only every second, third, or fourth atrial wave is
followed by a ventricular complex (.RJ'-waves) ; after the others, there is
ventricular silence.
In partial block due to vagal influences, the block can be made to pass
off by giving a stiff dose of atropin. In an interesting case reported by
Thayer and Peabody, the administration of atropin in partial block was
followed first by a complete cessation of ventricular activity for 10 sec-
onds; a few minutes later, the rhythm became normal (see Figs. 267-268).
iii. Complete Block
When complete obstruction occurs in the bundle, the ventricles can no
longer depend upon stimuli conducted from the atria, and they must
initiate their own contractions. There thus arise two independent rhythms,
which are simultaneously maintained in the same heart. While the atria
are receiving impulses from the Kleith-Flack node and contracting at a
rate of from 70-80 beats per minute, the ventricles, in accord with their
own, slow, automatic rhythm, make only some 30 contractions per minute.
CLINICAL DISORDERS OF THE HEART BEAT 851
852 DISEASES OF THE CIRCULATORY APPARATUS
This condition has been called complete dissociation or complete heart
block.
ZO 2O 20 20 20 20 2O 2O 2O 20
ii i i ii i rrn
Fig. 209. — Heart Block. Complete Dissociation Between the Contractions of the Auricles
and Those of the Ventricles. (After K. F. Wcnckebach, "Arch, des maladies du cceur,"
published by Bailliere et Fils, Paris.)
Pulse Tracings (Fig. 270). — The arteriogram in total block shows a
series of very slow, forcible pulsations coincident with the ventricular
rhythm ; the pulse waves are separated by long diastolic pauses. A simul-
taneous jugular tracing shows c- and T-waves synchronous with each
pulsation on the arteriogram, but in addition there are many small waves
(scattered at regular intervals throughout the curve), which represent the
Fig. 270. — Jugular Phlebogram and Radial Arteriogram in a Case of Complete Heart Block.
There are Three Pulsations in the Neck During Each Radial Cycle. Two of Each Group
of Three Neck Waves Result from Atrial (or Auricular) Contractions, a, while the
Third is the Result of Ventricular Systole, c ; when a and c Fall Together an Exagge-
rated Wave is Produced and is Visible as such in the Neck : it is Due to Discharge of
the Atrial Contents into the Veins. (After T. Lewis, "Clinical Disorders of the Heart
Beat," published by P. B. Hoeber, New York.)
a-waves of the atrial rhythm. In differentiating total block from partial
block, the main point to note is the complete independence of the two
rhythms — atrial and ventricular — in the former condition. While there
may be places where an a-wave and a c-wave seem to be associated in the
usual relation, if the tracing be examined through a number of beats it
will be seen that this relationship does not recur with any constancy.
Electrocardiograms (Fig. 271). — The features of the two rhythms can
be much more readily demonstrated in electrocardiograms. The ventricu-
lar systoles, occurring as a regular rhythm, are marked by the R- and
T-waves of the normal form of ventricular complex. This indicates that
the ventricular rhythm is not due to contractions of extrasystolic type,
CLINICAL DISORDERS OF THE HEART BEAT 853
and that the inherent rhythm of the ventricles originates well up in the
ventricular conduction-system. The rhythm of the atria, as evidenced by
Fig. 271. — Electrocardiogram in Complete Heart Block. The Ventricular Rhythm is Shown
by the High, Sharp #-Waves. The Smaller Atrial or Auricular Waves, p, can be Seen
at Regular Intervals on the Curve. The Two Rhythms are Absolutely Independent of
One Another. The T-Waves are Easily Distinguishable from the P- Waves.
the P-waves, seems to he superimposed upon, but completely dissociated
from, the ventricular rhythm.
(&) Intraventricular Block
Normally, the right and left ventricles are stimulated simultaneously
through the two branches of the atrioventricular bundle of His, but, in
some instances, the path of conduction to either the right or the left side
may be obstructed, in which event, the stimulus passes to one ventricle only
and is thence transmitted through the muscular wall of the heart to the
other ventricle. This muscular connection between the two ventricles is,
however, so intimate that no asynchronism of the ventricles can be demon-
strated by clinical observation of the heart itself or by any of the simpler
mechanical methods of registration. It is only by means of a study of the
electrical variations that we become aware of this change in the form of
the ventricular contraction.
Electrocardiograms (Fig. 272). — The curve in intraventricular block
shows a regular rhythm, each cycle of which is made up of an atrial P-
wave, followed, after the usual interval, by a ventricular wave. This in-
dicates that, in every instance, the ventricular contraction is the result of
a stimulus conducted from the atrium after the preceding atrial systole.
The ventricular part of the curve, however, does not exhibit the features
of normal supraventricular stimulation, but is of the form produced in
heterogenetic beats, or extrasystoles, of the ventricle. The diphasic wave of
an extrasystole of ventricular origin is explained by the fact that a hetero-
genetic beat arises in the wall of one ventricle and is thence transmitted
to the wall of the other. The same principle, it is believed, holds good for
the curve seen in intraventricular block, the stimulus from the atrium be-
ing able to reach one ventricle directly and not the other owing to the
854 DISEASES OF THE CIECULATOEY APPAKATUS
existence of an obstructive lesion in one branch of the bundle of His.
We have seen that we can decide, by a study of the form of the electrical
curve in a ventricular extrasystole, which ventricle is first stimulated ; in
intraventricular block we can also, from a study of the electrocardiogram,
Fig. 272. — Electrocardiogram from a Patient with a Lesion of One Branch of the Bundle of
His. This Peculiar Form of Electrocardiogram is Observable in Partial Lesions of the
Bundle of His. The Atria (or Auricles) Contract in the Usual Manner as Shown by
the Normal Form of P-Wave. Each Atrial Wave, however, is Followed by the Ventricular
Complex that is Usually Associated with a Ventricular Extrasystole. This Indicates
that though the Ventricles Receive the Impulse from Above, One Ventricle Contracts
Before the Other, as in an Extrasystole. This Phenomenon is Explicable by Assuming
a Lesion of the Bundle of such a Sort that the Stimulus to One Side is Blocked, though
that to the Other is Not. In the Curve Above, the Block is in the Right Ventricle and
the Left Ventricle Contracts First. (Heart Station, J. H. H.)
make out which ventricle contracted first, and thus locate the lesion that
causes the block in the branch of the bundle on the opposite side.
Etiology of Heart Block. — Heart block may be due either to functional
disturbance (reflex vagus inhibition, overdose of digitalis or strophanthin),
or to organic changes in the His bundle (fatty degeneration, fibrosis,
gumma, atherosclerosis, calcification, tumor, anemic necrosis from throm-
bosis, or acute inflammatory infiltrations). In cases that have come to
autopsy, the lesion has most often been found either in the Aschoff-Tawara
node, or in the main trunk of the bundle.
In 1909, Hirschfelder and I reported experiments in which we were
able in animals to cut one branch of the bundle (Fig. 273).
The Adams-Stokes Syndrome. — For decades it has been known that
patients with marked bradycardia are subject to characteristic attacks of
fainting, arrested respiration, and epileptiform convulsions. The syndrome
was described in 1827 by Adams, and, later on, also, by Stokes. In 1897,
His observed the syndrome, and found by studies of the venous and
arterial pulse that, in the bradycardia, the atria and the ventricles were
contracting at different rates, and that many atrial contractions occurred
without any corresponding ventricular contractions. His gave the name
"Heart Block" to this condition. Block in animals had been known be-
fore to the physiologists Gaskell (1883) and Engelmann. The whole
subject was later on illuminated by the brilliant experimental researches
CLINICAL DISOEDEKS OF THE HEABT BEAT 853
of Erlanger, who, in Howell's laboratory, devised an ingenious method
by which all forms of conduction disturbance, from delay, through partial
block, to total block, could be produced experimentally. It seems probable
that when the typical syncopal attacks occur in human beings there is a
sudden change from partial to total block.
A syncopal attack may be very transient; as a rule, it lasts 5 to 10
Fig. 273. — Wall of the Left Ventricle, Showing a Cut Through All the Ramifications of the
Left Branch of the Atrioventricular Bundle, which Appear Lighter than cthe Rest of
the Heart Muscle. (After L. F. Barker and A. D. Hirschf elder, Arch. Int. Med.)
seconds. Attacks are prone to occur in groups. A patient may be free
from attacks for months or years, then have a period of a few days or
weeks in which single attacks or groups of attacks occur, to be followed
again by a free period. The number of attacks varies much. Some patients
have only a single attack in a month; some have 20 attacks per day;
and His has reported a case in which a patient had 143 attacks within
856 DISEASES OF THE CIRCULATORY APPARATUS
twenty-four hours. The pulse is usually 28-34 at the time of attacks;
but as low a rate as 8-17 per minute has been observed.
Diagnosis of Heart Block. — The condition may be suspected clinically
when there are "dropped beats," or when there is a permanent bradycardia
of high grade, or if the patient gives a history of syncopal attacks. But,
to make an accurate diagnosis, graphic methods are essential. Electro-
cardiograms are the most satisfactory, but if they are unobtainable, the
condition can be analyzed, with the use of the polygraph, in simulta-
neously-recorded phlebograms and arteriograms (see above).
In addition to the accurate information afforded by graphic methods, certain
clinical features are worthy of attention. In delayed conduction, if the As- Vs
intervals be long, the sounds of the atrial contractions may be audible, separate
from those of the ventricular contractions; when a "reduplicated first sound" is
audible, or when a "double second sound" can be heard, the possibility of delayed
conduction should be kept in mind.
In cases where single beats are "dropped" the phenomenon may be due either
to a silence of the whole heart (sinus irregularity) or to a ventricular silence after
an atrial contraction; in the latter instance, the dropped beat is not regularly
associated with a definite respiratory phase.
In 2:1 heart block, the ventricular rate is usually between 40 and 50 per minute.
When this occurs in mitral stenosis, there may be two thrills and two diastolic
murmurs (due to atrial contraction) for each single ventricular cycle (T. Lewis).
In complete heart block, the pulse rate is often quite regular at a rate of 28-34
per minute. Listening over the heart, a first and a second sound are audible for
each ventricular beat, but on listening attentively, faint muffled sounds, due to
atrial systoles, may be heard in the long diastoles. Moreover, waves synchronous
with the atrial systoles may be visible in the jugular veins.
It should, of course, be emphasized that heart block and the Adams-Stokes'
syndrome are not synonymous terms; "the majority of patients who exhibit heart
block never have fits" (T. Lewis). I have observed one patient who has had com-
plete heart block for years without syncopal attacks; in addition to his regular
ventricular automatic rhythm, he has many ventricular extrasystoles.
References
1. Experimental Physiological
Cohn (A. E.) & Lewis (T.). The predominant influence of the left vagus nerve upon con-
duction between the auricles and ventricles in the dog. J. Exper. M.,
Lancaster, Pa., 1913, xviii, 739-747.
Erlanger (J.). On the physiology of heart-block in mammals, with especial reference to the
causation of Stokes-Adams disease. J. Exper. M., New York. 1905.
vii, 676-724. •
Lewis (T.}, White (P. D.) & Meakins (/.)• The susceptible region in A-V conduction.
Heart, London, 1914, v, 289-299.
Meakins (/.)• Experimental heart-block with atrio-ventricular rhythm. Heart, London.
1914, v, 281-286.
2. Clinical
Adams (/?.)• Cases of diseases- of the heart, accompanied with pathological observations.
Dublin Hosp. Rep., 1827, iv, 353-453.
CLINICAL DISOEDEES OF THE HEAET BEAT 857
Allen (H. W.}. The occurrence of heart block in acute diseases. Calif. State J. M., San
Francisco, 1915, xiii, 310-312.
Bachmann (George}. Sphygmographic study of a case of complete heart-block: a con-
tribution to the study of the action of strophanthus on the human heart.
Arch. Int. Med., Chicago, 1909, iv, 288-253.
Barton (W. M.)« Removal by caffein of some digitalis arhythmias: illustrated by tracings.
Am. J. M. Sc., Philadelphia, 1915, cl, 352-358.
Christian (H. A.). Transient auriculo-ventricular dissociation with varying ventricular
complexes caused by digitalis. Arch. Int. Med., Chicago^ 1915, xvi, 341-
355.
Cohn (A. E.). A case of transient complete auriculo-ventricular dissociation, showing con-
stantly varying, ventricular complexes. Heart, London, 1913-14, v, 5-14-
Cohn (A. E.) & Fraser (F. R.). The occurrence of auricular contractions in a case of in-
complete and complete heart-block due to stimuli received from the contract-
ing ventricles. Heart, London, 1913-14, v, 141-146. 1 pi.
Eyster (J. A. E.} & Evans (J. S.). Sino-auricular heart block, with report of a case in man.
Arch. Int. Med., Chicago, 1915, xvi, 832-845.
Falconer (A. W.). Note on a case showing the frequent occurrence of an auriculo-ventricular
rhythm associated with a long a-c interval. Lancet, London, 1915, i, 747-
749.
Gallavardin (£.)• Contractions auriculaires percepiibles a Voreille dans le block total.
Arch. d. mal. d. coeur [etc.], 1914, vii, 171-173.
Hart (T.S.}. Functional heart-block. Am. J. M. Sc., Philadelphia, 1915, cxlix, 62-77.
Heineke (A.), Muller (A.) & von Hosslin (//.)• Zur Kasuistik des Adams-Stokes' schen
Symptomkomplexes und der Ueberleitungsstorungen. Deutsches Arch. f.
klin. Med., Leipzig, 1908, xciii, 459-484.
His (W.), Jr. Ein Fall von Adams-Stokes' scher Krankheit mit ungleichzeitigem Schlagen
der Vorhofe und PlerzLammern (IlerzUocl}. Deutsches Arch. f. klin.
Med., Leipzig, 1899, Ixiv, 316-331.
Hume (W. E.). A case in which a high speed of the auricles did not produce tachycardia.
Quart. J. M., Oxford, 1913, vi,. 235-241.
Laslett (E. E.}. A case exhibiting a slow atrio-ventricular rhythm. Heart, London, 1914-
15, vi, 81-86.
Naish (A. E.). Premature ventricular beats in heart block. Quart. J. M., Oxford, 1913,
vi, 196-208.
Naish (A. E.) & Kennedy (A. M.). Heart-block in acute rheumatic carditis. Lancet,
London, 1914, ii} 1242-1245.
Osier (Sir W.) & Keith (A.). Stokes-Adams disease. In: Syst. Med. (Allbutt & Rolle-
ston). 8°. London, 1909, vi, 180-156.
Peabody (F. W.}. Heart-block associated with infectious diseases. Arch. Int. Med.,
Chicago, 1910, v, 252-262.
Pletnew (/>.)• Der Morgagni-Adams-Stokessche Symptomenkomplex. Ergebn. d. inn.
Med. u. Kinderh., Berlin, 1908, i, 46-67.
Riesman (D.) & Austin (J. H.). Poly graphic tracing of complete heart-block, with rapid
ventricular rate. Proc. Path. Sec., Philadelphia, 1914, xvi, 53.
Robinson (G. C.). A case of heart block illustrating the mode of action of the vagus nerve
on the heart. J. Missouri M. Ass., St. Louis, 1915, xii, 863-368.
Sakai (S.). Zur Kenntnis der Dissoziation des Herzens. Mitt. a. d. med. Fakult. d. k.
Univ. zu Tokyo, 1914, xiii, 213-229. 5 pi.
Schmoll (E.). Adams-Stokes' disease. J. Am. M. Ass., Chicago, 1906, xlvi, 361.
Stokes (W.). The diseases of the heart and aorta. Dublin, 1854, Hodges & Smith. 689
p. 8°. Also: Philadelphia, 1855, Lindsay & Blakiston. 710 p. 8°.
Thauer (W. 5.) & Peabody (F. W.}. A study of two cases of Adams-Stokes' syndrome
heart-block. Arch. Int. Med., Chicago, 1911, vii, 289-347,
858 DISEASES OF THE CIRCULATORY APPARATUS
Van Zwaluwenburg (J. G.)» Some observations on heart-block. Arch. Int. Med., Chicago,
i9iit via, 141-149.
Waller (A. !).)• Prolongation of the aumculo-ventricular interval, with increased pulse-
frequency. Tr. Internal. Cong. Med., 1913, London, 1914, Sect. Ill, Gen.
Path. & Path. AnaL, pt. 2, 119-121.
Wilkinson (K. D.). On the value in clinical medicine of graphic methods of investigating
disorders of the heart's rhythm, with a record of seven cases of heart block,
four of whom showed Adams-Stokes' syndrome. Birmingham M. Rev.,
1913, Ixxiii, 53; 126; 183.
3. Pathological-Anatomical
Armstrong (H.). Lymphangio-endothelioma of the A. -V. -node, causing heart-block. Liver-
pool Med.-Chirurg. J., 1913, xxxiii, 100-104.
Ashton (T. G.), Norris (G. W.) & Lavenson (R. S.). Adams-Stokes disease (heart-
block) due to a gumma in the intervenlricular septum. Am. J. M. Sc.,
Philadelphia & New York, 1907, n. s., cxxxiii, 28-49.
Cohn (A. E.) & Lewis (T.). Auricular fibrillation and complete heart-block: a description
of a case of Adams-Stokes' syndrome, including the post-mortem exami-
nation. Heart, London, 1912-13, iv, 15-30.
A description of a case of complete heart-block, including the post-mortem
examination. Heart, London, 1912-13, iv, 7-12. 1 pi.
The pathology of bundle-branch lesions of the heart. Proc. N. Y. Path.
Soc., New York, 1914, n. s., xiv, 207-216.
Fahr. Ueber die musculdre Verbindung zwischcn Vorhof und Venlrikel (das His'sche
Bundel) im normalcn Herzen und bcim Adams-Stokes' schen Symptom-
komplex. Virchow's Arch. f. path. AnaL [etc.], Berl., 1907, clxxxviii,
562-575. 1 pi.
Griffith (T. W.) & Kennedy (A. M.). A case of complete auriculoventricular heart-block,
with a report of the pathological condition of the heart. Brit. M. J., Lon-
don, 1913, 1203-1205.
Krumbhaar (E. B.). Adams-Stokes' syndrome, with complete heart-block, without de-
struction of the bundle of His. Arch. Int. Med., Chicago, 1910, v, 583-595.
Oppenheimer (Adele) & Oppenheimer (B. S.). Three cases of Adams-Stokes syndrome,
with histological findings. Arch. Int. Med., Chicago, 1914, xiii, 957-969.
Oppenheimer (B. S.) & Williams (H. B.). Prolonged complete heart-block, without
lesion of the bundle of His and with frequent changes in the idioventricular
electrical complexes. Proc. Soc. Exper. Biol. & Med., New York, 1913,
x, 86-87.
Par dee (H. E. B.). The relation of heart-block to lesions of the auriculoventricular bundle,
with report of a case. Arch. Int. Med., Chicago, 1913, xi, 641-652.
Renon (L.), Geraudel (E.) & Thibaut (D.}. Syndrome d' Adams-Stokes mortel sans
lesion anatomique du cceur ni du systeme nerveux. Bull, et mem. Soc.
med. d. hop., Paris, 1913, xxxv, 56-72.
Stengel (A.). A fatal case of Stokes-Adams disease with autopsy showing involvement
the auriculoventricular bundle of His. Am. J. M. Sc., Philadelphia
New York, 1905, cxxx, 1083-1091.
= 4. Intraventricular Block
, Barker (L. F.) & Hirschfelder (A. D.). The effects of cutting 'the branch of the His bundle
going to the left ventricle. Arch. Int. Med., Chicago, 1909, iv, 193-200.
, Carter (E. P.}. Clinical observations on defective conduction in the branches of the auriculo-
ventricular bundle: a report of 22 cases in which aberrant beats were ob-
tained. Arch. Int. Med., Chicago, 1914, xiii, 803-840.
Eppinger (H.) & Rothberger (C. /.)• Ueber die Folgen der Durchschneidung der Ta-
wara' schen Schenkel des Reizleitungssystems. Ztschr. f. klin. Med., Berlin.
— lxx,l-20.
CIECULATOKY INSUFFICIENCY 859
v. Leyden (#.)• Ueber Hemisystolie. Deutsche med. Wchnschr., Leipzig u. Berlin, 1908,
xxxiv, 137-139.
Rothberger (C. /.) & Winterberg (H.). Zur Diagnose der einseitigen Blockierung der
Reizleitung in den Tawara'schen Schenkeln. Zentrcdbl. /. Herzkrankh.
[etc.], Wien & Leipz., 1913, v, 206-208. 1 pi.
B. Circulatory Insufficiency
The circulation may become insufficient, either through failure of the
motor (myocardial insufficiency) or through failure of contraction of the
peripheral arterioles (vasomotor paralysis).
In myocardial insufficiency, the reserve force of the heart is the first
to suffer; the heart may do its work fairly well when the body is at rest,
but it is unable to meet tho extra demands for work that muscular
effort throws upon it. It loses its "power of accommodation."
Myocardial insufficiency is usually responsible for chronic insufficiency
of the circulation.
In acute infectious diseases, vasomotor paralysis is most often the cause
of the acute insufficiency of the circulation that sometimes develops; it
was formerly believed to be due to "heart failure." An acute insufficiency
of the circulation may, however, occasionally be due to acute dilatation of
the heart from myocardial injury following overexertion or intoxications.
In order that the blood pressure may be kept sufficiently high, two fac-
tors are necessary: (1) a sufficient amount of blood must be expelled into
the aorta, the minute-volume here depending upon (a) the systolic output
and (b) the frequency of ventricular contraction; and (2) a sufficient
peripheral resistance must be maintained through contraction of the
arterial musculature under the influence of the vasomotor nerves.
In the processes of "compensation," therefore, delicate adjustments
have to be made between the minute-volume on the one hand and the,
peripheral resistance on the other. In a given case of circulatory insuffi-
ciency, it may be very difficult to decide in how far each of the several
factors concerned in the maintenance of the circulation under normal
circumstances may be involved. Now that we have begun to realize,
through the researches of K. Hasebroek and others, the active part played
by the muscle of the arteries, not only in the regulation of the peripheral
resistance and the distribution of the blood, but also in supplying a part
of the driving energy of the circulation, the difficulty increases.
1. Chronic Circulatory Insufficiency
Definition. — This is a condition in which the power of accommodation
of the heart is impaired or lost ; in the milder cases, the reserve force of
,the heart is lessened; in the severer cases, the heart is unequal to the tasks
860 DISEASES OF THE CIRCULATORY APPARATUS
thrown upon it even when the patient is completely at rest — the state of
"decompensation" exists.
Etiology. — The causes of chronic circulatory insufficiency lie either
in the heart itself (organic diseases of this organ, especially of the myo-
cardium), or in disturbances of the heart secondary to diseases elsewhere
in the body (e. g., atherosclerosis, chronic nephropathies, thyreointoxica-
tions, pulmonary emphysema).
The varied causes of chronic circulatory insufficiency may well be considered
in relation to their effect upon the heart. To one class of etiological factors the
heart shows little or slight adaptative reaction; myocardial insufficiency is primary
and myocardial hypertrophy is absent or but imperfectly developed. In a second
type of case, however, the stage of circulatory insufficiency is preceded by a
period in which; by hypertrophy, the heart has remained competent in the pres-
ence of conditions that increased its work above normal limits.
To the first class belong those cases in which progressive circulatory insuffi-
ciency develops as a result of some toxic action, as in hyperthyroidism, or in infec-
tious diseases such as typhoid fever. Here also should be classed the gradually
developing circulatory insufficiency seen in acute endocarditis, and in acute myo-
carditis. The more active cases of luetic aortic insufficiency show this same
tendency to progressive myocardial failure, the compensatory hypertrophy being
unable to keep pace with the development of the valvular lesion. In the so-called
''fatty heart," and in the senile fibroses of the myocardium, a slower, but similarly
unchecked, march of events takes place.
In certain of the above cases the heart may recover upon the disappearance
of the cause of myocardial failure. Apparently, normal function may be re-
gained, or a chronic valvular or myocardial lesion may remain against which the
heart protects itself by adaptative reactions.
The second class of causes of circulatory insufficiency includes those whose
nature is such as to place an extra burden of work upon the heart. Insufficiencies
and stenoses of the cardiac valves; pericardial adhesions; hypertension of nephritic
or atherosclerotic origin; increased resistance in the pulmonary circulation due
to fibrosis of the lungs or to emphysema; increase in the volume of blood, plethora
vera. At first, in all these cases, the extra demands made upon the heart are met
by hypertrophy of one or both sides of the organ, but as increasing age tends to
multiply these burdens, the reserve power of the heart becomes ever smaller.
Symptoms. — These vary greatly in single cases, for reasons which we
do not as yet know. The stasis in the several organs varies, and the resist-
ance to stasis by the organs seems also to be an individual affair.
Of the SUBJECTIVE SYMPTOMS complained of, dyspnea, distress in the
region of the heart or liver, digestive disturbances, and abnormal feelings
in the head are most common. Cough is a very common 'symptom.
Dyspnea is the most constant symptom, being noticed first on exer-
tion. In severer cases, paroxysmal attacks of dyspnea — the so-called "car-
diac asthma"— may be very disturbing; they point to a failing left ven-
tricle, and, sometimes, herald the onset of pulmonary edema.
Distress in the region of the heart may cause considerable suffering.
It seems to be due either to dilatation of the ventricles or to anemia of
CIRCULATORY INSUFFICIENCY 861
the cardiac muscle, either of which can give rise to "referred pain." Out-
spoken stenocardiac attacks, or angina pectoris, point to sclerosis of the
coronary vessels.
Pain, or soreness, in the right hypochondrium is probably due to the
stretching of Glisson's capsule, as the liver enlarges, owing to chronic
passive congestion.
The digestive disturbances are doubtless due chiefly to stasis in the
venous system. They include anorexia, bloating after eating, and con-
stipation. Vomiting and diarrhea are frequently present.
Abnormal feelings in the head include headaches and dizziness.
Many patients complain that they cannot concentrate their minds prop-
erly arid that they feel depressed.
Of the OBJECTIVE FINDINGS, may be mentioned (1) changes in the
heart itself and (2) stasis phenomena elsewhere in the body.
In the heart, the signs of hypertrophy, of dilatation, or of both are
present (q. v.). These are easily made out by physical methods and by
x-ray examinations. Changes in pulse rate are nearly always met with
and arhythmia is common. In many cases, evidences of valvular lesion
are present.
Of the stasis phenomena, the commonest are edema, oliguria (with
albuminuria and cylindruria), cyanosis (with tachypnea and dyspnea),
and palpable enlargement of the liver and, sometimes, of the spleen.
Soon, or later, signs of edema of the lungs appear, and we can make out
dullness at the bases, rales, and diminution of the breath sounds. The
sputum contains "heart-failure cells."
The edema of cardiac decompensation shows the effects of gravity, be-
ing most marked in dependent parts. Patients that are up and about
show it, first, at the ankles, about the malleoli ; those that lie in bed may
manifest it over the sacrum or in the backs of the thighs. Sometimes the
scrotum is very edematous. In contrast with edema of renal origin, the
face is less affected than the extremities. As the circulatory insufficiency
develops, general anasarca may appear, with dropsy of the serous cavities.
Sometimes, a hydrothorax or an ascites may precede the subcutaneous
edema.
The oliguria is one sign of a stasis nephropathy; other urinary changes
include a high color and high specific gravity and the presence of albumin
and casts. Formerly there was difficulty in distinguishing such a stasis
nephropathy secondary to chronic circulatory insufficiency from other
nephropathics, but with the use of the renal test diet (q. v.) and of func-
tional tests, differentiation is easier.
Cyanosis of the lips, cheeks, and other acra (fingers, toes) is often
present. It is due to venous stasis, and is often associated with polycy-
themia rubra (q. v.) and increased viscosity of the blood. The respiratory
rate is increased (tachypnea) and the respirations are labored (dyspnea) ;
862 DISEASES OF THE CIKCTJLATOKY APPAKATUS
often the patient is compelled to sit up in bed, or to be propped up, through
the night, a condition known as orthopnea. In such cases, besides lung-
stasis, the possibility of hydrothorax should be kept in mind. Cheyne-
Stokes' breathing is not uncommon. Acute edema of the lungs is rarely
seen in chronic myocardial insufficiency except as a terminal phenomenon.
The swelling of the liver, due to chronic passive congestion, often be-
comes demonstrable, by palpation, early. The lower edge may be felt below
the costal margin, the consistence is firm, and the organ is tender. In
.advanced cases, the 1'ver edge may be as low as the umbilicus. The en-
largement of the liver .nay also extend upward, dislocating the diaphragm
^percussion, rontgenoscopy). Occasionally, there is slight icterus. The
rspleen may, or may not, be palpable.
The actual onset of the chronic circulatory insufficiency may be gradual, or
it may follow as a direct sequel of an acute decompensation of the heart due to
sudden demands in excess of its reserve power. In either case, if the causal
•condition is not of a rapidly progressive nature, or if the damage done is not
already too extensive, the freeing of the heart from all unnecessary work may
allow it to became competent again, temporarily. Chronic circulatory insuffi-
ciency, in these cases, is, characteristically, a disease of remissions.
Patients in whom the onset is gradual often present, over a long period of
time, the clinical picture of a MILDER GRADE OF RELATIVE CARDIAC INSUFFICIENCY.
Such patients notice shortness of breath on slight exertion, or after eating a heavy
meal. They may wake suddenly at night with a choking sensation, which passes off
when they sit up. A chronic cough often develops; this may occur in paroxysms.
A feeling of oppression, or even of pain, in the cardiac region is frequently noted.
Sudden exertion, or change in position, causes marked dizziness. Sooner or later the
patients usually discover the presence of some edema about the ankles; appearing
toward the end of the day. In appearance, they are often slightly cyanotic.
'Traces of breathlessness may show in their speech, and a nervous manner is not
uncommon. The findings upon e amination of the heart will depend upon the
condition responsible for the myocardial insufficiency. Hypertrophy may or may
not be present, but a moderate dilatation of one side of the heart is a frequent
finding. Evidence of organic valvular lesions may be present. A relative insuf-
ficiency of the mitral valve is common. The rhythm may be regular but it is more
usual to find some extrasystolic arhythmia, or a gallop-rhythm at the apex (espe-
cially in nephritic hearts). Some degree of tachycardia is the rule. The blood
pressure will depend largely upon the condition to which the cardiac signs are
primarily due. At the base of the lungs, posteriorly, a slight impairment of the
percussion note may be found, along with a few moist rales. A palpable, tender
liver-margin, when present, is a valuable confirmatory sign. A trace of albumin
and occasional casts in the urine are to be expected as a result of renal stasis.
The edema of the lower extremities may be very slight or absent. It should be
carefully looked for; it is often earliest discovered over the lower end of the tibia
or behind the malleoli. It may be more marked on the left leg. The pitting of
the tissue on pressure is characteristic.
The clinical picture of COMPLETE CARDIAC DECOMPENSATION is a far more strik-
ing one. The dyspnea reaches higher grades; the patient must remain constantly
in the sitting position (orthopnea) ; during the frequent pseudo-asthmatic attacks,
the accessory respiratory muscles are all brought into play, the nostrils dilate,
the countenance is livid, the extremities cold, and cold perspiration appears on the
CIKCULATOKY INSUFFICIENCY 863
forehead. There is often Cheyne-Stokes respiration. Cough is frequent and
exhausting. The edema is usually very marked. The legs, the external genitalia,
the abdominal wall, and the lower back, are greatly swollen. The hands and arms
may be likewise involved. The face is often spared, but infra-orbital edema and
chemosis are common. The edema shifts, with changes of position of the patient,
to the dependent parts. In cases of long standing, a distinct icteric color of the
skin and conjunctivae is often present. Cyanosis is variable in degree. A marked
pallor characterizes many cases. The heart is dilated; the apex impulse is diffuse
and wavy; the right and left cardiac borders are displaced lateralward. The heart
sounds are blurred and softened. If murmurs of organic valvular disease were
previously present, they have usually grown much fainter, or have disappeared.
Blowing murmurs of relative mitral and tricuspid insufficiency may be detected.
Marked disturbances in the cardiac rhythm are the rule ; of these the most common
are those due to auricular fibrillation or to extrasystoles. The heart rate is rapid
and varies with changes in the patient's condition (100-140). The pulse is often
difficult to count, since many beats do not reach the wrist ("pulse-deficit") and
the volume is small. The blood pressure is usually lowered. There occur cases,
however, in which a rise in blood pressure accompanies decompensation of the
heart. This is, occasionally, strikingly evident in cases of aortic insufficiency of
luetic origin, and in cases of hypertensive renal disease. Engorgement of veins
in the neck, and the systolic venous wave, due to tricuspid insufficiency, may be
observed.
Throughout the body, functional disturbances and physical signs appear,
indicative of the effects of passive congestion upon the viscera. The bases of the
lungs show impaired resonance, the breath sounds are diminished, and crackling
rales are heard. The sputum may be tinged yellowish-brown. Right-sided, or
bilateral, hydrothorax is common. In cases of long standing, infarcts of the lung,
often of considerable extent, should be watched for; they may develop with out-
spoken symptoms and signs, or may be cryptic. Whenever, in such a case, obscure
signs of consolidation, accompanied by pleural friction, appear over a lower lobe,
infarction should be suspected. Terminal bronchopneumonias are common. Hydro-
pericardium is more frequently present than detected. Only careful daily obser-
vation of the outline of cardiac dullness and of the intensity of the heart sounds
enables the physician to appreciate the appearance of this complication. The
enlarged liver, tender especially in the earlier stages, may extend below the level
of the umbilicus. The surface is smooth. When the edge can be grasped and pul-
sation felt, the diagnosis of tricuspid insufficiency is certain. Pain, due to hepatic
distention, is, in some cases, a very prominent symptom. The congestion of the
walls of the stomach and small intestine gives rise to many g Castro-intestinal symp-
toms. The commonest of these are anorexia and constipation. Belching and
flatulence, meteorism, and persistent vomiting, may all occur. In extreme conges-
tion, hemorrhage per diapedesis occurs in the intestine, and the stools contain
macroscopic blood. An acute colitis is, not infrequently, ai, terminal infection.
The abdominal cavity, in all severe cases of myocardial insufficiency with edema,
contains an excess of peritoneal fluid; but it is often difficult to detect this
fluid until the amount is very considerable. The urine is scanty (300-700 c.c.),
usually high-colored and of high specific gravity. Albumin, hyaline and granular
casts, and a few red blood-cells are found. In addition to the stasis-kidney, the
presence of an underlying nephritis, should it exist, may be discoverable only by
means of a careful study of the renal function (q. v.) and by the presence of the
extrarenal features of this disease. Psychical symptoms are common in myo-
cardial insufficiency, and may closely resemble those seen in uremia. Nocturnal
delirium and restlessness may necessitate a close watch over the patient.
864 DISEASES OF THE CIKCULATOKY APPAKATUS
The diagnosis of chronic circulatory insufficiency should always be considered
by the physician as only the first step in his attempt at a complete understanding
of the case. Only after he has discovered the underlying cause of the myocardial
failure will he be able to employ rational therapeutic measures, or to offer a logical
opinion as to the prognosis.
Course of Myocardial Insufficiency. — All depends upon (1) the cause,
and (2) the management. If the cause be removable, or if the injury
to the heart muscle be relatively slight, brilliant results can be obtained
from therapy. Even in the severer forms of myocardial insufficiency judi-
cious management may achieve most gratifying results over a long period.
Sudden death may, occasionally, occur from coronary disease, or, more
rarely, from pulmonary edema. In slow cardiac death, the stasis phe-
nomena increase, atrial fibrillation is common, and, at the end, a pneu-
monia, or some other infection, may supervene.
Diagnosis of Chronic Circulatory Insufficiency. — The existence of the
insufficiency of the circulation is easily made out from the symptoms and
signs described above. But the diagnosis of the underlying cause and
of the exact pathological anatomy and physiology may be exceedingly diffi-
cult. Each case should be exhaustively studied by physical and graphic
methods, and the study should not be confined to the circulatory organs
but should include all the systems of the body.
In the milder grades (relative insufficiency} , symptoms appear only
on exertion, and the clews to diagnosis have to be gained largely from the
anamnesis and from functional tests of capacity. In the severer grades
(absolute insufficiency), the diagnosis "leaps to the eyes"; the dyspnea,
the cyanosis, the edema, the abnormalities of the pulse, the changes in the
heart, and the swollen, tender liver leave, as a rule, no room for doubt. In
every case, besides confirming the signs of the circulatory insufficiency, an
attempt should be made to explain its pathogenesis, in order that the
therapy may be intelligently planned.
References
Aschoff (L.) & Tawara (5.). Die heutigeLehre von den pathologisch-anatomischen Grund-
lagen der Herzschwache. Kritische Bemerkungen auf Grund eigener
Untersuchungen. Jena, 1906, A. Fischer. 81 p. 8°.
Alter (/.). On the action of digitalis and digitalis-like substances on the right ventricle. Tr.
Ass. Am. Phys., Philadelphia, 1912, xxvii, 96-99.
Barker (L. F.). Some comments upon the increase of precision in the methods of studying
cardiovascular states and upon the application of the principle of protec-
tion and the principle of exertion in the treatment of the failing heart.
Cleveland M. J., 1911, x, 269-282.
On the treatment of some of the forms of cardiac failure. Virginia M.
Semi-Monthly, Richmond, 1911, xv, 457; 486.
Barringer (T. B.), Jr., & Teschner (J.). The treatment of cardiac insufficiency by a new
method of exercise with dumb bells and bars. Arch. Int. Med., Chicago,
1915, xvi, 795-808,
CIECULATOKY INSUFFICIENCY 865
Bittorf (A.). Die verschiedenen Ursachen der Atmungsinsuffizienz und ihre Wirkungen.
Handb. d. allg. Pathol. (Krehl & Marchand), Leipzig, 1912, ii, 1, 554-
625 .
Cameron (P. /).)• Physiological and pharmacological studies on cardiac tonicity in mam-
mals. Johns Hopkins Hosp. Rep., Baltimore, 1911, xvi, 549-670.
Chapman (C. W.). Diagnosis in relation to prognosis in diseases of the heart and circula-
tion. Clin. J., London, 1914, xliii, 702-704.
Cohn (A. E.}. Clinical and electrocardiographic studies on the action of digitalis. J Am
M. Ass., Chicago, 1915, Ixv, 1527-1532.
Cotton (T. F.)» Dyspnoea in cardio-renal disease. Canadian M. Ass. J., Toronto, 1915,
v, 972-980.
Eggleston (C.). The present status of digitalis therapy. Internal. Clin., Philadelphia
1915, 25. s., ii, 87-97.
Ehrenberg (!/.)• The tying off of the extremities according to Tornai, a noteworthy method
of treatment in weak hearts. Detroit M. J., 1915, xv, 14~22.
Fulton (F. T.). Observation upon Cheyne-Stokes breathing. Heart, London, 1914-15, vi
77-80.
Goulston (Arthur). Cane sugar and heart disease. London, 1914, Bailliere, Tindall &
Cox. 114 p. 8°.
Greene (C. L.). Avoidable errors in the diagnosis of cardiac insufficiencies. Journal-
Lancet, Minneapolis, 1915, xxxv, 322-328.
Hasebroek (K.). Physikalisch-experimentelle Einwdnde gegen die sogenannte arterielle
Hypertension; zuqleich einBeitrag zur Frage der aktiven Arterienbewegung.
Arch. f. d. 0es. PhysioL, Bonn, 1911-12, cxliii, 519-559.
Hering (H. E.). Die Patholoqie der Herzschwdche. Deutsche med. Wchnschr., 1913,
xxxix, 1769-1774.
Die Pathologic der Herzschwdche. Tr. Internal. Cong. Med.. 1913,
London, 1914, Sect. VI, Medicine, 215-230.
[Discussion], 187-193.
Hirschfelder (A. D.). The clinical use of digitalis. St. Paul M. J., 1915, xvii, 255-263.
Hofbauer (L.)« Ursachen der Orthopnoe. 2. Die kardiale Orthopnoe. Ztschr. f. klin.
Med., Berlin, 1913, Ixxix, 128-134.
Honan (J. H.). What heart patients should know and do: suggestions for persons suffer-
ing from diseases of the heart and blood-vessels, etc. New York, 1913,
Dodd, Mead & Co. " 215 p. 8°.
J oneway (T.}. The use and abuse of digitalis. Am. J. M. Sc., Philadelphia & New
York, 1908, n. s., cxxxv, 781-790.
Janeway (T. C.). The comparative value of cardiac remedies. Tr. Internal. Cong. Med.,
1913, Lond., 1914, Sect. V, Therap., 1-22.
Kiilbs (F.). Die Kreislaufsinsuffizienz. Handb. d. inn. Med. (Mohr & Slaeheliri) , Ber-
lin, 1914, ii, 958-1011.
Lenhartz (//.)• Ueber Herzfehlerzellen. Deutsche med. Wchnschr., Leipzig u. Berlin,
1889, xv, 1039-1041.
Lewis (T.), Ryffel (J. H.}, Wolff (C. G. L.}, Cotton (T.) & Barcroft (/.)• Observa-
tions relating to dyspnea in cardiac and renal patients. Heart, London,
1913, v, 45-92.
Moritz (F.). Ueber klinische Zeichen beginnender Herzschwdche. Munchen. med.
Wchnschr., 1915, Ixii, 1-4-
Neilson (C. H.). Treatment in heart disease. J. Missouri M. Ass., St. Louis, 1914-15.
xi, 212-214.
Osborne (Oliver T.). Ed. Disturbances of the heart. Chicago, 1913, Am. M. Ass. 216
p.* 12°.
Parkinson (J.) & Rowlands (R. A.). Strychnine in heart failure. Quart. J. Med.t
Oxford, 1913, vii, 42-60.
DISEASES OF THE CIRCULATOKY APPARATUS
Peabody (F. W.}. Studies on acidosis and dyspnea in renal and cardiac disease. Arch.
Int. M., Chicago, 1914, xiv, 236-262.
Pratt (J. H.). On the causes of cardiac insufficiency. Johns Hopkins Hosp. Bull., Balti-
more, 1904, xv, 801-309.
Steell (G.). Heart failure as a result of chronic alcoholism. 24 p. 1 ch. 8°. Manches-
ter, 1893. Repr. from Med. Chron., Manchester, 1893. L. B. Collection,
clxiv, No. 24.
Steiner (W. R.}. Digitalis; its action and its uses. Boston M. & S. J., 1913 , clxix, 828-
833.
Stern (H.}. Das hygienische AB C fur Herzkranke. Wurzburg, 1914. 156 p. 8°.
Taussig (A. E.). The present status of the treatment of advanced cardiac decompensation.
Interstate M. J., St. Louis, 1914, xxi, 1317-1322.
Vaquez (H.). Les grands syndromes de Vinsuffisance cardiaquc. Arch. d. malad. d. coeur,
[etc.]. Paris, 1913, vi, 753-776.
Les causes de Uinsujfisance cardiaque. Arch. d. mal. du cceur [etc.].
Paris, 1915, viii, 317-342.
Wenckebach (K. F.). Herzinsufficienz und Herzschwdchs. Tr. Internal. Cong. Med.,
1913, London, 1914, Sect. VI, Medicine, 199-214; [Discussion], 187-193.
Wilson (T. S.). The early diagnosis of heart failure and oilier essays on the heart and circu-
lation. London, 1915. 638 p. 8°.
Windal (D. J.). The action of digitalis in rheumatic heart disease with dropsy and normal
heart rhythm. Tr. Internal. Cong. Med., 1913, London, 1914, Sect. V.
Therap., pt. 2, 228-232.
Wood (H. C.), Jr. The newer ideas concerning digitalis. Therap. Gaz. [etc.], Detroit, 1915,
xxxi, 381-385.
2. Acute Circulatory Insufficiency
Definition. — A state in which there is a sudden development, within
a few minutes or a few hours, of symptoms pointing to vasomotor paralysis,
to acute myocardial insufficiency, or to both.
Etiology. — The commonest cause of acute circulatory insufficiency is
intoxication of the vasomotor center, with vasomotor paralysis, in acute in-
fectious processes (e. g.7 in pneumonia, sepsis, typhoid). Sometimes, a
sudden injury to the cardiac muscle may be responsible as in infections
like diphtheria, in coronary embolism or thrombosis, or in violent over-
exertion (acute overstrain of the heart of athletes) ; in many of these cases,
however, the heart muscle, supposedly healthy, has been the site, earlier,
of a chronic inflammatory or degenerative process.
Symptoms. — These are exceedingly variable, depending upon the
cause. In the rapidly developing VASOMOTOR PARALYSIS of acute infections,
there is sudden collapse, the blood pressure (both maximal and minimal)
falls, the pulse becomes dicrotic, sometimes monocrotic, the pulse is accel-
erated, and the vessel feels empty ; the skin is pale, cool, and often bathed
in cold sweat; the patient is prostrated, often delirious or comatose. The
heart's action may still be regular, and there is no overfilling of the veins —
in marked contrast with myocardial insufficiency.
In ACUTE DILATATION OF THE HEART in acute infections, or after violent
EEPAKATIVE AND ADAPTIVE PEOCESSES 867
overexertion, the veins become overfull and the increase in the size of the
heart can be made out by percussion and by rontgenoscopy. The right
margin of the heart is often rapidly displaced to the right as the right
ventricle dilates. Stasis phenomena quickly appear (crackles at the bases
of the lung; swelling of the liver; scanty, high-colored, albuminous urine).
References
Gordon (G. A.). Observations on the effect of prolonged and severe exertion on the blood
pressure in healthy athletes. Edinb. M. J., 1907, n. s., xxii, 58-56.
Gunn (J. A.} & Martin (P. A.). Intrapericardial medication and massage in the treatment
of arrest of the heart. J. Pharmqcol. & Exper. Therap., Baltimore, 1915-
16, vii, 31-55.
His (W.). Ermudungsherzen im Felde. Med. Klin., Berlin, 1915, xi, 293-298.
Kordny (Baron A.}. Die Therapie der akuten Insufficienz der Blutzirkulation, unter
besonderer Berucksichtigung der im Verlauf der akuten fieberhaften Krank-
heiten • vorkommenden Zirkulationsinsufficienz. Pest med.-chirurg. Presse.
1913, xlix, 213-217.
Lademan (O. E.) Management of acute decompensation-cases in cardio-renal disease.
Med. Fortnightly, St. Louis, 1915, xlvii, 211-213.
MacCallum (W. G.}. The mechanism of the circulatory failure in diphtheria. Am. J.
M. Sc., Philadelphia & New York, 1914, cxlvii, 37-44.
Monckeberg (T. G.). Herzschwdche und plotzlicher Herztod als Folge von Erkrankungen
des At"ioventrikular systems. In:Ergebn. d. allgem. Pathol. [etc.] (Lubarsch
& Ostertag), Wiesbaden, 1910, xiv, Abt. i, 594-705.
Pdssler (//.) & Roily (F.). Experimentelle Unter suchungen iiber Kreislaufstorungen bei
acuten Infectionskrankheiten. Deutsches Arch. f. klin. Med., Leipzig,
1903, Ixxvii, 96-167.
Romberg (E.). . Ueber die Erkrankungen des Herzmuskels bei Typhus abdominalis,
Scharlach und Diphtherie. Deutsches Arch. f. klin. Med., Leipzig, 1891,
xlviii, 369-413; 1892, xlix, 413-441.
Schott (T.). Zur acuten Ueber anstrengung des Herzens und deren Behandlung. 4- Aufl.
Wiesbaden, 1908, J. F. Bergmann. 59 p. 8°.
Socin (C.). Experimentelle Unter suchungen uber akute Herzschwdche. Arch. f. d. ges.
Physiol, Bonn, 1914, clx, 132-182.
Willson (R. N.}. The diagnosis between primary and secondary acute cardiac pictures. Am.
J. M. Sc., Philadelphia, 1915, cl, 258-264.
Zueblin (E.). The action of pituitrin on acute heart-failure and incompensate heart-lesions.
Boston M. & S. J., 1914, clxxi, 962-970.
C. Reparative and Adaptive Processes in
the Heart
The heart muscle undergoes hypertrophy in adapting itself to in-
creased work. The wall of the ventricle may become twice as thick as nor-
mal. The thickening is due to enlargement of the individual fibers, not to
a multiplication of them. When the chambers of the heart undergo dilata-
tion, this is due to the increased amount of blood that they are forced to
contain. Dilatation is closely related to the function of tonicity of the
heart muscle; it is, in some cases, a cardiac hypotony.
868 DISEASES OF THE CIKCULATORY APPARATUS
The heart, as a whole, may be enlarged from dilatation, from hyper-
trophy, or from both ; but, more often, one, or two, of its chambers will be
found enlarged alone, or more than the other chambers.
1. Hypertrophies ol the Heart
(a) Hypertrophy of the Left Ventricle
Physical Signs. — Here we see displacement of the apex beat downward
and lateralward. The impulse is stronger and more heaving than normal.
There is no marked change in the cardiac dullness unless there is dilatation
II
III
Fig. 274. — Electrocardiograms in Hypertrophy of the Left Ventricle. Derivations I, II, and
III Shown in Order. The Characteristic Feature, in this Condition, is the Inversion of
the 72-Wave, as One Goes from Derivation I to Derivations II and III.
REPARATIYE AKD ADAPTIVE PROCESSES 869
as well as hypertrophy. Sooner or later, however, the dilatation accom-
panying the hypertrophy gives rise to an enlargement perceptible on per-
cussion. On x-ray examination, the heart occupies a more horizontal posi-
tion than normal, the third curve on the left side projects prominently, and
the apex looks rounded and plump. The condition is often associated
with arterial hypertension and with an accentuated aortic second sound.
The electrocardiograms are characteristic.
Etiology. — The more important etiological factors include: (1) in-
creased work due to valvular disease (most marked in aortic insufficiency
and in aortic stenosis) ; (2) arterial hypertension in prolonged muscular
overexertion (athlete's heart), in pregnancy, in nephritis, in some cases
of arteriosclerosis, and in plethora vera; (3) sometimes "idiopathic" (no
cause being ascertainable) .
(6) Hypertrophy of the Right Ventricle
Physical Signs. — The apex beat is not more forcible than normal, but
is rather diffuse, and is displaced to the left rather than downward. Rotary
undulation is often visible in the precordium. The superficial and the
deep areas of cardiac dullness are widened, especially to the right (due
to accompanying dilatation). The pulmonary second sound is accentuated.
On x-ray examination, the "median position" of the heart is striking ;
and there may be noticeable projection of the lower of the two curves on
the right, often due in part to accompanying dilatation of the right
atrium. The pulse may be but little changed. The maximal blood pres-
sure is often low.
Etiology. — This hypertrophy may be the result of various causes,
including: (1) organic valvular disease, especially mitral disease, and (2)
obstructions in the pulmonary system (stenosis of the pulmonary artery,
emphysema, kyphoscoliosis, chronic bronchitis, arteriosclerosis of the pul-
monary vessels). Hypertrophy and dilatation of the right ventricle
accompany (3) insufficiency of the pulmonary valves and (4) tricuspid-
valve lesions. In (5) congenital anomalies (patent ductus Botalli and
patent foramen ovale), the right ventricle hypertrophies.
(c) Atrial Hypertrophy
The walls of the atria may also hypertrophy, in which case an exag-
gerated a-wave may be seen upon the jugular plebogram (right atrium),
or upon the esophageal cardiogram (left atrium). The high P-wave in
the electrocardiogram of mitral stenosis believed to be associated with
atrial hypertrophy.
870 DISEASES OF THE CIKCULATOBY APPARATUS
Fig. 275. — Electrocardiogram in Hypertrophy of the Atria (or Auricles). The Characteristic
Feature of this Electrocardiogram is the Comparative Size and Height of the P-Wave.
It is Almost Double that of the Normal P-Wave.
References
Bridgman (E. W.). The value of the electrocardiogram in the diagnosis of cardiac hyper-
trophy. Arch. Int. Med., Chicago, 1915, xv, 487-500,
Gibson (A. G.). Hypertrophy of the heart. Mod. Med. (Osier). 8°. Philadelphia &
New York, 1908, iv, 151-172.
Moore (Norman). Observations on the shape of the chest in cases of hypertrophy of the heart.
London, 1873, Bradbury, Agnew & Co. 32 p. 2 pi. 8°.
Moritz (F.). Anomalien des Lumens und der Masse des Herzens undGefdsse. Handb. d.
allg. Pqthol. (Krehl & Marchand). Leipzig, 1913, ii, 2, 67-85.
Stewart (H. A.}. An experimental contribution to the study of cardiac hypertrophy. J.
Exper. M., Lancaster, Pa., 1911, xiii, 187-209.
Wider be (5.). Die Massenverhdltnisse des Herzens unter pathologischen Zustanden.
Christiania, 1911. 148 p. 8°.
2. Dilatation of the Heart (Failure of Tonicity)
The heart is limited in its power of adaptation by hypertrophy. Sooner
or later, disturbances appear (decompensation due to myocardial insuffi-
ciency). When the left ventricle is weak, the blood will tend to be
dammed back upon the lungs; when the right ventricle "veakens, chronic
passive congestion in the veins of the body sets in.
As the heart muscle weakens, the cavities surrounded by it dilate
(dilatation of the heart from failure of tonicity). Hypertrophy of the
heart, by itself, causes very little increase in the size of the heart demon-
strable by physical methods; when the areas of cardiac dullness are in-
creased from enlargement of the heart, or when on x-ray examination a
larger volume than normal is visible, dilatation exists. The areas of per-
cussion dullness and the fluoroscopic views (as orthodiagrams) are char-
acteristic for dilatation of the single heart chambers (q. v.). Arhythmia
is common. The dilatation may involve all four cavities simultaneously ;
usually, however, either the left heart or the right heart is predominantly
affected.
THE INFLAMMATORY CARDIOPATHIES 871
Causes of Dilatation. — (a) In the HEART MUSCLE itself:
(1) From recurring inflammations in the heart muscle, espe-
cially those involving the conduction system; or
(2) From chronic intoxications (bacterial, alcohol, catfein, nico-
tin).
(3) From multiple infarctions (due to emboli, or to thrombosis) ;
(b) OUTSIDE THE HEAET MUSCLE. The hypertrophic myocardium
may fail on account of too great disproportion between
the force of the heart and the resistance to be overcome.
This disproportion may arise:
(1) At the cardiac orifices (from organic changes in the
valves) ; or
(2) in the peripheral vascular system (general or pulmonary),
from bodily overexertion, from infections, from arterio-
sclerosis, or from nephritis.
The real cause of dilatation, however, if there is not an actual leak
back from the arteries, lies in overfilling of the heart from high venous
pressure.
The symptoms are those of chronic circulatory insufficiency (q. v.).
References
Cameron (P. D.}. Physiological and pharmacological studies on cardiac tonicity in mam-
mals. Johns Hopkins Hosp. Rep., Baltimore, 1911, xvi, 549-370.
Delbet (P.) & Vaquez (//.)• De la chondrectomie dans certaines dilatations irreductibles
du cceur droit. Corn-pi, rend. Acad. d. Sc., Paris, 1915, clx, 456-458.
Fraser (F. R.). Experimental cardiac enlargement and accompanying electrocardiographic
changes. Proc. N. Y. Path. Soc., New York, 1914, n. s., xiv, 216-218.
Gibson (A. G.). Insufficiency and dilatation of the heart. Mod. Med. (Osier). 8°.
Philadelphia & New York, 1908, iv, 173-204.
Often (M.). Die Bedeutung der Orthodiagraphie fur die Erkennung der beginnenden Herz-
weiterung. Deutsches Arch. f. klin. Med., Leipzig, 1912, cv, 370-439.
West (5.). On the murmurs in dilated hearts, and their exp^nations. Proc. Roy. Soc. Med.,
London, 1913-14, vii, Med. Sect., 193-204.
D. The Inflammatory Cardiopathies
These may be acute or chronic, and may involve the endocardium, the
myocardium, or the pericardium. When all three are simultaneously in-
volved, we speak of a carditis or of a pan-carditis.
1. Endocarditis
Definition. — An inflammation of the lining membrane of the heart.
Etiology. — In the majority of cases, if not in all, the cause lies in
bacterial infection, though a toxemia may predispose to localization of
872 DISEASES OF THE CIKCULATOKY APPAKATUS
the bacteria on the endocardium. The bacteria get into the blood stream
from some primary focus of infection (tonsils, teeth, paranasal sinuses,
urethra, lung, etc.). Any one of several bacterial forms may set up an.
endocarditis. That most frequently responsible is the virus of acute rheu-
matic fever, the Streptococcus rlieumaticus; but the Streptococcus Jiemo-
lyticus, the Pneumococcus, the Streptococcus viridans, the Gonococcus,
the Stapliylococcus aureus, or the Bacillus influenzae, may be responsible.
Less common agents are the meningococcus, the typhoid bacillus, and the
colon bacillus. Endocarditis has been experimentally produced by inject-
ing bacteria into the blood stream after mechanical injury to the heart
valves.
Pathology. — Endocarditis may follow an acute, a subacute, or a chronic
course. The left side of the heart is much more often involved than the
right. The membrane over the valves is most often involved (valvular
endocarditis] ; or the localization may be chiefly elsewhere, say on the
chordae tendineae (chordal endocarditis), on on the walls of the atria or
ventricle (parietal, or mural, endocarditis). The mitral valve is most
frequently involved (60 per cent of the cases), the mitral and aortic to-
gether (30 per cent of the cases), aortic alone (3 per cent of the cases),
tricuspid or pulmonary alone very rarely.
(a) Acute Endocarditis
Varieties. — Acute endocarditis may be classified on an etiological basis
(rheumatic, gonococcal, etc.), or on a pathological-anatomical basis. The
following main types are distinguishable :
(1) SIMPLE VEGETATIVE AND BENIGN ENDOCARDITIS (Thrombo-endo-
carditis super ficialis, Endocarditis verrucosa, Endocarditis simplex). —
This is frequent as a complication of tonsillitis, rheumatism and other
infectious diseases (chorea, scarlet fever, measles, gonorrhea, pneumonia,
diphtheria). Numerous, minute, grayish-white deposits occur at the line
of closure of the valves, on the chordae tendineae, or on the parietal endo-
cardium ; the warty deposits (or vegetations) are minute thrombi made up
of blood platelets, white and red corpuscles and a little fibrin. The endo-
thelium beneath them is dead; they lie on the subjacent connective tissue,
which, proliferating, may later invade them; hence adhesions, thicken-
ings, scarring and retractions develop and lead to chronic valvular diseases
(stenosis, insufficiency) especially in recurring endocarditis.
(2) SEPTIC, ULCERATIVE., OR MALIGNANT ENDOCARDITIS (TJirombo-
endocarditis septica, Endocarditis ulcerosa). — Here one sees a similar
process, but the thrombi are larger and coarser and there is more extensive
destruction of valve tissue. Ulcers occur on the valves, and smears from
these at autopsy show many bacteria, usually cocci ; the parietal ulcers,
especially on the septum over the left branch of the His bundle, are not
THE IJSTFLAMMATOKY CARDIOPATHIES
873
uncommon. Occasionally, a heart aneurism occurs and even perforation.
Many bacteria (streptococci, pneumococci, staphylococci, gonococci) have
been isolated during life in blood cultures from these cases. Septic emboli
are formed, which cause infarction of the kidneys, spleen, heart muscle and
brain, with the formation of miliary abscesses. JSTo hard and fast line can
be drawn between the severer forms of rheumatic endocarditis and ordi-
nary septic thrombo-endocarditis. Differences may depend upon degrees
of virulence of the invading bacteria.
Symptoms. — In the SIMPLE, BENIGN FORM, subjective symptoms, other
than those of the primary infection with its fever and leukocytosis, may
be slight or absent, or there may be oppression and pain in the precordicl
region with tachycardia and a sense of palpitation. Objectively,
soft systolic murmurs are audible at the apex or, more rarely, over
the aorta. There is usually accentuation of the pulmonic second sound.
There is danger, in the acute stage, of embolism and of infarction (brain,
heart, spleen, kidneys, intestine). There may be cyanosis of the face,
arms and legs, associated with pallor due to anemia. The maximal and
minimal blood pressures
fall. The size of the heart
often increases, owing to
more or less dilatation.
Pericarditis, myocarditis
and pleuritis are common
complications. In the rheu-
matic cases, the endocardi-
tis may be associated with
tonsillitis, polyarthritis, or
chorea. There is nearly al-
ways a leukocytosis. Lesions
in the parietal endocardium
may lead to fibrosis and to
conduction disturbances.
Most cases of chronic in-
flammatory cardiopathy are
sequels of acute endocardi-
tis and acute myocarditis.
In the SEVERE, SEPTIC,
TJLCERATIVE FORM, the
symptoms are usually more
stormy at onset, though they
may sometimes resemble
those in the milder form.
Usually, there is high fever,
with joint pains, chills,
Fig. 276. — Erythema multiforme with Chorea, Mitral
Insufficiency and Stenosis and Chronic Tonsil-
litis. (Med. Service, J. H. H.)
874 DISEASES OF THE CIECULATOEY APPARATUS
sweats, and outspoken polymorphonuclear leukocytosis and anemia. Tachy-
cardia, palpitation, dyspnea, and prostration are prominent phenomena.
Not infrequently, conjunctival, retinal, or subcutaneous hemorrhages occur,
the latter often in petechial form. The urine contains albumin, casts, and,
sometimes, blood. The spleen is usually palpable (acute splenic tumor).
Murmurs (systolic or diastolic) become audible over the heart. Signs of
acute circulatory insufficiency may be present, or the signs of myocardial
insufficiency with dilatation of the heart gradually develop. As a result
of septic emboli, the signs of infarction of the kidneys, spleen, intestine,
brain, lungs, or heart may appear.
Clinically, several types are distinguishable (Osier) : (1) septic type,
with rigors, sweats, irregular fever and bacteriemia; (2) typhoid type,
with more continuous fever, early prostration, delirium, diarrhea, drench-
ing sweats and petechiae; the heart signs may be insignificant; (3)
cardiac type of Bramwell, with the acute infection superimposed upon an
old valve lesion; (4) cerebral type, simulating meningitis; (5) the more
chronic or subacute infective type, resembling recurring malarial attacks
extending over many months (6 to 13), in which there are fever, recurring
chills, and progressive weakness. (See Endocarditis lenta).
Diagnosis. — The condition will be discovered, in the majority of cases,
if the patient be carefully studied by physical and by laboratory methods.
The fever, the tachycardia, the leukocytosis, the development of heart
murmurs, and the presence of a primary focus of infection, are clews to
diagnosis. The mildness or the severity of the symptoms and the course,
but, more particularly, the character of the bacteria found in the blood by
cultural methods, will help to distinguish the simple from the ulcerative
form. In the cases resembling typhoid fever, the pulse rate, the leukocy-
tosis, and the blood culture differentiate. In the cerebral type, the positive
blood culture and the negative findings in the cerebrospinal fluid obtained
by lumbar puncture will rule out meningitis. The blood culture is essen-
tial, and media of different kinds should be employed in order that the
etiological agent may be discovered ; the gonococcus, the influenza bacillus,
and the rheumatic coccus of Rosenow are difficult to grow except on special
media. It would be unfortunate, too, to miss the streptococcus viridans
of endocarditis lenta, on account of the grave prognosis in the latter condi-
tion.
It should be remembered that the occurrence of "accidental" murmurs
in acute febrile infections may mislead, when no endocarditis exists.
Again, if an old valvular lesion be present, the murmur may be mistaken
for that of acute endocarditis, if the previous condition of the patient be
unknown. Not infrequently, however, an acute endocarditis is superim-
posed upon an old valvular lesion.
THE IKFLAMMATOKY CAEDIOPATHIES 875
References
Babcock (R. H.). Endocarditis due to streptococcus rheumaticus and that due to strepto-
coccus viridans, illustrated by specimens, together with discussion of etiology
and prognosis. J. Mich. M. Soc., Grand Rapids, 1913, xii, 645-647.
Cautley (!?.)• The modern treatment of heart disease in children. Clin. J London 1913-
14, xlii, 486-489.
Dreschfeld (/.)• Revised by T. M'Crae. Acute simple endocarditis. In- Syst Med
(Allbutt & Rolleston). 8°. London, 1909, vi, 261-275.
Dunn (C. #.)• Cardiac disease in childhood, with special reference to prognosis. Am J
Dis. Child., Chicago, 1913, vi, 104-116.
Gaskell (J. F.). The lesions of the kidney in ulcer alive endocarditis. Proc. Roy Soc Med
London, 1913-14, vii, Path. Sect., 109-118.
Lamb (A. R.) & Paton (E. W.). A case of vegetative endocarditis caused by a hitherto
undescribed spirillum (Spirillum surali N. £.). Arch. Int. Med 1913
xii, 259-272.
Norris (G. W.). The infectious febrile heart. Penn. M. J., Athens, 1912-13, xvi, 97-104.
Oille (J. A.}, Graham (D.) & Detweiler (H. JK.). Streptococcus bacteremia in endocardi-
tis; its presence before and during the development of endocardial signs.
J. Am. M. Ass., Chicago, 1915, Ixv, 1159-1163.
Osier (TF.). The Goulstonian lectures on malignant endocarditis. Brit. M. J., London
1885, i, 467; 522; 577; 607.
Osier (Sir William}. Acute endocarditis. Mod. Med. (Osier & McCrae). 2. ed.
Philadelphia & New York, 1915, iv, 148-165.
Thayer (W. S.) & Blumer (G.). Ulcerative endocarditis due to the gonococcus; gonor-
rhoeal septiccemia. Johns Hopkins Hosp. Butt., Baltimore, 1896, vii,
57-63.
Weber (F. P.}. Osier's sign and certain cutaneous phenomena sometimes associated with
heart disease. Quart. J. Med., Oxford, 1913, vi, 384-890.
(6) Subacute Infective Endocarditis (Endocarditis lento)
Definition. — A subacute inflammation of the lining membrane of the
heart, due to infection with the Streptococcus viridans, almost always
terminating fatally after months of illness.
Pathology. —The portal of entry is often an infected tooth, or a pyorrhea
alveolaris, though other portals may, in some instances, be responsible. Rigid,
warty, masses develop on the heart valves, and there is a pronounced tendency
for the process to extend to the mural endocardium; thus, when the mitral valve
is attacked, the endocarditis often spreads to the posterior wall of the left atrium,
and when the aortic valve is diseased, the process goes on to involve the endo-
cardium of the wall of the left ventricle and the ventricular surface of the mitral
cusps. At autopsy, the signs of embolic glomerulo-nephritis are almost always
present (Baehr). Infarctions of various organs (brain, spleen, kidneys) are
usually found.
Symptoms. — The patients have fever over a long period. They become
anemic, sallow, develop petechial hemorrhages, and, sometimes, tender
nodules in the skin of the hands and feet. The urine contains albumin
and casts, and frequently blood, owing to the embolic glomerulo-nephritis
that is nearly always associated. The temperature may become almost
876 DISEASES OF THE CIECULATOEY APPAKATUS
normal for a time, only to recur later on. The duration is from 4 to 18
months, and the possibility of its existence should be thought of in long-
continued fever, with chills, sweats, and leukocytosis, that is otherwise
unexplained. The disease is almost uniformly fatal, though now and then
a case recovers, as has been proven by Libman of New York, who has
made a very careful study of the disease.
Diagnosis. — Failure to diagnose this disease is very common among
general practitioners. Mistaken diagnoses of malaria, pulmonary tuber-
culosis, and subacute rheumatism are often made. Even when an endo-
carditis is recognized, its grave nature often goes unsuspected. And yet,
as a rule, the diagnosis is relatively easy, if malaria and typhoid be ruled
out by blood examinations, if a careful physical examination be made,
if the leukocytes be counted, and especially if endocarditis lenta be thought
of and a search made for the streptococcus viridans by suitable cultural
methods in blood taken by syringe from a vein at the bend of the elbow.
If the first blood culture be negative, others should follow at intervals;
the streptococcus viridans will sooner or later be recovered, if endocarditis
lenta exists. The patients may, for a long time, not seem to be very ill,
and a consultant that makes the diagnosis often has a hard time in con-
vincing the less-experienced practitioner that an exceedingly grave malady
is before him.
References
Baehr (G.). Glomerular lesions of subacute bacterial endocarditis. J. Exper. M.,
Lancaster, Pa., 1912, xv, 330-347.
Billings (Frank}. Chronic infectious endocarditis. Arch. Int. Med., Chicago, 1909, iv,
409-431.
Cautley (/?.). Chronic infective endocarditis. Arch. Pedialr., New York, 1913, xxx,
Coleman (W.). The pseudomalarial types of infective endocarditis. Aw.. J. M. Sc., Phila-
delphia & New York, 1905, n. s., cxxix, 381-390.
Gordinier (H. C.). Pernicious endocarditis. A report of six cases, with four autopsies.
Albany M. Ann., 1913, xxxiv, 317-335.
Hastings (T. W.}. Concerning a polyvalent antigen for the complement-fixation test for
streptococcus viridans infection. J. Exper. Med., Lancaster, Pa., 1914,
xx, 72-80.
Hemsted (H.). Recovery from infective endocarditis (streptococcal) . Lancet. London,
. 1913,10-14*
Border (T. J.). Infective endocarditis, with an analysis of 150 cases and with special refer-
ence to the chronic form of the disease. Quart. J. Med., Oxford, 1908-09,
Libman (/?.). A study of the endocardia! lesions of subacute bacterial endocarditis, with
particular reference to healing or healed lesions; with clinical notes. Am.
J. M. Sc., Philadelphia & New York, 1912, cxliv, 313-327.
The clinical features of cases of subacute bacterial endocarditis that have
spontaneously become bacteria-free. Am. J. M. Sc., Philadelphia & New
York, 1913, cxlvi, 625-645.
Observations on subacute bacterial endocarditis, with special reference to cases
that have become spontaneously bacteria-free. Tr. Internal. Cong. Med.,
1913, London, 1914, Sect. VI, Medicine, pt. 2, 195-211.
THE INFLAMMATORY CARDIOPATHIES 877
Libman (E.} & Celler (H. L.). The etiology of subacute infective endocarditis. Am J
M. Sc., Philadelphia & New York, 1910, cxl, 516-527.
Major (R. H.}. Clinical and bacteriological studies on endocarditis lenta. Johns Hopkins
Hosp. Bull., Baltimore, 1912, xxiii, 326-332.
Osier (W.). Chronic infectious endocarditis. Quart. J. M., Oxford, 1909, ii, 219-230.
(c) Chronic Endocarditis
Definition. — A chronic inflammation of the lining membrane of the
heart.
Etiology. — This probably always begins as acute endocarditis due to
some bacterial infection. In many cases, after the acute process is over,
a slow, more or less slumbering, inflammation continues, with occasional
flare-ups (endocarditis recurrens), resulting gradually in fibrosis of the
valves. Sometimes, the process is insidious from the start, especially in
nephropathic or in tuberculous patients that become infected secondarily
with streptococci of low virulence.
Symptoms. — The signs of valvular disease (q. v.) gradually develop.
Diagnosis. — When signs of a valvular lesion exist without fever, it may
be hard to decide whether a chronic endocarditis is present, or whether
one is dealing with an arrested process. A gradual increase of the signs of
valvular involvement speaks for a continuance of the inflammatory
process.
Atherosclerotic valvular lesions may simulate those due to chronic
endocarditis; formerly, no distinction was made between them.
2. Myocarditis
Definition. — An inflammation of the musculature of the heart.
Etiology. — Two groups of cases are known: (1) myocarditis due to
metastatic infection from some distant primary focus (tonsillitis, diph-
theria, influenza, oral sepsis, etc.) ; and (2) myocarditis due to extension
per continuitatem from an endocarditis or a pericarditis. In some in-
stances, doubtless, the endocardium, the myocardium and. the pericardium
are simultaneously involved as a result of the bacteriemia.
Pathology. — Histologically, several varieties of inflammation of the myo-
cardium are recognizable; clinically, it is difficult enough, as yet, to be sure that a
myocarditis exists, let alone to differentiate the several varieties.
(a) PARENCHYMATOUS FORM (M. parenchymatosa] . — Very common in diph-
theria; more rarely in typhoid and streptococcus infections. Hyaline and waxy
degeneration of heart-muscle fibers ; healing by minute scars. Occasionally, sudden
death in acute stage.
(b) PURULENT FORM (M. purulenta). — Usually a complication of ulcerative
endocarditis, due to infected emboli.
(c) ACUTE INTERSTITIAL MYOCARDITIS (M. inter stitialis acuta). — Minute foci
878 DISEASES OF THE CIRCULATORY APPARATUS
of primary proliferation of fixed tissue cells with aggregations of lymphocytes,
plasma cells and eosinophils; degenerative changes in muscle fibers; healing by
small scars (typhoid, streptococcus and other infections).
(d) RHEUMATIC MYOCARDITIS (M. rheumatica). — Peculiar, submiliary nodules
in interstitial tissue; cells with large nuclei, of connective-tissue origin; some
lymphocytes and eosinophils. Sub-endocardial distribution of nodules, often
destroying parts of conduction system.
(e) TUBERCULOUS AND SYPHILITIC FORMS (M. tuberculosa; M. syphilitica). —
Rare, though gummata of the septum occasionally cause heart block.
Symptoms. — The disease is nearly always a complication of some infec-
tion, especially of rheumatism, diphtheria, sepsis, .typhoid, or scarlet fever.
Fever, pressure or pain in the cardiac region ; pallor or cyanosis, tachycar-
dia or bradycardia, or arhythmia may suggest its development. The heart
is often dilated. Systolic murmurs may be due to relative insufficiency or
to a complicating endocarditis. In severe cases, the stasis phenomena of
decompensation (albuminuria, edema, dyspnea, enlarged liver) appear.
Death may occur suddenly (as in the children who fall over dead in con-
valescence from diphtheria), or gradually through progressive dilatation.
Mild cases recover in a few weeks or months with little or no residue ;
others go on to productive changes (myocarditis chronica) with scar forma-
tion, a form of chronic inflammatory cardiopathy, often spoken of as
chronic fibrous myocarditis.
The senile heart, at autopsy, nearly always contains patches of fibrous
change in the myocardium.'
References
Bard (L.) & Phillippe (€.}. De la myocardite interstilielle chronique. Rev. de med.,
Paris, 1891, xi, 345; 608; 660.
Bricout. (C.). La syphilis du coeur. Paris, 1913, Leclerc. 218 p. 8°.
Fleisher (M. S.) & Loeb (Leo}. Further investigations in experimental myocarditis.
Arch. Int. Med., Chicago, 1910, vi, 427-438.
Huchard (//.) & Flessinger (N.). Syphilis gommeuse du cceur. Rev. de med., Paris,
1907, xxvii, 948-969.
Liebmann (E.). Untersuchungen iiber die Herzmuskulatur bei Infekfionskrankheiten. I.
Zur Frage der eosinophilen Myokarditis. Deutsches Arch. f. klin. Med.,
Leipzig, 1915, cxvii, 488-44?.
Loeb (/>.). Ueber experimentelle Myokarditis. Arch. f. path. Anal., [etc.], Berlin, 1913,
ccxii, 475-476.
Pearce (R. M.). Experimental myocarditis: a study of the histological changes following
intravenous injections of adrenalin. J. Exper. M., New York, 1906,
viii, 400-409.
Ribbert (//.)• Ueber experimentelle Myo- und Endocarditis. Fortschr. d. Med., Berlin,
1886, iv, 1-13.
Thalhimer (W.) & Rothschild (M. A.). Experimental focalized myocardial lesions pro-
duced with streptococcus mitis. J. Exper. M., Lancaster, Pa., 1914, xix,
429-443.
Warthin (A. S.). Primary tissue-lesions in the heart produced by Spirochete pallida. Am.
J. M. Sc., Philadelphia & New York, 1914, cxlvii, 667-672.
THE IOTLAMMATOKY CARDIOPATHIES 879
3. Pericarditis
Definition. — An inflammation of the pericardium, or closed serous sac
that surrounds the heart.
Etiology. — This is always due to bacterial infection ; the fibrinous and
serofibrinous forms are often due to the virus of rheumatic fever. The
bacteria most often responsible are streptococci, staphylococci, pneumo-
cocci and tubercle bacilli.
The bacteria reach the pericardium: (a) through the lymph vessels
(lymphogenous form), as a complication of pleuritis, subphrenic periton-
itis, myocarditis, or mediastinitis ; or more often (b) through the blood
vessels (hematogenous form), as a metastatic infection complicating tonsil-
litis, typhoid or pyogenic infections of various sorts.
Chronic nephritis strongly predisposes the pericardium to infection.
Tuberculous pericarditis is not uncommon, especially as a part of a
polyserositis.
Classification and Pathology. — The acute forms are classified according
to their exudates, since these give rise to different clinical symptoms.
1. FIBRINOUS OK DRY PERICARDITIS (Pericarditis fibrinosa s. sicca)
is the most common form. The fibrinous exudate may be very slight ; when
more abundant, it forms ridges or villi on the epicardium (cor villosum).
On healing, the fibrin may be entirely absorbed, or it may undergo organ-
ization in places, leaving sclerotic patches on the surface of the heart.
Sometimes, pericardial adhesions unite the visceral to the parietal layer.
Occasionally, the whole pericardial cavity is obliterated (total synechia or
concretio pericardii).
2. PERICARDITIS WITH EFFUSION" (Pericarditis exudativa). — Here,
the fibrinous exudate is accompanied by serous, hemorrhagic, purulent, or
putrid effusion.
Symptoms. — In a sharp attack, the patient complains of violent pain
in the region of the heart, shortness of breath, oppression, and a feeling
of anxiety. Sometimes, however, the rxnset is insidious with weakness,
headache, anorexia, and chilly sensations; in such cases, the patient may
experience no pain in the region of the heart.
Dyspnea and cyanosis are nearly always present, even when there is
no marked effusion. There is usually some fever and tachycardia ; some-
times, the pulse is irregular. Over the heart, a pericardial friction rub
(q. v.) may be palpable and audible (pericarditis sicca). If pericarditis
be suspected, one should listen carefully, especially at the base of the
heart, the patient being told to hold his breath after a full inspiration.
If a fluid exudate be poured out (pericarditis exudativa), the friction
rub will disappear. The effusion leads to enfeeblement of the apex beat
and to its displacement downward and to the left. The apex beat some-
880 DISEASES OF THE CIKCULATOEY ' APPAKATUS
times lies medial from the left margin of the area of cardiac dullness. The
areas of cardiac dullness, both superficial and deep, are broadened, since
the fluid tends to collect in the lateral regions of the pericardial sac. As
the effusion grows, the areas of superficial and deep cardiac dullness coin-
cide. One of the earliest signs of pericardial effusion is obliteration of the
Heart
Wall of
pericardial sac
Diaphragm
Fig. 277. — Frontal Section Through a Pericardial Exudate (Half Schematic), Showing the
Pushing Down of the Left Side of the Diaphragm, the Position of the Heart and its
Apex, and their Relation to the Right and Left Portions of the Exudate. (After Cursch-
mann in J. Schwalbe's "Therap. Technik," published by G. Thieme, Leipzig.)
cardiohepatic angle ; instead of being a right angle, it becomes very obtuse.
When the effusion is large, a triangular area of dulness, a little rounded
at the apex, can be made out ; this corresponds to the equilateral triangular
shadow seen on rontgenoscopy.
As the effusion accumulates, the left lung becomes compressed; dulness
can be made out on percussion over the left lower lobe, enfeebled or bron-
chial breathing becomes audible under the angle of the left scapula and
there is increased vocal fremitus.
Pericarditis may cause irritation of the neighboring nerves. Thus,
irritation of the E". vagus or of the !N". recurrens may lead to laryngeal
paralyses or to dysphagia ; irritation of the !NT. phrenicus may cause hic-
cough, paroxysmal eructations, or vomiting.
When a pericardial effusion occurs in young children, an outspoken
heart-boss or voussure may develop. In adults, especially in those that
suffer from emphysema, an effusion may cause a bulging in the epigas-
trium.
3. The signs of adherent pericardium (PERICARDITIS ADIIAESIVA) in-
clude: (1) fixation of apex beat, (2) systolic retraction of the apex and of
THE INFLAMMATOBY CARDIOPATHIES
881
the lower part of the sternum, (3) Broadbent' s sign (q. v.), and (4) dias-
tolic collapse of the veins of the neck. A pulsus paradoxus, in which the
pulse becomes smaller, or actually disappears, during full inspiration, is
occasionally present but is by no means constant.
The diastolic shock or rebound accompanying the second sound may be
markedly exaggerated
over the cardiac area in
adherent pericardium
(Broadbent) ; an in-
tense shock may, in ad-
dition, accompany the
protodiastolic third
heart sound (W. S.
Thayer).
Murmurs are often
present, most often ow-
ing to associated valvu-
lar lesions. But even
in the absence of valvu-
lar disease, a presystol-
ic rumble may be audi-
ble, due perhaps to
stretching of strands of
adhesions when the
atria contract.
When the pericardi- '•i\./ '•'.'•.•;••.
iim is adherent to the $&>£;'£,
diaphragm we may, on /y.V:\ \;:
listening over the stom- ' V.-:';\
ach, hear heart-sounds ''X;.v.-:\
that are loud and metal- ''*&)'•••:
lie in quality (Reiss;
Frangois-Franck) .
If, in adherent peri-
cardium, the anamnesis Fig< 278.
be carefully gone into,
it will often be possible
to get a history of an
earlier febrile attack
accompanied by pains
in the chest and palpi-
tation. . .
Adherent pericardium, if associated with mediastino-pericarditis,
leads, sooner or later, to symptoms of chronic circulatory insufficiency
\ .• ,:-^:v:;-'-:>:--N^
\ . * ...•;'.*.••:••' /. I.-..--'---/ v;;;-
Diagram Showiug Factors that May Affect the
Cardiohepatic Angle (Continued). Displacement of
the Lower Part of the Right Wall of the Pericardium,
either by Effusion or Great Dilatation of Right Auricle,
the Front Projection of the Organs in Mitral Stenosis
is Shown. A, Anterior Medial Border of Right Lung;
B, Right Wall of Superior Cava and Right Atrium;
C, Pulmonic Veins; D, Right Wall of Left Atrium;
E, Right Atrium; F, Diaphragm; G, Right Ventricle.
(After W. J. Calvcrt, J. II. II. Bull.)
882 DISEASES OF THE CIKCULATORY APPAKATUS
(cyanosis, dyspnea, cardiac arhythmia, stasis phenomena). Such symp-
toms are due to atrophy or degeneration of the myocardium and are to
be regarded as danger signals. Unless the adhesions uniting the peri-
cardial sac to the sternum be severed, the outlook is grave; but with
Brauer's operation of cardiolysis, which Kocher calls "thoracolysis peri-
,-v;\v--.\
/.:•;/ V •:/. \
f'f ";v^:>-... • ^:£)W
i§ "^Q^li^fe"'-'
,^lfe^>.., ^/ .Ipti. °
if ^^vS^^iil^M^^ r "
A;:/\ ••-•^~£igfe'~-;'& vx^v;^~
;v;^x- V*4^?:^^i^i'^.^v^:-S']^> ''••-.
fei^' ^f^^fe.;.-^^'-.* '
'Sll^^3^^®^^^
Fig. 278a. — Diagram Showing Factors that May Affect the Cardiohepatic Angle ; Displace-
ment of the Root of the Lung. The Front Projection of an Enlarged Heart in Aortic
Stenosis is Shown, and also the Right Wall of the Pericardium and the Diaphragm in
Two Cases of Pericarditis. A, Jugular Vein ; B, Anterior Medial Border of Lung ;
C, Right Wall of Pericardium, with J, its Corresponding Diaphragm in One Case of
Pericarditis; E, Left Wall of Right Atrium; F, Right Wall of Right Atrium; O, Dia-
phragm of Heart Case ; H, Lower Portion of Pericardial Wall at Point of Maximal
Displacement; /, Inferior Vena Cava. (After W. J. Calvert., J. H. H. Bull.)
cardiaca," many of these patients can he rescued. Kecently, surgeons
have advised removing the sternum and its anterior periosteum, leaving
the posterior periosteum behind (Konig, Blauel), an operation that yields
even better results.
THE INFLAMMATORY CAKDIOPATHIES
883
Fig. 279. — Case of Pericarditic Pseudo<
cirrhosis. (After Cabot, from A. D.
Hirschfeldcr's "Diseases of the
Heart and Aorta," published by
J. B. Lippincott Co., Philadelphia.)
If mediastino-pericarditis exist, the abdomen should also be carefully
examined, for the thoracic condition may be complicated by chronic pro-
ductive perihepatitis (icing-liver)
and ascites (Pick's syndrome). Sec
Part VIII.
Diagnosis. — Pericarditis will
scarcely be overlooked, provided a
careful physical examination be made.
If effusion be present, paracentesis
of the pericardium may be under-
taken and the character of the fluid
determined by bacteriodiagnostic and
cytodiagnostic methods (See Explor-
atory Punctures).
Rontgenoscopy and rontgenogra-
phy are valuable aids in the diagnosis
of adherent pericardium (M. Bene-
dikt ; Stuertz ; Lehmann and
Schmall). The strands of adhesions
are directly visible, though care must
be taken not to be misled by shadows normally present in the lung areas
near the pericardium. When in doubt, an examination should be made
when the structures are rendered tense by a deep inspiration; in adher-
ent pericardium, the margin of the sac will be pulled downward and out-
ward by the strands of adhesions.
References
1. General
McPhedran (A.). Diseases of the pericardium. Mod. Med. (Osier & McCrae). 2. ed.
Philadelphia & New York, 1915, iv, 41-77.
Roberts (F. T.}. Diseases of the pericardium. /;;: Syst. Med. (Allbutt & Rolleston).
8°. London, 1909, vi, 26-104.
2. Surgical
Brauer (L.)« Die Kardiolysis und ihre Indicationen. Arch. f. klin. Chir., Berlin , 1903-04,
Ixxi, 258-267.
Curschmann (H.). Zur Beurtheilung und opsrativen Behandlunj grosser Herzbeutelergusse.
Deutsche Klinik, Berlin u. Wien, 1905, iv, 401-452.
Delatour (H. B.}. Surgery of the pericardium and heart. Am. J. Surg., New York,
1909, xxiii, 114-121.
Bock (€?.)• Paracentesis of the pericardium. Brit. M. J., London, 1906, ii, 1026-1028.
von Eiselsberg (A. F.). Ueber einen Fall von Incision des Herzbeutels wegen eiteriger
Pericarditis. Wien. klin. Wchnschr., 1895, viii, 21-24.
Tessier (J.-P.}. La paracentese du pericarde par la voie postcrieure. Bull, et mem. Soc. m6d.
d. hop. de Paris, 1915, 3. s., xxxix, 413-416.
von Walzel (P. U.)« Ueber Pericardiotoiric. Mitt. a. d. Grenzgcb. d. Med. u. Chir.t
Jena, 1913, xxv, 264-277.
884 DISEASES OF THE CIKCULATORY APPAKATUS
3. Medical
Billings (F.). Clinical observations in pericarditis. J. Am. M. Ass., Chicago, 1901,
xxxvii, 1503-1507.
Blechmann (CV). La dyspnee pericardiaque ; le signe de Hirtz ou "signe des attitudes."
Paris med., 1912-13, xi, 431-435.
Blechmann (Germain). Les epanchements du pericarde, etude dinique et therapeutique ;
la ponction epigastrique de Marfan. Paris, 1913, J. B. Bailliere. 367 p.
No. 172. 8°.
Calveri (/.) & Pigg {T. S.}. Calcification of pericardium following suppurative pericarditis.
Tr. Path. Soc., London, 1897-98, xlix, 31.
Calvert (W. /.)• Position of the heart in pericarditis with effusion. Johns Hopkins
Hosp. Bull, Baltimore, 1907, xviii, 403-409.
A possible means of differentiation between cardiac dilatation and peri-
carditis with effusion. Arch. Int. Med., Chicago, 1909, in, 92.
A possible differential sign between cardiac dilatation and pericarditis
with effusion. J. Am. M. Ass., Chicago, 1910, Iv, 763-767.
Pericarditis with effusion. J. Missouri M. Ass., St. Louis, 1900-07, ill,
389-392.
Gordon (A. R.). Pericarditis with partial heart block. Univ. Toronto Med. Bull., Toron'i,
1915, ii, 9-11.
Still (G. F.). Observations on suppurative pericarditis in children, rdlalrics, New Fc.v,
1901, xii, 332-339.
Taussig (A. E.). The inspiratory exaggeration of the dicrotic wave i:i pericarditis. Tr. AJS.
Am. Phys., Philadelphia, 1914, 535-546.
Warthin (A. S.). Accentuation of the pulmonary second sound an important sign in f':.s
diagnosis of pericarditis. Med. News, Philadelphia, 1895, Ixvi, 395-300.
4. Adhesive Pericarditis
Babcock (R. //.)• Adherent pericardium. J. Am. M. Ass., Chicago, 1301, xxxvii, 1578-
1584.
von Bamberger (//.)• Ueber zwei seltene Herzaffektionen mil Bezujnahme auf die Theorie
des ersten Herztons. Wien. med. Wchnschr., 1872, xxii, 1-4; 25-28.
Brauer (L.). Die Kardiolysis und ihre Indicalionen. Arch. f. klin. Chir., Berlin, 1933,
Ixxi, 258-267.
Broadbent (J. F. //.). Adherent pericardium. London, 1895. 12°.
Broadbent (Sir W.}. Adherent pericardium. Brit. M. J., London, 1898, i, 147-149.
Cabot (R. C.)« Obliterative pericarditis a cause of hepatic enlargement and ascites, with re-
port of a case. Boston M. & S. J., 1898, cxxxviii, 463; 471.
Cooper (C. M.}. The respiratory ratio; a preliminary note. J. Am. M. Ass., Chicago, 1909,
Hi, 1182.
Duroziez (P.). Signes de V adherence du pericarde. Bull. Soc. de med. de Paris (1880],
1881, xv, 60-69.
Francois-Franck (A.}. Des bruits extracardiaques en general, et en particulier des bruits
gastriques rythmes avcc le cceur; contribution au diagnostic de I' adherence
du pericarde. Gaz. hebd. de med., Paris, 1885, 2. s., xxii, 757-760.
Head (G. />.)• Chronic adherent pericarditis (a study of 55 cases}. St. Paul M. J., St. Paul,
Minn., 1905, vii, 251-259.
Hoist (P. F.}. Adhaerent perikardium. Norsk. Mag. f. Laegevidensk., Kristiana, 1914,
Ixxv, 1105-1142. 1 pi. 1 ch.
Kussmaul (A.). Ueber schwielige Mediastino-Pericarditis und den paradoxen Puls.
Berl. klin. Wchnschr., 1873, x, 433; 445; 461.
Lehmann. Pericarditis adhoesiva im Rontgenogramm; kasuislische Mitteilung. Fortschr.
a. d. Geb. d. Rontgenstrahlen, Hamburg, 1905-06, ix, 196-202.
HYDEOPEKICABDIUM 885
Manges (M.). Adherent Pericardium. Internal. Clin., Philadelphia. 1905. 15 s *t
67-73.
Nove-Josserand (G.) & Pehu (M.}. Sur un cas de symphyse cardiaque chez une enfant
de 7 ans, remarquablement amelioree par une operation de Brauer Lyon
med., 1914, cxxii, 1481-1485.
Pick (F.). Ueber chronische, unter dem Bilde der Lebercirrhose verlaufende Pericarditis
(pericarditische Pseudolebercirrhose) nebst Bemerkungen uber die Zucher-
gussleber (Curschmann) . Ztschr. f. klin. Med.. Berlin. 1896. xxix, 385-
410.
Rieder (H.). Das Panzerherz. Fortschr. a. d. Geb. d. Rontgenstrahl.. Hamburg. 1913,
xx, 50-57.
Riess (.£.)• Ueber ein neues Symptom der Herzbeutelverwachsung. Berl. klin. Wchnschr.t
1878, xv, 751.
Weitere Beobachtungen uber einer die Herztone begleitende Magenconsonanz
bei Herzbeutelverwachsungen. Berl. klin. Wchnschr., 1878, xvi, 333.
Salvetti (G.). Contributo allo studio clinico della sinfisi del pericardio mell' eta infantile.
Riv. crit. di din. med., Firenze, 1915, xvi, 17, 33.
Stuertz. Zur Diagnose der Pleuraadhdsionen an Pericard. und Zwerchfell. Fortschr.
a. d. Geb. d. Rontgenstrahlen, Hamburg, 1904, vii, 265-272. 1 pi.
Vaquez (H.) & Bardet (E.}. Etude radiologique de la symphyse cardiaque et des adherences
partielles du pericarde. Arch. d. mat. d. cceur, [etc.], Paris, 1913, vi, 1-22.
von den Velden (R.). Rechtsseitige Cardiolyse. Zentralbl. f. Herzkrankh. [etc.], Dresden
u. Wien, 1915, vii, 10-18. 1 pi.
Venus (E.). Die chirurgische Behandlung der Pericarditis und der chronisch-adhdsiven
Mediastinopericarditis (Cardiolysis). Centralbl. f. d. Grenzgeb. d. Med.
u. Chir., Jena, 1908, xi, 401-416.
Wells (H. G.). The pathology of the healed fibrous adhesions of the pericardium. Am. J.
M. Sc., Philadelphia, 1902, n. s., cxxiii, 241-261.
The pathology of active tuberculosis of the pericardium. J. Am. M. Ass.,
Chicago, 1901, xxxvi, 1451-1458.
Wenckebach (K. F.). Remarks on some points in the pathology and treatment of adherent
pericardium. Brit. M. J., London, 1907, i, 63-68.
5. Tuberculous Pericarditis
Osier (IF.). Tuberculous pericarditis. Am. J. M. Sc., Philadelphia, 1893, n. s. cv, 20-87.
Riesman (D.). Primary tuberculosis of the pericardium. Am. J. M. Sc., Philadelphia
& New York, 1901, n. s. cxxii, 6-21.
E. Non-inflammatory Diseases of the
Pericardium
Among those of chief clinical interest are: (1) hydropericardium, (2)
hemopericardium, and (3) pneumopericardium.
Hydropericardium. — By this is meant a non-inflammatory accumula-
tion of serum within the pericardial sac. It is due either to venous
stasis, to a pathologically increased permeahility of the hlood vessels,
or to hoth. It is met with in chronic circulatory insufficiency (in associa-
tion with hydrothorax, ascites, and general anasarca), in chronic neph-
ropathies, and in cachectic states (carcinoma, chronic tuberculosis). Clin-
886 DISEASES OF THE CIKCULATOEY APPAEATUS
ically, the signs of pleural effusion are present. On paracentesis, the
fluid is found to be a transudate, not an inflammatory exudate.
Hemopericardium. — Blood may accumulate in the pericardial cavity
as a result (1) of partial rupture into it of an aneurism of the heart, of
the ascending aorta, or of the pulmonary artery; (2) of oozing in states
of hemorrhagic diathesis; or (3) of trauma.
If the hemorrhage be large and occur quickly, the patient becomes
dyspneic, cyanotic, and arhythmic, loses consciousness and dies. Should
it be smaller, or occur slowly, the dyspnea and cyanosis are slower in
developing, the area of cardiac dullness increases, and the heart sounds
become, distant. Paracentesis of the pericardium reveals blood.
Pneumopericardium. — An accumulation of air or of gas in the pericar-
dial cavity may be due (1) to trauma in which the chest wall is perfor-
ated; (2) to rupture of a pneumothorax, of a lung cavity, or of a gastric
or esophageal ulcer into the sac; or (3) to putrefactive decomposition of
a pericardial exudate. The area of cardiac dullness is replaced by an area
of resonance or of metallic tympany when the patient is in the recumbent
posture; dullness may appear in the same area when the patient sits up.
The heart sounds have an amphoric or a metallic quality. When liquid
and air are both present, the water-wheel sound (bruit de moulin), may be
heard, and, sometimes, if the patient be shaken, a Hippocratic succussion-
splash may become audible. Pneumopericardium may resemble gaseous
distention of the stomach or a partial pneumothorax near the heart, but
rontgenoscopy and rontgenography will differentiate.
F. Valvular Diseases of the Heart
Definition. — By valvular disease of the heart is meant an interference
with the function of the heart valves due to some organic disease of the
heart.
When the valves close incompletely and allow blood to leak back
through them, we speak of regurgitation or of insufficiency of the valve;
when the valve-edges grow together, or when for any other reason an
orifice is narrowed, we speak of obstruction or stenosis of the valve. In-
sufficiency of a valve will reveal itself during those phases of the cardiac
revolution in which the orifice is normally closed ; a stenosis, on the other
hand, during those in which the orifice is normally open and the blood cur-
rent passing through it. Sometimes insufficiency of a valve is combined
with stenosis of the same valve, though, clinically, one or the other is
usually the more prominent lesion.
Etiology. — Valvular insufficiency and valvular stenosis are usually
endocarditic in origin, though changes in the aortic valve, and sometimes
also in the mitral valve, may be atherosclerotic or luetic in origin. In-
VALVULAK DISEASES OF THE HEART 887
sufficiencies may be due also to widening of the orifices from relaxation
of the muscle ring about the valve in myocardial weakness and in failure
of tonicity (so-called relative or muscular insufficiencies), or they may
follow changes in the papillary muscles (fatty degeneration, inflamma-
tion, fibrosis). Rarer forms of valvular defect are due to congenital anom-
alies, to trauma, or to tumors.
Effects of Valvular Disease. — In valvular disease, the normal mechan-
ism of the heart is disturbed, in that the portion of the heart "down-
stream" from the diseased valve receives less blood than normal, whereas
the portion of the heart "up-stream" gets more. The latter then attempts
to "compensate" for the disturbance ; in valvular insufficiency, it will send
forward a larger amount of blood than normal at each beat, whereas in
valvular stenosis an effort is made to force the blood through the narrowed
orifice with increased force. The insufficiency will thus lead to hyper-
trophy together with dilatation, stenosis (at first) to hypertrophy alone.
As long as the heart muscle is able to adapt itself to these disturbed con-
ditions, the heart is in the stage of compensation. Sooner or later the
heart becomes unequal to the task and there is failure of compensation
(decompensation).
The heart muscle has, normally, remarkable POWERS OF ADAPTATION
to the variable demands made upon the heart for work. The heart can vary
(1) its systolic output and (2) its frequency of contraction; on these two
factors, the amount of blood pumped into the aorta each minute, the so-
called minute-volume, depends.
It is asserted that simply in walking on the level the heart has to
do four times as much work as when the person is at rest, and that
when the body is exerting itself to the utmost the heart does 13 times
the amount at rest (Zuntz). No wonder then that the heart muscle, con-
fronted by a valvular defect that throws more work upon it, can easily
and quickly adapt itself to the new conditions as long as the heart muscle
itself remains uninjured. The increased work calling continuously upon
the reserve force of the heart causes HYPERTROPHY of the musculature of
its walls. In animal experiments, the volume and weight of the muscle
may be demonstrably increased within a month after a valvular lesion
has been produced. The individual muscle fibres enlarge and there
is also an increase in the number of heart-muscle cells. For a long time
it was thought that such hypertrophied hearts have less reserve force than
the normal heart, but recent studies indicate that the reserve forces of
the hypertrophic and of the normal heart are equal in amount.
The increased diastolic filling of the heart in each cardiac cycle accounts
for the increased systolic output ; such a DILATATION of the heart is neces-
sary as a compensatory process, and is spoken of, sometimes, as a physio-
logical or compensatory dilatation. But in larger valve defects, and when
the heart muscle is weakened, the increased diastolic filling is not perina-
888 DISEASES OF THE CIRCULATORY APPARATUS
nently compensated for by increased systolic output and then a pathologi-
cal dilatation occurs, known also as systolic dilatation, or stasis dilatation.
In such cases, the intramuscular connective tissue is stimulated to pro-
liferation and myofibrosis cordis develops.
Sooner, or later, the adaptive powers of the heart begin to fail and
symptoms of DECOMPENSATION begin to appear. This may result from
(1) an extension of the valvular injury (endocarditis recurrens, mesaorti-
tis luetica, atherosclerosis), but more often decompensation sets in because
of (2) degenerative processes in the heart muscle, due to prolonged over-
work, to intoxications, or to infections.
Decompensation may be manifested in the pulmonary circuit by stasis
phenomena in the lungs (heart failure cells in the sputum or a tendency
to chronic bronchitis; later, infarction of the lungs, or pulmonary edema).
Decompensation in the systemic circulation may reveal itself by cya-
nosis, dyspnea and signs of chronic passive congestion in the organs (tender
palpable liver; scanty, dark, albuminous urine; ascites; right-sided hydro-
thorax), by edema of the ankles, or by the occurrence of embolic infarc-
tions (brain, spleen, kidneys). These phenomena have already been dis-
cussed under Chronic Circulatory Insufficiency.
Frequency of Defects of the Several Valves.— Hirschfelder has analyzed
1,781 cases of valvular disease of the heart studied in -the medical clinic at the
Johns Hopkins Hospital (1899-1908), and found the following incidence:
Mitral insufficiency 29 per cent.
Aortic insufficiency 22 "
Mitral stenosis and aortic insufficiency 14 "
Mitral stenosis alone 8 "
Aortic and mitral insufficiency with mitral stenosis. . . 4 "
Aortic insufficiency and aortic stenosis 3 "
Other valvular defects 20 "
Kiilbs, in a collective review, estimates the incidence of the several valvular
diseases as follows:
Mitral insufficiency 20-40 per cent.
Mitral insufficiency and mitral stenosis 6-33 "
Aortic insufficiency 10-22 "
Mitral stenosis alone 5-21 "
Aortic insufficiency and mitral stenosis 3-14 "
Aortic and mitral insufficiency 4-5 "
Other valvular lesions 9-25 "
Age. — In the first decade of life, the valvular lesions found are nearly
all congenital ; in the second and third decades, they are chiefly endocar-
ditic, and, indeed, largely rheumatic in origin and are most often mitral
lesions ; in the third and fourth decades occur the majority of luetic lesions,
VALVULAK DISEASES OF THE HEAKT 889
involving chiefly the aortic valves; and in later life (after the 40th year)
the atherosclerotic lesions, involving the aortic valve or the aortic and
mitral together, predominate.
Recognition. — The existence of valvular disease is recognized largely
by means of auscultation, though percussion and x-ray examinations help
to reveal the changes in the various cavities of the heart that result
from the processes of accommodation and of compensation of the lesion.
In the stage of compensation, an exact diagnosis is usually easily made ;
after the stage of decompensation has set in, there may he more* difficulty,
owing to the complications arising from muscular insufficiencies and the
modifications of the auscultatory signs resulting from the enfeeblement of
the heart muscle.
References
Dean (G.) & Falconer (A. W.}. Primary tumors of the valves of the heart. J. Pathol.
& Bacterial, Cambridge, 1913-14, xviii, 64-74-
Gerhardt (D.). Die Endokarditis. Wien, 1914, 130 p. 8°.
Kent (A. F. S.). On the mechanism of the cardiac valves; a preliminary communication.
Proc. Roy. Soc., London, 1915, Ixxxviii, s. B, 537-541. 1 pi.
Kiilbs (F.). Herzklappenfehler. Handb. d. inn. Med. (Mohr & Staehelin). Berlin, 1914,
a, 1042-1077.
Moritz (F.). Anomalien in der Funktion der Ventileinrichtungen des Kreislaufs. Handb.
d. allg. Pathol. (Krehl & Marchand). Leipzig, 1913, ii, 2, 93-108.
Robinson (G. C.) & Draper (G.). Studies with the electrocardiograph on the action of
the vagus nerve on the human heart. II. The effects of vagus stimulation
on the hearts of children with chronic valvular disease. J. Exper. M.,
Lancaster, Pa., 1912, xv, 14~47.
Stadtler (E.). Die Mechanik der Herzklappenfehler. Ergebn. d. inn. Med. u. Kinderh.,
Berlin, 1910, v, 1-37.
Stengel (A.). Extracardiac causes of failure of compensation in valvular diseases of the
heart. Am. J. M. Sc., Philadelphia & New York, 1913, cxlv, 17-28.
Weichsel (/.). Ueber Mitral- und Anrtenklappenfehler. Report, d. prakt. Med., Berlin,
1915, xii, 177-182.
1. Aortic Stenosis
Narrowing at the aortic orifice gives the left ventricle more work to
do when it empties itself; hence hypertrophy of its walls, with only
moderate, dilatation follows. The right ventricle becomes an appendage
to the left, the wall of the latter bulging into the former.
The apex beat is slightly displaced downward and to the left, and is
not markedly increased in strength; there is very little enlargement of
the heart to the left until dilatation occurs. A loud systolic murmur is
audible in the aortic area; it is propagated especially toward the vessels
of the neck. A palpable systolic thrill is demonstrable in the second right
intercostal space. The second sound in the aortic area is feeble or absent.
The pulse is small, prolonged, and anacrotic; bradycardia is common.
890 DISEASES OF THE CIKCULATOEY APPAEATUS
Orthodiagrams and electrocardiograms point to hypertrophy of the left
ventricle. Syncopal attacks are common.
Reference
Manges (M.). Aortic stenosis; adherent pericardium. Internat. Clin., Philadelphia,
1905, 15. s., I, 62-73.
2. Aortic Insufficiency
Some blood regurgitates from the aorta into the left ventricle during
diastole. Since, in diastole, the ventricle also receives its normal amount
from the left atrium, its cavity dilates. At each systole, a larger amount
of blood is thrown into the aorta and the wall of the left ventricle hyper-
trophies.
The apex beat is forcible, resistant, circumscribed (choc en dome),
displaced markedly to the left and often downward to the sixth intercostal
space. The areas of cardiac dullness are enlarged to the left and upward.
A horizontal position of the heart with dynamic dilatation of the aorta
(large systolic output) can be made out on rontgenoscopic examination.
The electrocardiogram also points to hypertrophy of the left ventricle. A
characteristic blowing murmur, soft, aspirative, commencing with the
beginning of diastole and replacing the sound due to closure of the aortic
valves, or following immediately upon this, can be heard ; this murmur
is sometimes short, occupying only a part of the long pause, but ordinarily
it is long and decrescendo in character, lasting through diastole ; it is
audible in the course of the blood current giving rise to it, i. e., in the
aortic area, along the left margin of the sternum, as far as the xiphoid ;
occasionally, it is maximal at the apex, and, rarely, it can be heard in
the axilla and along the left margin of the heart (Rufus Cole.) Occa-
sionally, the murmur is musical, especially when the insufficiency is due
to rupture of a valve, or to atherosclerosis. The murmur is sometimes
scarcely audible at all, or it may be heard only when the patient sits,
or stands, or takes exercise; it is sometimes heard better with the naked
ear than with the stethoscope. A systolic murmur at the apex, due to
relative mitral insufficiency, is frequently associated with it. The first
sound at the apex is often indistinct. Occasionally, a presystolic mur-
mur near the apex can be heard; this is the "Flint murmur of aortic insuf-
ficiency." Other phenomena pointing to aortic insufficiency include the
pulsus celer or Corrigan pulse, throbbing of carotids, tones (q. v.) and
Duroziez's double murmur in the peripheral arteries ; pallor of the face ;
and a capillary pulse.
Many of the cases of aortic insufficiency are due to luetic aortitis
(Wassermann reaction) ; many to atherosclerosis ; some to endocarditis.
VALVULAR DISEASES OF THE HEART 891
If the Wassermann reaction be positive, especial pains should be taken to
ascertain if an aneurism coexist.
References
Bensaude (R.) & Monod (Mme. Robert). Insuffisance aortique par rupture valvulaire,
chez un soldat ayant recu, au cours d'un corps a corps, un coup de crosse sur
la region precordiale. Bull, et mem. Soc. med. d. hop. de Paris. 1915. 8 s
xxxix, 484-489.
Cohn (A. E.). The formation of endothelial pockets in aortic insufficiency. Proc. N. Y.
Path. Soc., 1914, xiv, 24-27.
Corrigan (D. J.). On permanent patency of the mouth of the aorta or inadequacy of tlie
aortic valves. Edinb. M. & S. J., 1832, xxxvii, 225-245.
Edwards (A. R.). Relative aortic insufficiency caused by chronic fibrous myocarditis. Am.
J. M. Sc., 1895, n. s., ex, 488-444-
Greene (C. L.). Misleading factors in aortic regurgitalion. Arch. Diagn., New York,
1908, i, 124-127.
MacCallum (W. G.)» The changes in the circulation in aortic insufficiency. Johns Hop-
kins Hosp. Bull, Baltimore, 1911, xxii, 197-209.
Saltykow (S.). Beginnende Atheroskkrose der Herzklappen. Beitr. z. path. Anal. u. z.
attg. Path., Jena, 1915; Ix, 321-336.
Stewart (H. A.). Experimental and clinical investigation of the pulse and blood pressure
changes in aortic insufficiency. Arch. Int. Med., Chicago, 1908, i, 102-
147.
Taussig (A. E.) & Cook (J. E.). The determination of the diastolic pressure in aortic
regurgitation. Arch. Int. Med., Chicago, 1913, xi, 542-550.
Thayer (W. S.). Observations on the frequency and diagnosis of the Flint murmur in aortic
insufficiency. Tr. Ass. Am. Physicians, 1901, xiri, 393-409.
Also: Am. J. M. Sc., Philadelphia & New York, 1901, cxxii, 538-552.
Traube (L.). Ueber zwei eigenthiimliche Phdnomene bei Insufficienz der Aortenklappen.
Berl. klin. Wchnschr., 1867, iv, 455; 467.
Also: Ges. Beitr. z. Path. u. Physiol, Berlin, 1871, ii, pt. 2, 793-806.
Wiggers (C. /.). Reflex vasodilalion is not the cause of the collapsing pulse of aortic insuf-
ficiency. Proc. Soc. Exper.Biol. & Med., New York, 1914, xii, 55.
Zollinger (F.). Zur experimentellen Pathologic und Therapie der akuten Aorteninsuffizienz.
Arch. f. exper. Path. u. Pharmakol, Leipzig, 1909, Ixi, 193-209.
3. Mitral Stenosis
The mitral orifice is obstructed and too little blood flows from the left atrium
into the left ventricle in ventricular diastole and, consequently, into the aorta in
ventricular systole. Hypertrophy and dilatation of the left atrium develop; in-
creased pressure in the pulmonary circulation, and hypertrophy of the right ven-
tricle are results of the effort to overcome this. Later, the right ventricle dilates,
when it becomes insufficient for the work required of it. In pure mitral stenosis,
the left ventricle atrophies and becomes an appendage of the right ventricle.
The apex beat is feeble unless the apex is formed by the right ventricle,
when it may be stronger. Visible rotary or wavelike pulsation can be seen
in the precordium. There is enlargement of the area of cardiac dullness
to the right, and Krb'nig's "steplike line" bounding the area of superficial
cardiac dullness on the right, can be made put. A chimney-shaped area.
892 DISEASES OF THE CIRCULATORY APPARATUS
of dullness along the left sternal margin is due to the dilated pulmonary
artery and the enlarged left atrium. Relative dullness over the left atrium
may be demonstrable in the left interscapular space. Mitral configuration
of the heart is characteristic on x-ray examination. Epigastric pulsation
due to the hypertrophied right ventricle is common. A diastolic rumble,
a presystolic murmur, or both, can be heard at the apex, often accompanied
by palpable thrill in the apex region. The first sound at the apex is a
loud snap, with corresponding abrupt palpable shock (durete cloturale) ;
the pulmonary second sound is strongly accentuated. Double, or split,
second sounds are audible at the base and, sometimes, at the apex. The
pulse is small, soft, and often irregular. There is a high P-wave on the
electrocardiogram when the atrium is hypertrophied and active.
In both mitral stenosis and mitral insufficiency, the patients may ex-
hibit a "high color" in the cheeks and slight cyanosis of the lips (mitral
fades) .
Most important in making the diagnosis are (1) the palpable thrill
and the rumble, in diastole, (2) the snapping first sound, (3) the accen-
tuated and split second sound in the pulmonary area. In the late stages,
a pulsus irregularis perpetuus, due to atrial fibrillation, is common. Em-
bolism is a very common complication in mitral stenosis.
References
Cabot (R. C.). Mitral stenosis: observations on 200 cases. Before and after death. Also
on 116 cases not autopsied. Tr. Ass. Am. Physicians, Philadelphia,
1914, xxix, 22-48.
Fetterolf (G.) & Norris (G. W.). The anatomical explanation of the paralysis of the left
recurrent laryngeal nerve found in certain cases of mitral stenosis. Am.
J. M. Sc., Philadelphia & New York, 1911, cxli, 625-638.
Goodhart (Sir J. P.). The right-sided murmurs of mitral stenosis; their bearing on the
course of the disease. Lancet, London, 1915, ii, 7-10.
Hirschf elder (A. D.}. The volume curve of the ventricles in experimental mitral stenosis,
and its relation to physical signs. Johns Hopkins Hosp. Bull., Baltimore,
1908, xix, 319-322.
Lewis (7\). The time relations of heart sounds and murmurs, with special reference to the
acoustic signs in mitral stenosis. Heart, London, 1913, iv, 241-254.
MacCallum (W. G.) & McClure (R. D.}. On the mechanical effects of experimental
mitral stenosis and insufficiency. Johns Hopkins Hosp. Bull., Baltimore.
1906, xvii, 260-265.
Osier (W.). De la paralysie du nerf recurrent gauche dans les affections mitrales. Arch,
d. mal. du coeur [etc.], Paris, 1909, ii, 73-76.
Pegler (L. H.). X-ray photograph illustrating the thoracic appearances in a case of left
recurrent paralysis associated with mitral stenosis. Proc. Roy. Soc. Med.,
London, 1914-15, viii, Laryngol. Sect., 80-82.
Pezzi (C.) & Lutembacher (R.). Sur le mecanisme du rythme a trois temps de la stenose
mitrale. Arch. d. malad. d. coeur, etc., Paris, 1913, vi, 561-573.
Ritchie (W. T.}. The absence of certain mitral murmurs in mitral disease. Edinb. M. J.,
1913, x, 410-414.
Steell (G.). Mitral stenosis. Internal. Clin., Philadelphia, 1898, 8. s.. Hi, 144-154-
VALVULAR DISEASES OF THE HEART 893
4. Mitral Insufficiency
During systole, part of the blood from the left ventricle regurgitates
through the insufficient mitral valve into the left atrium; hence, dilata-
tion of the left atrium occurs and there is increased pressure in the pul-
monary circulation, which, in turn, leads to hypertrophy (and later to
dilatation) of the right ventricle and accentuation of the pulmonary second
sound. An increased amount of blood passes from the dilated left atrium,
during diastole, into the left ventricle, and leads to dilatation of the
latter. The left ventricle, pumping out larger amounts of blood than
normal, hypertrophies.
The apex beat is forcible and diffuse ; it is displaced somewhat lateral-
ward. The areas of cardiac dullness are enlarged to the left and, in severe
cases, also to the right. A chimney-shaped area of dullness may be demon-
strable near the sternum in the second intercostal space. Mitral configura-
tion of the heart is visible on x-ray examination. A systolic murmur of
blowing quality is audible ; it is maximal at the apex, often replacing the
first sound there. This murmur is decrescendo in character, usually holo-
systolic, and is propagated toward the axilla and the angle of the scapula in
the back. The pulmonary second sound is accentuated. The pulse is of
normal volume and tension in the stage of compensation, becoming small
and irregular when decompensation sets in. Symptoms of chronic passive
congestion of the lungs are common ; there is a tendency to bronchitis and
the sputum contains cells filled with brown pigment ("heart-failure cells").
There may be dyspnea on slight exertion, and cyanosis, even when the
heart is fairly-vell compensated. The distinction between mitral insuffi-
ciency due to valvulitis and that due to muscular relaxation has been re-
ferred to above (see Heart Murmurs).
References
Gerhardt (/>.)• Uber die Compensation von Mitralfehlern. Arch. f. exper. Path. u.
PharmakoL, Leipzig, 1900-01, xlv, 186-209.
Prince (M.). Physiological dilatation and the mitral sphincter as factors in functional and
organic disturbances of the heart. Am. J. M. Sc.} Philadelphia & New
York, 1901, n. s. cxxi, 188-208.
5. Pulmonary Stenosis
This is a rare lesion, usually congenital, and then often combined with
other anomalies in so-called "blue babies" (morbus caeruleus). There is
hypertrophy and, later, dilatation of the right ventricle. A systolic mur-
mur is audible ; it is maximal in the pulmonary area, and is accompanied
by a palpable thrill. The pulmonary second sound is feeble or absent
Dyspnea is present on exertion. The child has Hippocratic fingers.
894 DISEASES OF THE CIBCULATOKY APPAEATUS
All forms of endocarditis in fetal life tend to affect the right side of
the heart; in postnatal life, it is only the gonococcic form of endocarditis
that shows this tendency.
References
Carrel (A.}. Experimental operations on the sigmoid valves of the pulmonary artery. J.
Exper. Med., Lancaster, Pa., 1914, xx, 9-18.
Tuffier (T.) & Carrel (A.}. Patching and section of the pulmonary orifice of the heart. J.
Exper. Med., Lancaster, Pa., 1914, xx, 3-8.
6. Pulmonary Insufficiency
This lesion, too, is often congenital, though, occasionally, it is acquired.
The mechanical effects on the right ventricle, here, are similar to those on
the left ventricle in aortic insufficiency. Dilatation and hypertrophy of
the right ventricle occur, as shown by percussion and on x-ray examina-
tion. A chimney-shaped area of dullness may be demonstrable in the
second and third left intercostal space, close to the sternum, due to the
dilated pulmonary artery. A loud, aspirative, diastolic murmur is audible
in the pulmonary area and over the right ventricle. The pulse is usually
small in volume.
References
Barie (#.)• Recherches sur Vinsuffisance des valvules de Vartere pulmonaire. Arch. gen. de
med., Paris, 1891, i, 650; ii, 80; 83.
Cautley (E.). Case of pulmonary regurgilation. Proc. Roy. Soc. Med., London, 1914-15,
viii, Sect. Stud. Dis. Child., 65-69.
Rudolf (R. />.)• Passing leakage of the pulmonary valve. Am. J. M. Sc., Philadelphia
& New York, 1911, n. s. cxlii, 328-334.
7. Tricuspid Stenosis
This is an extremely rare lesion. It leads, first, to hypertrophy and,
later, to dilatation of the right atrium. General venous stasis develops
early. Enlargement of the right atrium may be demonstrable on per-
cussion and on x-ray examination. A diastolic, or a presystolic, murmur
is audible, sometimes accompanied by a palpable thrill, in the tricuspid
area. A presystolic wave can be made out on the hepatic pulse ; and a
high a-wave is seen on the jugular phlebogram in the early stages before
the atrium is paralyzed.
CONGENITAL DISEASES OF THE HEART 895
References
Fenwick (#.). On tricuspid stenosis. Lancet, London, 1881, i, 653.
Futcher (T. #.)• Tricuspid stenosis, with a report of five cases. Am. J. M. Sc., Phila-
delphia & New York, 1911, cxlii, 625-636.
Herrick (J. /?.)• Tricuspid stenosis, with reports of three cases wiih autopsies, together with
abstracts of forty cases reported since Leudet's thesis (1888). Boston M.
& S. J., 1897, cxxxvi, 245-252.
8. Tricuspid Insufficiency
This is most often a relative insufficiency, due to dilatation of the
right ventricle ; occasionally, an insufficiency of endocarditic origin occurs.
Blood regurgitates from the right ventricle through the right venous orifice
into the right atrium at each systole. Dilatation of the right atrium and
atrial paralysis follow, and there is general venous stasis.
Marked increase of the area of cardiac dullness to the right can be
made out, and there is broadening of the heart shadow on x-ray examina-
tion. A systolic blowing murmur can be heard in the tricuspid area
and over the right ventricle ; it is not transmitted to the left beyond the
apex, and is not audible in the axilla or in the back. When the insuffi-
ciency is relative, the murmur varies with the degree of dilatation of the
right ventricle. The pulmonary second sound is feeble. The jugular
phlebogram is of the "ventricular type." Enlargement and pulsation of
the liver can be made out. The spleen may be palpable. The pulse is
small.
References
Calvert (W. /.)- Rok of venous congestion in compensation of tricuspid insufficiency.
Arch. Int. Med., Chicago, 1908, i, 277-284.
Esmein (C.). Les symptomes caracteristiques de V insuffisance tricuspidienne et particuliere-
ment le pouls veineux ventriculaire. Ann. de med., Paris, 1914, ii, 193—
221.
Hering (H. E.). Kann man klinisch die Trikuspidalinsuffizienz diagnostizieren. Med.
Klin., Berlin, 1909, v, 1426.
G. Congenital Diseases of the Heart
Pulmonary stenosis and pulmonary insufficiency, as congenital lesions,
have been referred to above under Valvular Diseases.
Persistent ductus arteriosus Botalli occurs, usually along with other
anomalies of the heart. The right ventricle hypertrophies; a chimney-
shaped dullness can be made out to the left of the sternum in the first, sec-
ond, and third intercostal spaces (dilated pulmonary conus). On rontgeno-
896 DISEASES OF THE CIKCULATOKY APPAKATUS
scopy, marked systolic dilatation of the second of the three curves on the
left margin of the cardiovascular stripe can be seen. A systolic thrill and
a systolic murmur are demonstrable over the pulmonary area.
Patent interventricular septum and patent foramen ovale, are defects
that rarely occur singly, and the diagnosis may be difficult to establish
intra vitam. In defect of the interventricular septum, a loud, rough, high-
pitched systolic murmur, often obscuring the two heart sounds, is audible at
the level of the third left intercostal space, or at the level of the fourth
chondrosternal articulation, on
the same side (Eoger) ; it is
sometimes audible in the whole
precordial region. It is propa-
gated in a transverse direction
— never toward the left clavicle
— a fact that distinguishes it
from the murmur of pulmonary
stenosis. The murmur begins
with systole and is audible dur-
ing both of the normal sounds
of the heart. A thrill may, or
may not, accompany it. Hyper-
trophy and dilatation of the
Fig. 280.— Distribution and Character of the Mur- . £ J
mur Due to a Patent Interventricular Septum right heart OCCUr.
(Roger's Murmur). (From A. D. Hirsch- P/j//»W iornmp'n nvnlp miv
felder's "Diseases of the Heart and Aorta," aa7
published by j. B. Lippincott Co., Phiia- yield no physical signs as long
as the pressure relations in the
two atria are normal. When the pressure rises in either atrium, blood
will. flow through the orifice and may produce murmurs (systolic, dias-
tolic, or both). Occasionally, paradoxical embolism occurs; by this is
meant transport of thrombi from the body veins directly into the general
arterial circulation. Another peculiarity is the occurrence of a "ven-
tricular type'7 of jugular phlebogram in mitral insufficiency associated
with patent foramen ovale ; it is due to regurgitation of blood from the left
ventricle into the left atrium, and, thence, through the foramen ovale into
the right atrium, the vena cava superior and the jugular vein.
Stenosis of the Isthmus of the Aorta. — This anomaly is usually easily
recognizable, from
(1) Signs of dilatation of aorta (dullness in the second and third
right intercostal space ; high pulsation of the aorta in jugular fossa ; rela-
tive insufficiency, with marked dilatation and hypertrophy of the left ven-
tricle) ;
(2) Marked dilatation and visible pulsation of the arteries in the
upper half of body, with small, delayed pulse in the vessels of the lower
half of the body ;
CONGENITAL DISEASES OF THE HEAKT
897
(3) Collateral circulation between
the upper half and the lower half of
the body in the form of visible, tortu-
ous, pulsating, superficial arteries on
the trunk (there may be a systolic
thrill and a murmur in these).
Transposition of the Heart (Situs
inversus cordis). — Congenital dextro-
cardia is usually a part of a general
situs viscerum inversus. The apex-
beat is in the fifth intercostal space
between the right parastcrnnl and
mammillary lires. The areas of car-
diac dullness, and the cardiovascu-
lar stripe on x-ray examination, pre-
sent a mirror picture of the normal
relations. The electrocardiogram is
characteristic.
Ectopia cordis. — As a congenital
anomaly the heart may be so displaced
as to lie no longer within the thorax.
Thus it may lie (1) high up in the
neck (cervical heart), (2) on the front
of the chest, when there is fissure of the
sternum (pectoral heart), or (3) in the
abdominal cavity, when the diaphragm
is defective (abdominal heart).
Fig. 281. — Ectopia cordis Secondary to
Malformation of the Sternum — Pec-
toral Heart. (After G. Fay, "Arch,
des Maladies du coeur," published
by Bailliere et Fils, Paris.)
References
Abbott (Maude E.}. Congenital cardiac disease. Mod. Med. (Osier & McCrac). 2. ed.
Philadelphia & New York, 1915, iv, 823-448.
Abelmann (M.}. Diagnose und Prognose der angeborenen Herzfehler. Ergebn. d. inn.
Med. u. Kinderh., Berlin, 1913, xii, 143-159.
Black (D. />.). Two cases of cardiac malformation; more especially of the infundibular
region. J. Anat. & Physiol., London, 1913-14, xlviii, 274-^79.
Campergne (Berthe). Contribution d V etude de la cyanose congenitale. Paris, 1913,
Oilier & Henry. 67 p. No. 249. 8°.
Clarac (G.}. Origine infectieuse des malformations congenitales du coeur et des vaisseaux,
d'apres M. Letulle. Arch. d. mal. du coeur [etc.], Paris, 1914, vii, 664-
566.
Einthoven (P. H.). Das Elektrokardiogramm bei angeborenen Herzfehlem. Zentralbl. f.
Herzkrankh. [etc.], Dresden & Leipzig, 1915, vii, 101-108. 1 pi.
Foster (N. /?.)• A. study of the nitrogen- and sulphur-metabolism in morbus ceruleus. Arch.
Int. Med., Chicago, 1910, vi, 24-27.
898 DISEASES OF THE CIKCULATOEY APPAKATUS
Hamilton (W. F.) & Abbott (Maude E.}. Patent ductus arteriosus with acute infective
pulmonary endarleritis. Tr. Ass. Am. Phys., Philadelphia, 1914, xxix,
294-308.
Hotz (August). S chs Fdlle von Transposition der grossen Herzarterienstdmme. Zurich,
1913, Leeman & Co. 39 p. 8°.
Kocemba (Josef). Ein Fall von Stenose am Isthmus aortas. Bonn, 1913, H. Trapp.
28 p. 8°.
Loeser (A.). Ueber kongenitale Aortenstenose und fotale Endokarditis. Arch. f. path.
Anat. [etc.] (Virchow), Berlin, 1915, ccxix, 309-319.
Miller (R.) & Orton (G. H.). A case of patent ductus arteriosus, with skiagram. Brit.
J. Child. Dis., London, 1913, x, 109-111.
Miiller (H.). Zwei Fdlle von Offenbleiben des BotalWschen Ganges. Cor.-BL f. Schweiz.
Aerzte, Basel, 1915, xlv, 85.
Drei Fdlle von angeborener Liicke der Kammerscheidewand. Cor.-BL f.
Schweiz. Aerzte, Basel, 1915, xlv, 86.
Neuhof (S.). A case of congenital familial dexirocardia. J. Am. M. Ass., Chicago, 1913,
Ix, 1064-1065.
Powell (Sir R. D.}. On a case of congenital disease of the heart, presumably constriction with
arrested development of the infundibulum (bulbus cordis) and pulmonary
artery and patent septum ventriculorum. Clin. J., London, 1915, xliv, 121-
126.
Robertson (J. /.)• The comparative anatomy of the bulbus cardis, with special reference
to abnormal positions of the great vessels in the human heart. J. Pathol.
& Bacterial, Cambridge, 1913, xviii, 191-210.
Roger (//.)• Recherches cliniques sur la communication congenitale des deux caeurs, par
inocclusion du septum interventriculaire. Bull. Acad. de mcd., Paris,
1879, 2. s., viii, 1074; US9.
Vierordt (H.). Die angeborenen Herzkrankheiten. Wien, 1898, A. Holder. 225 p. 8°.
Forms pt. ii, vol. xv, of Spez. Path. u. Therap. (Nothnagel).
H. The Chronic Toxic-degenerative
Cardiopathies
Under valvular diseases and chronic myocarditis, above described, are
included the chronic cardiopathies of inflammatory origin (cardiopathia
chronica inflammatoria) . In contrast with these are the chronic cardi-
opathies that are degenerative or circulatory, and not inflammatory, in
origin (cardiopathia chronica degenerativa s. circulatoria) . This group
includes :
(1) The atherosclerotic cardiopathy (C. atherosclerotica) .
(2) The fatty cardiopathy or heart of obesity (C. adipositatis) .
(3) The nephropathic cardiopathy (C. nephropathicorum).
(4) The thyreotoxic cardiopathy (C. thyreotoxica) .
In these different forms of myodegeneratio cordis, it is not uncommon,
toward the end, to see an atrial fibrillation, with pulsus irregularis per-
petuus, develop.
CHKOOTC CAKDIOPATHIES 899
References
Longcope (W. 7\)« The effect of repeated injections of foreign protein on the heart muscle.
Arch. Int. Med., Chicago, 1915, xv, 1079-10S4.
Powell (Sir R. /).). Diseases of the myocardium. In: Syst. Med. (Allbutt & Rolleston)
8°. London, 1909, vi, 105-129.
Williamson (C. S.). The effects of exercise on the normal and. pathological heart; based
upon the study of one hundred cases. Am. J. M. Sc., Philadelphia, 1915.
cxlix, 492-503.
1. The Atherosclerotic Cardiopathy (Cardiopathia
atherosclerotica)
This may depend (a) partly upon increased resistance to the arterial
flow due. to the sclerosis of the peripheral vessels and to the arterial hyper-
tension often accompanying it, leading especially to hypertrophy of the
Jeft ventricle; (b) upon sclerosis of the coronary arteries, leading to sec-
ondary thrombosis of their smaller branches with necrosis of the heart
muscle, and; later, scarring; (c) upon atherosclerosis of the aortic and
mitral valves and of the annulus fibrosus, the sclerosis and calcification of
these valves and of the fibrous ring leading to stenoses and insufficiencies.
Atherosclerotic cardiopathies rarely become noticeable before the for-
tieth year. The predisposing causes include potatorium, syphilis, lead-
poisoning and physical overexertion. The early hypertrophy gives way,
later, to dilatation and to all the signs of myocardial, or chronic circulatory,
insufficiency. Marked bradycardia, cardiac asthma and stenocardiac at-
tacks (angina pectoris) are suggestive of the atherosclerotic heart and
particularly of the form due to coronary sclerosis. Sudden death often
follows upon thrombosis or embolism of one of the larger coronary vessels.
The His bundle is frequently involved in the atherosclerotic cardi-
opathy, the lesions revealing themselves by delay of conduction (or by
partial or complete heart block) and the Morgagni- Adams-Stokes syndrome.
2. The Fatty Cardiopathy or Heart of Obesity
(Gardiopathia adipositatis)
This is due to a marked proliferation of the epicardial adipose tissue
arid a growth of fatty tissue between the, muscle fibers of the myocardium,
especially in the conus of the right ventricle. The injury to the heart is
probably due less to the local fatty infiltration than to the demands made
by the general obesity of the body upon a heart relatively too small to
meet them.
The obesity is usually complicated also by myodegeneratio cordis and
by atherosclerotic lesions.
900 DISEASES OF THE CIKCULATOKY APPAKATUS
The hypertrophy and dilatation of the heart are best made out on x-ray
examination, since obesity interferes with satisfactory percussion and
localization of the apex beat. Dyspnea on exertion, cardiac asthma, steno-
cardiac and syncopal attacks are. common. The blood pressure is often ele-
vated, especially in patients with associated arteriolar sclerosis.
References
Borchers (E.). Die Rolle der Fettphanerose bei der krankhaften Verfettung der Herzmusku-
latur. Arch. f. path. Anal, [etc.] (Virchow), Berlin, 1914, ccxviii, 37-47.
Dickey (W. A.). Myocardial changes following the acute infectious fevers. Med. Rec., New
York, 1915, Ixxxvii, 142-145.
Eyselein (K.). Untersuchungen uber den Fettgehalt der Herzmuskulatur. Arch. f. path.
Anat. [etc.] (Virchow), Berlin, 1914, ccxviii, 80-37.
Kisch (E. H.). ZurLehre vom Mastfettherzen. Wien. med. Wchnschr., 1902, Hi, 545-548.
Krehl (L.). Ueberfettige Degeneration des Herzens. Deutsches Arch.f. klin. Med., Leipzig,
1892-93, li, 416-450.
von Noorden (C.). The treatment of obesity complicated by diseases of the circulatory organs.
Internat. M. Mag., New York, 1902, xi, 400-404.
Satterthwaite (T. E.). Corpulence and the fatty heart, with cases. Postgraduate, New
York, 1899, xiv, 197-208.
3. The Nephropathic Cardiopathy (Cardiopathia
nephropathicorum)
(Traube's Heart)
The nephropathic cardiopathies are most marked in patients that suffer
from contracted kidneys with continuous arterial hypertension. In addi-
tion to the hypertension as a cause of the heart hypertrophy, direct toxic
factors have to be considered, since the hypertrophy affects the whole heart
and not merely the left ventricle. Hypertrophy of the adrenal medulla
has been pointed out recently as an accompaniment of the heart hypertro-
phy in contracted kidney and it has been suggested that an increased secre-
tion of epinephrin may explain the arterial hypertension. The proof has,
however, yet to be brought. The permanent vasoconstriction tends soon to
be accompanied by general atherosclerosis, which, in turn, hastens the de-
velopment of myocardial insufficiency. The signs of decompensation of
the heart begin with dyspnea, malleolar edema and uremic phenomena.
References
Pdssler (H.}. Ueber Ursache und Bedeutung der Herzaffektion Nierenkranker. Samml.
klin. Vort., Leipzig, 1906, n. F., No. 408. (Inn. Med., No. 123, 525-548.)
Riesman (/>.)• High arterial pressure: high pressure hypertrophy of the heart. Am. J.
M. Sc., Philadelphia & New York, 1913, cxlv, 487-494-
ANGINA PECTOKIS 901
4. The Thyreotoxic Cardiopathy
(Cardiopathia thyreotoxica)
There is every transition from the mild tachycardia of slight grades of
hyperthyroidism to the grave cardiopathies with hypertrophy, dilatation
and ultimate asystole of the severer cases. In every unexplained tachy-
cardia, hyperthyroidism and thyreo-intoxication should be kept in mind
as a possible cause. Whether the thyreotoxic substances act directly uoon
the heart muscle, or chiefly upon the nervous system (stimulation of the
accelerators) is not known. The diagnosis is usually easy. (See Graves's
Disease and Thyreotoxicosis). Atrial fibrillation may be a late phe-
nomenon.
References
Dernini (G.). II cuore nel morbo di Basedow. Riforma med., Palermo- Napoli, 1906.
xxii, 1177-1187.
Kraus (F.). Ueber das Kropfherz. Wien. klin. Wchnschr., 1899, xii, 416-421.
Minnich (W.). Das Kropfherz und die Beziehungen der Schildrusenerkrankungen zu dem
Kreislaufapparat. Leipzig & Wien, 1904. F. Deuticke. 172 p. 8°.
5. Other Forms of Chronic Cardiopathy
Under this designation are included the chronic degenerative cardi-
opathies due. to various infections and intoxications. Many of the cases
described clinically as "chronic myocarditis" or "idiopathic heart-hyper-
trophy" are really instances of toxic degeneration of the heart muscle.
The whole group of chronic cardiopathies depends upon injury to the car-
diac muscle, the noxa causing degeneration of the muscle fibers, scar for-
mation, hypertrophy of the remaining fibers and, finally, failure of
tonicity. In each patient studied, the effort should be made to ascer-
tain the various mechanical, infectious and toxic factors that may have
been responsible for the injury to the heart muscle. Small foci of chronic
infection (e. g., oral sepsis, infected paranasal sinuses, chronic prostatitis)
have to be considered here, just as when studying chronic polyarthritis.
J. Angina pectoris
(Stenocardiac Attacks)
Definition. — An affection in which, on slight exertion, paroxysms of
retrosternal or, less often, precordial pain occur, sometimes extending into
the left arm, accompanied by a sense of constriction due to contraction of
the intercostal muscles, and by characteristic mental anxiety or a sense of
impending death.
902 DISEASES OF THE CIRCULATORY APPARATUS
Nature. — The pathogenesis is not wholly clear. In most cases, there is sclerosis
of the coronary arteries or a luetic lesion at the root of the aorta. In the angina
that follows exertion, the cause is most often a narrowing of the coronary arteries
(stenocardia)', in the angina pectoris of decubitus, the cause is usually an acute
dilatation of the heart.
Etiology. — The causes of atherosclerosis and of lues must be looked upon as
the causes of the lesions that underlie angina pectoris. It is believed that tobacco,
alcohol, tea and coffee, in excess, may be important contributing factors. Gout,
obesity, and infections predispose.
In patients over 45, the commonest cause of angina pectoris is atherosclerosis;
in younger people, the condition is most often due to aortitis associated with lues,
rheumatism or influenza.
Symptoms. — A sudden pain is felt in the region of the heart, behind
the sternum, or in the epigastrium ; it rapidly increases in violence and
may be so severe as scarcely to be bearable. It is rather vaguely localized,
is cramplike in character, and often extends down the medial side of the
left arm to the elbow, wrist, and little finger. It is accompanied by great
anxiety, by a pinched look to the face, and a grayish pallor, .sometimes by
lachrymation and sweating. The patient stands stock-still when attacked
and anxiously awaits the passing of the attack. The duration is from a
few minutes to a half-hour or longer. The attacks nearly always follow
Fig. 282. — The Shaded Area Shows the Dis- Fig. 283. — After Repeated Attacks of Angina
tribution of the Cutaneous Hyperalgcsia.
After the First Attack of Angina pectoris.
(After J. Mackenzie, "Symptoms and Their
Interpretation," published by Shaw & Son,
London.)
pectoris the Pain and Hyperalgesia Ex-
tended to the Regions Shaded Here. Note
the Area in the Neck and Medial Side of
Right Elbow. Compare with the Preceding
Illustration. (After J. Mackenzie, "Symp-
toms and Their Interpretation," published
by Shaw & Son, London.)
exertion, though this may be slight. Many patients cannot walk a block
without an attack. Walking after a meal, or against a cold wind, seems
especially likely to excite an attack. Sometimes the increased work thrown
on the heart by digestion will provoke a paroxysm,
ANGINA PECTORIS
903
Fig. 284. — Blood Pressure Curve Showing
Crises of Hypertension During Attacks
of Angina pectoris. (From A. D.
Hirschfelder's "Diseases of the Heart
and Aorta," published by J. B. Lip-
pin cott Co., Philadelphia.)
Abortive attacks occur ; some of these are So slight that no actual pain
is experienced (angina sine dolore). The blood pressure of patients who
suffer from angina is often low;
it may rise 30-60 mm. in an attack, or
may not change at all. Physical ex-
amination of the heart may reveal no
abnormalities.
Differential Diagnosis. — The
most common error is to look upon
a paroxysm of angina pectoris as
an attack of "acute indigestion."
Attempts are often made to dis-
tinguish true angina (angina vera)
from false angina (angina spuria).
Certain it is that the attacks of
angina vasomotoria that occur in
Graves's disease, and the attacks of
angina nervosa that occur in young
women, have a different significance
and gravity than the attacks of argina pectoris associated with lesions of
the aorta and of the coronary arteries. The aorta should be examined
rontgenologically in cases of angina pectoris.
References
1. Physiology and Pharmacology of Coronary Arteries
Barbour (H. G.). The constricting influence of adrenalin upon the human coronary arteries.
J. Exper. M., Lancaster, Pa., 1912, xv, 404-414.
Bond (G. S.). Effect of various agents on the blood flow through the coronary arteries and
veins. J. Exper. Med., Lancaster, Pa., 1910, xii, 575-585.
Markwalader (J.) & Starling (E. H.}. A note on some factors which determine the blood-
flow through the coronary circulation. J. Physiol., Cambridge, 1913,
xlvii, 275-285.
Miller (J. L.) & Matthews (S. A.}. Effect on the heart of experimental obstruction of the
left coronary artery. Arch. Int. Med., Chicago, 1909, Hi, 476-484-
Prince (A. L.). Variations in coronary pressure, and their bearing on the relaxation rate of
the ventricles. Am. J. Physiol., Baltimore, 1915, xxxvii, 43-49-
Spalteholz (W.). Die Coronararterien des Herzen. Anat. Anz., Jena, 1907, xxx,
ErgnzngshfL, 141-153.
Voegtlin (C.) & Macht (D. /.). The a-ction of nitrites and drugs of the digitalis group on
the isolated coronary artery. J. Pharmacol. & Exper. Thcrap., Baltimore,
1913, v, 77-86.
2. Clinical
Allbutt (Sir Clifford). Diseases of the arteries, including angina pectoris. New York,
1915, Macmillan Co. 2 vols. 8°.
Herrick (J. B.}. Certain popular but erroneous notions concerning angina pectoris. J.
Am. M. Ass., Chicago, 1910, Iv, 1^-1^6.
Clinical features of sudden obstruction of the coronary arteries. J. Am.
M. Ass., Chicago, 1912 , lix, 2015-2020.
904 DISEASES OF THE CIKCULATOKY APPAKATUS
Hoover (C. F.). Angina pectoris. In: Mod. Med. (Osier & McCrae), 2. ed., Phila.
& N. Y., 1915, iv, 289-295.
Kisch (E. H.)» Ueber Mors subita der Herzkranken. Munchen. med. Wchnschr., 1908,
Iv, 721-722.
Kohn (#.). Die Angina pectoris. Berl. klin. Wchnschr., 1915, Hi, 509-516.
Moritz (F.). Anomalien in den Beziehungen des Nervensy stems zu den Kreislaufsorganen.
Handb. d. allg. Pathol. (Krehl & Marchand). Leipzig, 1913, ii, 2. 108-
112.
Munzer (E.). Die Erkrankungen des Herzgefasssy stems imLichte moderner Untersuchungs-
methoden. Zentralbl. f. Herzkrankh. [etc.]. Dresden u. Leipzig, 1913. v.
484; 537.
Neusser (E.). Ausgewdhlte Kapitel der klinischen Symptomatologie und Diagnostik.
Hft. 2. Angina pectoris. Wien u. Leipzig, 1904, W. Braumuller. 33 p. 8°.
Osier (W.). Lectures on angina pectoris and allied states. New York, 1897, D. Appleton
& Co. 160 p. 8°.
Pulley (W. /.)• The reflex or protective phenomena of angina pectoris. New York M J
1913, xcviii, 918-920.
Rochester (De L.). Angina pectoris. Tr. Am. Climat. & Clin. Ass., Philadelphia, 1914,
xxx, 258-272.
Steell (£?.)• Angina pectoris and transient pericardial friction-sound: a clinical experience
Med. Chron., 1913, xxvi, 97-107.
Vaquez (#.)• L'angine de poitrine. Arch. d. mal. du cceur [etc.], Paris, 1915, viii, 45-85.
K. Diseases of the Arteries
Certain disturbances of development have been referred to above under
diseases of the heart. The most important arterial diseases met with
clinically are: (1) atherosclerosis; (2) syphilitic arteriitis; (3) thrombo-
sis and embolism; (4) aneurisms; (5) thromboangeitis obliterans; and
(6) periarteriitis nodosa.
1. Atherosclerosis, or Arteriosclerosis
Definition. — A primary degeneration (atheroma nodules, chiefly in the
intima and partly in the media), with secondary sclerotic connective-tissue
formation ; a progressive disease, the commonest and most varied lesion in
the vascular system.
Pathology. — The disease is rare before middle life, but juvenile arterio-
sclerosis occurs. The distribution of the lesions is extremely variable (local
or general). The process may affect the aorta chiefly, or the peripheral
arterial system chiefly, or it may be limited almost entirely to single
arterial domains (atherosclerosis or the cerebral arteries, of the coronary
arteries, of the renal arteries, of the mesenteric arteries, or of the leg
arteries).
The relation of the degenerative process to the sclerotic process may
vary greatly. When the former predominates, the walls of the artery are
weakened, undergo diffuse dilatation, and are subject to total and par-
DISEASES OF THE ARTERIES
905
tial ruptures (e. g., of the cerebral arteries). The degenerative process
may reach the lumen and break through (atheromatous ulcer) ; the contents
of an ulcer may be swept off as emboli, or may become the seat of platelet-
and fibrin-deposits (thrombosis). An atheromatous ulcer may rupture
externally (hemorrhage), or blood may become extravasated between the
arterial walls (dissecting aneurism), especially in the aorta and larger
arteries.
When the sclerotic process predominates over the atheromatous, the
course may be more benign, though gradually, through alteration of the
general conditions of the circulation leading to changes in the velocity of
the blood flow and often to arterial hypertension, great strain is thrown
upon the heart and large vessels.
In the smaller vessels, the sclerotic process may take the form of an
obliterating endarteritis. This, combined with calcifications of the media
and thrombosis in the lumina of the small vessels, may cause: (1) gangrene
in the extremities; (2) cerebral softening; (3) myomalacia cordis, with
rupture of the heart; or (4) fatal degenerations of the heart muscle (coro-
nary sclerosis).
Etiology. — The process has been supposed to be due chiefly to chronic
intoxications (alcohol, lead, gout, diabetes, syphilis and other infectious
diseases, nephritis, adrenal hypertrophy, digestive disturbances). Cer-
tainly, such intoxications may play a part. As one's clinical experience
grows, however, one is more and more impressed with the importance of
the quality of tubing a person starts with, and the character of his endo-
crine glands.
Diagnosis. — (1) GENERAL PERIPHERAL ARTERIOSCLEROSIS. — The
radial, brachial, temporal and crural arteries are accessible to palpation.
The arteries roll under the fingers ; hardening and thickening of the walls is
285. — Marked Peripheral Arteriosclerosis ; Br.achial .Ajtery.
- Service, ). II. II. >
906 DISEASES OF THE CIKCULATOKY APPAEATUS
easily felt; the arteries are elongated and tortuous; a calcified radial may
liave a "goose-neck" feel. X-ray examinations will reveal the calcified
arteries as shadows. The blood pressure is sometimes increased; but not
always.
(2) AORTIC SCLEROSIS OR CENTRAL SCLEROSIS. — This may occur
even when the peripheral arteries are unaffected. The patients may com-
plain of a burning feeling behind the sternum and of anginal symptoms,
Physical examination reveals retrosternal dullness ; a dilated aorta is vis-
ible on x-ray examination ; there is a ringing aortic second sound ; some-
times, aortic insufficiency develops and, occasionally, aortic aneurism.
The most common form of sclerosis of the aorta is one in which the atheroma-
tous lesions are most marked at the level of the abdominal aorta. In this portion,
the normal intima may be almost entirely replaced by atheromatous ulcers and
calcified atheromatous plaques while, higher up, at the level of the aortic arch, only
a few, early, smooth, yellow nodules are to be seen. The condition is not usually
discoverable clinically. In other cases, the upper portion of the aorta may be
extensively involved.
(3) SCLEROSIS OF AUTERIES SUPPLYING SPECIAL DOMAINS. — Athero-
sclerosis in the smaller arteries supplying individual organs disturbs their
nutrition and may give rise to important symptoms.
(a) Cerebral Atherosclerosis. — This is common after the sixtieth year.
The patients complain of headache, of an indescribable "numb feeling"
in the head, of vertigo and of depression. After a time, cerebral apoplexy,
or softening due to thrombosis, causes paralysis, aphasia, apraxia, etc.
Ophthalmoscopy reveals retinal atherosclerosis. Mental reduction is com-
mon (atherosclerotic dementia). See Part XII.
(&) Coronary Sclerosis. — This has been referred to under diseases of
the heart (q. v.).
(c) Eenal Atherosclerosis. — This leads to the atherosclerotic con-
tracted kidney when the larger renal vessels are involved, or to hyperten-
sive nephropathy when the small arterioles are diffusely involved (see
Part X).
(d) Atherosclerosis of the Mesenteric Vessels. — This may give rise
to attacks of violent colic with meteorism (dyspraxia intermittens alhero-
sclerotica or angina abdominis). If the vessels supplying the pancreas
are involved, pancreatic atrophy may result (diabetes, or pancreatic
hemorrhage).
(e) Atherosclerosis of the Arteries of the Lower Extremity. — The
patients may be comfortable when resting, but feel pain and weakness on
walking. They begin to limp and soon have to sit down and rest (intermit-
tent claudication of Charcot; dysbasia intermittens angiosclerotica of Erb).
The foot becomes pale in the attack and the pulse disappears in the foot.
The symptoms are probably due to a tonic spasm of the diseased vessels
DISEASES OF THE AETEKIES 907
(vascular crises of Pal) . If the lumen of a peripheral artery he completely
obliterated, gangrene results (senile gangrene, diabetic gangrene, etc.).
References
1. General
Brunton (Sir L.}. Funktionelle Krankheiten der Arterien. Berl. klin. Wchnschr., 1913,
I, 193-196.
Mott (F. W.). Arterial degenerations and diseases. In: Syst. Med. (Allbutt & Rolleston).
8°. London, 1909, vi, 549-620.
Osier (Sir William}. Diseases of the arteries. Mod. Med. (Osier &: McCrac.) 2. ed.
Philadelphia & New York, 1915, iv, 449-471.
2. Pathological- Anatomical «
Adami (J. G.). The nature of the arteriosclerotic process. Am. J. M. Sc., Philadelphia &
New York, 1909, cxxxviii, 485-504.
Aschoff (L.). Ueber Atherosklerose und andere Sklerosen des Gcfdsssy stems. Beihefte z.
Med. Klin., Berlin u. Wien, 1908, iv, 1-22.
Arteriosklerose. Beihefte z. Med. Klin., Berlin u. Wicn, 1914, x, 1-16.
Jores (/.). Wesen und Entwicklung der Arleriosklerose auf Grund anatomischer und
experimenteller Untersuchungtn. Wiesbaden, 1903, J. F. Bergmann.
173 p. 8°.
Klotz (O.). Arteriosclerosis: diseases of the media and their relation to aneurysm. Lan-
caster, Pa., 1911, New Era Print. Co. 105 p. 4°.
3. Experimental
Adler (/.). Studies in experimental atherosclerosis. Tr. Ass. Am. Physicians, Philadelphia,
1914, xxix, 512-527.
Bailey (C. H.}. Cholesterol atheroma in rabbits. Proc. Soc. Exper. Biol. & Med., New
York, 1914, xii, 68-70.
Denny (G. P.] & Frothingham (C.)» Jr. Experimental arterial disease in rabbits. J.
Med. Research, Boston, 1914-15, xxxi, 277-283.
Erb, Jr. (W.}. Experimentelle und histologische Studien iiber Arteriencrkrankung nach
Adrenalininjektionen. Arch. f. exper. Path. u. PharmakoL, Leipzig,
1905, liii, 173-212.
Heubner (W.). Experimentelle Arteriosklerose. Ergebn. d. inn. Med. u. Kinderh., Ber-
lin, 1908, i, 273-297.
Hildebrandt (F.). Experimentelle erzeugte lokale Atherosklerose und Hire Beziehungen zur
Niere. Heidelb., 1912, J. Horning. 46 p. 8°.
Josue (O.). Alherome aortique experimental par injections repetees d1 adrenaline dans les
veines. Corn-pi, rend. Soc. de biol., Paris, 1903, Iv, 1374-1376.
Klotz (O.). Fatty degeneration of the intima of arteries. J. Med. Research, Boston, 1915,
xxxii, 27-43. 1 pi.
Pearce (R. M.) & Stanton (E. M.}. Experimental arteriosclerosis. J. Exper. Med.,
New York, 1906, viii, 74~86.
4. Eiiological
•
Cabot (R. C.). The, relation of alcohol to arteriosclerosis. J. Am. M. Ass., Chicago, 1904,
xliii, 774-775.
Fisher (Irving} & Fisk (Eugene L.}. How to live: rules for healthful living fco.so/ on
modern science. Neu, York, 1915, Funk <fc Wagnalls Co. 845 p. pi.
908 DISEASES OF THE CIKCULATOKY APPAKATUS
Frothingham (C.). Etiology of arteriosclerosis. Johns Hopkins Hosp. Bull, Baltimore,
1913, xxiv, 323-326.
Goodman (C.). Arteriovenous anastomosis for impending gangrene; a report of personal
experience with fifteen- operated cases. Tr. Internal. Cong. Med., 1913,
London, 1914, Sect. VII, Surg., pt. 2, 101-123.
Noorden (C. u.)- On the etiology and treatment of arteriosclerosis. Postgraduate, New
York, 1913, xxviii, 415-431.
Pel (P. K.}. 1st das Rauchen schadlich? Ein Brief an PaulEhrlich. Berl. klin. Wchnschr.,
1914, li, 490-491.
Thayer (W. S.) & Brush (C. E.). The relation of acute infections to arteriosclerosis. J.
Am. M. Ass., Chicago, 1904, xliii, 726-729.
Wenckebach (K. F.). Ueber den Mann vonfiinfzigJahren. Wien. med. Wchnschr., 1915,
Ixv, 689-696.
5. Clinical
Bernheim (B. M.). Surgery of the vascular system. Philadelphia, 1913, J. B. Lippincott
Co. 104 P- 12°.
Birt (A.}. Vascular crises and angiospasm. Canad. Med. Ass. J., Toronto, 1914, iv, 853-864.
Bishop (Louis Faugeres). Arteriosclerosis; a consideration of the prolongation of life and
efficiency after forty. 2. Impression. London, 1914, H. Frowde.
393 p. 8°.
Bissell (J. B.}. The field of surgery in arteriosckrosis. N. York M. J. [etc.], 1915, ci, 993-
995.
Campbell (C. M.). Arterio-sclerosis in relation to mental disease. Am. J. Insan., Bal-
timore, 1907-08, Ixiv, 553-561.
Cramer (A.)- Die nervosen und psychischen Storungen bei Arteriosklerose. Deutsche med.
Wchnschr., L ipzig u. Berlin, 1909, xxxv, 1595-1600.
Fremont-Smith (F.). Arteriosclerosis in the young. Am. J. M. Sc., Philadelphia &
New York, 1908, cxxxv, 199-207.
Garrod (A. E.} & Evans (G.). Sclerosis of the arch of the aorta, leading to obliteration of
the pulses in the neck and upper limbs. St. Barth. Hosp. Rep., London,
1914, l,pt. 1, 65-75.
Ljungdahl (3f.)« Untersuchungen uber die Arteriosklerose des kleinen Kreislaufs. Wies-
baden, 1915. 203 p. 8°.
Longcope (W. 7\) & McClintock (A. T.}. The effect of permanent constriction of the
splanchnic arteries and the association of cardiac hypertrophy with arterio-
sclerosis. Arch. Int. Med., Chicago, 1910, vi, 439-448.
Marple (W. B.}. Arteriosclerosis as seen by the ophthalmologist. N. York M. J. [etc.],
1915, ci, 988-993.
McCrae (T.). Dilatation of the aorta. Am. J. M. Sc., Philadelphia & New York, 1910,
cxl, 469-487.
M tiller (H.). Die Arteriosklerose und ihre Behandlung. Univ. Zurich, Festgabe, 1914, pt.
a> <j)oa> ff>x/n
O, &.<Jd—&Q4.
Osier (W.). Transient attacks of aphasia and paralysis in states of high blood pressure and
arteriosclerosis. Canad. M. Ass. J., Toronto, 1911, i, 919-926...
Pal (/.)• Gefdsskrisen. Leipzig, 1905, S. Hirzel. 279 p. 8°.
Price (S. B.}. The diagnosis and treatment of arteriosclerosis. Internal. Clin., Philadelphia,
1915, 25 s., ii, 17-38.
Schlesinger (Hermann). Die Krankheiten des hoheren Lebensalters. Bd. I. Wien &
Leipzig, 1914, A. Holder. 8°.
Thayer (W. S.) & Fabyan (M.). Studies on arteriosclerosis, with special reference to the
radial artery. Tr. Ass. Am. Physicians, Philadelphia, 1907, xxii,
694-715.
Also: Am- J. M- Sc., Philadelphia $ New York, 1907, cxxxiv, 811-829.
DISEASES OF THE ARTEKIES 909
Veale (P. J.) & Coombs (C.). Cardiac failure in a child aged six years, associated with
atheroma of the pulmonary artery and extreme dilatation of the right ven-
tricle. Brit. J. Child. Dis., London, 1915, xiii, 72-77.
Zesas (D. G.). Die angiosklerotische Gangrdn der unleren Extremitdten und die neueren
chirurgischen Bestrebungen zu ihrer Behandlung. Centralbl. f. d. Grenzgeb.
d. Med. u. Chir.} Jena, 1912, xv, 382-458.
6. Intermittent Claudication
Char cot (J. M.). Sur la claudication intermittente par obliteration arterielle. Progres.
med., Paris, 1887, 2. s., vi, 99; 115.
Dehon (M.) & Heitz (J.). Syphilis et arterite obliterante des membres inferieurs (Claudi-
cation intermittente). Arch. d. malad. d. cceur, etc., Paris, 1914. vii,
381-394.
Erb (W.). Ueber das intermittierende Hinken und andere nervose Storungen in Folge von
Gefdsserkrankungen. Deutsche Ztschr. f. Nervenh., Leipzig, 1898, xiii,
1—76.
Favre (/.). Zur Frage der Dystasia angiosclerotica (intermittierendes Hinken). Deutsche
Ztschr. f. Nervenheilk., Leipzig, 1913, xlix, 293-304.
Rosenbusch (/.). Zur Diagnose der arteriosklerotischen Erkrankungen der unteren Ex-
tremital. Berl. klin. Wchnschr., 1911, xlviii, 1712-1714.
Zoege von Manteuffel (W.). Die Arteriosklerose der unteren Extremitaten. Mitt. a. d.
Grenzgeb. d. Med. u. Chir., Jena, 1902, x, 343-410.
2. Syphilis of the Arteries
(Arteriitis syphilitica)
The most important of the infectious diseases of the blood vessels is
syphilis. The veins and lymph vessels may be affected in all stages of
the disease; syphilitic arteriitis is most common in tertiary lues, though
it may occur within six months after infection. The arteries at the base
of the brain are especially predisposed to involvement, and the adjacent
arachnoid is nearly always simultaneously diseased (distinguished from
atherosclerosis).
The ascending aorta is very frequently involved (mesaortitis produc-
tiva syphilitica). There is frequent involvement of the orifices of the
coronary arteries, with angina pectoris. Aneurismal dilatation of the aorta
is common between the thirty-fifth and the forty-fifth years of life. Symp-
toms of aortic syphilis resemble those of atherosclerosis of the aorta, but
they appear earlier in life, though often years after the external symp-
toms of syphilis have disappeared. The Wassermann reaction is usually
positive, and is a great help in recognition.
Patients with syphilis, especially with congenital syphilis, show a defi-
nite tendency to early general atherosclerosis of a non-specific type. The
radials feel like rubber tubes. In any young person showing general
arteriosclerosis, syphilis as an etiological factor should be strongly sus-
pected. (Nonne.)
910 DISEASES OF THE CIECULATOKY APPAKATUS
True syphilitic arteriitis, as at present recognized, is less widely generalized.
It is usually seen as a process localized in the aorta or in the cerebral vessels ; very
often, it may be active in both situations in the same patient.
In the smaller arteries, infiltration about the vasa vasorum, in the media
(mesarteritis) , and in the adventitia (periarteritis) , leads to disturbances of nutri-
tion of the vessel wall. A compensatory proliferation of the intima occurs
(obliterative endarteritis) ; and complete occlusion of the vessel by thrombosis is the
usual end-result.
In larger arteries, especially in the aorta, an infiltration of the media and
adventitia occurs in circumscribed patches in the wall. Destruction of muscle-
fibers and elastic tissue is found in such areas, with substitution of granulation
tissue (mesaortiiis productive*}. The media undergoes compensatory proliferation.
As retraction of the granulation tissue in the media occurs, the intima is drawn
down. It is this process that gives these patches of syphilitic aortitis their
characteristic wrinkled or puckered appearance. .The destructive processes in the
media result in thinning and weakening of the vessel wall; the ultimate result of
this is a general dilatation of the vessel, or, in some cases, the production of a true
aneurism.
In both smaller and larger vessels, the infiltrative process may assume the
form of true gummatous nodules. The Treponema has been demonstrated in
these lesions.
Syphilis of the Aorta. — Syphilitic aortitis (Heller-Dohle) shows a marked
tendency to localization at the root of the aorta, in contradistinction to the usual
aortic atherosclerosis, which is chiefly developed in the aorta descendens (Mb'nke-
berg). It is most common in the later stages of syphilis. It is not usually dis-
covered clinically until, by its extension, complications are produced, the symp-
toms of which are more obvious. Such, in order of frequency, are: (1) involve-
ment of the aortic valves (aortic insufficiency) (q. 1?.), (2) aneurism formation,
(3) extension to the coronary arteries (stenocardiac attacks).
It is important to recognize aortic syphilis earlier, before the occurrence of
these complications. It should be looked for in every case of syphilis of more
than a few months' standing. The dilatation of the ascending aorta can often be
suspected from the presence of retro- and parasternal dullness at the- level of the
first to the third interspace. The rontgenoscopic examination gives more definite in-
formation. It is often combined with some hypertrophy of the left heart even
before any valvular lesion can be discovered. A moderate hypertension is common.
This condition, in a patient below 45 and without nephritis, should in itself be
considered very suspicious of vascular syphilis. A history of luetic infection, or
a positive Wassermann, are valuable for confirmation. Babinski states that in
cases of syphilitic aortitis the slowing of the heart that is a normal reflex response
to pressure on the eyeballs is absent. Serological or clinical evidence of coincident
luetic cerebral endarteritis is present in a high percentage of cases of syphilitic
aortitis.
Syphilis of Cerebral Arteries. — Two chief forms are described. Heubner's
endarteritis of the larger arteries of the base of the brain leads more commonly
to partial or complete obliteration of the vessel lumen with resultant atrophies
or softening of corresponding portions of the brain. Hemiplegias, aphasias, etc.,
are the common clinical results. (In some cases, the diseased vessel ruptures and
an apoplexy occurs.) At times, however, aneurism formation occurs in the course
of one of these cerebral arteries. Such luetic aneurisms are usually single and
large as opposed to the numerous miliary aneurisms on atherosclerotic vessels. The
symptoms are those of cerebral tumor.
DISEASES OF THE AETERIES 911
Nissl and Alzheimer's endarteritis of the smaller vessels of the brain is believed
by these authors to be the commonest cause of syphilitic epilepsy.
References
Blunter (G.). The pathogenesis and symptomatology of syphilitic aortitis. Albany M.
Ann., 1914, xxxv, 415-422.
Colombe (/.)• L'aortite abdominale. Gaz. d. hop., Paris, 1913, Ixxxvi, 805; 853.
Darling (S. T.) & Clark (H. C.). Arteritis syphilitica obliterans; a pathological report of
several cases of complete occlusion of large arteries; aorta, carotid and sub-
clavian, in which syphilis was the causative factor. J. Med. Research,
Boston, 1915, xxxii, 1-26. 1 pi.
Dbhle (K. G. P.}. Ueber Aortenerkrankung bei Syphilitschen und deren Beziehung zur
Aneurysmenbildung. Deutsches Arch. f. klin. Med., Leipzig, 1895, Iv,
190-210.
Eisler (F.) & Kreuzfuchs (5.). Die Rontgendiagnose der Aortensyphilis. Deutsche med.
Wchnschr., 1913, xxxix, 2145-2146.
Fukushi (M.). Ueber die pathologische Flistologie der syphilitischen Aortitis mil besonderer
Berucksichtigung des Vorkommens von Plasmazellen. Virchow's Arch. f.
path. Anat. [etc.], Berlin, 1913, ccxi, 331-423.
Gilbert (A.} & Brim (L.). Reaction de Wassermann et lesions de Vaorte. Paris med.,
1912-13, xi, 461-465.
Goldscheider (A.}. Ueber die syphilitische Erkrankung der Aorta. Med. Klin., Berlin,
1912, viii, 471-475.
Halsey (J. T.}. The importance of the recognition of syphilis in circulatory disease. South.
M. J., Nashville, 1913, vi, 23-25. [Discussion], 32-35.
Heller (A.). Die Aortensyphilis als Ursache von Aneurysmen. Munchen. med. Wchnschr.,
1899, xlvi, 1669-1671.
Aorten-Aneurysma und Syphilis. Virchow's Arch. f. path. Anat. [etc.],
Berlin, 1903, clxxi, 177-179.
Kraus (F.). Ueber die Aortenerweilerung bei der Heller-Doehleschen Aortitis. Deutsche
med. Wchnschr., Leipzig u. Berlin, 1914, xl, 577-579.
Kulbs (F.). Arteriosklerose. Handb. d. inn. Med. (Mohr & Staehelin). Berlin, 1914, ii,
1104-1129.
Syphilis der Gefdsse. Handb. d. inn. Med. (Mohr & Staehelin).
Berlin, 1914, ii, 1129-1140.
Legout (P.-A.). Contribution d Vetude de Vaortite abdominale. Paris, 1913, A. Legrand.
94 p. No. 180. 8°.
Longcope (W. T.}. Syphilitic aortitis: its diagnosis and treatment. Arch. Int. Med.,
Chicago, 1913, xi, 14-51.
Mallory (F. B.). The infectious lesions of blood vessels. The Harvey Lectures, Philadelphia
& London, 1912-13, 150-166. J. B. Lippincott Co.
McCrae (T.). Dilatation of the aorta. Tr. Ass. Am. Physicians, Philadelphia, 1910,
xxv, 344-366.
McPhedran (A.). Syphilis of the heart and aorta. Canad. M. Ass. J., Toronto, 1915, v,
680-683.
Neuhof (5.). Diagnosis, symptomatology and theory of dilatation of the descending thoracic
Aorta. Med. Rec., New York, 1915, Ixxxvii, 540-542.
Rebaudi (S.}. Die Aortitis bei kongenitalsyphilitischen Kindern. Monatschr. f. Geburtsh.
u. Gynaek., Berlin, 1912, xxxv, 681-702.
Rolleston (H. D.}. Malignant aortitis; hypoplasia of the aorta. Lancet, London, 1915, ii,
912 DISEASES OF THE CIKCULATOKY APPAKATUS
Stadler (/?.)• Die Klinik der syphilitischen Aortenerkrankungen. Jena, 1912, G. Fischer.
93 p. 8°. i
Thiem (H.). Die syphilitischen Aortenerkrankungen. Zentralbl. f. Herzkrankh. [etc.],
Dresden u. Leipzig, 1914, vi, 405; 417; 429.
Turnbull (H. Af.). Alterations in arterial structure and their relation to syphilis. Quart.
J. Med., Oxford, 1915, viii, 201-254.
Vinit (Antony}. De Vinegalite des pouls radiaux dans les aortites chroniques syphilitiques.
Paris, 1913, Jouve & Cie. 44 p. No. 323. 8°.
Wiesner (R.). Ueber Erkrankung der grossen Gefdsse bei Lues congenita. Centralbl. f.
allg. Path. u. path. Anat., Jena, 1905, xvi, 822-829.
Winternitz (M. C.)« The pathology of syphilitic aortitis; with a contribution to the forma-
tion of aneurysms. Johns Hopkins Hosp. Bull., Baltimore, 1913, xxiv,
3. Aneurisms
Definition. — An aneurism is a chronic dilatation of the lumen of an
artery with new formation of the wall, thus differing from mere ectasia
of an artery (dilatation through stretching of an atrophic wall) and from
an intra- or extramural hematoma (communication of the lumen of the
artery with another blood cavity through a ruptured wall).
Varieties. — An aneurism may be circumscribed or diffuse. Circum-
scribed aneurisms may be saccular, circular, boat-shaped or funnel-shaped.
The diffuse aneurisms may be spindle-shaped or cylindrical.
A dissecting aneurism develops through the rupture of the inner and
middle coats and the spread of the blood for long distances between them
and the outer coat of the vessel ; it would be better described as an intra-
mural hematoma.
Sites. — An aneurism may occur in any artery in the body. It is most
common in .the ascending aorta and in the aortic arch. Popliteal aneurisms
are common. In the viscera, aneurisms are not uncommon in the cerebral,
pulmonary, and splenic arteries. They are more rarely found in the
mesenteric and the coronary arteries. The so-called miliary aneurisms
on the cerebral arteries are not true aneurisms but are small hemorrhages
into the arterial sheaths. In the peculiar disease known as periarteritis
nodosa (q. v.) a very large number of aneurisms of the small arteries are
met with. The nature of this disease is obscure.
Size. — An aneurism may be microscopic in size, or, in the aorta, may
be as large as a child's head. (Fig. 287.)
Walls. — The wall of the aneurism always shows a break in the continuity in
the coats of the artery. In circumscribed aneurisms, these breaks are at the
margin of the dilatation. In diffuse aneurisms there are many smaller breaks
intercalated among islands of fairly-normal lamellated wall. The breaks affect
the elastic lamellae predominantly, but the connective tissue and muscle coats are
also interrupted. As a rule, the intima breaks first, then the media, and, lastly, the
DISEASES OF THE AKTEKIES
913
adventitia. The lacunae due to the breaks are filled up in all
aneurisms with new connective tissue. Owing to the changes
in the wall, this yields to the blood pressure, which causes a
bulging. If new connective tissue be formed in sufficient
amounts, rupture may be long postponed. Most aneurisms are
progressive, though in rare instances they become stationary.
Etiology. — The causes are manifold (trauma, ather-
osclerosis, gummatous syphilitic arteritis, and other in-
fectious forms of arteritis). Lues is by far the most
common caus,e of aneurism of the aorta. (Fig. 286.)
Complications. — Aneurisms may invade neighbor- „
. . i< ig. Job. — Ireponema
ing organs (adhesions, erosions, compressions), and may paiiidum from the
finally rupture externally, or into a body cavity or a
canal. Rupture into a vein causes varicose aneurism.
(a) Aneurism of the Thoracic Aorta
Wall of an Aneu-
rism. (After Wright
and Richardson, In
A. D. Ilirschfelder's
"Diseases of the
Heart and Aorta,"
published by 3. B.
Lippincott Co.)
The most common, cause is syphilis. Most cases of
aortic aneurism are to be looked upon as complica-
tions of a preexisting syphilitic aortitis by which the wall of the aorta has
been weakened (vide supra). These aneurisms are frequently fusiform,
but clinically the most common form is the saccular. The symptoms and
signs of aortic aneurism vary markedly with the site of the aneurism, in
the ascending, transverse, or descending portions of the arch of the aorta or
in the descending aorta.
In cases of ANEURISM OF THE ASCENDING PORTION OF THE ARCH the
Pig. 287.— Unuj
illy Large Aortic Aneurism. Photographed the Day Before Death.
(After W. H. Hough, J. H. H. Bull.)
914 DISEASES OF THE CIRCULATORY APPARATUS
physical signs are usually more prominent than the symptoms. The aneu-
rism tends to grow into the right pleural cavity reaching the chest wall
usually in the second or third interspace where pulsation is early to be
made out on inspection. On palpation, this pulsation is felt to be expan-
sile in character. A thrill and diastolic shock are often felt over this area.
A loud aortic second sound is heard on auscultation. An aortic systolic
murmur is common and a diastolic murmur is present when the aortic
valves have been involved by the luetic process. An abnormal area of
dullness is made out above and usually somewhat to, the right of the cardiac
dullness. The left border of the heart is usually forced to the left of the
mammillary line. The chief symptom associated with this type of aneu-
rism is the pain resulting usually from pressure on, and erosion of, the- an-
terior chest wall. In time, a large tumor, projecting from the chest wall,
may result from such erosion. Anginal pain may likewise result from in-
volvement of the orifices of the coronaries. Pressure on the superior vena
cava may cause engorgement of the vessels of the head and arms. Hoarse-
ness may be caused by injury to the right recurrent laryngeal nerve.
In ANEURISM OF THE TRANSVERSE AND DESCENDING ARCH of the aorta
symptoms arising from pressure are more prominent than physical
signs. Small aneurisms in this location may cause symptoms by pres-
sure, when yielding no signs on palpation, percussion, or auscultation.
They tend to grow posteriorly, but may point against the anterior chesV
wall in the midline or to the right of the sternum. In some cases, they
form pulsatile tumors, posteriorly, in the left interscapular region. In-
volvement of the large arteries given off from the arch may cause inequality
in the radial pulses, due to retardation, or diminished volume, on one side.
A distinct pulsatile downward jerk may be transmitted to the trachea
(tracheal tug). Pressure on the sympathetic may lead to inequality of the
pupils. The commoner symptoms are cough (often brassy in character),
bronchorrhea, and fever, due to compression of a bronchus (usually the
left) ; hoarseness, or aphonia, due to pressure on the left recurrent laryn-
geal nerve ; pain due to erosion of the vertebrae, or of the posterior or ante-
rior chest wall ; dysphagia, from pressure on the esophagus.
ANEURISMS OF THE DESCENDING THORACIC AORTA are often latent.
They may give rise to pressure effects ; pain due to erosion of the vertebrae
(often, when involving the nerve roots, this pressure causes intercostal neu-
ralgia) ; dysphagia ; symptoms and signs of pulmonary compression.
(b) Diagnosis of Aortic Aneurism
It should be suspected and looked for in every patient that has had
syphilis, especially when oppression in the chest, intercostal neuralgia,
Loarseness, or difficulty in swallowing are complained of. If there be
any suspicion of the existence of an aortic aneurism, a thorough x-ray
DISEASES OF THE ABTEBIES
915
examination (rontgenoscopy) should be made. If an aortic aneurism
exists, an abnormal, dark, pulsating shadow will be recognized. The
borders of the shadow are sharply circumscribed. The expansile pulsa-
tion, if seen in two different spots of the same shadow, can be regarded
as pathognomonic. The rontgenoscopic examination should be made not
only in the sagittal direction, but also with oblique transillumination. With
rontgenography, a permanent record may be made. (Figs. 288 and 289.)
Fig. 288. — Large Thoracic Aneurism. Outline is Indicated by Outer Set of Arrows; Wire in
Sac Indicated by Inner Set of Arrows. (X-ray Dept, J. H. H.)
Physical Signs. — Visible pulsation is met with in the first, second or
third right or left intercostal space; on palpation, pulsation may be ex-
pansile and accompanied by thrill and by diastolic shock. If adherent to
the trachea, a distinct tracheal tug may be felt when the fingers are pressed
under the cricoid when the patient sits up with his head thrown slightly
backward (Oliver-Cardarelli sign). Among the other important signs are
dilatation of the superficial veins of the chest or in front of one shoulder,
dislocation of the trachea, inequality of the pupils, paralysis of left N.
recurrens (hoarseness, brassy cough, laryngoscopic examination), dyspnea,
dysphagia, and inequality of the two radial pulses. A systolic murmur,
916 DISEASES OF THE CIRCULATOEY APPARATUS
sometimes also a diastolic, may be audible over the aneurism. The left
ventricle is not hypertrophied in aneurism, unless there be accompany-
ing aortic insufficiency or other special cause.
Fig. 289. — Aneurism of Descending Portion of Arch of Aorta. (X-ray Dept, J. H. H.)
(c) Aneurism of the Abdominal Aorta
These aneurisms are rare in comparison with those of the thoracic
aorta. The commonest site of occurrence is in the epigastric region. Gas-
tric symptoms, especially vomiting, are frequent. More characteristic are
severe neuralgic pains in the back, often radiating to the legs. Paraplegia
may occur. In these cases erosion of the vertebrae has occurred. Large
retroperitoneal masses may be formed by infiltration of the tissues. In
these masses, which are largely composed of laminated clot honeycombed
with blood spaces, little or no pulsation may be evident. The diagnosis is
less difficult where a definite saccular tumor with expansile pulsation can
be isolated, on palpation. Thrills and murmurs, both systolic and diastolic,
may be made out over such tumors. The throbbing abdominal aorta, often
found in neurasthenia, should not lead to errors in diagnosis, since the pul-
sation can be traced the length of the aorta and no localized tumor is
present.
(d) Diagnosis of Aneurisms of the Pulmonary Artery
The mass may cause bulging, pulsation, systolic thrill and dullness
in the second and third left intercostal space and behind the sternum. A
DISEASES OF THE AKTERIES 917
systolic murmur is audible. The signs are similar to those yielded by
aneurism of the aorta. The murmurs of aortic aneurism are, however,
propagated into the carotid arteries ; those of pulmonary aneurism are not.
Moreover, aneurism of the pulmonary artery does not affect the radial or
the femoral pulse.
(e) Arteriovenous Aneurisms
In these cases, an abnormal communication exists between an artery
and a vein. The etiological factor is usually trauma. The condition is
accordingly found most often in the extremities. Rupture of an aneurism
of the ascending portion of the arch of the aorta into the superior vena
cava has been observed in a number of cases. There is cyanosis of the
upper half of the body and, often, edema in the same area. In such cases,
too, the ventricular type of jugular phlebogram is seen. Pulsation, marked
venous engorgement, palpable thrill, and a continuous loud murmur with
systolic intensifications, are characteristic of all cases of arteriovenous
aneurism.
References
Baetjer (F. H.}. The X-ray diagnosis of thoracic aneurisms. Johns Hopkins Hosp.
Bull., Baltimore, 1906, xvii, 24-27.
The X-ray diagnosis of thoracic aneurism. Internal. J. Surg., New
York, 1907, xxiv, 133-138.
Ballance (C. A.). The treatment of aneurism. Tr. Internal. Cong. Med., 1918, London,
1914, Sect. VII, Surg., pt. 2, 173-175.
Barker (L. F.}. A case of healed aneurism of the aorta. Johns Hopkins Hosp. Bull.,
Baltimore, 1894, v, 31.
Bernheim (B. Af.) & Worth (P.), Jr. Arteriovenous aneurism of the external iliac vessels
with wound of the external iliac vein. Ann. Surg., Philadelphia, 1914, lix,
558-562.
The newer blood vessel operations; who should do them? Interstate M. J.,
St. Louis, 1915, xxii, 9-15.
Bier (A.). Ueber Kriegsaneurismen. Deutsche med. Wchnschr., Leipzig u. Berlin, 1914,
Chirurg'ie der Gefasse; Aneurismen. Beitr. z. klin. Chir., Tubingen, 1915,
xcvi, 556-560.
Carman (R. />.). The X-ray diagnosis of thoracic aneurism. J. Missouri M. Ass.,
St. Louis, 1912-13, ix, 389-395.
Finneu (J. M. T.). The miring of otherwise inoperable aneurism, with report of cases.
Ann. Surg., Philadelphia, 1912, Iv, 661-681.
Gessner (H. B.). My experience with the Matas operation of endoaneurismorrhaphy.
N. Orleans M. & S. J., 1914-15, Ixvii, 598-607.
Gordinier (H. C.). Aneurism of the thoracic aorta. Fourteen cases with seven autopsies.
Albany M. Ann., 1902, xxiii, 423-436.
Groedel (F. M.). Anonyma und Subclavia im Rontgenbilde. Fortschr. a. d. Geb. d. Ront-
genstrahlen, Hamburg, 1911-12, xviii, 183-187.
von Haberer (H.}. Weitere Erfahrungen iiber Kriegsaneurismen, mil besonderer Beruck-
sichtigung der Gefdssnaht. Wien. klin. Wchnschr., 1915, xxviii, 435; 471.
Halsted ( W. S.} . Der partielle Verschluss grosser Arterien. Verhandl. d. Deutsch. Gesellsch.
f. Chir., Berlin, 1914, xliii, 2. Teil, 349-367.
918 DISEASES OF THE CIRCULATORY APPARATUS
Hare (H. A.}. Three cases of wiring with electrolysis for aortic aneurism; one heretofore in
part reported. Tr. Coll. Phys. Philadelphia, 1914, xxxvi, 60-70.
Hay thorn (S. R.). Tuberculosis of the large arteries. With the report of a case of tuber-
culous aneurysm of the right common iliac artery. J. Am. M. Ass., Chi-
cago, 1913, Ix, 1413-1416.
Heller (A.). Die Aortensyphilis als Ursache von Aneurismen. Munchen med. Wchnschr.
1899, xlvi, 1669-1671.
Aorten-Aneurysma und Syphilis. Arch. f. path. Anat. [etc.], Berlin,
1903, clxxi, 177-179.
Hewlett (A. W.) & Clark (W. R. P.}. The symptoms of descending thoracic aneurism.
Am. J. M. Sc., Philadelphia & New York, 1909, cxxxvii, 792-805.
Horsley (J. S.}. A new method of lateral anastomosis of blood vessels and an operation fir
the cure of arteriovenous aneurism. Ann. Surg., Philadelphia, 1915, Ixi,
597-603.
Horsley (John Sheltori). Surgery of the blood vessels. St. Louis, 1915, C. V. Mosby Co.
304 p. 8°.
Horsley (J. S.) & Whitehead (R. H.}. A study of reversal of the circulation in the lower
extremity. J. Am. M. Ass., Chicago, 1915, Ixiv, 873-877.
Hough (W. H.). A case of unusually large aortic aneurism. Johns Hopkins Hosp. Bull.,
Baltimore, 1905, xvi, 331-333.
Kuemmel (H.). Operative treatment of aortic aneurism. Tr. Am. Surg. Ass., Philadelphia,
1914, xxii, 457-461. [Discussion], 483~483d.
Lemann (I. /.). The diagnosis of aneurism of the thoracic aorta. N. Orleans M. &
S. J. 1912, Ixv, 420-425.
Lindbom (O.)» Beitrag zur Kenntnis der embolischen Aneurismen als Komplikationen der
akuten Endocarditiden. Mitt. a. d. Grenzgeb. d. Med. u. Chir., Jena, 1914,
xxvii, 912-933.
Mat as (#.)• The suture of the arterial system; the suture as applied to the surgical cure of
aneurism. Tr. Internal. Cong. Med., 1913, London, 1914, Sect. VII, Surg.,
pt. 2, 149-172. [Discussion], 173-190. 3 pi.
McCrae (J.). A case of multiple mycotic aneurysms of the first part of the aorta. J. Path.
& BacterioL, Edinburgh <fe London, 1905, x, 373-379.
McGlannan (A.). Aneurism oj the posterior libial artery, with report of two cases. J.
Alumni Ass. Coll. Phys. & Surg., Baltimore, 1915, xviii, 11-15.
McNeil (H. L.}. Report of case of multiple mycotic aneurism of the aorta. South. M. /.,
Nashville, 1914, vii, 540.
McPhedran (A.}. Aortic aneurism with recurrent fever. Am. J. M. Sc., Philadelphia,
1915, cxlix, 101-103.
Moore (C. H.) & Murchison (C.). On a new method of procuring the consolidation of
fibrin in certain incurable aneurisms. With the report of a case in which
an aneurism of the ascending aorta was treated by the insertion of wire.
Med.-Chir. Tr., London, 1864, xlvii, 129-149.
Murphy (J. B.). Aneurism of the brachial artery; endoaneurismorrhaphy. Surg. Clin.,
Chicago, 1915, iv, 53-75. 1 pi.
Murray (W.). An account of a case of aneurism of the abdominal aorta which was cured by
compression of that artery immediately above the tumor. Med.-Chir. Tr.,
London, 1864, xlvii, 187-194.
Oehlecker (F.). Zur Operation der sogenannten falschen Aneurismen. Zentralbl. f. Chir..
Leipzig, 1914, xli, 1745-1750.
Oliver (W. S.}. Physical diagnosis of thoracic aneurism. Lancet, London, 1878, ii, 406.
Osier (Sir W.}. Remarks on arteriovenous aneurism. Lancet, London, 1915, i, 949-955.
Osier (W.). Aneurism of the abdominal aorta. Lancet, London, 1905, ii, 1089-1096.
Aneurism. Mod. Med. (Osier & McCrae). 2.ed. Philadelphia & New
York, 1915, iv, 472-525.
Aneurism. In: Syst. Med. (Allbutt & Rolleston). 8°. London, 1909,
vi, 620-681.
DISEASES OF THE ARTERIES 919
Ower (J. J.}. Early aneurism of the aorta (report of a case). J. Med. Research Boston
1914-15, xxxi, 251-254. 1 pi.
Rolleston (H. D.) & Grellier (E. F. W.}. Unilateral clubbing of the fingers associated
with an axillary aneurism on that side. Proc. Roy. Soc. Med. London
1913-14, vii, Clin. Sect., 154-156.
Roques (Elie}. Contribution a V etude des anevrysmes de Vaorte. Paris, 1913, H. Paulin
& Cie. 150 p. 8°.
Shennan (7\). Dissecting aneurisms. Tr. Internal. Cong. Med., 1913, London 1914
Sect. Ill, Gen. Path. & Path. Anat., pt. 2, 805-307.
Tufnell (T. J.). The successful treatment of internal aneurism by consolidation of the con-
tents of the sac. 2. ed. London, 1875, J. & A. Churchill. 71 p. 8°.
Weitz. Beitrdge zur Kenntnis des Bauchaortenaneurysmas. Deutsches Arch f klin
Med., Leipzig, 1911, civ, 455-480.
Winternitz (M. C.). The pathology of syphilitic aortitis, with a contribution to the forma-
tion of aneurysms. Johns Hopkins Hosp. Bull., Baltimore, 1913. xxiv
212-216.
Woloschin (A. D.). Zur Frage der spontanen Aortenrupiur. Mitt. a. d. Grenzgeb. d. Med.
u. Chir., Jena, 1913, xxvi, 701-709.
von Ziemssen (H.}. Ueber den Pulsus differens und seine Bedeutung bei Erkrankungen
des Aortenbogens. Deutsches Arch. f. klin. Med., Leipzig, 1889-90,
xlvi, 285-295.
4. Thrombosis and Embolism
Thrombi or emboli lead to occlusion of vessels and anemia (when end-
arteries, necrosis) of the parts they supply. Thus arise infarctions of the
lung, heart, brain, spleen, kidney and intestine (see these organs).
References
Aschoff (L.)- Thrombosis. Arch. Int. M., Chicago, 1913, xii, 503-525.
Beneke (/?.)• DieEmbolie. In: Krehl (L.) u. Marchand (F.}, Handbuch der allegemeinen
Pathologic, Leipzig, 1912, S. Hirzel, 2 Abt., U, 300-371.
Die Thrombose. Handb. d. allg. Pathol. (Krehl & Marchand). Leipzig,
1913, U, 2, 130-299.
Bernheim (B. M.}. Threatened and real gangrene of the extremities as seen by the modern
surgeon; its causes and treatment. South. M. J., Nashville, 1915, viii,
512-517.
Blumer (£.)• Thrombosis. Embolism. Phlebitis. Mod. Med. (Osier & McCrae). 2. ed.
Philadelphia & New York, 1915, iv, 526-578.
Buerger (L.) & Oppenheimer (Ad&le). Gangrene without organic vascular disease. Med.
Rec., New York, 1914, Ixxxvi, 1083-1085.
Gallavardin (L.) & Dufourt (P.). Embolie de I'arlere coronaire anterieure avec brady-
cardie d 22-28. Contribution a V elude de la mort rapide par obliteration
coronarienne. Lyon med., 1913, cxxi, 141—149'
Kleinschmidt (O.). Experimentelle Untersuchungen uber Luftembolie. Arch. f. klin.
Chir., Berlin, 1915, cvi, 782-822.
Renter (W.). Experimentelle Untersuchungen uber Fcttembolic. Frankfurt.Ztschr.f. Path.,
Wiesbaden, 1915, xvii, 205-217.
Stetten (/>.)• The futility of arteriovenous anastomosis in the treatment of impending gan-
grene of the lower extremity, Surg. Gynec. & Obst., Chicago, 1915, xxt 381-
920 DISEASES OF THE CIKCULATOKY APPAEATUS
Stewart (F. T.). The operative treatment of arterial thrombosis and embolism. Ann. Surg..
Philadelphia, 1915, Ixi, 519-634.
Warthin (A. S.}. Traumatic lipcemia and fatty embolism. Internal. Clin., Philadelphia,
1913, 23. s., iv, 171-227.
Welch (W. H.}. Revised by H. D. Rolleston. Thrombosis. In: Syst. Med. (Allbutt &
Rolleston). 8°. London, 1909, vi, 691-762.
Wilson (L. /?.)• Fatal post-operative embolism. Ann. Surg., Philadelphia, 1912, Ivi, 809-
817. 2 tab.
5. Thrombo-angeitis obliterans
Definition. — A condition in which parietal, red thrombi occur in the blood
vessels, especially in the arteries of the lower extremities, though the veins may
also be involved.
Incidence. — The process is much more common in males than in females. It
is a disease of middle life, and is especially common in Jewish people. For full
description, see the papers of Leo Buerger of New York.
References
Buerger (£.)• Concerning vasomotor and trophic disturbances of the upper extremities,
with particular reference to thrombo-angiitis obliterans. Am. J. M. Sc.,
Philadelphia, 1915, cxlix, 210-229.
Thrombo-angiitis obliterans; a study of the vascular lesions leading to pre-
senile spontaneous gangrene. Am. J. M. Sc., Philadelphia & New York,
1908, cxxxvi, 667-680. 8 pi.
Is thrombo-angiitis obliterans related to Raynaud's disease and erythro-
melalgia* Am. J. M. Sc., Philadelphia, 1910, n. s., cxxxix, 105-107.
Recent studies in the pathology of thrombo-angiitis obliterans. J. Med.
Research, Boston, 1914-15, xxxi, 181-194. 5 pi.
Putnam (C. R. L.)» Arteriovenous anastomosis for thrombo-angiitis obliterans. Med. Rec.,
New York, 1915, Ixxxvii, 332.
Thompson (J. E.). Study of the collateral circulation in some cases of spontaneous gan-
grene of the foot. J. Am. M. Ass., Chicago, 1913, Ixi, 171-174.
Weber (F. P.}. Non-syphilitic arteritis obliterans ("thrombo-angiitis" of Leo Buerger} , with
gangrene of toes; remarks on the occasional connexion with traumata.
Proc. Roy. Soc. Med.,Lortdon, 1914-15, viii, Clin. Sect., 49-52.
6. Periarteritis nodosa
Definition. — A disease characterized by inflammatory infiltrations and fibrinous
deposits beginning in the media and adventitia of the medium-sized arteries (espe-
cially the coronaries and mesenteric) ; minute aneurisms are formed and become
thrombosed; sometimes, marked proliferation of the intima also occurs (Verse).
Etiology. — This is not yet clear, though lues and other infectious processes
have been held responsible.
Symptoms. — These vary according to the arteries predominantly
affected, since the blood supply is partly cut off in the domains of dis-
tribution of the diseased vessels. Among the symptoms described are
DISEASES OF THE VEI^S 921
hemorrhage from the intestines and kidneys, cerebral hemorrhage, paral-
ysis, muscular pains, and severe anemias. The disease is fatal in a few
weeks, though a patient may, sometimes, recover after vigorous antiluetic
treatment.
There is outspoken tachycardia, but no fever. When palpable vessels
are involved, the nodules may be felt in their course.
Diagnosis. — This can only occasionally be made during life, when the
symptoms above described are prominent and nodules are palpable on
the peripheral arteries.
References
Block (Vera). Ueber Periarteriitis nodosa. Zurich, 1913, J. J. Meier. 42 p. 8°.
Guldner (#.). Zwei neue Beobachtungen von Periarteriitis nodosa beim Menschen und beim
Hausrinde. Arch. f. path. Anat. [etc.], (Virchow) Berlin, 1915, ccxix,
366-376. 1 pi.
Klotz (O.). Nodular endarteritis of the aorta about the intercostal arteries. J. Med. Re-
search, Boston, 1914-15, xxxi, 409-430.
Lamb (A. R.). Periarteritis nodosa; a clinical and pathological review of the disease, with
a report of two cases. Arch. Int. Med., Chicago, 1914, xiv, 481-516.
L. Diseases of the Veins
1. Phlebitis and Thrombophlebitis
Definition. — An inflammation of the walls of the veins, often leading
to thrombosis.
Etiology. — Nearly always, the disease is due to bacterial infection
(streptococci). Infection may occur by direct extension, or it may be
hematogenous or lymphogenous in origin. A peculiar luetic phlebitis is
also described (B. Hoffmann).
Symptoms. — In the superficial veins, there is redness in the skin over
the vein, and a tender cord is palpable where the deep veins are involved.
The symptoms are vague at first (burning, formication, itching) ; later,
intense boring pains may develop. Swelling and redness of the neighbor-
ing tissues appear. The danger of embolism is great, unless the part be
kept at rest.
Thromboses may form and may extend into the larger veins, even to
the vena cava.
Thrombophlebitis is common after childbirth (phlegmasia alba dolens)
rand in typhoid fever. There is a form of recurring thrombophlebitis that
occurs in women, attacking, successively, the veing in different parts
pf the body ; it is a grave malady.
922 DISEASES OF THE CIBCULATOKY APPAKATUS
Fig. 290. — Diagram of a Case of Latent Cancer of
the Stomach with Multiple Thrombi in the Veins.
(After W. Osier and T. McCrae, "Cancer of the
Stomach," published by P. Blakiston's Sons Co.,
Philadelphia.)
2. Varicose Veins
Definition. — Varix is a pathological dilatation of a vein.
Etiology. — Mechanical factors, obstructing the venous flow, are usually
responsible. Varicose veins of the legs may be due to wearing tight garters
or to pressure on the veins within the abdomen (pregnancy, tumors) or
to occupations requiring long standing. Varicose veins of the esophagus
may be due to the formation of a collateral circulation after portal obstruc-
tion (cirrhosis hepatis).
Symptoms. — In the legs, the enlarged and tortuous veins appear as
prominent swellings, and they may be painful, especially on long stand-
DISEASES OF THE VEINS 923
ing. Pigmentations and atrophy of the skin accompany them, and often
"varicose ulcers."
Varicosities of the hemorrhoidal veins are known as piles or hemor-
rhoids. They may cause great discomfort (itching, pain, hemorrhage).
In esophageal varix, profuse hemorrhage is not uncommon and may first
lead one to suspect a cirrhosis of the liver. (See Part VIII.)
3. Phlebosclerosis
The walls of the veins are sometimes palpably thickened, a process akin to
atherosclerosis. The condition is, as yet, of but little clinical importance.
References
Bennett (W. H.). Clinical lectures on varicose veins of the lower extremities. Lancet,
London, 1889, i, 1071; 1123; 1231.
Buerger (L.). Thrombophlebitis migrans der oberfldchlichen Venen bei Thromboangiitis
obliterans. Mitt. a. d. Grenzgeb. d. Med. u. Chir., Jena, 1909-10, xxi,
353-376.
Edinger (L.). Ueber phlebogene Schmerzen. Berl. klin. Wchnschr., 1914, li, 521-523.
Forst (A. W.}. Ueber kongenitale V arizen. Verblutung aus einem kongenitalen Varixkno-
ten der Venajugularis. Frankfurt. Ztschr. f. Path., Wiesbaden, 1915, xxii,
137-157.
Foster (G. 5.). Phlebectasis ; description of a newly modified instrument for use in operative
cases. Surg., Gynecol. & Obst., Chicago, 1912, xiv, 202-205.
Haward (H.). Phlebitis and thrombosis. The Hunterian lectures delivered before the Royal
College of Surgeons of England in March, 1906. London, 1906. 8°.
Jeger (E.) & Israel (W.). Ueber Ersetzung eines Stuckes der Vena cava inferior durch
frei transplantierte Vena jugularis externa desselben Tieres. Arch f klin.
Chirurg., Berl., 1913, c, 1018-1028.
Lydston (G. F.}. A review of varicocele and its treatment. West. M. Reporter, Chicago,
1891, xiii, 129; 153.
Murphy (J. #.). Varicocele. Surg. Clin., Chicago, 1912, i, 17-23.
Parker (E. C.). Varicose veins with special reference to Schede's operation. Mississippi
M. Month., Vicksburg, 1911-12, xvi, 131-134-
Schum (#.). Beitrag zur Kenntnis der septischen Thrombophlebitis. Arch. f. path. Anal,
[etc.] (Virchow), Berlin, 1914, ccxviii, 300-350. 1 pi.
Secher (K.). Behandlung von Varicen an den unteren Extremitaten nach der Methode von
Kuzmik-Schede. Berl. klin. Wchnschr., 1915, Hi, 608-610.
Tavel (E.}. Die Behandlung der Varicen durch die kunstliche Thrombose. Deutsche Ztschr.
f. Chir., Leipzig, 1912, cxvi, 735-738. 2 pi.
Vorner (H.). Ueber Phlebitis moniformis ectatica und den Zonalismus. Arch. f. Dermat.
u. Syph., Wien u. Leipzig, 1914, cxx, Orig., 877-888.
Weichert (M.). Sapheno-femorale Anastomose (Delbet) bei Varicm. Berl. klin. Wchnschr.,
1913, I, 1396-1400.
Widal (F.), Bezancon (F.) & Labbe (M.). Maladies des veines et des lyniphatiques.
Paris, 1911, J. B. Bailliere & fils. 169 p. 8°. [Nouv. Traite de Med.
de Therap., xxv.]
INDEX TO REFERENCES
Abbott (A. C.) 259, 363, 551
Abbott (F. C.) 198
Abbott (Maude E.) 897, 898
Abbott (W. J.) 591
Abderhalden (E.) 4
Abel (J.) 804
Abel (R.) 96, 555
Abelmann (M.) 897
Abraham (P. S.) 296
Abrami (P.) 307
Abrams (A.) 547
Achard (C.) 249, 667
Acker (G. N.) 444
Adam (A.) 694
Adam (J.) 591
Adami (J. G.) 6, 118, 652, 681, 907
Adams (R.) 854
Adamson (H. A.) 378
Adamson (H. G.) 318, 325
Addis (T.) 108
Adler, 123
Adler (I.) 652, 716, 907
Agasse-Lafont, 647
Agramonte (A.) 389, 391
Ahnmaner, 402
Albers-Schonberg (H. E.) 63, 716
Albert- Weil (E.) 63, 690
Albrecht (E.) 822
Albrecht (W.) 469
Alden (A. M.) 260
Alexander (A.) 558
Alexander (D. M.) 553
Allan (W.) 305
Allard (E.) 77
Allbutt (Sir T. C.) 2, 5, 739, 807, 825, 903
Allen (H. W.) 843, 857
Allen (R. W.) 109, 540
Alwens, 65, 643
Ames (J. C.) 133
Ameuille (P.) 691
Amoss (H. L.) 402, 403
Anderes (E.) 603
Anders (A.) 822
Anders (H. S.) 3
Anders (J. M.) 2, 3, 188, 674
Anderson (F. A.) 305
Anderson (J.) 681
Anderson (J. F.) 123, 126, 218, 290, 298,
300, 301, 304, 305, 394, 395, 404, 416,
440, 441
Andr&s (A.) 679
Andrews (E. W.) 591
Angerer (K) 176
Anglada (J.) 739
Anthony (H. G.) 421
Aoyama (T.) 666
Apelt, 81
Arima (R.) 245
Armande-Delille (P. A.) 288, 672
Armbruster (G.) 638, 647
Armstrong (D. B.) 624
Armstrong (G. E.) 188
Armstrong (II.) 858
Armstrong (S. T.) 298
Armstrong (V. A.) 184
Arndt (J.) 843
Arning, 293
Arnold (J.) 646, 647
Arnsperger (II.) 679
Arnsperger (II. E. R.) 64
Arrhenius (Svante) 105
Arthur (D.) 64
Artus, 123
Aschoff (L.) 6, 457, 864, 907, 919
Ascoli (M.) 176
Ashburn (P. M.) 391, 392
Ashford (B. K.) 307
Ashton (T. G.) 858
Ashurst (A. P.) 218
Assmann (H.) 64, 547
Astrowski (S.) 504
Atkinson (I. E.) 188
Auche (B.) 407
Audrain (J.) 378
Audustere, 670
Auer (J.) 123, 126, 130, 218, 804, 823,
824, 864
Aufrecht (E.) 596
Augenbrugger (L.) 495
Augustin (G.) 391
Aumann, 298
Austen (E. E.) 331
Austin (J. H.) 722, 857
Austin (R. S.) 121, 179
Austrian (C. R.) 123, 127, 163, 175, 289
Avellis (G.) 476
Avenches (M.) 421
Avery (0. T.) 145, 606
Axenfeld (T.) 201, 221, 5G3
Azoulay, 735
B
Baas (J. H.) 5
Babcock (R. H.) 591, 596, 602, 698, 875,
884
925
926
INDEX TO REFERENCES
Babes (V.) 214, 292, 296, 329, 388
Baccelli (G.) 218
Bachmann (G.) 780, 792, 795, 857
Bacmeister (A.) 615
Bacon (C. S.) 189
Bacot (A. W.) 227
Baehr (G.) 301, 302, 305, 874, 876
von Baerensprung (F. W.) 312
Baermann (G.) 377
Baeslack (F. W.) 378
Baetjer (F. H.) 53, 61, 624, 630, 711, 917
Baetjer (W. A.) 163, 247, 332, 334, 335
Bail (0.) 96, 103
Bailey (C. H.) 164, 907
Bailey (H. C.) 780
Baillie (M.) 613
Baker (C. H.) 555
Baldwin (E.) 624
Baldwin (E. R.) 175, 289
Balfour (A.) 362, 391
Ballance (C. A.) 917
Ballance (H. A.) 670
Bailenger (W. L.) 476, 548, 563
BalliSre (J. B.) 665
von Bamberger (H.) 884
Bandelier (B. E. G.) 287
Banks (C. E.) 673
Bannerman (W. B.) 227
Barach (J. H.) 224, 804
Barany (R.) 459
Barber (M. A.) 106, 227
Barbier (H.) 548, 629
Barbour (H. G.) 485, 903
Barclay (A. E.) 64
Barcroft (J.) 488, 865
Bard (L.) 4, 652, 666, 667, 703, 725, 726,
727, 758, 759, 761, 765, 780, 781, 847,
878
Bardet (E.) 885
Bardswell (N. D.) 291, 625
Barfurth (W.) 184
Bargeduhr (A.) 675
Barie (E.) 894
Barker (B. A.) 87, 88
Barker (L. F.) 26, 203, 210, 227, 245,
261, 363, 699, 757, 788, 807, 858, 864,
917
Barker (W. W.) 179
Barling (J. E. V.) 330
Barlow (T. W. N.) 596
Barr (J.) 703
Barrett (G. M.) 216
Barringer (T. B.) 813
Barringer (T. B., Jr.) 864
Barrington-Ward (L. E.) 611
Bartel (J.) 287
Barth (E.) 555
Barth (H.) 478
Barthelemy, 547
Bartlett (F. H.) 628
Barton (A. L.) 382
Barton (W. M.) 825, 857
Baruch (S.) 602
Barwell (H.) 574
von Basch (S.) V51, 797, 811
Basile, 344
Bass (C. C.) 122, 363, 364
Bassett (V. H.) 247
Bassoe (P.) 457
Bastianelli (G.) 363
Bates (J. P.) 364
Battaerd (P. J. T. A.) 722
Batten (F. E.) 400, 404
Batzdorff (E.) 594
Bauer (W.) 634
Baugher (A. H.) 216
Baumler (C.) 667
Baumann, 280
Baumann (A.) 638
Baumann (F. L.) 629
Baur (J.) 670
Bawetetz (A.) 640
Bayle, 5, 613
Bayliss, 813
Beall (K. H.) 191, 669
Beardsley (E. J. G.) 244
Beattie (J. M.) 195
Beau (J. H. S.) 525
Beaurepaire (H.) 434
Bechold (H.) 383
Beckmann (E. H.) 670, 671
Beckmann (K.) 487
BeclSre (A.) 648, 669, 671, 672, 679, 690
BeclSre (J.) 547
Bedos (J.) 476
Behrend (E. B.) 244
von Behring (E.) 112, 218, 260, 283, 287,
290, 615
Beitzke (H.) 287
Belfanti (S.) 116
Bell (A. J.) 411
Bellot, 170, 211
Belot (J.) 672
Benario (J.) 377
Benda (C.) 290
Benedek (L.) 177
Benedik.t, 883
Beneke (R.) 643, 919
Benjamins (C. E.) 762
Bennecke (H.) 218
Bennett (W. H.) 923
Bensaude (R.) 891
Bentley, 343
Berg (*A. A.) 198
Bergeat (H.) 559
Bergengriin (P.) 476
Berger (V.) 843
Bergmann, 807
von Bergmann (E.) 476
von Bergmann (G.) 683, 687, 688, 689
Bergonie (J.) 669
Beriel (L.) 482
Berkart (J. B.) 591
Berkeley (W. N.) 775
Berkowitz (S.) 379, 634
Bernard (C.) 6
Bernard (L.) 288
Bernhardt (G.) 410
Bernhardt (M.) 451
Bernheim (B. M.) 908, 917, 919
Berry (F. H.) 638
INDEX TO REFERENCES
927
Berry (H. M.) 564
Berry (Jane L.) 290
Bert (P.) 457
Bertier (J.) 701
Resnier, 17
Besredka (A.) 103, 109, 130, 218, 246,
627
Besson (A.) 137
Bettmann (M.) 589
de Beurmann (C. L.) 307, 313, 322, 325
Bevan (A. D.) 685
Bezangon (F.) 531, 535, 602, 923
Bezold (F.) 574
Bibb (L. B.) 547
Biedl (A.) 126, 130
Bien (G.) 482
Bier (A.) 917
Bierast (W.) 251
Bierger, 292
Biermer, 513
Biernacki (J.) 411
Bierring (W. L.) 403
Bies (C.) 648
Bigelow (O. P.) 85
Biggs (H. M.) 625, 681
Bignami (A.) 362
Billings (F.) 101, 378, 876, 884
Billings (J. S., Jr.) 291
Bing, 794
Birsch-Hirschfeld (F. V.) 615
Bisgard (A.) 93
Bishop (L. F.) 908
Bishop (S. S.) 574
Bissell (F. S.) 629
Bissell (J. B.) 908
Bittorf (A.) 488, 789, 865
Black (D. D.) 897
Black (J.) 209, 211
Blackfan (K. D.) 164, 166
Blacklock (B.) 341
Blackstein (A. G.) 245
Blaizot (L.) 368
Blanc (F.) 559
Blanc (G.) 368
Blanchard (M.) 340
Blanchard (R.) 362
Blauel, 799, 882
Blecher, 613
Blechman (C.) 884
Blechman (G.) 77
Bliss (M. A.) 564.
Bloch (B.) 326
Bloch (Vera) 921
Bloodgood (J. C.) 809
Bloomfield (A. L.) 163, 192, 193
Blue (R.) 227
Blumenfeld (F.) 574
Blumenthal (J. M.) 259
Blumer (G.) 204, 214, 261, 669, 718, 911,
919
Boardman (W. L.) 61, 174
Boardman (W. W.) 540, 547
Boas (H.) 166, 378
Bodin (E.) 309
Boeck, 293
Boehm (E.) 604
Boelter (W. R.) 227
Boer (O.) 260
Boggs (T. R.) 221, 397, 594
Bohme (A.) 116, 11V
Bohne (A.) 388
Bohr (C.) 487, 489
Boine, 557
Boinet (E.) 698
Boinot, 344
Bois (G.) 672
du Bois-Reymond (R.) 487
Bolduan (C. F.) 625
Bellinger (O.) 326, 421, 434, 607
Bolton (H. C.) 133
Bolton (R. M.) 217
Bond (C. J.) 701
Bond (G. S.) 721, 788, 821, 823, 903
Bonhoff (F.) 247
Bonney (S. G.) 625, 629
Boothby (W. M.) 487, 638, 823
Borchardt (L.) 591
Borchers (E.) 900
Bordet (J.) 105, 112, 115, 117, 122, 155,
221, 224
Bordier (H.) 65
Bordone-Uffreduzzi, £02
Borel, 219
Bornstein (A.) 457
Boruttau (H.) 542, 789
Bosquet, 261
Bosworth (F. H.) 548, 551, 564
Bottler (R.) 166
Bougault, 671
Bouveret (L.) 837
Bovaird (D., Jr.) 2, 209, 670, 679
Bowditch (V. Y.) 667
Bowen (C. F.) 477
Bowman (F. B.) 627
Boyce (R. W.) 328, 329
Boyd (H.) 602
Boykott, 455
Bradford (Sir J. R.) 341
Bramwell (B.) 6, 718
Brand (E.) 117
Brannan (J. W.) 24,
Brauer (L.) 666, 679, 883, 884
Brault (J.) 329
Braun (L.) 698, 758, 764
Bray (H. A.) 210
Brebeck (C.) 321
Breinl (A.) 336
Bricheteau (M.) 742
Bricout (C.) 878
Bridge (N.) 634
Bridgman (E. W.) 718, 721, 785, 788,
821, 849, 870
Brieger (L.) 103
Brigham (F. G.) 244
Brill (N. E.) 305
Brim (L.) 911
Brinkerhoff (W. R.) 423, 434, 439
Broadbent (J. F. H.) 767, 884
Broadbent (Sir W.) 670, 781, 881, 884
Brocq, 17
Brodie (T. G.) 752
Brodmann (K.) 751
928
INDEX TO REFERENCES
Broek (W.) 293
Bronfenbrenner (J.) 289, 629
Brons (C.) 564
Broussais (F.-J.-V.) 613
Brown (A.) 177
Brown (A. G., Jr.) 607
Brown (G. L.) 127
Brown (G. V. I.) 549
Brown (L.) 288, 625, 627, 629
Brown (P. K.) 290, 296, 318, 560, 625
Brown (R. O.) 403
Brown (T. R.) 243, 261
Brown (W. G.) 625
Brown (W. H.) 363
Brown (W. T.) 625
Browning (C. H.) 118
Bruce (C. E.) 804
Bruce (Sir D.) 211, 212, 337, 338, 339,
340, 341
Bruce (Lady) 340
Bruce (R. B.) 814
Bruck (C.) 155, 203, 378
Brudzinski (J.) 210
Bruen (E. T.) 741
Brues (C. T.) 381, 403
Briigelmann (W.) 591
Brugsch (T.) 3, 4, 137, 378, 716, 722,
817
Brumpt (E.) 342
Brunings (W.) 473
Brunton (Sir L.) 907
Brush (C. E.) 798, 804, 908
Brush (N.) 84, 94
Bruynoghe (R.) 210
Bryan (J. H.) 564
Buchanan (Florence) 784, 789
Buchner (H.) 103, 108
Buckner (G. D.) 127
Budde (W.) 65
Buerger (L.) 919, 920, 923
Bulkley (L. D.) 17
Bull (C. G.) 201
Bullock (W.) 118, 195, 291, 625
Bullock (W. E.) 171
Bundesen (H. N.) 260
Bunting (C. H.) 90, 690
Burdon-Sanderson (Sir J.) 136
Burkhart (J. L.) 607
Burnam (C. F.) 453, 689
Burnet (E.) 667
Burnett (C. H.) 548
Burnham (F. W. E.) 362
Burns (J. E.) 191
Burns (N. B.) 640
Burrows (H. A.) 558
Burton (A. H. G.) 625
Burton -Opitz, 812
Busacchi (P.) 261
Buschke (A.) 305, 318
Buscinco (A.) 652
Bushby (T.) 679
Buswell (H. C.) 316
Butler (G. R.) 3, 681, 701
Butterfield (H. G.) 837, 846
Bythell (W. J. S.) 64
C. (J.) 690
Cabot (R. C.) 4, 6, 87, 500, 525, 647, 673,
708, 804, 814, 825, 884, 892, 907
Cade (A.) 667
Cadel (A.) 583
Caiger (F. F.) 410
Caldwell (G. W.) 574
Calkins (G. N.) 331, 334, 423, 440
Callender (G. R.) 629
Calmette (A.) 112, 175, 288, 619, 620
Caloe (J.) 290
Calvert (J.) 884
Calvert (W. J.) 227, 247, 669, 670, 679,
884, 895
Camac (C. N. B.) 5, 243, 341, 744, 767
Cameron (P. D.) 865, 871
Caminitti (R.) 330
de la Camp (O.) 679, 690
Campbell (C. M.) 908
Campbell (J. M. H.) 487, 489
Campergue (Berthe) 897
Canfield (R. B.) 78
Cannata, 344
Canon, 149
Cantieri (C.) 807
Capitan, 700
Capps (J. A.) 191, 666, 809
Carbone (T.) 116
Carlson (A. J.) 823
Carman (R. D.) 65, 669, 917
Carnot (P.) 96
Caro (A.) 583
Caronia (G.) 345
Carpenter (H. C.) 175
Carr (J. W.) 670, 679
Carrel (A.) 596, 894
CarriSre (G.) 669
CarriSre (II.) 434
Carrieu (M.) 730
Carrington (C. S.) 291
Carrington (P. M.) 627
Carrion (D.) 382
Carroll (J.) 389, 391
Carrougeau (J.) 330, 331
Carson-White (E. P.) 378
Cartaz (A.) 548
Carter, 328
Carter (E. P.) 788, 858
Carter (H. R.) 391
Carter (H. S.) 667
Carter (H. V.) 329
Cartier (P.) 666
Cary (C.) 201, 605, 682
Gary (E. G.) 119
Casamajor (L.) 87
Case (J. T.) 64, 65
Caspar (M.) 404
Cassarini (D.) 673
Casselberry (W. E.) 551, 559, 578, 58S
Castellani (A.) 5, 121, 122, 331. 340, 341,
345, 380, 540
Castex (A.) 548
Cathcart (E. P.) 804
Cattermole (G. H.) 175
INDEX TO REFERENCES
929
Cautley (E.) 875, 876, 894
Cazzaniga (A.) 690
Cecil (A. B.) 739
Cecil (R. L.) 166, 210, 540
Celler (H. L.) 189
Celli (A.) 362, 364
Cerf (L.) 421
Chagas (C.) 342
Chalier (J.) 626
Chalmers (A. J.) 5, 331, 540
Chantemesse (A.) 179
Chapin (C. V.) 434
Chapin (H. D.) 244, 603
Chapin (W. S.) 118
Chapman (C. W.) 865
Chapman (E. D.) 296
Charcot (J. M.) 400, 909
Chatard (J. A.) 341, 603, 604
Chauffard (A.) 334, 672, 673
Chauveau (A.) 3£3, 758, 761
Cheadle (C. M.) 629
Cheinisse (L.) 444
Chesley (A. J.) 403
Cheyne (W. W.) 185
Chiari (0.) 548, 556, 574, 577, 585
Chick (H.) 227
Chickering (H. T.) 120, 201, 603
Chillingworth (F. P.) 490
Chisolm (R. A.) 485
Chowning (W. M.) 441
Christen (T. F.) 818
Christian (H. A.) 122, 368, 683, 688, 857
Christiansen (J.) 638
Christie (A. C.) 64
Christophers, 343
Church (Sir W. S.) 195, 603
Churchman (J. W.) 185
Citron (J.) 103, 150, 166
Claisse (P.) 586, 596
Clarac (G.) 843, 8f>7
Clarague, 5
Clark (Sir A.) 596
Clark (A. H.) 813
Clark (G. H.) 804
Clark (H. C.) 911
Clark (Hilda) 625
Clark (J. M.) 606
Clark (L. P.) 404
Clark (P. F.) 394, 395, 396, 402, 403
Clark (W. M.) 251
Clark (W. R. P.) 918
Clarke (J. A.) 343
Claude (H.) 672
Clay (J. V. F.) 690
Claypole (Edith J.) 246, 329, 330
Claytor (T. A.) 825
Clegg (M. T.) 329, 334
Cloetta (M.) 591, 603
Clough (F. E.) 804
Clough (P. W.) 123, 166, 200, 201, 316,
405
Clowes (G. H. A.) 155, 553
Cnopf (J.) 631
Coakley (C. G.) 469, 476, 54S
Cobb ("F. C.) 558
Coca (A. F.) 117, 127, 130, 166
Cockayne (E. A.) 383
Cody (E. F.) 434, 813
Coffin (B. H.) 775
Cohen (J. S.) 476
Cohen (S. S.) 549, 629
Cohn (A. E.) 697, 763, 822, 823, 828, 837,
843, 856, 857, 858, 865, 891
Cohn (E.) 325
Cohn (J. S.) 145
Cohn (M.) 117
Cohn (T.) 537
Cohnheim, 614
Cohoe (B. A.) 220, 221
Cole (H. N.) 378
Cole (R. I.) 69, 122, 171, 184, 195, 200,
201, 203, 205, 603, 606, 739
Coleman (W.) 245, 249, 876
Collier, 807
Collier (W.) 672
Collins (K. R.) 122
Collis (E. L.) 647
Colliver (J. A.) 403, 629
Colombe (J.) 911
Comby (J.) 670
Corite (C.) 305
Concetti (L.) 345
Conner (L. A.) 244, 493, 595, 643
Conor (C.) 305
Conradi (H.) 147, 251
Conseil (E.) 305, 368, 442, 444
Conte (R.) 613
Cook (F. C.) 247
Cook (H. W.) 605
Cook (J. E.) 891
Cooke (Jean V.) 318
Cooke (R. A.) 553
Coolidge (W. D.) 27
Coombs (C.) 421, 744, 909
Coombs (C. F.) 844
Cooper (C. M.) 672, 884
Cooper (W. F.) 331
Cope (T. A.) 175
Coplin (W. M. L.) 645, 666
Corda, 325
Cordier (V.) 607
Coriat (I. H.) 667
Corica (A.) 690
Corner (E. M.) 378
Cornet (G.) 288, 290
Cornwall (E. W.) 79 J.
Corre (G.) 694
Corrigan (D. J.) 647, 891
Corvisart (J. N.) 495, 708
Cort (E. C.) 351
Cotoni (L.) 603
Cotton (T.) 865
Cotton (T. F.) 865
Cotton (W.) 64
Councilman (W. T.) 210, 332, 334, 363,
421, 423, 439, 633
Couret (M.) 296
Courmont (J.) 186
Courmont (P.) 627, 667
Cowan (J. M.) 670
Cowie (D. M.) 118, 127
Cragg (F. W.) 331
930
INDEX TO KEFEKENCES
Craig (C. F.) 164, 332, 334, 362, 364, 391,
392
Cramer (A.) 908
Craster (C. V.) 416
Crede-Horder (C. A.) 204
Crehore (A. C.) 750, 775
Creighton (Sarah R.) 724
Crile (G. W.) 244, 585, 807, 809
di Cristina (G.) 344, 345
Crocker (H. R.) 17
Crombie (D. W.) 631
Crombie (R. H.) 547
Cross (J. G.) 603
Crossonini (E.) 88
Crow (G. B.) 629
Crowe ( S. J. ) 565
Cullis (W.) 822
Cumberbatch (E. P.) 65
Cummer (C. L.) 166, 679
dimming (J. G.) 389
Cummins (W. T.) 318
Cumston (C. G.) 244
Curschmann (H.) 243, 534, 591, 883
Cushing (H.) 77, 210, 244, 883
Cushing (H. W.) 805
Cushny (A. R.) 823, 843
Czerny (A.) 224, 284, 290
D
Dabney (W. M.) 204
Da Costa (J. C.) 4
Da Costa ( J. C., Jr.) 510
Da Costa (J. M.) 825
Dale (G.) 789
Dale (H. H.) 807
Dally (J. F. H.) 788, 792
Damant, 455
D'Ambrosio (A.) 690
Damoiseau (H.) 508, 668
Dana (C. L.) 451
Danielssen (D. C.) 293
Danysz (J.) 227
Darier (J.) 17
Darling (S. T.) 345, 368, 382, 911
David (V.) 558
Davidson (A.) 253, 391
Davies (B. C.) 592
Davies (H.) 720
Davies (H. M.) 595, 627, 629
Davies (J. R:) 791
Davies (L. G.) 645
Davis (B. J.) 251
Davis (D. J.) 191, 196, 210, 221, 325, 330
Davis (N. S.) 607
Davis (W. B.) 564
Davison (J. T. R.) 739
Dawson (G. D.) 245
Dawson (P. M.) 805, 816
Day (J. M.) 411
Dayton (H.) 78, 672
Deaderick (W. H.) 362
Dean (G.) 889
Dean (H. R.) 156
Dearholt (H. E.) 629
Debains (E.) 629
Debove (G. M.) 2
Dcbre (R.) 211
Decloux (L.) 547
Decks (W. E.) 334
Dehio (K.) 725, 744, 763
Dehon (M.) 909
Delamarre (A.) 558
Delatour (H. B.) 883
Delavan (D. H.) 564
Delbet (P.) 871
Delorme, 627
Demmer (F.) 609
Dench (E. B.) 574
Denison (H. S.) 246
Denny (G. P.) 907
Denys (J.) 119
Dcperer, 344
Dernini (G.) 901
De Sautelle (W. T.) 253, 739
Dessauer (F.) 64, 65
Determann (H. A.) 701
Detweiler (H. K.) 875
Devoto (L.) 629
Dexter (P.) 166
Dexter (R.) 483, 672
Deycke (G.) 292, 296
Dibourg (E.) 691
Dick (G. F.) 150, 166
Dickey (W. A.) 900
Dickie (J. K. M.) 574
Diday, 375
Dieck (W.) 65
Dietlen (H.) 672, 701, 716
Dieudonne (A.) 150, 227
Dieulafoy (G.) 2, 633, 648, 668, 671, 672,
688
Di Jorio (E.) 788
Dittrich, 534
Dixon (S. G.) 625
Dixon (W. E.) 93, 487, 807
Dobbie (W. J.) 629
Dochez (A. R.) 87, 200, 201, 402, 604, 606
Dock (G.) 91, 557, 675, 883
Doehle (P.) 410
Dohle (K. H. P.) 911
Doerr (R.) 125, 405
Doflein (F.) 331
Dold (H.) 120, 127
Doll (K.) 703
Dominguez (M.) 652
Donald (R.) 85
Donaldson (M.) 805
Donovan, 343
Dorendorff (H.) 583
Dormoy, 574
Dorn (M.) 592
Doming (J.) 603
Dorr (R.) 253
Dorset (M.) 383
Doty (A. H.) 305
Douglas (C. G.) 484, 487, 48>
Douglas (K. M.) 188
Douglas (S. R.) 107, 118
Dowling (0.) 378
INDEX TO REFERENCES
931
Downing (A. F.) 633
Draper (G.) 400, 402, 411, 761, 889
Dresbach (M.) 836
Dreschfeld (J.) 243, 603, 875
Dreyer (G.) 112
Drigalski, 147
Dubois (E.) 245
Duckworth (D.) 745
Ducrey (A.) 253
Dudgeon (L. S.) 289, 410, 666, 747
Dudley (W. H.) 592
Duffey (G. F.) 682
Dufourt (A.) 604
Dufourt (P.) 919
Duhring (L. A.) 17
Dukes (C.) 418
Dumas (L. E.) 547
Dunbar (W. P.) 298, 553, 554
von Dungern (E.) 117
Dunges (A.) 627
Dunham (E. K.) 549
Dunham (H. K.) 547
Dunham (K.) 61, 629
Dunn (C. H.) 875
Dupuich (A.) 630
Durand (P.) 482
Durham, 121, 122
Duroziez (P.) 744, 884
Dutton (J. E.) 336, 337, 341
Duval (C. W.) 292, 296
Duval (H. R.) 319
Dyer (L) 296
Dykes (A. L.) 411
E
Earhart (T. W.) 296
Earl (H. C.) 668
Eastman (J. R.) 668
von Eberts (E. M.) 244
Ebstein (E.) 11, 12
Ebstein (W.) 405, 482, 504, 708, 759
Eckard (B.) 340
Eckhardt (E. A.) 526, 668
Edelmann (M.) 500
Edelmann (M., Jr.) 757
Edgeworth (F. H.) 603
Edie (E. S.) 363
Edinger (L.) 923
Edington (G. H.) 670
Edlavitch (B. M.) 652
Edmunds (C. W.) 843
Edsall (D. L.) 447, 605
Edwards (A. R.) 2, 739, 891
Egbert (J.) 109
Eggleston (C.) 865
Eggstein (A. A.) 127
Ehrenberg (L.) 865
Ehrlich (P.) 103, 105, 107, 110, 112, 114,
115, 117, 156, 288, 378, 614
Eichelberg, 395
Einthoven (P. H.) 897
Einthoven (W.) 697, 722, 754, 757, 784,
788, 789
von Eiselsberg (A. F.) 883
Eisenberg (P.) 122
Eisenbrey (A. B.) 127, 166, 809
Eisendrath (D. N.) 218
Eisler (F.) 669, 911
von Eisler (M.) 122
von Elischer (J.) 753
Elliott (J. B.) 260, 291
Ellis (A. W. M.) 94, 378
Ellis (C.) 508
Elsberg (C. A.) 198, 680
Elsberg (L.) 583
Elser (W. J.) 210
Emanuel (J. G.) 666
Emerson (C. P.) 4, 603, 680
Emerson (H.) 809
Emmerich (E.) 297
Emrys-Roberts (E.) 554
Endriss (G.) 549
Eng-Kiu Chiu (S.) 378
Engel, 284, 290
Engel (H.) 547
Engel (K.) 454
Engelbach (W.) 669
Engelmann, 697
Entin (M.) 647
Eppinger (H.) 3*3, 330, 483, 789, 858
Epstein (D.) 288
Erb (W.) 378, 909
Erb (W., Jr.) 907
Erben (N.) 764
Erlanger (J.) 697, 792, 798, 800, 803,
804, 805, 816, 823, 853, 856
Esbach, 81
Escherich (T.) 286, 290
Esmein (C.) 847, 895
D'Espine (A.) 290
Ettinger (W.) 803
Eulenburg (A.) 3
Eustis (A.) 213, 245
Evans (C. L.) 487, 816
Evans (G.) 908
Evans (G. H.) 175
Evans (H. M.) 627
Evans (J. S.) 857
Ewald (W. F.) 824
Ewart (W.) 595, 668, 669, 680
Ewing (E. M.) 781, 809
Ewing (J.) 245, 363, 440, 604
Exchaquet, 726
Eyre (J. W. H.) 201, 212
Eyselein (K.) 900
Eyster (J. A. E.) 485, 781, 784, 788, 789,
805, 809, 811, 823, 824, 825, 836, 857
Faber (H. K.) 195
Fabyan (M.) 510, 628, 669, 908
Faguet, 330
Fahr (G.) 789, 823
Faisans, 670
Falconer (A. W.) 857, 889
Falk (F.) 531
Fantham (H. B.) 334, 336, 337, 339, 341,
346, 549
932
INDEX TO EEFEEEXCES
Farnell (F. J.) 319
Faught (F. A.) 4, 791, 798
Favre (J.) 909
Fayerweather (R.) 804
Fayrer (Sir J.) 447
Fehleisen (X.) 188
Feiling (A.) 444
Feldstein (S.) 210
Feletti (R.) 349, 350, 362
Felton (L.) 94
Fenwick (B.) 895
Ferrannini (L.) 629
Ferrata (A.) 117
Ferre. 330
Festerling (E. G.) 805
Fetterolf (G.) 510, 583, 629, 674, 720, 892
Ficker (M.) 96, 110
Field (G. H.) 399
Filatow (N.) 418
Fildes (P.) 166
Finger (E.) 378
Fink (E.) 557
Finlay (C.) 391
Finlay (D. W.) 680
Finlayson (J.) 739
Finley ( F. G.) 680
Finney (J. M. T.) 244, 917
Finzi*(N. S.) 564
Firth (R. H.) 382
Fisch (C.) 217
Fischer (B.) 321, 643
Fishbein (M.) 411
Fisher (I.) 907
Fisher (L.) 559
Fisk (E. L.) 907
Fitz (R.) 244
Fitz (R. H.) 2
Fitzgerald (M. P.) 487
Fitzsimons (F. W.) 247
Flack (M.) 792, 822, 827
Flack (M. W.) 822
Fleischer (M. S.) 878
Fleischner (E. C.) 603
Flessinger (N.) 668, 878
Flexner (S.) 117, 210, 226, 227, 253, 259,
329, 330, 392, 393, 394, 395, 398, 400,
402, 403, 634
Flick (L. F.) 291
Fliess (W.) 549
Flint (A.) 2, 4, 478, 500, 525, 698, 739
Flint (J. M.) 226, 227
Flohil (A.) 722
Florand (A. L.) 590
Flournoy (T.) 440
Floyd (C.) 179, 184, 626, 668
Flurin (H.) 590
Foley (H.) 368
Fontaine (B. W.) 318
Forbat (A.) 629
Force (J. N.) 179, 246
Forchheimer (F.) 130,605
Ford (W. W.) 110, 117, 247, 259
Forgue, 557
Forlanini (C.) 630
Fornet (W.) 247, 434
Forrest (J.) 548
| Forssell (G.) 65
Forst (A. W.) 923
Forster (A. M.) 470
Foshay (P. M.) 742
Foster (A. D.) 627
Foster (G. B.) 177
Foster (G. B., Jr.) 305
Foster (G. S.) 923
Foster (H.) 558
Foster (N. B.) 806, 897
Fotheringham (J. T.) 218
Foubertin, 329
Foulcrton (A. G. R.) 330
Fournier (A.) 376, 377, 379
Fournier (E.) 379
Fowler (J. K.) 633, 638
Fowler (0. S.) 627
Fox (G. H.) 434
Fox (T. C.) 188, 199
Fraenkel (A.) 289, 592, 596, 603, 652, 681
Fraenkel (E.) 65, 547, 605
Frankel, 221, 329
Frlinkel (B.) 577, 585
Frankel (M.) 612, 630
France (J. I.) 699
Franck (A. J. H.) 342
Francis (E.) 403
Frangois (M. L.) 590
Frangois-Franck (A.) 742, 744, 844, 881
Frank, 812
Frank (I.) 535
Frank (0.) 722, 750
Franz (K.) 405
Franze (P. C.) 716
Fraser (F. R.) 94, 394, 403, 837, 857, 871
Fraser (J.) 290
Fraser (J. S.) 574
Frazer (T.) 625
Frazier (C. H.) 94
Fredericq (E.) 697, 761, 762, 784
Fre'de'ricq (H.) 824
Freeman (A. W.) 247
Freeman (J.) 554
Freer (0. T.) 555, 559
Fremont-Smith (F.) 908
French (H.) 6
French (H. S.) 4
French (T. R.) 477
Freund, 43
Freund (A.) 586
Freund (E.) 444
Freund (W. A.) 280, 482, 615, 638
von Frey (M.) 761, 775
Frick (A.) 643, 672
Fridericia (L. S.) 487
Fried (G. A.) 149
Friedberger (E.) 117, 122, 127, 137
Friedenberg (S. A.) 477
Friedenwald (H.) 574, 630
Friedman (G. A.) 305
Friedman (U.) 176
Friedreich (N.) 2, 268, 512
Friedrich (0.) 547
Friedrich (P. L.) 691
Fritsch (G. T.) 6
Frosch (P.) 259, 405
TO REFERENCES
933
Frost (W. H.) 394, 395, 404
Frothingham (C.) 845, 908
Frothingham (C., Jr.) 121, 907
Frothingham (L.) 263
Fukushi (M.) 592, 911
Fuller (C. A.) 184
Fullerton (R.) 557
Fulton (F. T.) 865
Funaro, 786
Funk (E. H.) 671
Fussell (M. H.) 3, 605, 680
Futcher (T. B.) 500, 604, 698, 895
G
Gabbi (U.) 345
Gairdner (W. T.) 739
Galeotti (G.) 788
Gallavardin (L.) 698, 725, 836, 857, 919
Gammon (J. E.) 487
Ganter (G.) 824
Gardere, 670
Garland (C. H.) 291
Garland (G. M.) 508
Garre (C.) 198
Garre (K.) 596
Garrey (W. E.) 843
Garrison (F. H.) 5
Garrod (A. E.) 583, 908
Garrod (A. H.) 761
Garvin (A. H.) 627, 666
Gaskell, 697, 854
Gaskell (J. F.) 875
Gaskell (W. H.) 824
Gasser (H. S.) 816
Gastou (P.) 383
Gatch (W. D.) 809
Gaucher (E.) 17
Gauckler (E.) 404
Gautier (L.) 309
Gautier (P.) 127
Gay (F. P.) 115, J17, 123, 127, 166, 179,
201, 226, 246, 403
Gee (S.) 4, 478, 500, 525, 531, 666
Geigel (R.) 500, 716, 725, 739
Geisbock (F.) 791, 807
Geissler (W.) 85
Gelien (Johanna) 175, 260
Geluk (M. A. J.) 722
Gengou (O.) 108, 117, 221, 223
Georgesco-Carpatiano ( M. ) 682
Geraghty (J. T.) 145
Geraudel (E.) 823, 858
Gerber (P. H.)) 551, 557
Gerhard (G. S.) 665
Gerhard (W. W.) 300
Gerhardt, 268
Gerhardt (C.) 4, 513, 525, 668
Gerhardt (D.) 478, 494, 502, 504, 506,
512, 520, 605, 666, 670, 703, 761, 781,
825, 889, 893
Gerhartz (H.) 80, 625, 721, 722
Gessner (H. B.) 917
Ghoreyeb (A. A.) 643
Gibbs (H. D.) 447
Gibier (P.) 214
Gibson (G. A.) 485, 592, 698, 763, 825,
870, 871
Giemsa (G.) 91, 363
Giffin (H. Z.) 630, 694
Gilbert (A.) 2, 307, 911
Gilbert (G. B.) 470, 680
Gilchrist (T. C.) 318
Gilder, 782
Gillespie (L. J.) 200, 201
Gillet (H.) 721
Gillet (J.) 64
Gilliland (C. E.) 547
Gins (H. A.) 259
Ginsberg (G.) 260
Giraud (C.) 645
Giraud (Marthe) 645
Githens (T. S.) 485
Gittings (J. C.) 803
Glas (E.) 288, 578
Glenny (A. T.) 103
Glover (E. G.) 630
Gocht (H.) 64
Goddard (C. H.) 788
Goedeler (G.) 288
Goppert (F.) 210, 548, 638
Gott (T.) 753
Goldberger (J.) 300, 301, 305, 416
Goldie (W.) 605
Goldmann (E. E.) 560
Goldscheider (A.) 499, 500, 505, 516, 708,
Golgi (C.) 364
Golla (F. L.) 592
Goodale (J.) 555
Goodale (J. L.) 463, 557, 592
Goodall (E. W.) 127
Goodall (J. S.) 788
Goodhart (Sir J. F.) 485, 592, 892
Goodman (C.) 908
Goodman (E. H.) 531, 802, 809
Gordinier (H. C.) 669, 847, 876, 917
Gordon (A.) 378, 447
Gordon (A. R.) 884
Gordon (G. A.) 867
Gordon (W.) 739
Gorgas (W. C.) 363, 391
Gorham (L. W.) 816
Gorse (P.) 630
Gossage (A. M.) 843
Gotch (F.) 788, 789
Gottlieb (M. J.) 554
Gottstein (J.) 574
Gougerot (H.) 307, 317, 324, 325, 326,
330, 668, 671
Gouget (A.) 698
Goulston (A.) 865
Grabower (H.) 476
Graef (C.) 260
Graham (D.) 699, 875
Graham (D. A. L.) 174, 176
Graham (E. A.) 319
Graham (G. F.) 368
Graham (L. W.) 340
Graham-Smith (G. S.) 259
934
INDEX TO KEEEEENCES
Grail, 5
Grant (D.) 575
Grass! (B.) 349, 350, 362
Graupner (S. C.) 814
Graves (M. L.) 245
Graves (R. J.) 2
Graves (W. W.) 378
Gravier (L.) 847
Gray, 337, 338
Gray (E. A.) 630
Green (A. B.) 440
Green (J., Jr.) 560
Greene (C. L.) 3, 668, 670, 699, 865, 801
Greene (J. B.) 578
Greig, 338
Grellier (E. F. W.) 919
Grey (E. G.) 487, 739
Griffith (J. P. C.) 418
Griffith (T. W.) 858
Grimbert (L. L.) 4
Grober (J. A.) 645, 666
Grocco (P.) 669
Groedel (F. M.) 64, 65, 547, 716, 753, 805,
917
Groedel (T.) 753, 789, 837
Gross (S. D.) 5
Grosser, 383
Grosskopf (W.) 555
von Gruber (M.) 96, 118, 121, 122
Griinwald (L.) 555
Grulee (C. G.) 627
Grulle, 84
Guarnieri (G.) 423, 434, 440
Guttich (A.) 577
Guiart (J.) 4
Guillain (G.) 81, 94, 260
Guillemot (L.) 671
Guldner (E.) 921
Gulland (G. L.) 668
Gundrum (E.) 403
Gunn (J. D.) 789
Guthrie (C. G.) 260, 341
Guthrie (L. G.) 605
Gwynn (N. B.) 330, 483
Oy (A.) 669
Haase (M.) 318
von Haberer (H.) 917
Hachtel (F. W.) 299
Handel (L.) 156, 200, 201
Haenisch (G. F.) 691
Haeser (H.) 5
Haffkine (M. M. W.) 299
Hagedorn (M.) 574
Hagner (F. R.) 205
Hahn (M.) 103, 108, 487
Halm (R.) 411
Hajek (M.) 549, 556, 564, 578, 580
Halberstadter (L.) 377
Haldane (J. S.) 455, 487, 489, 638
Hale (C. H.) 405
Hall (C. R.) 742
Hall (F. de H.) 548
Hall (J. N.) 670
Halle (J.) 671
Halliburton (W. D.) 93
Hallock (W.) 549
Hallwachs (W.) 213
Halsey (J. T.) 911
Halsted (W. S.) 917
, Hamburger (F.) 286, 290, 627, 669
Hamburger (L. P.) 191
Hamburger (W. W.) 179
Hamerton (A. E.) 340
Hamilton (W. F.) 670, 672, 837, 897
Hamman (L.) 61, 173, 175, 247, 280, 624,
630
Hammers (J. S.) 84, 94
Hammill (S. M.) 175
Handford (H.) 727
Hanford (J. M.) 411
Hanes (F. M.) 201, 606
von Hansemann (D.) 65
Hansen (G. A.) 292
Harbitz (F.) 296
Hare (H. A.) 3, 244, 603, 805, 918
Harms (F.) 627
Harrass (P.) 64
Harris (A.) 288
Harris (D. F.) 742
Harris (D. L.) 388
Harris (N. M.) 203, 204, 300
Harris (T.) 681
Harris (W. H.) 296
Hart (C.) 587, 627, 630
Hart (T. S.) 825, 843, 857
Barter (A. G.) 318
Hartley (P. H. S.) 531, 675
Hartmann (C.) 818
Hartmann (M.) 334
Hartoch (Q.) 340
Hartshorn (W. M.) 630
Hartwel\ (J. A.) 670
Harvey (D.) 340
Harvey (W. F.) 389
Hasebroek (K.) 699, 791, 859, 865
Haskell (L. W.) 203
Haskell (R. H.) 196
Haslebacher, 592
Hasselbach (K. A.) 486, 487
Hassell (A.) 541
Hassin (G. B.) 403
Hastings (T. W.) 26, 540, 604, 876
Hauti£re (E.) 577
Havens (L. C.) 680
Haward (H.) 923
Hawes (J. B.) 530, 625
Hawes (J. B., Jr.) 630
Hawes (J. B., 2d) 625
Hawley (M. C.) 805
Hawn (C. B.) 780
Hay (J.) 775, 837
Haythorn (S. R.) 647, 918
Hazen (H. H.) 378
Head (G. D.) 884
Head (H.) 699
Healy (D. G.) 127
Heard (J. D.) 843
Heckenroth (F.) 340
ISTDEX TO BEFEKENCES
935
Hecker (R.) 413, 416
Hegler (C.) 444
Heim (F.) 647
Heim (R.) 487
Heiman (H.) 210, 2G1
Heine, 392
Heine (J.) 401
Heineke (A.) 857
Heinemann (P. G.) 441
Heise (F. H.) 627
Heitler (M.) 720
Heitz (J.) 843, 909
Hekman (J.) 627
Hektoen (L.) 96, 108, 117, 118, 119, 120,
318, 322, 324, 325, 412, 416, 560, 607
Hellendall (H.) 652
Heller, 615, 636
Heller (A.) 911, 918
Heller (0.) 112, 261, 389
Heller (R.) 643
Helmholz, 123
Hemenway (J.) 86, 87, 277, 290
Hemsted (H.) 876
Henderson (D. K.) 85
Henderson (F. F.) 224
Henderson (L. J.) 487
Henderson (M. S.) 482
Henderson (T.) 813
Henderson (Y.) 487, 489, 807, 809, 816
Henes (E., Jr.) 166
Henry (A.) 188
Henry (F. P.) 670
Henschen (C.) 630
Henson (G. E.) 362
Hericourt (J.) 123, 127
Bering (H. E.) 697, 780, 789, 824, 836,
843, 847, 865, 895
Herisset (A.) 558
Herlitzka (A.) 383
Herrick (A. B.) 296
Herrick ( J. B.) 210, 603, 668, 895, 903
Herringham (W. P.) 665, 837
Hertz (J.) 843
Heryng (T.) 466
Hess (A. F.) 418, 444
Hetsch (H.) 299, 388
Hett (G. S.) 564
Heublein (A. C.) 691
Heubner, 413
Heubner (W.) 907
Heuter (C.) 638
Hewes, 204
Hewetson (J.) 17
Hewlett (A. W.) 752, 762, 775, 781, 825,
843, 918
Hewlett (R. T.) 383
Heynsius (A.) 744
Hibbert (P.) 703
Hicks (J. A. B.) 843
Higgins (H. L.) 487
Higley (G. 0.) 487
Hildebrandt (F.) 907
Hill (E. W.) 218
Hill (L.) 457, 490, 792
Hindle (C. F.) 755
Hinds (W.) 741
Hinsdale (G.) 627
Hippocrates, 442, 525, 613
Hiramatsu (T.) 483
Hirsch (A.) 5
Hirschfelder (A. D.) 487, 607, 697, 698,
699, 718, 750, 779, 781, 788, 789, 813,
821, 836, 837, 843, 854, 858, 865, 892
Hirst (B. C.) 189
His (W.) 867
His (W., Jr.) 857
Hiss (P. H.) 119, 137, 253
Hobson (F. G.) 487, 489
•Hochhaus (H.) 494
Hogyes (A.) 388
von Hosslin (H.) 547, 857
Hofbauer (L.) 482, 487, 491, 493, 583,
592, 596, 638, 666, 680, 699, 865
Hoffman (C. G.) 633
Hoffman (F. A.) 65, 696, 691
Hoffmann (A.) 784, 785, 786, 789, 814,
825, 837
Hoffmann (E.) 377
Hoffmann (W. H.) 341
Hoke (£.) 263
Holden (S. J. C.) 625
Holitscher (A.) 627
Hollman (C.) 633
Holmes (B.) 564
Holmes (C. R.) 555
Holmes (0. W.) 189
Holsclaw (F. M.) 379
Hoist (P. F.) 884
Holt (L. E.) 166, 379, 540, 603, 605
Holzknecht (G.) 30, 65, 630, 688, 691, 711
Hommel (W.) 595
Honan (J. H.) 865
Honeij (J. A.) 293, 296
Hooker (D. R.) 792, 804, 811, 813, 816
Hoover (C. F.) 378, 482, 483, 487, 603,
638, 680, 699, 727, 798, 825
Hope (C. W. M.) 579
Hopkins (J. G.) 377
Horder (T. J.) 876
Horn (H.) 555
Homer (A.) 791
Homer (A. A.) 222, 224
Horsley (J. S.) 918
Horsley (Sir V.) 583
Horton-Smith-Hartley (P.) 597
Hoskins (R. G.) 805
Hotz (A.) 898
Hough (W. H.) 87, 164, 918
Howard (C. P.) 201, 595, 691, 694
Howard (C. W.) 396, 403, 423
Howard (W. T.) 564
Howard (W. T., Jr.) 434
Howell (A. A.) 603, 802, 813
Howell (Katherine) 551
Howell (W. H.) 798, 824, 855
Huber (F.) 634
Huber (G.) 218
Huchard (H.) 668, 698, 721, 742, 878
Hudelo (L.) 221
Hiibener (E.) 249
Htickel (A.) 424. 440
Huerthle (K.) 700
936
INDEX TO KEFEKENCES
Huismans (L.) 716
Hume (W. E.) 260, 857
Hun (H.) 780
Hunt (G. H.) 837
Hunt (J. M.) 476
Hunter (W.) 391
Hunton (F. M.) 210
Huntress (L., Jr.) 500
Hutchinson (J.) 376, 378
Hutchinson (R. H.) 247, 340
Hutchinson (R.) 3, 837
Hutinel, 555
Iglauer (S.) 471
Immerman ( H. ) 434
Ingals (E. F.) 476, 477, 558, 585
Ingersoll (J. M.) 564
Irons (E. E.) 170,203, 213, 214, 249, 263,
319, 442
Israel (J.) 327
Israel (W.) 923
Israeli (C.) 434
Issaeff, 299
Jackson (C.) 477, 559
Jackson (L.) 191
Jacob (L.) 251
Jacobsohn (O.) 595
Jacoby (J.) 156
Jacquet, 17
Jacquet (L.) 345
Jadassohn (J.) 296
Jaeggy (E.) 305
ron Jagic (N.) 698
von Jaksch (R.) 4
James, 788
James (A.) 666
James (T. L.) 680
James (W. B.) 789, 825, 843
James (W. M.) 364
Janeway (E. G.) 2, 672
Janeway (H. H.) 809
Janeway (T. C.) 791, 793, 798, 799, 805,
806, 808, 865
Janowski (W.) 762, 814
Janus (F.) 39, 59, 64
Janvrin (E. R. P.) 762
Japhe (F.) 666
Jaquet (A.) 750, 760, 775
Jardry (H.) 669
Jarisch (A.) 843
Javal (A.) 80
Jeanselme (E.) 330, 331
Jeger (E.) 923
Jehle (L.) 253, 588
Jehn (W.) 644, 691
Jellinek (S.) 451
Jemma (R.) 344, 345
Joachim (G.) 722
Jobling (E.) 383
Jobling (J.) 127, 201, 210, 627
Jobs (A.) 122
Jochmann (G.) 96, 149, 185, 188, 196,
197, 201, 204, 210, 221, 251, 434, 680
John (R. L.) 218
Johns (F. M.) 364
Johnson, 726
Johnson (W.) 485
Jolly (W. A.) 789
Jones (E.) 81, 94
Jones (Edith P.) 528
Jones (F. A.) 378, 674, 791
Jones (F. W.) 482
Jones (J. H. M.) 548
Jones (T.) 742
Jones (W. S.) 585
de Jong (S. I.) 531, 535, 602
Joppich (0.) 592
Jordan (A. C.) 630
Jordan (E. O.) 137, 249, 300
Jordan (M.) 198
Jores (J.) 907
Jores (L.) 645
Jores (R.) 843
Josue (0.) 700, 907
Jousset (A.) 666
Judd (C. C. W.) 149, 166
von Jiirgensen (T.) 434, 698
Jump (H. D.) 792
Jupille (F.) 629
Kampfer, 328
Kilstle (C.) 65
Kahler (0.) 638
Kalin (F.) 66
Kahn (II.) 560
Kahn (M.) 476
Kahn (R. H.) 789, 847
von Kahlden (C.) 605
Kaiser (F.) 627
Kaiser (M.) 247
Kaliski (D. J.) 177
Kammerer ( II. ) 434
von Kanffl-Lenz (E.) 117
Kapff (W.) 780
Kaplan (D. M.) 87
Karewski (F.) 634
Karsner (H. T.) 643
Kartulis (S.) 332, 334
Kassel (K.) 548, 560
Kassowitz (K.) 261
Kast (A.) 578, 613, 647, 652, 666, 681
Kastle (J. H.) 127
Kato (F.) 634
Katz (L.) 559, 574
Katzenstein (M.) 817
Kaufmann (L) 291, 745
Kawamura (K.) 595
Kaye (G. W. C.) 64
Kayser (C.) 592
Kedrowsky, 292
Keen (W. W.) 482
Keilty (R. A.) 288
INDEX TO REFERENCES
937
Keiper (G. F.) 592
Keith (A.) 667, 781, 822, 827, 857
Keitschewsky, 292
Kelber (C.) 177
Keller, 598
Kellogg (J. H.) 494
Kelly (H. A.) 5, 452, 689
Kemp (C. G.) 19G
Kennedy (A. M.) 857, 858
Kent (A. F.) 822
Kent (A. F. S.) 889
Ker (C. B.) 411
Ker (C. H.) 96
Kerley (C. G.) 587
Kernig (W.) 210
Kessel (L.) 823
Kesson (J. E.) 752, 792, 805
Keyes (E. L., Jr.) 376
Keysser (F.) 96
Kidd (P.) 6-25, 680
Kilborne (F. L.) 345
Killian (G.) 470, 476, 477, 560, 564, 578,
595, 652
King (A. F. A.) 363
King (H. M.) 625
King (W. W.) 441
Kinghorn (A.) 338, 340, 341
Kinghorn (H. M.) 289, 630
Kinyoun (J. J.) 201, 260, 298
Kirchheim, 86
Kirstein (A.) 473, 476
Kisch (E. H.) 900, 904
Kitasato (S.) 112, 216, 218
Ivjeldahl (J.) 81
Klebs (A. C.) 434
Klebs (E.) 259, 288
Klein (B. G.) 203
Klein (H.) 120
Kleine (F. K.) 340
Kleinschmidt (0., 91&
Klemensiewicz (R.) 645
Kline (B. S.) 606
Kling (C.) 401, 402
Klopstock (F.) 200
Klotz (O.) 196, 216, 647, 907, 921
Klotz (W. C.) 630
Knapp (P. C.) 451
Knapp (R. E.) 368
Knauer (A.) 494
Knight (C. H.) 556, 557
Knopfelmacher (W.) 411
Knopf (S. A.) 288, 625
Knorr (A.) 112, 218
Knox (D. N., Jr.) 602
Knox (R.) 64
Kobelew (E.) 404
Kober (G. M.) 625
Kocemba (J.) 898
Koch (J.) 203
Koch (R.) 137, 172, 185, 214, 242, 289,
299, 368, 614
Koch (W.) 843
Kocher, 882
Kocher (R. A.) 136
Kohler (A.) 630, 670, 716
Koehler (0.) 331
Konig, 882
Koeniger (H.) 89, 91
Korner (O.) 549
Koessler (K. K.) 130, 554, 592
Kohlisch (H.) 403
Kohn (H.) 904
Kolle (W.) 3, 98, 109, 137, 166, 299, 340
Kolmer ( J. A.) 96, 150, 224, 260, 341, 411,
436
Koplik (H.) 210, 404, 412, 416, 418, 603,
670
von Koranyi, 385
von Korfmyi (A.) 668, 669, 867
von Koranyi (F.) 214
Korotkow, 803
Korsakoff (N. S.) 191
Kossel (H.) 260, 288, 289
Kovacs (J.) 630
Kudicke, 337
Krannhals (H.) 261
Kraus, 137, 395, 547
Kraus (E.) 288, 573
Kraus (F.) 630, 645, 784, 789, 790, 792,
901, 911
Kraus (H.) 378
Kraus (R.) 105, 120, 127, 130, 253
Krause (A. K.) 175
Krause (P.) 3, 64, 65, 137, 224, 259, 288,
299, 547
Krause (R.) 389
Krehbiel (O. F.) 713
Krehl (L.) 698, 7CO, 900
Kretschmer (M.) 410
Kretz (R.) 643
Kreuzfuchs (S.) 691, 911
Kriege (II.) 727
von Kries (J.) 752
Krogh (Marie) 488
Kronig ( G. ) 505, 508
Kronig, 453
Krumbein (F.) 112
Krumbhaar (E. B.) 175, 858
Krumwiede (C., Jr.) 299
Kruse (W.) 96, 332
Kiilbs (F.) 611, 699, 713, 792, 813, 814,
822, 824, 825, 8C5, 889, 911
Kumrnel, 666
Kuemmel (H.) 918
Kiipferle (L.) 630
Kuhn (E.) 630
Kundrath, 309
Kure (K.) 483
Kussmaul (A.) 2, 434, 694, 884
Kuster (E.) 549
Kuthy (D. O.) 631
Kutscher (K. H.) 210, 243
Kuttner (A.) 549
Kyes (P.) 114, 117, 167
Kyle (D. B.) 548, 549, 560, 578
Kyle (J. J.) 555
Laache (S.) 670
Labbe (M.) 923
938
INDEX TO REFERENCES
Lade (F.) 88
Ladernan (O. E.) 867
Laederich (L.) 319
Laennec (R.-T.-H.) 2, 495, 513, 525
Lafleur (H. A.) 332, 334
Lagriffoul, 261
Lahy (J. M.) 751
Laird (A. T.) 289
Lake (R.) 578
Lakin (C. E.) 652
Lamac, 574
Lamacq, 726
Lamar (R. V.) 606
Lamb (A. R.) 166 875, 921
Lambart (H. C.) 5
Lambert (A.) 46, 448, 603, 605
Lambert (H. C.) 331
Lambert (R. A.) 434
Lambert (S. W.) 189
La Motte (Ellen M.) 625
Lampe (A. E.) 631
Landis (H. R. M.) 291, 611, 628, 631, 633,
674, 745
Landsteiner (K.) 110, 117, 122, 393, 394,
395, 402
Lange (C.) 379
Lange (L. B.) 406
Langenbeck (C. J. M.) 327
Langeron (M.) 362
Langmead (F.) 745
Lapham (Mary E.) 291, 626, 631, 680
Lapinski (J.) 603
Large (S. H.) 596
Larned (C. W.) 718, 737
Laroche (G.) 260
Larrabee (R. C.) 609
Laslett (E. E.) 836, 857
Latham (A.) 291
Lau (H.) 631
Laurens (G.) 575
Lautmann ( S. ) £55
Lavenson (R. S.) 858
Laveran (A.) 337, 340, 346, 362, 364
Lavinder (C. H.) 364
Lawrence (C. H.) 808
Lawson (M. R.) 364
Lazarus-Barlow (W. S.) 66, 769
Lazear (J. W.) 204, 389
Leared, 540
Leathes (J. B.) 667
Lebard (R.) 634
Leblanc (A.) 247
Leclerq (A.) 698
Le Count (E. R.) 652
Lectef (J.) 119
Le Dantec (A.) 331
Ledoux, 634
Lee (A. W.) 296
Lee (R. I.) 808
Lee (R. L.) 305, 326, 330
Lee (W. E.) 805
Leftwich (R. W.) 6
Legout (P.- A.) 911
Legendre (J.) 363
Lehmann, 670, 883, 884
Leimdorfer (A.) 486, 488
Leiner (K.) 393, 397, 402
Leishman (Sir W. B.) 345
Lelievre (H.) 290
Lemann (I. I.) 592, 611, 652, 918
Lemcke, 135
Lemierre (A.) 251
Lemoine (G.) 721
Le Monnier (Jean) 681
Lenhartz (H.) 4, 434, 535, 865
Lentz, 387
Lentz (0.) 253
Leon-Kindberg (M.) 290
Leopold (J. S.) 416
Leopold (S.) 404
Lepere (E.) 261
Le Prince (J. A.) 363
Lermoyer (N.) 593
Leschly (W.) 378
Lesieur (C.) 531
Leslie (R. M.) 631
L'Esperance (Elsie S.) 166
Lesser (E.) 17, 164
Letulle (M.) 628
Levaditi (C.) 106, 137, 393, 394, 395, 401,
402
Levi (E.) 672
Levine (S. A.) 845
Levy (L.) 607, 670
Levy (R.) 578
Levy (R. L.) 94
Levy-Dorn (M.) 547
Lewandowsky (F.) 288
von Lewin (A.) 227
Lewis (C. J.) 564
Lewis (D. D.) 666, 681
Lewis (M. J.) 305
Lewis (P. A.) 123, 126, 127, 289, 393,
394, 397, 398, 400, 628, 633
Lewis (T.) 488, 697, 699, 700, 722, 763,
775, 782, 788, 824, 825, 837, 839, 842,
843, 845, 856, 858, 865, 892
von Leyden (E.) 536, 859
Lexer (E.) 198
Lian (C.) 583, 781
Libman (E.) 149, 189, 416, 876
Lichty (M. J.) 808
Liebermeister (G.) 251
Liebmann (E.) 878
Liebmeister (C.) 434
Liefmann (H.) 117
Lilienthal (H.) 595, 611, 671, 691
Limbeck (R. R.) 926
Lind (S. C.) 260
Lindbom (0.) 918
Lindemann (L.) 500
Lindhard (J.) 487, 817
Lindsay (J.) 597
Lindstedt (F.) 691
von Lingelsheim (H. A. W.) 184, 218
Lipliawsky (S.) 66
Lippo-Cramer, 65
Lipschutz (P.) 383
Lipskerow (M.) 259
Litten (M.) 483
Liverato (S.) 88
Ljundahl (M.) 908
INDEX TO REFERENCES
939
Llopart (P.) 587
Lloyd (J. J.) 626
Lloyd (L.) 340, 341
Locke (E. A.) 411, 626, 631
Loeb (J.) 824
Loeb (L.) 878
Loffler (F.) 259, 405, 540
Loeper (M.) 763
Loesch, 332
Loeser (A.) 898
Loevenhart (A. S.) 824
Lowenbein (L.) 531
Lowenstein (E.) 289, 290
Loewenthal (W.) 368
Loewy (A.) 488
Lombard (W. P.) 718, 781
Lommel (F.) 77, 463
Longcope (W. T.) 117, 899, 908, 911
Lord (F. T.) 221, 540, 597, 611, 661, 666,
668, 680
Loughnan (W. F. M.) 405
Louria (L.) 305
Lovett (R. W.) 395, 399, 403
Low (G. C.) 340, 343
Lowden (M. M.) 386, 388
Lubarsch (O.) 643, 652
Lucas (W. P.) 123, 403, 417
Ludlum (S. D. W.) 378
Liidke (H.) 136
Luetscher (J. A.) 138, 222, 538, 540
Luff (A. P.) 681
Lukas (Christine) 403
Lungwitz (P.) 66
Lutembacher (R.) 727, 892
Luttinger (P.) 224
Lutz, 292
Lutz (B. R.) 803
Lyall (H. W.) 244
Lydston (G. F.) 923
Lyman (D. R.) 626
Lynch (K. M.) 296, 334, 378
Lyon (I. P.) 201, 605, 682
Lyons (R.) 211, 246
M
M'Aldowie (A. M.) 739
Macalister (C. J.) 667
McBride (P.) 548, 577
MacCallum (J. B.) 822
McCallum (W. G.) 136, 263, 362, 364,
740, 867, 891, 892
McCampbell (E. F.) 305
McClintock (A. T.) 908
McClure (R. D.) 892
McCollum (J. H.) 259, 410
MacCombie (J.) 434
McCord (C.) 592
McCoy (G. W.) 226, 227
McCrae (J.) 411, 647, 918
McCrae (T.) 2, 166, 195, 243, 244, 305,
605, 908, 911
McCurdy (J. H.) 805
M'Donagh (J. E. R.) 203, 378
MacDonald (G.) 464, 57.7
MacDonnell (H.) 761
M'Fadyean (J.) 263
Macfadyen (J.) 211
MacFarland (J.) 440, 822
Macfie (J. W. S.) 341
McGill (C.) 847
McGlannan (A.) 918
Macht (D. I.) 804, 805, 806, 903
Mclnnes (B. K.) 378
Mclnnes (G. F.) 378
Mclntosh (J.) 127, 166, 246
Macintyre (J.) 541, 583
McKendrick (A.) 389
Mackenna (R. W.) 379
Mackenzie (H.) 479, 607
Mackenzie (J.) 24, 698, 747, 750, 760,
768, 773, 824, 829, 836
Mackenzie (J. N.) 476, 549, 585
McKernon (J. F.) 574
Mackie (F. P.) 345
McKisack (H. L.) 6, 24
McLeod (J. W.) 184
McLoone (J. J.) 564
McNaught (J.) 343
MacNeal (W. C.) 341
MacNeal (W. G.) 319
MacNeal (W. J.) 336, 341
McNee (J. W.) 184
MacNeil (A.) 167, 168, 169, 170
McNeil (H. L.) 918
McPeek (C.) 805
McPhedran (A.) 244, 586, 652, 672, 883,
911, 918
McPhedran (F.) 605
McQueen (J.JV1.) 246,792
MacWilliam (J. A.) 752, 791, 792, 805
Madsen (T.) 103, 112, 218
Maes (U.) 611
Mager (W.) 643
Magnussen (G.) 167
Mairinger (E.) 424, 434, 436
Major (R. H.) 88, 163, 166, 211, 253,
876
Makins (G. H.) 198
Makuen (G. H.) 476
Malcolm, 534
Mall (F. P.) 822
Mallory (F. B.) 137, 210, 222, 224, 386,
615, 911
Maloney (W. J. M. A.) 494
Manasse (P.) 411
Manceaux, 344
Manges (M.) 611, 672, 885, 890
Mann (M.) 477
Mann (T. A.) 191
Mannaberg (J.) 362
Maiming (E. T.) 554
Manning (W. J.) 528
Manoukhine (J.) 627
Manson (Sir P.) 5, 343, 392, 641
Mantoux (Dora) 691
Manwaring (W. H.) 117, 127
Maragliano (V.) 631
Marchand (F.) 448, 700, 813
Marchand (L.) 119
Marchiafava (E.) 364
940
IJSTDEX TO EEFEKENCES
Marchoux (E.) 296, 389
Marcinowski (J.) 592
Marcorelles (E.) 583
Maresch (R.) 388
Marey (E. J.) 700, 747, 701
Marfan (A.-B.) 77, 691
Margot (A. G.) 289
Marie (A.) 112, 218
Markovici (E.) 486, 488
Marks (H. K.) 156
Marks (W. L.) 804
Markwalader (J.) 903
Marland (L.) 560
Marlowe, 332
Marple (W. P.) 908
Marshal] (H. T.) 117, 118, 343
Martin (C. J.) 227
Martin (E. B.) 404
Martin (E. G.) 824
Martin (H. H.) 191, 557, 579
Martin (S.) 288, 585
Martius (F.) 483, 739, 761
Marx, 299, 385
Massini (M.) 410
Matas (R.) 918
Mathias (H. H.) 845
Matthes (M.) 479
Matthews (J.) 592
Matthews (S. A.) 645, 903
Matthewson (G. D.) 822
Mautner (H.) 541
Max (O.) 66
Maxey (E. E.) 441
von Maximowitsch (J.) 7C2
May (R.) 500
Mayer (G. S.) 288 •
Mayer (M.) 331, 341, 345
Mayo (C. H.) 671
Mays (T. J.) 603, 626
Meakins (J. C.) 156, 184, 205, 788, 824,
856
Means \J. H.) 487
Meara (F. S.) 602, 750, 755
Medigreceanu (F.) 605
Medin (0.) 392, 402
Meek (W. J.) 789, 816, 823, 825
Meek (W. O.) 289
Meier (G.) 166
Meiklejohn (J.) 822
Meillon (A.) 583
Melcher (R.) 292
Meltzer (S. J.) 218, 261, 485, 576, 587,
592, 597, 606, 607, 609, 682, 804
Melvin (G. S.) 752, 791, 792, 803
Mendel (K.) 482
Mendl (J.) 218
Mense (C.) 5, 331
Merck, 147
von Mering (J. Frhr.) 2
Mesnil (F.) 337, 340
Messerschmidt (T.) 247
Metchnikoff (E.) 106, 108, 245, 377, 423
Meunier (L.) 5
Meyer (E.) 549, 575
Meyer (F.) 790
Meyer (H.) 218
Meyer (W.) 595
Meyer-Lierhei'm, 789
Michaelis (G.) 119
Michaelis (L.) 110, 120, 122, 127, 667 •
Middleton (W. S.) 791
Millard (C. K.) 440
Miller (F. E.) 577
Miller (Florence W.) 378
Miller (J. A.) 604, 626
Miller (J,L.) 80, 645, 903
Miller (J. R.) 804
Miller (R.) 898
Miller (S. R.) 84, 94, 163
Mills (C. K.) 404
Milroy (T. H.) 485, 488
Minchin (E. A.) 331, 549
Minerbi (C.) 680
Mines (G. R.) 789, 824
Minet (J.) 78
Minkowski (0.) 488, 542, 762
Minor (C. L.) 558, 578, 626
Minot (G. R.) 603
Mi not (J. J.) 244
Mircoli (S.) 631
Mita (S.) 127
Mitchell (R. H.) 318
Mitchell (W. J., Jr.) 629
Mitzmain (M. B.) 363
Miura (M.) 540, 648
Moczutkowski (0. O.) 301, 305
Modrakowski (G.) 645
Mailers (B.) 293
Monckeberg (T. G.) 867
Moftitt (H. C.) 136
Mohler (J. R.) 263
Mohr (L.) 2, 448, 451, 454
Monod (Mme. Robert) 891
Monro (T. K.) 2, 602
Montgomery (C. M.) 526, 628, 668
Montgomery (D. W.) 296
Montgomery (F. H.) 319
Moody (A. M.) 84, 94
Moody (E. E.) 260
Moon (V. H.) 246
Moore (A. B.) 631
Moore (A. E.) 221
Moore (C. H.) 918
Moore (Sir J.) 305, 671
Moore (J. J.) 441
Moore (J. W.) 94
Moore (X.) 739, 870
Moore (V. A.) 137
Moorhouse (V. H. K.) 824
Mora (R.) 602
Morawitz (P.) 751
Morax (V.) 218
Moreschi (C.) 156
Morgan (A. C.) 671
Morgan (E.) 260
Morgenroth (J.) 88, 112, 117, 118, 122
Morison (A.) 718, 823
Moritz (F.) 597, 643, 708, 716, 805, 808,
817, 825, 865, 870, 889, 904
Morland (E. C.) 175
Moro (E.) 127, 174
Morris. (Sir M.) 3H
INDEX TO REFERENCES
941
Morris (R. E.) 789
Morris (R. S.) 79, 80
Morrow (A. S.) 3
Morrow (H.) 296
Morse (J. L.) 668
Morton (E. R.) 64, 631
Morton (R.) 631
Mosenthal (H. O.) 224
Mosny (E.) 91, 288, 331, 586, 596
Moshage (Emily) 260
Moss (W. L.) 115, 127, 260, 289, 628, 680
Mott (F. W.) 339
Mouisset (F.) 509
Mouriquand (G.) 604
Much (H.) 150, 289, 292, 293
Miihlens (P.) 368, 377, 382
Miihsam (R.) 595
Miiller (A.) 857
Miiller (E.) 395, 396, 397, 399, 400, 401,
402
Miiller (Franz) 799, 817
von Miiller (Friedrich) 26, 494, 500, 501,
530, 531, 727, 825
Miiller (H.) 898, 908
Miiller (0.) 751, 792, 816
Miiller (P. T.) 88, 96, 108, 122
Miiller (R.) 167, 170, 177
Muir (J.) 64
Muir (R.) 106, 118, 137
Muirhead (W.) 85
Mumford (J. G.) 5, 595
Munford (S. A.) 836
Munk (F.) 64
Munson (E. L.)' 299
Murchison (C.) 918
Murphy (F. T.) 611
Murphy (J. B.) 406, 482, 671, 918, 923
Murphy (J. K.) 376
Murphy (T. J.) 626
Murray (J. R.) 803
Murray (R. M.) 718
Murray (W.) 918
Musgrave (W. E.) 253, 263, 328, 329, 334
Muskens (L. J.) 847
Musser (J. H.) 3, 330
Musser (J. H., Jr.) 175, 79.2
Myerson (A.) 94
N
Nabarro (D.) 341
Naegeli (T.) 164, 667
Naish (A. E.) 857
Naito (H.) 483
Nammack (C. E.) 603
Napier (A.) 681
Naunyn (B.) 77, 739
Navarro '(D.) 211
Negri (A.) 388, 428, 440
Neilson (C. H.) 865
Neisser (A.) 203, 377
Neisser (E.) 77
Neisser (M.) 108, 155, 167, 198, 259, 292
Netter, 671
Netter (A.) 211, 221, 223, 224, 331, 401,
404
Neuburger (M.) 5
Neufeld (F.) 119, 156, 184, 200, 201, 607
Neuhof (S.) 898, 911
Neuman (L.) 244
Neuman (R. O.) 331
Neumann (J.) 558
Neumann (R.) 556
Neurath (R.) 444
von Neusser (E.) 763, 806 904
Neustaedter (M.) 395
New (C. F.) 542
Newburgh (I.) 604
Newburgh (L. H.) 603, 604, 606
Newcomet (W. S.) 66
Newell (L. B.) 305
Newham (H. B.) 340
Newman (D.) 542
Newsholme (A.) 292
Newton (R. C.) 708
Nichol (K.) 628
Nicholas (J.) 667
Nicholls (A. G.) 6, 645
Nichols, 164
Nichols (E. H.) 198
Nichols (H. J.) 87, 377, 647
Nicholson (P.) 791, 792
Nicholson (S. T., Jr.) 166
Nicolai (G. F.) 697, 699, 784, 785, 788,
789, 790
Nicolaier (A.) 216, 218
Nicoll (M.) 260, 411
Nicolle (C.) 301, 305, 344, 368, 385, 442,
444
Nieriker (A.) 675
Niles (W. L.) 540, 631
Nissl, 94
Nitsch (G.) 682, 683
Noble (E.) 88, 253
Noblecourt (P.) 251
Nocard (E.) 325
Noguchi (H.) 81, 88, 94, 117, 118, 149,
157, 162, 163, 164, 166, 177, 178, 219,
369, 377, 379, 383, 384, 388, 392, 393,
402
Nokanishi (K.) 648
Nolf (P.) 118
Nonne (M.) 81, 909
von Noorden ( C. ) 900, 908
Norris (C.) 120
Norris (G. W.) 219, 510, 583, 602, 604,
611, 626, 720, 751, 791, 798, 799, 813,
858, 875, 892
Northrup (W. P.) 211, 576, 604
Nothnagel (H.) 2
Notter (J. L.) 213
Novak (E.) 644
Nove-Jusserand (G.) 885
Novy (F. G.) 103, 226, 227, 336, 341, :'.»:?,
344, 345, 368, 3SU
Nuttall (G. H. F.) 108, 171, 216, 259, 331
Obermeier (O.) 365
O'Carroll (J.) 724
Ochsner (A. J.) 188, 407
Oddo (C.) 739
942
IKDEX TO KEFEKENCES
Odell (Anna) 541
O'Dwyer (J.) 576
Oechsner (J. F.) 198
Oelecker (F.) 918
d'Oelsnitz, 691
O'Farrell (W. R.) 540
Otfenbacher (R.) 727
Ogawa (S.) 816
Ohm (R.) 775, 780
Oille (J. A.) 875
Olitsky (P. K.) 301, 302, 305
Oliver (Sir T.) 6, 451, 646, 668
Oliver (W. S.) 918
Olmstead (M.) 224
Olney (H. S.) 634
Onderdonk (W. A.) 667
O'Neill (0.) 109, 167, 169
Onodi (A.) 550, 564, 583
Ophttls (W.) 613
Opie (E. L.; 88, 119, 247, 362, 667
Oppenheim (H.) 542
Oppenheim (M.) 167, 170
Oppenheimer (Adole) 788, 824, 858, 919
Oppenheimer (B. S.) 788, 824, 858
Oppenheimer (C.) 110, 112
Oppenheimer (S.) 553, 554, 574
Ormerod (J. A.) 211'
Ortmann (P.) 292
Ortner (X.) 699, 764, 767
Orton (G. H.) 547, 898
Osborne (O. T.) 865
Oshida (T.) 389
Osier (Sir W.) 2, 16, 17, 26, 196, 211, 302,
308, 334, 425, 604, 606, 631, 672, 857,
874, 877, 885, 892, 904, 907, 908, 918
Ostenberg (Z.) 120
Oswald (F.) 341
Otis (E. 0.) 626
Otten (M.) 652, 716, 871
Otto (Isaac) 123, 136
Otto (M.) 391
Otto (R.) 127, 227
Overend (W.) 631
Owen (S. A.) 631
Ower (J. J.) 919
Pachetta, 691
Pachon (V.) 798
Packard (F. A.) 188
Packard (F. R.) 6, 549, 559
Passler (H.) 652, 867, 900
Pagel (J. L.) 6
Pagenstecher (E.) 674
Paine (A.) 191, 196
Painter (H. McM.) 189
Pal (J.) 807
Palmer (G. T.) 626
Paltauf (A.) 309, 384
Paltauf (R.) 122
Pandy, 81, 94
Pape (M.) 260
Pappenheim (A.) 411
Paraut (V.) 81, 94
Pardee (H. E. B.) 843, 858
Parfitt (C. D.) 631
Park (E. A.) 592, 805
Park (R.) 6
Park (W. H.) 122, 137, 219, 260, 550, 628
Parker, 293
Parker (E. C.) 923
Parkinson (J.) 604, 775, 837, 845, 865
Parsons-Smith (B.) 775, 839
Partsch (C.) 564
Paschen (E.) 435
Pasquale, 332
Pasteur (Louis) 96, 106, 199, 214, 215,
389, 395
Pastia, 393, 394, 395
Paton (E. W.) 875
Paton (J.) 668
Patrick (A.) 245
Patterson (H. S.) 334
Patton (W. S.) 331, 342, 343, 345
Paul (G.) 436, 440
Paviot (J.-M.) 3
Pawinski (J.) 721
Payne (J. F.) 5, 227
Peabody (F. W.) 245, 400, 402, 487, 488,
604, 839, 850, 857, 866
Pearce (Louise) 203
Pearce (R. M.) 103, 109, 123, 127, 160,
330, 564, 615, 636, 809, 873, 907
Pearson (K.) 292
Pearson (L.) 634
Peet (M. M.) 94
Pegler (L. H.) 892
Pehu (M.) 626, 885
Pel (P. K.) 534, 908
Pemberton (R.) 605
Perkins (C. F.) 322, 324, 325
Perrin (M.) 613
Peters (E. A.) 211
Peters (L. S.) 680
Petersen (H.) 667
Petersen (W. F.) 127, 627
Petroff (S. A.) 627, 628
Petruschky (J.) 288, 326
Pettenkofer, 297
Petter (J.) 750, 751
Petzetakis (M.) 670
Pezzi (C.) 727, 89-2
Pfahler (G. E.) 66
Pfeiffer (H.) 127, 448
Pfeiffer (L.) 423
Pfeiffer (R.) 154, 219, 299
Pfender (C. A.) 668
Philip (J. H.) SCO
Philpott (J. A.) 627
Pick (E. P.) 110
Pick (F.) 885
Pickmann (Olga) 630
Pigg (T. S.) 884
Pillsbury (W. B.) 718
Pinard (M.) 377
Pincussohn (L.) 597
Piorry (P. A.) 495, 500
Pirajoa da Silva, 342
von Pirquet (C. F.) 123, 129, 130, 175,
291, 415, 416, 417, 424, 437, 439, 440,
619, 628, 631
INDEX TO REFERENCES
943
Pitcliford (W. W.) 647
Pitie (H.) 611
Place (E. H.) 259, 410
Plantenga (H. W. G.) 417
Plaut (F.) 78, 88
Plaut (H. C.) 260; 308, 313, 321
Pleasants (J. H.) 18, 607
Plesch (J.) 488, 500, 505, 531, 708, 807,
817
Pletnew (D.) 857
Plimmer (H. G.) 341
Plotz (H.) 301, 302, 305
Podack (M.) 551
Poel (J.) 908
Pohl (R.) 66
Poncet (A.) 327
Poole (W. H.) 558
Popischill (D.) 410
Poppe (K.) 330
Popper (E.) 393, 402
Porges (O.) 166, 486, 488
Porter (A. E.) 290
Porter (W. G.) 469
Porter (W. T.) 260, 603
Portocalis (A.) 91
Posselt (A.) 244
Potain (C.) 703, 727
Potain (P. C. E.) 791
Pothet (R.) 441
Pottenger (F. M.) 631
Poulton (E. P.) ) 485
Powell (A. M.) 558
Powell (Sir R. D.) 597, 898, 899
Power (D'A.) 376
Powers (C. A.) 319
Poynton (F. J.) 191, 196, 698
Pratt (J. H.) 26, 260, 626, 866
Pratt (J. P.) 596
Pratt (J. S.) 299
Prausnitz ( C. ) 554
Preysing (H.) 574
Pribram (A.) 196
Price (S. B.) 908
Priestley (J.) 291
Priestley (J. G.) 487
Primrose (A.) 671
Prince (A. L.) 816, 903
Prince (M.) 893
Proescher (B. F.) 249, 387
Proescher (F.) 628
von Prowazek (S.) 331, 334, 341, 346,423,
424, 434
Prudden (T. M.) 108, 667
Pulleu (W. J.) 904
Purser, 682
Puschmann (T.) 6
Pusey (W. A.) 17, 379
Putnam (C. R. L.) 920
Putnam (Mary L.) 699
Pye-Smith (P. H.) 602
de Quervain (F.) 6
Quinnn (('.) 118
Quincke (H.) 72, 78, 596, 718, 781
R
Rabinowitsch (M.) 305
Each (E.) 343, 345, 547, 631, 670, 691
Radcliffe (J. A. D.) 628, 631
Rainy (H.) 3
Ranke (K. E.) 631
Ransom (F.) 218, 487
Ransome (A.) 494, 626
Raubitschek (H.) 253
Rauchfuss (C.) 669
Rautenberg (E.) 762
Ravaut (P.) 81, 669
Ravenel (M. P.) 388, 634
Rayer (P.) 263
Reagh (A. L.) 122
Reale (E.) 4
Rebaudi (S.) 911
von Recklinghausen (H.) 798, 811, 812
Reed (Margaret A.) 604
Reed (W.) 389, 391
Rehm (0.) 78
Reik (A. J. N.) 549
Reik (H. 0.) 464, 549, 572
Reinhold, 135
Reiter (H.) 137
Remlinger (P.) 329, 385
Renault (C.) 694
Rendu (R.) 557
Renon (L.) 309, 668, 823, 858
Retzer (R.) 823
Retzlaff (K.) 805
Reuter (W.) 919
Rey (C.) 167, 812
Reyher (P.) 224
Rhea (L. J.) 221
Ribbert (H.) 606, 878
Ribierre (P.) 243
Rice (C. C.) 557, 575
Richards (E. T. F.) 629, 789
Richards (J. H.) 164
Richards (J. K.) 788
Richards (T. W.) 377
Richardson (C. W.) 555
Richardson (G.) 411
Richardson (M. W.) 245
Richet (C.) 122, 123, 127
Richter (G.) 775
Ricketts (H. T.) 300, 301, 306, 319, 441,
442
Ridge (P. B.) 531
Ridpath (R. F.) 477
Riecke (E.) 17
Rieder (H.) 64, 65, 68, 691, 885
Riegel (P.) 694
Riesman (D.) 78, 119, 244, 537, 609, 645,
680, 741, 808, 857, 885, 900
Riess (L.) 885
Rietschel (II.) 379
Ri?gs (C. E.) 417
Rihl (J.) 776, 780, 781, 836
Rimpau (W.) 184
Ringer (S.) 745
Rios&re, 330
Rissler (J.) 400
Rist (E.) 290, 671, 691
944
INDEX TO REFERENCES
Ritchie (J.) 96, 137
Ritchie (W. T.) 845, 892
Ritter (J.) 631
Ritz (H.) 150
Riva-Rocci (S.) 798
Rivas (D.) 296
Riviere (C.) 175, 626
Roberts (F. T.) 683, 883
Roberts (S. R.) 808
Robertson (C. M.) 579
Robertson (H. E.) 219, 403
Robertson (J. I.) 898
Robertson (W. E.) 605
Robertson-Ross (J. E.) 640
Robinson (G. C.) 126, 211, 727, 761, 789,
824, 839, 843, 857, 889
Robinson (G. H.) 245
Robinson (L. E.) 331
Robinson (S.) 595, 671
Rochester (De L.) 904
Rockman (J.) 629
Roddy (J. A.) 249
Roe (J. O.) 476, 541, 586
Rohl (W.) 708
Romer (P. H.) 393, 394, 395, 398, 399,
400, 401, 402
Rontgen (W. C.) 41, 66
Roepke (0.) 287, 626
RSssle (R.) 103
Rover, 488
Roger (H.) 763, 898
Rogers (C. P.) 244
Rogers (L.) 5, 299, 333, 334, 345
Rogers (L. A.) 251
Rogers (M. H.) 247
Roget, 261
Roget (G. H.) 698
Rohdenburg (G. L.) 604
Roily (F.) 407, 867
Rolleston (H. D.) 911, 919
Rolleston (J. D.) 2, 200, 640, 652
Romberg (E.) 698, 867
Roque (G^) 607
Roques (E.) 919
Roseman, 395
Rosenau (M. J.) 6, 112, 123, 211, 403
Rosenbach (F. G.) 188
Rosenbach (F. J.) 219
Rosenbach (O.) 596
Rosenbusch (J.) 909
Rosenow (E. C.) 97, 119, 191, 192, 200,
201, 604, 607
Rosenthal, 688
Rosenthal (J.) 64, 753
Rosenthal (P. J.) 65
Ross (A.) 221
Ross (E. H.) 411
Ross (G. W.) 81, 94
Ross (J. N. M. B.) 691
Ross (R.) 339, 343, 363
Rosthorn (A.) 289
Rostoski (0.) 96, 290
Roth (Q.) 780, 845
Roth (P.) 488
Roth (W.) 557
Rothberger (C. J.) 697, 726, 789, 824,
836, 844, 858, 859
Rothermundt (M.) 389
Rothschild (M. A.) 196, 788, 878
Rous (F. P.) 86, 94
Roussy (G.) 404
Roux (E.) 219, 259, 377
Rowland (S.) 227
Rowlands (R. A.) 865
Rowlette (R. J.) 541
Rowley-Lawson (Mary) 304
Roy (D.) 580, 776
Rubenstone (A. I.) 667
Rubino (G.) 668, 791
Rubner (M.) 96, 445
Rubow (V.) 490
Rucker (W. C.) 227
Rudolf (R. D.) 244, 894
Ruediger (E. H.) 219, 246, 251, 389, 440
Ruediger (G. F.) 117, 118
Ruge (R.) 331, 339, 364
Ruhrah (J.) 196, 224, 417
Rumpel (T.) 578, 613, 647, 652, 666, 681
Rumpf (T.) 299
Runeberg (J. W.) 79, 80
Rusk (G. Y.) 118, 319
Russell (F. F.) 246
Russell (W.) 739, 742
Russell (W. W.) 364 .
Rutherford (E.) 66
Ryerson (E. W.) 319
Ryffel (J. H.) 485, 865
Rytina (A. G.) 178
Sabin (B.) 379
Sabouraud, 17
Sabourin (C.) 672, 680
Sabrazes (J.) 329
Sachs (H.) 110, 117, 118, 150, 167
Sachs (T. B.) 626, 632
Sachs-Miike, 211, 541
Sahli (H.) 3, 193, 508, 644, 608, 699, 725,
726, 727, 739, 776, 807, 809, 811, 817,
818
Sainsbury (H.) 745
Sakai (S.) 857
Salge (B.) 291
Salimbeni, 389
Sallard (A.) 2
Salmon (D. E.) 106
Salomonsen, 614
Salvetti (G.) 885
Salvin-Moore (J. E.) 336
Sambon (L. W.) 442
Samuely (F.) 103
Sam ways (D. W.) 780
Sand (A.) 293
Sanders (G.) 742
Sandwith (F. M.) 405
Sanfelice, 318
Satterthwaite (T. E.) 633, 701, 900
Sauer (L. W.) 671
Sauerbruch (F.) 597, 691
INDEX TO REFERENCES
945
Savill (T. D.) 698
Savy (P.) 672
Sawyer (Sir J.) 482
Sawyer (W. A.) 246, 247
Scales (F. M.) 247
Schade, 176
Schafer (Sir E.) 587
Schamberg (J. F.) 407, 436
Schapals (F.) 448
Schaudinn (F.) 332, 335, 377
Scheller (R.) 221, 222
Schenck (B. R.) 322, 324, 325
Schenck (F.) 484, 490
Schepelmann (E.) 459
Schereschewsky (J.) 377
Scheube (B.) 5, 331
Schick (B.) 107, 123, 260, 261, 408, 411,
418
Schiff (A.) 550
Schilling (C.) 341, 346, 362, 368
Schittenhelm (A.) 3, 4, 39, 59, 130, 137,
716
Schlegel (M.) 327
Schleicher (M.) 377
Schlesinger (E.) 592
Schlesinger (H.) 633, 668, 908
Schlesinger (M. J.) 629
Schley (O.) 418
Schlomovitz (B. H.) 825
Schlossmann (A.) 291
Schmall (B.) 727, 883
Schmidt (A.) 536, 668
Schmidt (M.) 549
Schmidt (R.) 652, 655
Schmoll (E.) 839, 857
Schmorl (G.) 615
Schneider (E.) 378
Schneider (E. C.) 805
Schochet (S. S.) 213
Schobl (0.) 299
Scholtze (O.) 132
Scholz (W.) 441
Schonemann '(A.) 555
Schoonmaker (H.) 844
Schoonmaker (P.) 477
Schorer (E. H.) 109
Schott (T.) 804, 867
SchottmUller (H.) 78, 184, 189, 243, 248,
249, 329, 609, 634
Schreiber (J.) 744
Schroder, 86
von Schrotter (H.) 456, 457, 613, 643
Schrotter (L.) 476, 579, 585, 632, 698
Schubert, 263
Schiiller (A.) 65
Schurmann (W.) 299, 340
Schiitze (A.) 156
Schultz, 263
Schultz (W.) 744
Schultz (W. H.) 628
Schulz (F. N.) 94
Schum (H.) 923
Schumacher (E. D.) 597, 644
Schut (H.) 547, 632
Schwab (S. I.) 560
Schwartz (G.) 825
Schwartz (H. T.) 167, 168, 169, 170
Schwarz, 43
Schwyzer (A.) 596
Scott, 488
Sears (G. G.) 667, 668, 672
Seifert (0.) 3, 476
Seligmann (R.) 290
Sellards (A. W.) 299, 332, 334, 335, 346,
381
Selling (T.) 500
Semmelweis (L P.) 189
Semon (Sir F.) 476, 575, 578, 583, 585
Senac-Lagrange, 556
Sergent (E.) 368, 632, 672
Seroia (H. M.) 260
Sewall (H.) 500, 526, 700
Sexton (L. A.) 411
Shaffer (P. A.) 245
Sharp (E. A.) 404
Shattuck (F. C.) 741
Shaw (H. B.) 526
Shaw (L. E.) 613, 672
Sheldon (W. D,) 630
Shennan (T.) 291, 919
Sheppard (P. A. E.) 395, 399, 402
Sherrington (C. S.) 485, 700, 739
Shiga (K.) 253-
Shircore (J. O.) 339, 341
Shurly (E. L.) 556, 577
Sicard (A,) 81
Siciliano (L.) 680
Siebeck (R.) 488
Siegel (J.) 404, 405
Siegert (F.) 417
Sieur (C.) 500
Silberberg (M. D.) 839
Sill (E. M,) 224
Simmona (D. G.) 671
Simon (C. E.) 3, 4, 90. 119, 149, 150, 156,
162, 171
Simon (G.) 385, 388
Simon (H.) 440
Simpson (C. A,) 177
Simpson (G, C,) 363
Sinkler (F, W.) 671
SJppy (B. W.) 84, 94
Sisco (D, L.) 805
Sison (A. G.) 263
Sjb'blom (J. C.) 488
Skillern (R. H.) 564
Skinner (E. H.) 547, 631
Skoda (J.) 496, 500
Skwirnsky (P.) 156
Sladen (F. J.) 210, 211
Slemons (J. M.) 189
Sluka (E.) 345, 632
Sly field (F.) 632
Smith (A. J.) 296
Smith (C. H.) 368
Smith (E.) 224, 444.
Smith (E. F.) 322
Smith (G. E.) 66ft
Smith (G. G.) 20a
Smith (H.) 685
Smith (H. L.) 499, 500, 505, 708, 7'M
Smith (J. C.) 742
946
INDEX TO REFERENCES
Smith (J. G.) 776
Smith (J. L.) 243
Smith (L.) 196
Smith (T.) 106, 109, 122, 123, 289, 345,
541, 607, 628
Smith (W. H.) 541 •
von Smolensk! (S.) 513
Snyder (C. D.) 763, 791
Sobernheim (G.) 268, 368, 377
Sobernheim (W.) 583
Sobotka, 437
Socin (C.) 867
Sonnenburg (E.) 448
Sophian (A.) 149, 209, 211
;Soulier (H.) 739
;Southard (E. E.) 123, 127, 373
iSpalteholz (W.) 903
;Speder (E.) 291, 691
;Spengler (L.) 679
Spriggs (E. I.) 391, 502
;Sprunt (T. P.) 163, 681
iSquire (J. E.) 510
:Stadtler (E.) 889, 912
'Stanley (D.) 691
:Staehelin (R.) 2, 80, 81, 457. 586, 592,
597, 616, 643, 659, 688, 699
Stanton (E. M.) 907
Stapler, 670
Stark (H. H.) 564
Starkenstein (E.) 847
Starling (E. H.) 487, 667, 813, 903
Starr (M. A.) 402
Steele (A. E.) 326
Steell (G.) 479, 604, 647, 698, 741, 866,
892, 904
Steffenhagen (K.) 170
Stein (R.) 404
Stein (R. O.) 177, 254
Steiner (R.) 578
Steiner (W. R.) 606, 866
Steinhardt (E.) 434
Steinhardt (J. D.) 410
Steinhaus (J.) 66
Steinitz (E.) 290
Stelwagon (H. W.) 17
Stengel (A.) 633, 739, 858, 889
Stephen (L.) 6
Stephens (J. W. W.) 337, 339, 340, 341,
364
Stephens (O. Z.) 805
Stern (H.) 866
Stern' (M.) 145
Sternberg (C.) 167, 199, 211
Stetten (D.) 919
Stevenard (L.) 379
Stevens (A. A.) 652
Stewart (F. T.) 920
Stewart (G. N.) 752, 825
Stewart (H. A.) 807, 870, 891
Stewart (J.) 681
Stewart (W. R. H.) 548
Sticker (G.) 293, 296, 434
Stiles (C. W.) 541
Stiles (H. J.) 632
Still (G. F.) 884
Stille (A.) 244
Stillman (R. G.) 493
Stimson (A. M.) 298, 388
Stimson (G. W.) 564
Stiner (0.) 166
Stitt (E. R.) 4, 5, 137, 605
Stober (A. M.) 319
Stocker (J. R.) 459
Stockton (C. G.) 606
S totter (H.) 176
Stokes (W.) 698, 742, 854 857
Stokes (W. A.) 247
Stokes (W. R.) 299
Stoll (H. F.) 632, 691, 808
Stone (A. K.) 632, 672
Stone (W. J.) 246, 792, 808
Strandberg (0.) 557
Strasburger (J.) 815
Straub (H.) 488, 7C4
Strong (R. P.) 227, 253, 299, 335, 346,
381, 382
Strouse (S.) 94, 201, 202, 607
von Striimpell (A.) 2, 3, 393
Stubbert (J. E.) 547
Stucky (J. A.) 550
Stueftz, 670
Sturm (M. J.) 407
Suner (E.) 609
Surmont (H.) 407
Surveyor (N. F.) 328, 329
Sutherland (G. A.) 482, 604, 844, K: >
Swain (H. L.) 476, 578
Swan (J. M.) 803, 814
Swann (A. W.) 762
Sweet (E. A.) 628
Swift (H. F.) 164, 166, 167, 185, 373
Sydenham (T.) 2, 407
Sylvius, 613
Symes (W. L.) 592
Szecsi (S.) 86
von Tabora (D.) 825
Takaki (T.) 219
Talbot (F. B.) 592
Tallant (Alice W.) 767
Talley (J. E.) 671, 789
Tanzk (F.) 632
Taussig (A. E.) 866, 884, 891
Taussig (S.) 405
Taute (M.) 339, 341
Tawara (S.) 822, 864
Taylor (F.) 3, 604, 652, 673
Taylor (G. G. S.) 379
Taylor (L.) 638
Taylor (R. M.) 319
Taylor (R. T.) 198
Teague (0.) 227, 259
Tecon (H.) 626
Teichmiiller (W.) 536
Tendeloo (N. P.) 586, 597, 615, 628, 638,
646
Terroine (E. F.) 288
Teschner (J.) 864
Tessier (J. P.) 883
INDEX TO BEFEREKCES
947
Thalhimer (W.) 196, 878
Thayer (W. S.) 26, 204, 244, 362, 510,
669, 708, 718, 726, 740, 786, 849, 850,
857, 875, 881, 891, 908
Theisen (C. F.) 541
Theobald (F. V.) 363
Thevenot (L.) 327
Thibaut (D.) 858
Thiem (H.) 912
Thillaye, 5
Thiroux (A.) 331
Thoinot (L.) 2, 243, 307
Thorn (W.) 528
Thomas (C.) 556
Thomas (G. F.) 691
Thomas (W. T.) 188
Thompson (E.) 632
Thompson (J. E.) 920
Thorn sen (O.) 167
Thomson (D. T.) 364
Thomson (J. G.) 346, 364
Thomson (H. H.) 292, 626
Thomson (Sir St. C.) 549, 550, 557, 578
Thorel (C.) 647, 823
Thorndike (P.) 216
Thornton (W. L.) 596
Thro (W. C.) 185, 395
Tlmdichum (J. L. W.) 559
Thursfield (H.) 221
Tice (F.) 78
Tidy (H. J.) 632
Tiffeneau (M.) 112
Tigerstedt (C.) 790
Tigerstedt (R.) 644, 700, 776, 825
Tileston (W.) 245, 291, 411, 417
Tilley (H.) 466, 548, 565
Tissier (L.) 364
Tobiesen (F.) 680
Todd (J. L.) 337, 339, 341, 342, 346
Tomarkin (E.) 4C4
de Toni, 325
Topley (W. C. C.) 330
Tornai (J.) 803
Torpey (J. H.) 444
Torrey (J. C.) 249
Tousey (S.) 64
Traube, 266
Traube (L.) 485, 891
Treadgold (H. A.) 531
Tresh, 424
Trevison, 325
Trevor (R. S.) 652
Trogu (G.) 652
Trousseau fA.) 2
Trudeau (E. L.) 123, 292, 626
Trumpp (J.) 804, 805
Tschistowitsch, 120
Tschuchiya, 81
Tiirk (W.) 897, 927
Tuffier (T.) 526, 632, 669, 691, 894
Tufnell (T. J.) 919
Tulloch, 337
Tunnicliff (Ruth) 119, 541, 551
Turnbull (H. M.) 912
Turner (A. D.) 564
Turner (A. L.) 469, 565
Tuttle (G. A.) 330
Twichell (D. C.) 289, 630
Twort (J. F.) 490
Tylecote (F. E.) 261
Tyrie (C. C.) 671
Tyson (J.) 3
Tyzzer (E. E.) 346, 381, 423, 434, 439,
44U
u
Uhle (A. A.) 167
Uhlenhuth (P.) 120, 170, 249, 379, 541
Ullman (J. S.) 592
Umber (F.) 80, 81, 88
Underhill (F. P.) 809
Ungermann (E.) 119
Unna (P. G.) 292, 420
Unruh (0.) 419
Urban (F. M.) 776
Uskoff (L. J.) 798
Vallardi (C.) 691
van der Kamp (C. J. G.) 440
Vander Veer (A., Jr.) 604
Van der Velde (H.) 119
Van Norman (K. H.) 174, 6"2
Van Slyke (D. D.) 125
Vaquez'(H.) 699, 806, 828, 866, 871, 885.
904
Vaschide (N.) 751
Vattuone (A.) 668
Vaughan (V. C.) 103, 106, 123, 130, 606
Vaughan (V. C., Jr.) 106
Veale (P. J.) 909
Veiel (E.) 780
von den Velden (R.) 885
Venus (E.) 885
Venza (A.) 488
Vernon (H. M.) 488
Verstraeten (C.) 745
Vianna (C.) 342
Viereck (H.) 332, 335
Vierordt (H.) 6, 724, 747, 776, 898
Villatte (C.) 368
Villemin (J.-A.) 613
Vincent (H.) 170, 211, 328, 329, 703
Vincent (M.) 196
Vinit (A.) 912
Virchow (R.) 613
Vischer (A.) 326
Visentini, 344
Vochting (K.) 816
Voeghtlin (C.) 805, 806, 903
Vogelmann (S.) 790
Vohsen (K.) 466
Volhard, 777, 780
Volk (R.) 122
Volpius (G.) 388
Vrijburg (A.) 341
Vuillemin (P.) 307, 313, 321, 325
Vulpius (O.) 604
948
INDEX TO KEFEKENCES
W
de Waart (A.) 789
Wade (E. M.) 263
Wadsworth (A.) 607
Waggett (E.) 473
Waggett (E. B.) 549
Wainwright (J. M.) 647
Walden (E. C.) 217
Waldron (C. W.) 469
Walker (E. L.) 335, 303
Walker (E. W. A.) 118
Walker (G.) 275, 291
Walker (I. C.) 167
Waller (A. D.) 754, 757, 788, 790, 857
Walpole (G. S.) 103
Walsh (D.) 64
Walsh (J.) 528
Walsham (H.) 547
Walsham (W. J.) 464
Walter (B. G. H. L.) 63
Walters (F. R.) 292
von Walzel (R. P.) 883
Wandel (O.) 24, 96
Wankel (J.) 289
Wanklyn (W. McC.) 435
Warburton (C.) 331
Ward (G. E. S.) 825
Ward (H. B.) 648
Ward (0.) 745
Ward (S. M.) 530
Warfel (F. C.) 593
Warfield (L. M.) 245, 878
Warnecke, 691
Warren (B. S.) 292
Warren (L. F.) 91, 593, 716
Warthin (A. S.) 66, 379, 634, 681, 878,
884, 920
Wash bourn (J. W.) 201
von Wasielewski (T.) 424, 440
von Wassermann (A.) 96, 103, 108, 112,
137, 155, 219, 379, 607
Wassermann (M.) 112
Waters (C. A.) 53, 469
Watkins (J. A.) 122
Watson (E. M.) 388
Watson-Wemyss (H. L.) 789
Watson-Williams (P.) 549, 565, 575, 578
Waueh (J. F.) 199
Weaver (G. H.) 186, 411
Weaver (J. P.) 419
Webb (F. C.) 441
Webb (G.) 106
Webb (G. B.) 290, 470, 680
Weber (A.) 823
Weber (E.) 593, 751, 798
Weber (F. P.) 875, 920
Webster (R. W.) 4, 162
Wechsberg (F.) 108, 198
Wedel, 451
Weed (L. H.) 94
Weichardt (W.) 130 150, 176, 177, 260
Weiehsel (J.) 889
Weichselbaum (A.) 211, 441, 606
Weidanz (O.) 120, 171
Weigert (C.) 137
Weil (A.) 547, 653
Weil (M. P.) 222, 224
Weil (R.) 130
Weill, 670
Weill (M. E.) 604
Weinberg (M.) 167, 648
Weinberg (W.) 291, 628
Weintraud (W.) 3
Weir (H. B.) 289
Weiss (F.) 410
Weiss (G.) 757, 814
Weiss (O.) 722
Weitz, 919
Weitz (W.) 790
Welch (D. A.) 330
Welch (W. H.) 102, 104, 106, 136, 186,
199, 201, 216, 259, 317, 644, 645, 920
Welcker (H.) 292
Weller (C. V.) 653
Wellman (C.) 213, 541
Wells (E. F.) 607
Wells (H. G.) 106, 123, 124, 885
Wells (R. T.) 335
Wenckebach (K. F.) 306, 547, 826, 866,
885, 908
von Werdt (F.) 215, 216
Werner (H.) 362
Wernicke (E.) 259
Wernstedt (W.) 390
Wertheim-Salomonson (J. K. A.) 700
Wesbrook (F. F.) 246, 259
Wesson (M. B.) 388
West (S.) 479, 597, 604, 653, 667, 669,
871
Western (G. T.) 118
Weston (P. G.) 167
Wetterer (J.) 65
Weysse (A. W.) 803
Wherry (W. B.) 226, 228, 289
Whipple (G. C.) 247
White (B.) 145
White (J. A.) 549
White (J. H.) 391
White (P. D.) 825, 846, 847, 856
White (T. W.) 100
White (W. C.) 174, 176, 632
White (W. H.) 485, 606, 647, 788
Whitehead (R. H.) 918
Whitelock (R. H. A.) 682
Whitfield (A.) 214
Whitmore (E. R.) 335
Whitney (J. L.) 175, 490
Wickmann (I.) 393, 396, 398, 399, 402
Widal (F.) 81, 122, 186, 251, 307, 593,
620, 669, 671, 923
Widal (V.) 530
Wideroe (S.) 870
Wiedemann (G.) 722, 727
Wiesner (B.) 64
Wiesner (R.) 912
von Wiesner (R. R.) 393, 397, 402
Wigham (J. T.) 290
Wiggers (C. J.) 700, 776, 781, 844, 891
Wilbur (R. L.) 404
Wilcox (H. L.) 260
Wilcox (H. W.) 245
INDEX TO KEFEKENCES
949
Wilde (A.) 805
Wilder (R. M.) 300, 301, 306, 442
Wile (U. J.) 88
Wilkinson (K. D.) 846, 858
Wilensky (A. O.) 671
Williams (A. W.) 137, 386, 388, 440
Williams (B. G. R.) 4
Williams (C. S.) 814
Williams (D.) 417
Williams (E. G. C.) 4
Williams (F. H.) 64, 66, 547, 716
Williams (H. B.) 754, 755, 788, 789, 858
Williams (P. W.) 419
Williams (T. A.) 808
Williams (W. R.) 604
Williams (W. W.) 106
Williamson (A. M.) 626
Williamson (C. S.) 541, 604, 806, 814,
899
Willis (T.) 523
Williss (B. C.) 245
Willson (R. N.) 604, 609, 808, 867
Wilson (F. N.) 829, 836, 843
Wilson (G.) 24
Wilson (H.) 488
Wilson (J. C.) 3, 673
Wilson (J. G.) 823
'Wilson (L. B.) 246, 441, 920
Wilson (W. J.) 306
Windle (J. D.) 847
Wingrave, 556
Winslow (R.) 188, 606
Winter, 593
Winterberg (H.) 697, 726, 824, 836, 843,
858
Winternitz (M. C.) 606, 607, 627, 912,
919
Wintrich (M. A.) 268, 495, 502, 505, 512,
513
Wishart (D. J. G.) 551, 583
Withington (C. F.) 606, 671
Withington (E. T.) 6
Withmore (E.) 334
Witt (W. H.) 699
Wittich (F. W.) 541
Witzel (W. F.) 681
Wladimiroff (A.) 263
Wolbach (S. B.) 184, 296, 342, 346
Wolbarst (A. L.) 205
Woley (H. P.) 6, 804, 806
Wolf (C. G. L.) 245, 605, 865
Wolfenden (R. N.) 585
Wolff, 289
Wolff (A.) 510, 667
Wolff-Eisner (A.) 88, 109, 123, 176, 554,
631
Wollstein (Martha) 211, 221, 222, 224,
246, 261, 379, 541. 607, 609, 628
Wolman (S.) 173, 175, 547
Woloschin (A. D.) 919
Wood (F. C.) 4, 632
Wood (F. M.) 554
Wood (H. C., Jr.) 866
Vvood (N. K.) 509
Woodhead (G. S.) 263, 388, 628
Woods (H. R.) 585
Wooley (P. G.) 24, 346
Worth (P., Jr.) 917
Wovschin (W.) 648
Wright (Sir A. E.), 107, 118, 119, 171
Wright (J.) 549, 550
Wright (J. H.) 137, 210, 307, 329, 345,
346
Wunderlich (C. R. A.) 136
Wurtz (R.) 331
Wydler (A.) 595
Wynkoop (E. J.) 604
Wynn (W. H.) 330
Xylander, 541
Yates (A. G.) 195
Yeardsley (M.) 464
Yerington (H. H.) 379
Yersin (A.) 259
Yorke (W.) 338, 340, 341
Youland (W. E., Jr.) 604
Young (C. L.) 762
Young (H. H.) 213
Zade (H.) 444
Zadek, 547
Zahn (A.) 824, 825
Zaloziecki (A.) 94
Zappert (J.) 402
Zarfl (M.) 343, 345, 694
Zbinden (T.) 628
Zesas (D. G.) 909
Ziegel (H. F. L.) 177
Ziegler (J.) 596
Ziegler (O.) 288
Zielinski (M.) 780
Ziemann (H.) 5, 362
von Ziemssen (H.) 669, 762, 919
Zingher (A.) 260, 411
Zinn (W.) 595
Zinsser (H.) 103, 104, 106, 108, 112, 118,
119, 120, 122, 123, 130, 137, 156, 246,
377, 379
Zoege von Manteuffel (W.) 909
Zol linger (F.) 891
Zsigmondy (R.) 94
Zuckerkandl (E.) 565
Zueblin (E.) 66, 246, 628, 867
Zuntz, 887
Zur Verth (M.) 331
Zwaardemaker (H.) 825
Zybell (F.) 671
INDEX
Abdominal pulsations, 767.
Abscess, amebic, of liver, 333.
of lung, 610.
Achorion-mycosis, human, 309.
Achorion schoenleinii, 308.
Acne syphilitica, 372.
Acosta's disease, 456.
Acremoniosis, 325.
Actinomyces, in lung, 647.
in sputum, 539.
Actinomycosis, diagnosis of, 327.
generalized, 327.
in human beings, 326.
of the intestines, 327.
of the lung, 633.
of the skin, 327.
oral, 327.
pulmonary, 327.
symptoms of, 327.
Adams-Stokes syndrome, 848, 854.
Adenoid vegetations, 464.
Adventitious sounds in the lungs, 517, 521.
Aestivo-autumnal malaria, 350.
Agglutination, 121.
saturation experiment in, 121.
Agglutination titer, 152.
Agglutinins, 121, 150.
tests for, 150.
Aggressins, 102.
Aggression, mechanisms of, 98.
Ague-cake, 355.
Air, breathing, 489.
complementary, 489.
inspired and expired, determination of
the volume of, 488.
reserve, 489.
residual, 489.
Air-hunger of Kussmaul, 484.
Air-pressure diseases, among balloonists
and aviators, 456.
Alcoholism and tuberculosis, 280.
Aleppo boil, 344.
Alexins, 106, 115.
Allergy, 109, 122.
characters of, 125.
theories of, 130.
Alopecia syphilitica, 372.
Alpha interval, in electrocardiogram, 786.
Altitude, as a factor in certain diseases,
456.
Amboceptor, 112.
hemolytic, 114.
Ameba coli, 332.
Ameba dysenteriae, 332.
Amebae, 97, 332.
Amebiasis, human, 332.
Amebic abscess of the liver, 333.
Amebic dysentery, 332.
Amebic pyorrhea, 334.
Amino-acid crystals in sputum, 537.
Amphibolous stage of fever, 136.
Amphoric echo, 520.
Amphoric sound, 503.
Amphorophony, 517.
Anamnesis, 7, 21.
Anaphylactic reaction, symptoms of, 125.
Anaphy lactic test for protein (Pfeiffer),
179.
Anaphylaxis, 122.
active, 125.
clinical conditions due to, 126.
passive, 125.
Anderson and Goldberger's test in typhus
fever, 304.
Anergy, 125.
Aneroid manometers, 795.
Aneurism, of abdominal aorta, 916.
arteriovenous, 917.
dissecting, 905, 912.
of the thoracic aorta, 913.
diagnosis of, 914.
physical signs in, 913, 914, 915.
varicose, 913.
Aneurisms, 912.
circumscribed, 912.
complications of, 913.
definition of, 912.
diffuse, 912.
etiology of, 913.
of the pulmonary artery, diagnosis of).
916.
sites of, 912.
size of, 912.
so-called miliary, on the cerebral ar-
teries, 912.
varieties of, 912.
walls of, 912.
Angina, streptococcal, 190.
Angina nervosa, 903.
Angina pectoris, 901.
definition of, <)01.
differential diagnosis of, 903.
951
952
1KDEX
Angina pectoris, etiology of, 902.
nature of, 902.
symptoms of, 902.
Angina sine dolore, 903.
Angina spuria, 903.
Angina vasomotoria, 903.
Angina vera, 903.
Angiology, clinical, 695.
Angiomata of the larynx, 585.
Angioneurotic edema, 19.
Animal inoculations, 149.
Anopheles mosquito as a carrier of mala-
ria, 349.
Anthracosis, of lung, 646.
Anthrax bacillus, 214.
diseases due to, 214.
Anthrax carbuncle, 214.
Anthrax edema, 214.
Anthrax, human, 214.
intestinal, 214.
pulmonary, 214.
Anthrax septicemia, 214.
Antianaphylaxis, 125.
Antibodies, bacteriogenic, 102, 109.
Antibody formation, theories of, 110.
Antiferments, 109, 122.
Antiformir method, 86, 144.
Antigens, 102, 109.
Antihemolysins, 115.
Antitoxins, 107, 109, 111.
Antritis, maxillary, 565.
Antrum disease, 565.
Aorta, abdominal, aneurism of, 916.
cinematography of, 753.
dynamic, 768.
pulsations over, 764.
rontgenoscopy of, 753.
stenosis of the isthmus of, 896.
syphilis of, 910.
thoracic, aneurism of, 913.
Aortic insufficiency, 890.
hypertension in, 807.
Aortic stenosis, 889.
Apex-beat of heart, 758.
graphic curves of, 760.
position of, 702.
Aphonia, 471.
hysterical, 582.
Apnea, 484.
Argyria, 16.
Arhythmia, 720.
cardiac, common examples of, 826.
cardiac, classification of, 821.
dependent upon abnormal premature im-
pulses arising in the heart, 829.
extrasystolic, 829.
perpetual, 771, 842.
sinus, 826, 827.
.Arterial hypertension, chronic, 806.
Arteries, auscultation of, 743.
cerebral, syphilis of, 910.
•diseases of, 904.
pulse in, 769, 770.
subcutaneous, pulsation of, 18.
syphilis of, 909.
Arteriograms, 746, 773.
Arteriosclerosis, 904. See also Athero-
sclerosis.
hypertension in, 807.
Arteriovenous aneurisms, 917.
Arteritis syphilitica, 909.
Artery, pulmonary, embolism of, 640, 641,
642.
diagnosis of, 641, 642.
symptoms of, 640, 641, 642.
thrombosis of, 643.
Arthralgia, in caisson disease, 455.
Arthritis, chronic streptococcal, 196.
meningococcal, 209.
syphilitic, 374.
tuberculous, 270.
Arthropoda, 97.
Ascomycetes, 319.
Asiatic cholera, 297.
Aspergillosis, 308.
of the lung, 633.
Aspergillus, 307.
in lung, 647.
in sputum, 539.
Aspergillus flavus, 307.
fumigatus, 307.
nidulans, 307.
pictor, 309.
Aspiration, in pleural effusion, 69.
Asthma, 486.
bronchial, 486, 590.
definition of, 590.
diagnosis of, 591.
etiology of, 590.
symptoms of, 590.
cardiac, 486.
nasal, 590.
nervous, 590.
sexual, 590.
uremic, 486.
wt-t, in chronic bronchitis, 589.
Asthmogenic substances, 590.
Atelectasis, 634.
acquired, 634, 635.
compression, 635.
congenital, 634.
definition of, 634.
diagnosis of, 635.
etiology of, 634.
due to feeble contraction of the muscles
of inspiration, 634.
marantic, 634.
of the new-born, 635.
stenotic or obstructive, 635.
symptoms of, 635.
Atelosaccharomycoses, 312.
Atheromatous ulcer, 905.
Atherosclerosis, 904. (See also Arterio-
sclerosis.)
definition of, 904.
diagnosis of, 905.
etiology of, 905.
pathology of, 904.
Atherosclerotic cardiopathy, 899.
Atmospheric pressure, diseases due to al-
terations of, 454.
INDEX
953
Atrial (or auricular) fibrillation, 779,
826, 839.
Atrial (or auricular) flutter, 826, 844.
Atrial hypertrophy, 869.
Attitude, 11.
Auscultation, 24.
of breath sounds, 517.
of lungs, 513.
Auscultation sites for heart valves, 719.
Autoscopy of Kirstein, 472.
Aviators, air-pressure diseases among,
456.
B
Babinski's phenomenon of the toes in
epidemic cerebrospinal menin-
gitis, 208.
Baccelli's sign, 516, 659.
Bacillary dysentery, 252.
chronic form of, 253.
Bacilli, diseases due to, 213.
Bacillus aerogenes capsulatus, 215.
anthracis, 214.
of Bordet and Gengou, 221.
diseases due to, 221.
cholerae asiaticae, 296.
coli, in bronchopneumonia, 608.
tiiphtheriae, 254.
cultures of 255.
of Ducrey, diseases due to, 254.
dysenteriae, 229, 252.
fecalis alcaligenes, 229.
Gartner's, 229.
of green pus, 261.
of hog-cholera, 229.
influenzae, 219.
in bronchopneumonia, 608.
lactimorbi, 299.
leprae, 292.
of malignant edema, 215.
mallei, 261.
diseases due to, 261.
of milk sickness, diseases due to, 299.
of mouse typhoid, 229.
mucosus capsulatus, 597.
of paratyphoid, 229, 248.
paratyphosus, diseases due to, 248.
pestis, 225.
in bronchopneumonia, 608.
phlegmonis emphysematosae, 215.
prodigiosus, 16.
proteus vulgaris, diseases due to, 300.
pyocyaneus, diseases due to, 261.
human infections due to, 261.
of rhinoscloroma (von Frisch), 213.
of soft chancre, 254.
tetani, 216.
tuberculosis, 263, 614.
tularense, 226.
typhosus (Eberth-Gaffky), 228.
gastroenteritis due to, 243.
typhi exanthematici, diseases due to,
300.
Bacillus carriers, in dysentery, 252.
in diphtheria, 255.
Bacteria, methods of cultivating, 146.
methods of staining, 142.
microscopic examination for, 140.
varieties found on examination, 139.
Bacterio-diagnosis, 86.
Bacteriological examination, collection of
material for, 137.
Bacteriological methods, clinical applica-
tion of, 137.
Bacterio-agglutinins, 121.
Bacteriolysins, 109, 112, 153.
Bacterioproteins, 102.
Bacteriotropins, 109, 118, 171.
Bacterium coli commune (Escherich), 251.
Bagdad sore, 344.
Balantidium, 97.
Balloonists, air-pressure diseases among,
456.
Barber's itch, 310.
Barrel-shaped thorax, 480.
Bartonia bacilliformis, 382.
von Basch's syhgmomanometer, 792.
Bathmotropic function of heart muscle,
821.
Bed-sores, 16.
Bendick's air-water sphygmomanometer,
795.
Benoist's penetrometer, 44.
Bert's thorakograph, 490.
Beta interval, in electrocardiogram, 786.
Biermer's change in pitch, 513.
Bigeminal pulse, 830.
Bing's sphygmomanometer, 797.
Biot's breathing, 484.
Black vomit, in yellow fever, 390.
Black-water fever, 357.
Bladder, tuberculosis of, 275.
Blastomyces in sputum, 539.
Blastomycetes, 97, 306, 312.
Blastomycosis, 312, 313.
definition and etiology of, 314.
diagnosis of, 317.
differential diagnosis of, 317.
forms of, 314.
of the lung, 633.
symptoms of, 314.
systemic, 313.
Blenorrhea, 551.
Blindness due to gonococcal infections,
204.
Blood, in malaria, 354.
in trypanosome fever, 338.
Blood culture, in typhoid fever. -j:5:J. -Jll.
Blood cultures, Rosenow's trclmie for, !!>:>.
Blood-pressure, in aortic insufficiency, 807.
arterial, instruments for determination
of, 792.
under normal conditions, 803.
maximal, 790.
palpatory method of determining,
798.
oscillatory and auscultatory meth-
ods of .determining, 799.
954
INDEX
Blood-pressure, minimal, 791.
auscultatory method of determin-
ing, 801.
Erlanger's method of determining,
800.
Janeway's method of determining,
799.
Korotkow's method of determining,
801.
oscillatory method of determining,
800.
palpatory method of determining,
799.
von Recklinghausen's method of de-
termining, 800.
in arteriosclerosis, 807.
in chronic cyanosis, 807.
in chronic polycythemia, 807.
in chronic diffuse renal disease, 806.
diastolic, 791.
in Graves' disease, 807.
in increased intracranial tension, 806.
instruments for graphic registration of,
796.
measurements of, 790.
in pathological states, 806.
systolic, 790.
variations of, under physiological con-
ditions, 804.
venous, determination of, 811.
normal, 812.
in pathological states, 812.
Blood-pressure apparatus of Erlanger, 749.
Hirschfelder's modification of, 748.
Blood-vessels, auscultation of, 743.
diagnosis of diseases of, 820.
instruments for mechanical registration
of movements of, 746.
movements of, 745.
sphygmomanometry of, 790.
tonometry of, 790.
Blue babies, pulmonary stenosis in, 893.
Boil, Aleppo, 344.
Delhi, 344.
Boils, 199.
Bones, caries of, 271.
tuberculosis of, 271.
Bordet and Gengou's bacillus, 221.
Bordet-Gengou phenomenon, 116, 154.
Botrytimycosis, 325.
Botrytideae, 322.
Botulismus, 95.
Bouba, 344.
Bouton d'Orient, 344.
Bradycardia, 771.
Bradypnea, 484.
Brauer's operation, in mediastino-pericar-
ditis, 882.
Brazilian trypanosomiasis, 339.
Break-bone fever, 391.
Breath sounds, auscultation of, 517.
variations in, in the normal chest, 518.
Breathing, Biot's, 484.
bronchial, 517, 519.
Cheyne-Stokes, 484.
cog-wheel, 518.
Breathing, costal type of, 482.
broncho-vesicular, 521.
feminine type of, 482.
indefinite, 521.
laryngeal, 519.
masculine type of, 482.
meningitic, 484.
metamorphosing, 521.
mixed, 521.
puerile, 518.
roughened, in bronchopneumonia, 608.
tracheal, 519.
tubular, 520.
vesicular, 517.
Brill's disease, 300.
Broadbent's sign, 767.
in adherent pericardium, 881.
Bronchi, anatomy of, 461.
diagnosis of diseases of, 586.
dilatation of, 593.
diagnosis of, 594.
complications of, 594.
etiology of, 593.
symptoms of, 503.
examination of, 470.
foreign bodies in, 595.
stenosis of, 595.
Bronchial asthma, 486, 590.
Bronchial breathing, 517, 519.
accidental, 520.
metallic, 520.
Bronchial catarrh, acute diffuse, 587.
definition of, 587.
diagnosis of. f>ss.
symptoms of, 588.
Bronchial casts, 532.
Bronchiectasia, 593.
cylindrical, 593.
saccular, 593.
spindle-shaped, 593.
Bronchiectasis, 593.
Bronchiolitis, 587.
Bronchiostenosis, 595.
Bronchitis, 586.
acute fibrinous, 588.
symptoms of, 589.
capillary, 587.
chronic, 589.
diagnosis of, 590.
etiology of, 589.
symptoms of, 589.
croupous, 588.
dry, 589.
fetid or putrid, 589.
obliterating, 588.
pseudomembranous, 588.
sicca, 589.
stasis, 638.
Broncho-blenorrhea, 589.
Bronchopathies, 585.
Bronchophony, 515.
in bronchopneumonia, 608.
pathological, 515, 516.
Bronchopneumonia, 607.
complications of, 609.
definition. of, 607.,
INDEX
955
Bronchopneumonia, differential diagnosis
of, 609.
etiology of, 608.
occurrence of, 608.
symptoms of, 608.
Bronchorrhea, serous, 589.
Bronchoscopy, 476.
Broncho-vesicular breathing, 521.
Brudzinski's contralateral reflex in epi-
demic cerebrospinal meningitis,
208.
Brudzinski's frog sign, in epidemic cere-
brospinal meningitis, 208.
Brugsch's sphygmotonograph, 797.
Bruit d'airain. 677.
Bruit de diable, 744.
Bruit de moulin, in pneumopericardium,
886.
of Bricheteau, 742.
Bubo, 77.
of plague, 226.
of syphilis, 371.
suppurative, in soft chancre, 254.
Build of patient, 12.
Bussenius' sphygmotonograph, 797.
Butcher-shop odor, in yellow fever, 390.
Cachectic fever, 343.
Cachexia, hypotension in, 809.
Caisson disease, 455.
California disease, 317.
Calmette's tuberculin test, 174.
Caloric diseases, 445.
Camp fever, 300.
Cancer, of the lung, 648.
of the pleura, 680.
Capillaries, pulse in, 769.
Capsules of bacteria, stains foT, 145.
Caput medusae, 17.
Carbuncle of plague, 226.
Carbuncles, 199.
Carcinoma of the larynx, 583, 584.
of the skin, from rontgen-injury, 452.
Carcinosis pleurae, 680.
Cardiac arhythmias, classification of, 821.
Cardiac asthma, 486.
Cardiac dullness, 703.
Cardiac hypotony, 867.
Cardiogram, 759, 760.
esophageal, 746, 762.
negative, 761.
Cardiopathia adipositatis, 899.
Cardiopathia atherosclerotica, 899.
Cardiopathia nephropathicorum, 900.
Cardiopathia thyreotoxiea, 901.
Cardiopathies, chronic degenerative, 901.
chronic toxic-degenerative, 898.
inflammatory, 871.
Cardiopathy, atherosclerotic, 899.
. chronic, other forms of, 901.
fatty, 899.
nephropathic, 900.
thyreotoxic, 901.
Cardiopneumatic murmurs, 524.
Cardiosphygmograms, 746.
Cardiosphjgmograph of Jacquet, 748.
Cardiovascular acoustics, 717.
Carditis, 871.
Careotrypanosis, 339.
Caries of bones, 271.
of the spine, 272.
Carphologia in typhoid fever, 234.
Carriers, of acute poliomyelitis, 394.
of the diphtheria bacillus, 255.
of disease germs, 99.
meningococcus, 207.
Carrion's disease, 382.
Car-sickness, 458.
Casts, bronchial, 532. 589.
Catamnesis, 7, 23.
Catarrh, apical, 617.
Cathode-rays, 35, 40, 41.
Cavity, signs of, in abscess of the lung,
610.
in chronic pulmonary tuberculosis,
619.
Cavities, tuberculous, 265, 619.
Cercomonas hominis, 335.
Cerebrospinal fever, 206.
Cerebrospinal fluid, pressure of, 75.
examination of, 81.
total protein content of, 81.
globulin content of, 81.
Cerebrospinal meningitis, epidemic, 206.
complications of, 208.
course of, 208.
definition of, 206.
diagnosis and differential diagnosis
of, 209.
epidemiology of, 207.
incubation period of, 207.
symptoms of, 207.
Cerebrospinal syphilis, 373.
Chagas' disease, 336, 339.
Chalicosis, of lung, 646.
Chancre, hard, 369.
Hunterian, 369.
soft, nature of, 254.
sites of, 254.
syphilitic, 369.
Charcot-Leyden crystals, in bronchial
asthma, 537, 591.
Chemotaxis, 106.
Chest, alar, 480.
flat, 479.
funnel, 480.
pterygoid, 480.
rickety, 480.
transversely constricted, 480.
Cheyne-Stokes breathing, 484.
in myocardial insufficiency, 862.
Chicken-pox, 419.
definition of, 419.
diagnosis of, 420.
hemorrhagic, 420.
immunity in, 419.
prognosis and complications of, 420.
susceptibility to, 419.
symptoms of, 419.
956
INDEX
Chicken-pox, the virus of, 419.
Chill, 134.
Chlamydozoan organisms, 423.
Chloasma uterinum, 15.
Cholera Asiatica, 297.
definition of, 297.
diagnosis of, 298.
epidemiology of, 297.
prophylaxis of, 298.
symptoms of, 297.
Cholera bacillus, 296.
diseases due to, 296.
Cholera nostras paratyphosa, 248.
Cholera typhoid, 297.
Cholerine, 298.
Cholesterin crystals in sputum, 537.
Christen's absolute hardness measurer, or
so-called "half-value layer," 45.
Christen's energometry, 818.
Chronotropic function of heart muscle,
821.
Chrystanzoon scarlatinae of Gamalia, 407.
Chylothorax, 674.
definition of, 674.
etiology of, 674.
syfnptomatology of, 675.
Cinematograms, of heart and aorta, 747.
Circulation, collateral, 17.
insufficiency of, 859.
Circulatory apparatus, diagnosis of dis-
eases of, 695.
Circulatory disturbances involving the
pleura, 673.
Circulatory insufficiency, 859.
absolute, 864.
acute, 866.
definition of, 866.
etiology of, 866.
symptoms of, 866.
chronic, 859.
definition of, 859.
diagnosis of, 864.
etiology of, 860.
symptoms of, 860.
relative, 864.
Cirrhosis of the lung, 646.
syphilitic, 374.
Cladiosis, 325.
Cladothrix, 97.
Clinical history, 1.
Clinical study of patient, general plan for,
Clinocoris rotundatus, as carrier of
Leishmania donovani, 343.
Cocci, diseases due to, 183.
Coccidia. 97, 382.
Coccidioidal granuloma, 313, 317.
Coccidioides pyogenes, 317.
Coccidiosis, 382.
Cog-wheel breathing, 518.
Coin-sound, 504, 513, 525, 677.
Cold abscess, differential diagnosis of, 273.
in caries of spine, 272.
Cold, diseases due to exposure to, 448.
in the head, 550.
local effects of, 448.
Coli-sepsis, 251.
definition of, 251.
symptoms of, 251.
Collar of Stokes, 685.
Collateral circulation, in space-occupying
processes in the mediastinum,
684.
in stenosis of the isthmus of the aorta,
896.
Collateral circulations, 17, 684, 896.
Colics' law in congenital syphilis, 375.
Colloidal gold test, 83.
Colon bacillus, diseases due to, 251.
Colpohyperplasia cystica, 215.
Compression apparatus, 58.
Condylomata, 371.
Congenital diseases of the heart, 895.
Congenital syphilis, 375.
Congo trypanosome fever, 338.
Conjunctivitis, gonococcal, 204.
Conorrhinus megistus, 337.
Conorrhinus rubrofasciatus, as carrier of
Leishmania donovani, 343.
Consumption, pulmonary, 265.
galloping, 266, 614, 619.
Contralateral reflex of Brudzinski, in epi-
demic cerebrospinal meningitis,
208.
Cook's sphygmomanometer, 784.
Coolidge tubes, 55, 56.
Comma bacillus, 296.
Compensation, of heart muscle, 887.
failure of, 887.
Complement, 112.
Complement fixation, 115, 116, 154, 167.
in the diagnosis of echinococcus, 167.
in the diagnosis of gonococcal infections,
107.
Complement fixation tests, 154.
for differentiation of human from ani-
mal blood, 167.
Complement deviation, 115.
Complementoid, formation of, 113.
Compressed-air manometers, 794.
Coryza, 550.
Coryza vasomotoria, 560.
Cough, 541.
in acute fibrinous bronchitis, 589.
in chronic pulmonary tuberculosis, 617,
618, 619.
Coughing sounds, 515.
Cow-pox, 421, 435.
Coxitis tuberculosa, 270.
Cracked-pot sound, 504, 513, 658.
Crackles, 522.
Craigia hominis, 332.
Crisis in fever, 136.
Croup, false, 575.
true, 576.
Crying sounds, 515.
Cryptococcus gilchristii, 313.
Cryptoradiometer, 45.
Cryptoscope, 45.
Cuff, of blood-pressure apparatus, 793.
Culex fatigans, as carrier of dengue fever,
391.
INDEX
957
Cultures, bacterial, for clinical diagnosis,
146.
Curschmann's spirals, 532.
in bronchial asthma, 591.
Cutaneous loishmaniasis, 342, 344.
Cyanosis, 15.
chronic, hypertension in, 807.
in emphysema, 637.
Cyclosterion scarlatinas of Mallory, 407.
Cyrtometer, 495.
Cysts, gas, 215.
of the larynx, 585.
Cytodiagnosis, 88, 89, 90, 91.
Cytolysins, 109.
Cytorrhyctes variolae, 423, 439.
Damoiseau's curve, in pleurisy with effu-
sion, 657.
Dandy fever, 391.
Death rattle, 587.
in edema of the lungs, 644.
Death from electrical injury, 449.
from freezing, 448.
from lightning, 449.
Decompensation, in chronic circulatory
insufficiency, 858.
in valvular disease of the heart, 887, 888.
Defense, mechanisms of, 105.
Defervescence, 136.
Defluvium capillorum, 371.
Delhi boil, 344.
Dementia paralytica, 374.
Dengue fever, 301.
definition of, 391.
diagnosis of, 392.
symptoms of, 391.
virus of, 391.
Dermacentor occidentalis, as a carrier of
Rocky Mountain spotted fever,
441.
Derm-actinomycosis, 327.
Dermatitis, blastomycetic, 313.
chronic, among rontgenologists, 452.
Dermatomycosis, 308.
Dhobie itch, 310.
Diabetes, bronzed, 15.
Diagnostic methods, 24.
Diaphragm, paradoxical movement of, in
pneumothorax, 677.
Diaphragm phenomenon, 483.
Diastolic blood-pressure, 791.
Diastolic shock or rebound, in adherent
pericardium, 881.
Diathesis, haemorrhagic, 16.
Diazo-reaction of Ehrlich in typhoid fever,
233.
Dilatation, of heart, 867, 870, 887.
physiological or compensatory, 887.
stasis, 888.
systolic, 888.
Diphtheria, conjunctival, 258.
cutaneous, 257.
complications and sequelae of, 258.
Diphtheria, diagnosis of, 258.
differential diagnosis of, 259.
forms of, 256.
gangrenous form of, 256.
iacunar form of, 256.
laryngeal,. 257.
membranous form of, 256.
mixed infections in, 255.
nasal, 257.
pharyngeal, 256.
symptoms of, 256.
progressive or spreading form of, 256.
susceptibility to, 256.
Diphtheria antitoxin, 255.
Diphtheria bacillus, diseases due to, 254.
pathogenicity of, 255.
Diphtheria toxin, 255.
Diplococcus intracellularis meningitidis,
205.
Diplococcus pneumoniae, 199.
Diplophonia, 471.
Discomyces mycoses, 330.
Dissecting aneurism, 905, 912.
Dissociation, complete, 852.
Dittrich's plugs, 533.
in bronchiectasia, 593.
in gangrene of the lung, 612.
in the sputum of chronic bronchitis, 589.
Diver's disease, 456.
Doer and Russ, filtrable virus of, 405.
Dromotropic function of heart muscle, 821.
Dry pleurisy, 654.
Ducrey's bacillus, 254.
Ductus arteriosus Botalli, persistent, 895.
Duke's fourth disease, 418.
Dum-dum fever, 343.
Dust as a carrier of germs, 99.
Dynamic aorta, 768.
Dysentery, amebic, 332.
diagnosis of, 333.
occurrence of, 332.
symptoms of, 332.
bacillary, 252.
complications of, 253.
definition of, 252.
diagnosis of, 253.
epidemiology of, 252.
epidemic, 252.
Dysentery bacillus, 229.
diseases due to, 252.
Dysphonia, 471.
Dyspnea, 485.
E
Ecchymoses, 16.
Echinococcus cyst, in lung, 648.
Echinococcus cysts in sputum, 534, 539.
Ecthyma, 372.
Ectopia cordis, 897.
Ectotoxins, 101.
Eczema marginatum, 310.
Edema, 18, 19.
of the glottis, 579.
inflammatory, 644.
958
INDEX
Edema, of lungs, 644.
malignant, 215.
mechanical, 644.
neural, 644.
non-inflammatory, 644.
Edsall's disease, 447.
Egophony, 516.
in pleurisy with effusion, 659.
Ehrlich's stain, 142.
Electrical injuries, diseases due to, 449.
general symptoms of, 450.
local effects of, 450.
sequelae of, 451.
Electricity, as a cause of death, 449.
Electrocardiogram of normal heart, 747,
782.
in heart block, 852, 853.
in pathological states, 787.
physiological variations of, 785.
in pulsus alternans, 846.
significance of, in pulsus alternans, 847.
Electrocardiograph, 753.
Electrocardiography, clinical value of, 785.
Electrons, 40.
Ellis's line, in pleurisy with effusion,
657.
Embolism, 919.
of pulmonary artery, 640. 641, 642.
Embolus, bland, 640.
blood-clot, 640.
cell, 640.
fat, 640.
gas, 640.
septic, 640.
Embryocardia, 720.
Emphysema, vesicular, 636.
chronic, true, or substantial, 636.
definition of, 636.
diagnosis of, 637.
etiology and pathogenesis of, 636.
symptoms of, 637.
mediastinal, false, 693.
precordial crackling of, 742.
subfascial, 693.
Emphysema pulmonum, 636.
Emphysematous thorax, 480.
Emprosthotonos, 217.
Empyema, bilateral, 663.
diaphragmatic, 662.
encapsulated, 662.
exploratory puncture in, 663.
gangrenous, 664.
interlobar, 662.
mediastinal, 662.
metapneumonic, 663.
necessitatis, 663.
parapneumonic, 663.
pulsating, 662.
putrid, 664.
following rupture of a lung abscess,
611.
tuberculous, 663.
Empyema pleurae, 661.
Enanthem, in chicken-pox, 420.
in measles, 412.
in small-pox, 424, 431.
Endarteritis, obliterative, 910.
Endocarditis, 871.
acute, 872.
diagnosis of, 874.
symptoms of, 873.
varieties of, 872.
bacterial infection as a cause of, 871.
of cardiac type, 874.
of cerebral type, 874.
chordal, 872*.
of chronic or subacute infective type,
874.
chronic, 877.
definition of, 877.
diagnosis of, 877.
etiology of, 877.
symptoms of, 877.
definition of, 871.
etiology of, 871.
gonococcal, 204.
lenta, 184, 186, 875.
definition of, 875.
diagnosis of, 18(5. 876.
pathology of, 875.
prognosis of, 187.
symptoms of, 186, 875.
parietal or mural, 872.
pathology of, 872.
of septic type, 874.
septic ulcerative or malignant, 872.
simple vegetative and benign, 872.
simplex, 872.
subacute infectious, 186.
of typhoid type, 874.
ulcerosa, 872.
valvular, 872.
verrucosa, 872.
Endomyces albicans, 319.
characteristics of, 320.
Endomycosis, 312, 313.
Endotoxins, 102.
Energometry, Christen's, 818.
Kiitnmcba buccalis, 334.
Entameba coli, 332.
Entameba histolytica, 332.
in sputum. 540.
Entameba tetragena, 332.
Epicrisis, 7, 24.
Epidemic dysentery, 252.
Epidemics, of acute poliomyelitis, 394.
Epidermophytia cruris, 310.
Epidermophyton, 310.
Epididymitis, gonococcal, as a cause of
sterility, 203.
tuberculous, 275.
Epigastric pulsations, 767.
Epilepsy, syphilitic, endarteritis of the
smaller vessels of the brain as
a cause of, 911.
Epiphanin reaction ( Weichardt ) , 176.
Epistaxis, 557.
in caisson disease, 455,
Equinia, 421.
Ergins, tests for, 171.
Erlanger's blood pressure apparatus,
749.
INDEX
959
Erlanger's method of determining the min-
imal arterial blood-pressure,
800.
Erlanger's and Hooker's method for esti-
mating heart-work, 815.
Erlanger's sph\ gmornanometer, 796.
Eruption. See* Hash.
Eruptions, skin, 16.
Erysipelas, 187.
definition of, 187.
symptoms of, 187.
Erysipelas migrans, 188.
Erysipeloid of Rosenbach, 188.
Erythrasma, 312.
Espundia, 344.
Ethmoidal sinusitis, 569.
Exanthem. See Rash.
Exanthems, 16.
Exanthemata, acute, 407.
Exascoses, 312.
Expectoration, albuminous, 70.
Expiration, prolongation of, 518.
Exploratory puncture, in empyema, 663.
of joint cavity, 77.
of kidney, 77.
of liver," 77.
of lymph glands, 77.
of pericardial cavity, 70.
of peritoneal cavity, 71.
of pleural cavity, 67, 68, 69.
in pleural thickening, 665.
in pleurisy with effusion, 660.
in pleurisy with putrid exudate, 664.
of skull cavity, 77.
of spleen, 77.'
of subarachnoid space, 72.
technic of, 67.
Expometer, 60.
External physical causes, diseases due to,
95.
Extrasystoles, atrial (or auricular), 832.
nodal, 833.
ventricular, 829.
Exudates, 80.
Fallopian tubes, tuberculosis of, 275.
Farcy, 262.
diagnosis of, 262.
symptoms of, 262.
Fatty acid crystals in sputum, 536.
Fatty cardiopathy, 899.
Faught's aneroid manometer, 795.
Faught's mercury sphygmomanometer,
794.
Favus, 309.
Febris miliaris, 441.
Febris recurrens, 365.
Fedde's oscillometer, 797.
Fever, 134.
in acute pulmonary tuberculosis, 619.
acute rheumatic, 191.
break-boiio, 391.
cachectic, 343.
Fever, camp, 300.
continued, 135.
in chronic pulmonary tuberculosis, 618.
619.
dandy, 391.
dengue, 391.
dum-dum, 343.
epidemic cerebrospinal, 206.
influenzal, 220.
intermittent, 135.
Malta, 212.
Mediterranean, 212.
Oroya, 382.
pappataci, 405.
recurrent, 136.
recurring, of Pel, 136.
relapsing, 365.
remittent, 135.
Rocky Mountain spotted, 441.
scarlet, 407.
spotted, 300.
trypanosome, 338.
typhoid, 229.
typhus, 300.
undulant, 212.
yellow, 389.
Fibrillation, atrial (or auricular), 779,
826, 839.
paroxysmal, 842.
Fick's thorakograph, 490.
Fission-fungi, 97.
Fistulae, tuberculous, 265.
Fistular murmur, in pneumothorax, 677.
Flagella, stains for, 146.
Flagellata, 97.
diseases due to, 334.
Fleas, as carriers of Leishmania infantum,
344.
Fleischer's turgograph, 797.
Flexneria noguchii, 392.
Flint murmur, of aortic insufficiency, 890.
Fluorescence, 43.
Fluoroscopy of lungs, 542.
Flutter, atrial (or auricular), 826, 844.
Fomites, 95.
Food-poisoning, typhoid form of, 248.
Foot and mouth disease, 404.
Foramen ovale, patent, 896.
Foreign bodies, in the bronchi, 595.
in larynx, 585.
pneumopathies due to, 645.
Fourth disease of Duke, 418.
Frambesia, 379.
Freezing, death from, 448.
Fremitus, pericardial friction, 767.
Friction, pleuropericardial, 5'J I.
Friction fremitus, pericardial, 767.
in pleurisy, 654.
Friction rub, in pleurisy, 654.
Friction sounds, pericardial, 740.
pleural, 524.
pleuropericardial, 741.
Friedliinder's pneumobacillus, 213, 598.
in bronchopneumonia, 608.
in pneumonia, 202.
von Frisch's bacillus, 213.
960
IISTDEX
Frog sign of Brudzinski, in epidemic
cerebrospinal meningitis, 208.
Frontal sinusitis, 567.
Fungi affecting the skin, 308.
diseases due to, 306.
fission, 97.
in sputum, 534, 539.
yeast, 306.
Funnel chest, 480.
Furunculosis, 199.
G
Gartner's bacillus, 229.
Gartner's tonometer, 792, 794.
Gait, 11.
Gallop rhythm, 725.
Gamma interval, in electrocardiogram,
786.
Gangosa, 380, 381, 557.
Gangrene, in abscess of the lung, 611.
hospital, 215.
gas, 215.
of the lung, 611.
Garland's triangle, in pleurisy with effu-
sion, 657.
Gas, in pleural cavity, 675.
Gas bacillus (Welch & Nuttall), diseases
due to, 215.
Gas cysts, 215.
Gas gangrene, 215.
Gastroenteritis paratyphosa B, 248, 249.
Gastroenteritis typhosa, 243.
Gengou-Moreschi phenomenon, 167.
German measles, 417.
Germinal infection, 100.
Gibbus, in Pott's disease, 272.
Gibson's recording sphygmomanometer,
796.
Glanders, 262.
diagnosis of, 262.
Glanders, of the lung, 633.
symptoms of, 262.
Glanders bacillus, 2G1.
Glands, enlargement of, in syphilis, 371.
Glass-rays, 36.
Glossina brevipalpalis, as carrier of try-
panosomes, 338.
Glossina morsitans, as carrier of trypan-
osomes, 337, 338.
Glossina palpalis, as carrier of trypano-
somes, 337.
Glottis, edema of, 579.
symptoms of, 580.
Gold-miner's phthisis, 646.
Gold-number method, 83.
Gonitis, fungous, 271.
tuberculous, 271.
Gonococcal conjunctivitis, 204.
Gonococcal endocarditis, 204.
Gonococcal inflammations of the urogeni-
tal organs, 203.
Gonococcal iritis, 205.
Gonococcal polyarthritis, 204.
Gonococci, diseases due to, 202.
Gonococcus complement-fixation test, re-
sults of, 169.
Gonorrheal rheumatism, 204.
Goose-neck radial, 906.
Gram's stain, 142.
Granulation, tuberculous, 614.
Granuloma, coccidioidal, definition and
etiology of, 317.
diagnosis of, 318.
symptoms of, 318.
ulcerating, 380.
Granuloma veneretim, 380.
Granulomata, infectious, 213, 262.
Graupner's test for functional capacity of
the heart, 814.
Graves' disease, hypertension in, 807.
Grocco's triangle, in pleurisy with effu-
sion, 657.
Guarnieri's corpuscles, in chicken-pox, 419.
in small-pox, 423.
Gumma, 374.
Habitus phthisicus, 266.
Hanging drop, 140.
Hardness-measurers, of x-ray tubes, 44.
Harrison's groove, 480.
Hay fever, 552.
Hay's pharyngoscope, use of, in direct lar-
yngoscopy, 473.
Head tetanus, 217.
Heart, abdominal, 897.
acute dilatation of, in acute infections,
866.
anatomy of, 701.
apex-beat of, 758.
changes in the contractile force of, 840.
cervical, 897.
cinematography of, 753.
congenital diseases of, 895.
delayed conduction time of, 848.
diagnosis of diseases of, 820.
dilatation of, 867, 870, 887.
causes of, 871.
disturbances in conduction in, 847.
dropped beats of, 828.
extrasystolic irregularity of, 826.
functional capacity of, 813.
hypertrophy of, 867, 868, 887.
hypertrophy of left ventricle of, 868.
etiology of, 869.
physical signs of, 868.
hypertrophy of right ventricle of, 869.
etiology of, 868.
physical signs of, 869.
instruments for mechanical registration
of movements of, 746.
movements of, 745.
of obesity, 899.
the pacemaker of, 827.
pectoral, 897.
position and size of, 700.
reparative and adaptive processes in,
867.
INDEX
961
Heart, rontgenoscopy of, 753.
thrills, 766.
transposition of, 897.
valvular diseases of, 886.
wandering, 702.
youthful irregularity of, 827.
Heart beat, clinical disorders of, 820.
Heart block, 771, 847.
atrioventricular, 848.
complete, 826, 850.
diagnosis of, S5t>.
electrocardiograms in, 852, 853.
etiology of, 854.
intraventricular, 848, 853.
partial, 849.
pulse tracings in, 852.
Heart-failure cells, in embolism of pul-
monary artery, 642.
in myocardial insufficiency, 861.
in sputum, 530.
of chronic bronchitis, 589.
of mitral insufficiency, 893.
in stasis bronchitis, 639.
Heart murmurs, 727.
accidental, 736, 738.
anemic, 737.
in aortic regurgitation, 731.
in aortic stenosis, 731.
cardiorespiratory, 738, 741.
direction and propagation of, 730.
extra-cardiac or exocardial, 736, 740.
functional, 736.
inorganic, 736, 737.
intensity of, 734.
mtra-cardiac; 736, 737.
locomotive, 740.
in mitral regurgitation, 732.
in mitral stenosis, 731.
multiple, 732.
organic, 736, 737.
quality or timbre of, 736.
pitch or tonality of, 735.
physical explanation of origin of, 736.
significance of, 736.
timing of, 728.
topography of, 729.
velocity, in fevers, 737.
Heart muscle, compensation of, 887.
failure of compensation of, 887.
powers of adaptation of, 887.
Heart-rate, phasic variations in, 827.
Heart sounds, 717.
alterations in intensity of, 722.
changes in number of, 724.
graphic registration of, 721.
identification of, 720.
normal, 717.
origin of, 717.
reduplicated, 724.
rhythm and accentuation of, 720.
splittings and doublings of, 724.
triple or gallop rhythms of, 725.
Heart-work, Erlanger's and Hooker's
method for estimating, 815.
Heat, diseases due to, 445.
Heat-prostration, 445.
Heat regulation of body, 131.
Heat-stroke, 445, 446.
diagnosis of, 447.
symptoms of, 446.
Height, 12.
Heine-Medin disease, 392. See also Polio-
myelitis.
abortive forms of, 399.
ataxic form of, 398.
bulbar and pontine forms of, 398.
cerebral form of, 397, 398.
contagiosity of, 395.
definition of, 392.
differential diagnosis of, 401.
historical note on, 393.
immunity in, 394.
Landry's paralysis in, 398.
meningitic form of, 399.
occurrence of, in epidemics, 395.
pathology of, 400.
polyneuritic form of, 398.
prognosis of, 399.
prophylaxis in, 396.
serodiagnosis of, 400.
symptoms of, 397.
Hemagglutinins, 121.
Hematemesis, in yellow fever. 390.
Hematoidin crystals in sputum, 536.
Hematoma, intramural, 912.
Hemisporosis, 325.
Hemolysins, 109, 112, 153.
Hemolysis, 113, 114.
Hemopericardium, 886.
Hemoptysis, 529, 639.
in bronchiectasia, 594.
in chronic pulmonary tuberculosis, 611
618.
in embolism of pulmonary artery, 642.
endemic, 648.
in pulmonary tuberculosis, 282.
in tumors of the lung, 649.
Hemorrhage, intestinal, in typhoid feveic
235, 239.
mediastinal, 693.
from the nose, 557.
pulmonary, 639.
Hemorrhagic diathesis, 16.
Hemorrhoidal veins, varicosities of, 923.
Hemorrhoids, 923.
Hemothorax, 674.
definition of, 674. '
etiology of, 674.
symptoms of, 674.
Hemosporidia, 382.
Hepatic abscess. See Liver abscess.
Hepatic pulsations, 768.
Herpes tonsurans maculosquamosus, 310.
Herpes tonsurans vesiculosus. :>!(>.
Hertz's sphygmomanometer, 795.
Heterolysins, 115.
Heterotopic stimuli, 697.
Hiccough, in dry pleurisy, 654.
Hill's sphygmomanometer, 794.
Hip-joint, tuberculosis of, 270.
Hippocratic fingers, in pulmonary steno-
sis, 893.
962
INDEX
Hippocratic succussion splash, 525, 677,
886.
History, clinical, 7.
of present illness, 8, 21.
previous, of patient, 9, 21.
of diseases of childhood, 9, 21.
of post-childhood diseases, 9, 21.
of general bodily functions and sexual
life, 10, 21.
of habits, education and experience, 10,
21.
family, 10, 22.
History-taking, 1.
combined plan of, 21.
Hog-cholera, bacillus of, 229.
Holzknecht's radiometer, 47.
Hooker and Eyster's method of determin-
ing venous blood-pressure, 811.
Horse-pox, 421.
Hospital gangrene, 215.
Howell's method of determining venous
blood-pressure, 812.
Humming-top murmur, 744.
Hunterian chancre, 369.
Hutchinsonian teeth in congenital syphilis,
376.
Hydrocephalus internus, 208.
Hydropericardium, 885.
Hydrophobia, 383.
Hydrothorax, 673.
definition of, 673.
etiology of, 673.
symptoms and signs of, 673.
Hyperesthesia, cutaneous, in epidemic
cerebrospinal meningitis, 207.
Hyperhydrosis of skin, 16.
Hyperpiesis, 807.
Ilyperpyrexia, rheumatic, 194.
Hypersusceptibility, 122.
Hypertension, in aortic insufficiency,
807.
in arteriosclerosis, 807.
chronic arterial, 806.
in chronic cyanosis, 807.
in chronic diffuse renal disease, 806.
in chronic polycythemia, 807.
in Graves's disease, 807.
in increased intracranial tension, 806.
Hyperthermia, 445.
Hypertrophy, atrial, 869.
of heart, 867, 868,- 887.
of left ventricle of heart, 868.
of right ventricle of heart, 869.
Hyphomycetes, 96, 306, 307.
diseases due to, 307.
Hypohydrosis of skin, 16.
Hypotension, acute arterial, 808.
in acute infections, 808.
in cachexia, 809.
chronic arterial, 808.
in pulmonary tuberculosis, 808.
in surgical shock, 809.
in tuberculous persons, 282.
Hysterical aphonia, 582.
Iclithyosis, 16.
Icing liver, 883.
Icterus. See Jaundice.
Ignisation, 445.
Immune body, 112.
Immunity, acquired, 105, 108.
acquired antitoxic, 105, 107.
in acute poliomyelitis, 31)4.
antibacterial "or bacteriolytic, 105, 106.
in chicken-pox, 419.
in general, 105.
natural, 105, 106.
phagocytic, 105.
in rabies, 383.
in small-pox, 424.
Immunization, active, 105.
passive, 105.
in diphtheria, 255.
Immunodiagnosis, 87.
Immunological methods, clinical applica-
tions of, 150.
Impetigo syphilitica, 371.
Incubation, 104.
Infantile kala-azar, 344.
Infantile leishmaniasis, 342, 344.
Infantile paralysis, 392.
Infantilism, in congenital syphilis, 376.
Infarction of lung, hemorrhage, 040.
Infection, congenital, in tuberculosis, 615.
definition of, 95.
extragenital, in syphilis, 369.
fetal, in syphilis, 369.
genital, in syphilis, .'5<>9.
germinal, in syphilis, 369.
inhalation or aerogenous, in tuberculo-
sis, 615.
intestinal, in tuberculosis, 615.
latent, 101.
modes of, in tuberculosis, 614.
mouth, in tuberculosis, (515.
tonsillar, in tuberculosis, 615.
Infections, acute, hypotension in, 808.
local, 101.
mixed, 101.
secondary, 101.
Infectious agents, 97.
sources of, 98.
Infectious diseases, diagnosis of, 95, 180.
etiological agents in, 180.
special diagnosis of, 180.
Influenza, 219.
of the central nervous system, 220.
complications of, 220.
definition of, 219.
gastro-intestinal, 220.
portals of entry of infection in, 219.
of respiratory tract, 220.
symptoms of, 219.
Influenza bacillus, 219.
in sputum, 538.
diseases due to, 219.
Infusoria, 97.
Ink-polygraph of Mackenzie, 747.
Inoculation, preventive, in rabies, 384.
in typhoid fever, 242.
INDEX
963
Inoscopy, 86.
Inotropic function of heart muscle, 821.
Insolation, 445.
Inspection, 24.
Intermediate hosts, 99.
Interrupter, 29.
Interventricular septum, patent, 896.
Intestinal anthrax, 214.
Intestinal hemorrhage in typhoid fever,
235, 239.
Intestinal ulcers, formation of, in typhoid
fever, 235.
Intestines, actinomycosis of, 327.
Intoxication diseases, 101.
Intracranial tension, hypertension in, 806.
Inverse discharge, 38.
lonto-quantimeter of Szillard, 43, 48.
Iritis, gonococcal, 205.
Iso-agglutinins, 121.
Iso-hemolysins, 115.
Itch, barber's, 310.
dhobie, 310
washerwoman's, 310.
Jaccoud's rheumatismus fibrosus, 195.
Jacquet's cardiosphygmograph, 748.
Janeway's method of determining the min-
imal arterial blood-pressure,
799.
Janeway's sphygmomanometer, 794.
Jaundice, epidemic catarrhal, 300.
in yellow fever, 390.
Jennerian vesicle, 437.
Joint-cavity, exploratory puncture of, 77.
Joints, tuberculosis of, 270.
K
Kala-azar, 342, 343.
definition of, 343.
diagnosis of, 343.
differential diagnosis of, 344.
infantile, 344.
symptoms of, 343.
Kaodzera, 337, 339.
Katzenstein's method of estimating the
functional capacity of the heart,
816.
Keratitis, interstitial, in congenital syph-
ilis. 376.
Kerion celsi, 311.
Kernig's sign in epidemic cerebrospinal
meningitis, 207.
Kidney disease. See Renal disease.
Kidney, exploratory puncture of, 77.
Kienbock's quantimeter, 43, 49.
Kinetoses, 458.
Kirstein's autoscopy, 472.
Klebs-Loeffler bacillus, 254.
Knee-joint, tuberculosis of, 271.
Koch's laws, 97.
Koplik's spots in the mouth, in measles,
413.
Korotkow's method of determining the
minimal arterial blood-pres-
sure, 801.
Kronig's fields of pulmonary resonance,
505.
Kronig's step-like line of cardiac dulness,
in mitral stenosis, 891.
Kussmaul's air-hunger, 484.
La grippe, 219.
Lamblia intestinalis, 335.
Laryngeal breathing, 519.
Laryngeal catarrh, chronic, 576.
diagnosis of, 577.
etiology of, 576.
symptoms of, 576.
Laryngeal muscles, paralyses of, 580.
Laryngitis, acute catarrhal, 57">.
acute pseudomembranous, 576.
etiology of, 576.
chronic catarrhal, 576.
diphtheritic, 576.
syphilitic, 578.
diagnosis of, 579.
symptoms of, 578.
tuberculous, 577.
typhoidal, 579.
Laryngoscopy, 472.
Larynx affection of, in secondary syphilis,
372.
anatomy of, 460.
angiomata of, 585.
auscultation of, 471.
chronic catarrh of, 576.
circulatory diseases of, 579.
cysts of, 585.
diagnosis of diseases of, 574.
examination of, 470.
foreign bodies in, 585.
growths in, 583.
inflammatory diseases of, 575.
inspection of, 470.
internal examination of, 472.
neoplasm of, 583, 584.
palpation of, 470.
papilloma of, 584.
paralytic diseases of, 580.
percussion of, 471.
polyp of, 584.
sarcoma of, 585.
stenosis of, 585.
tuberculosis of, 577.
tumors of, symptoms of, 583.
views of, in indirect larvngoscopy, 474,
475.
Leishmania, diseases due to varieties of,
342.
Leishmania donovani, 342.
Leishmania furunculosa sive tropica, 342,
344.
Leishmania infantum, 342, 244.
Leishmaniasis, cutaneous, 342, 344.
human, 342.
infantile, 343, 344,
964
IKDEX
Lenses, tuberculous, 533.
Lepra, 292.
Lepra mixta, 294.
Lepra nervorum, 294.
Lepra nodosa, 294.
Lepra tuberosa, 294.
Leprosy, experimental, 292.
human, 292.
complications of, 295.
diagnosis of, 295.
epidemiology of, 293.
symptoms of, 294.
Leprosy bacillus, diseases due to, 292.
Leptothrix, 97.
Leukocidin, 197.
Levy-Dohrn's thorakograph, 490.
Lice, as carriers of relapsing fever, 365.
as carriers of typhus fever, 301.
Lichen scrofulosum, 274.
Lichen syphilitica, 371.
Lightning, death from, 449.
Litten's phenomenon, absence of on af-
fected side, in pneumothorax,
677.
absence of, in pleural thickening, 665.
in pleurisy with effusion, 656.
Litten's sign, 483.
Liver, amebic abscess of, 333.
exploratory puncture of, 77.
icing, 883.
in malaria, 354.
in myocardial insufficiency, 861.
Lockjaw, 216.
Locomotor ataxia, 374.
Loeffler's stain, 142.
Lues. See Syphilis.
Lues, laryngeal, 578.
Luetin reaction, value of, 178.
Luetin test (Noguchi), 177.
Lumbar puncture, 72, 76.
Lung, abscess of, 610.
definition of, 610.
differential diagnosis of, 611.
etiology of, 610.
symptoms of, 610.
actinomyces in, 633, 647.
anatomy of, 461.
anthracosis of, 646.
aspergillus in, 633, 647.
blastomyces in, 633.
brown induration of, 639.
cancer of, 648.
chalicosis of, 646.
cirrhosis of, 646.
distension of, active, 636.
echinococcus cyst of, 648.
gangrene of, oil.
definition of, 611.
diagnosis of, 612.
etiology of, 612.
symptoms of, 612.
glanders in, 633.
hemorrhagic infarction of, 640, 641.
infiltrations of, in Hodgkin's disease,
633.
in leukemia, 633.
Lung, lymphosarcoma of, 649.
mucor in, 647.
red induration of, 639.
siderosis of, 646.
streptothrix in, 647.
streptotrichosis of, 633.
stones in, 534.
syphilis of, 632.
thrush-fungi in, 647.
tumors of, 648.
diagnosis and differential diagnosis of ;
649.
symptoms of, 649.
Lungs, auscultation of, 513.
chronic passive congestion of, 638.
definition of, 638.
etiology and pathogenesis of, 639.
symptoms of, 639.
diagnosis of diseases of, 596.
edema of, 644.
diagnosis of, 644.
symptoms and signs of, 644.
emphysema of, 636.
examination of, 478.
foreign bodies in, 645.
parasites in, 645, 647.
rontgenography of, 543.
rontgenoscopy of, 542.
stereoscopic views of, 544.
Lupus exfoliativus, 274.
Lupus hypertrophicus, 274.
Lupus maculosus, 274.
Lupus mutilans, 274.
Lupus nodule, 273.
Lupus serpiginosus, 274.
Lupus tuberosus, 274.
Lupus vulgaris, 273.
definition of, 273.
symptoms of, 273.
Lymphadenitis, generalized tuberculous,
269.
Lymphadenoid tuberculosis, 269.
Lymphosarcoma, of the lung, 649.
Lymph, kinds of, used in vaccination, 422.
Lymph glands, 19.
exploratory puncture of, in sleeping
sickness, 77.
tuberculosis of, 269.
Lysins, 107, 153.
tests for, 153.
Lysis in fever, 136.
Lyssa, 383.
M
Mackenzie's ink-polygraph, 747.
Maculae ceruleae, 15.
Macular syphilid, 371.
Madura foot, 328.
Malaria, aestivo-autumnal, 350.
cerebri, 355.
choleriform, 355.
diagnosis of, 355.
epidemiology of, 350.
human, 346.
parasites of, 346.
,1,1,1,
IXDEX
965
Malaria, pernicious, 350.
quartan, 349.
symptoms of, 351.
tertian, 340.
tropical, 350.
Malarial cachexia, 355.
Malarial diseases. 346.
Malarial parasites, life history of, 346.
Malarial paroxysm, 352.
Malignant edema. 215.
Malignant pustule, 214.
Malta fever, 2\'2.
Mammary gland, tuberculosis of, 275.
Manometer, aneroid, of Faught, 795.
Oliver's, 705.
Rogers Tycos. 795.
Manometers, aneroid, 795.
compressed-air, 704.
for measuring pressure within the cuff
of a blood-pressure apparatus,
704.
mercury, 704.
Marriage and tuberculosis, 279.
Mastigophora, pathogenic, diseases Sue to,
3:5.-).
Mastoiditis, 572.
complications of, 573.
diagnosis of, 572.
symptoms of, 572.
Maxillary antritis, 565,
Maxillary sinusitis, 565.
Measles, 412.
complications of, 416.
concurrent, 416.
definition of, 412.
diagnosis of, 416.
without eruption, 414.
etiology of, 412.
German. 417.
symptoms of, 412.
Meat-poisoning, typhoid form of, 248.
Mediastinitis, acute, 692.
definition of, 692.
etiology of, 692.
symptoms of, 692.
chronic, (593.
definition of, 693.
etiology of, 693.
symptoms of, 693.
phlegmonous, 694.
Mediastino-pericarditis, 882.
Brauer's operation in, 882.
diastolic sound in, 726.
Mediastinum, abscess of, 692.
anatomy of, 461. »
classification of diseases of, 683.
diseases involving the lymph spaces of,
(iO-2.
diagnosis of diseases of, 682.
displacements of, through pressure or
traction, 684.
emphysema, of, 603.
hemorrhage into, 693.
partial displacements of, 684.
rontgenography of, 687.
space-occupying processes in, 684.
Mediastinum, space-occupying processes
in, symptoms of, 684.
total displacements of, 684.
tumors of, 689.
diagnosis of, 689.
varieties of, 689.
Mediterranean fever, 212.
Megastoma entericum, 3:;r>.
Meiostagmin reaction (Ascoli), 176.
.Melanesia, arsenical, 16.
Meninges, tuberculosis of, 276.
Meningitic breathing, 484.
Meningitis, epidemic cerebrospinal, 206.
See also Cerebrospinal Meningi-
tis.
tuberculous, diagnosis of, 276.
differential diagnosis of, 277.
symptoms of, 276.
Meningitis meningococcica, 206.
Meningitis siderans, 208.
Meningococcal arthritis, 209.
Meningococcal sepsis, 209.
Meningococci, diseases due to, 205.
Meningococcus, 205.
in bronchopneumonia, 608.
Mensuration, 24.
Mental state, 13.
Mercury manometers, 794.
Mesaortitis, gummatous, 374.
Mesaortitis productiva syphilitica, 909.
Mesarteritis, 910.
Metallic bronchial breathing, 520.
Metastases, in staphylococcus sepsis, 197.
Miasmatic diseases, 96.
Miasmatic-contagious diseases, 96.
Microbes, virulence of, 104.
Micrococcus catarrhalis, in bronchopneu-
monia, 608.
Micrococcus lanceolatus, 199, 597.
Micrococcus melitensis, 211.
diseases due to, 211.
Micrograph of Crehore and Meara, 750.
Microorganisms, diseases due to, 331.
vegetable, diseases due to, 183.
Microsiphomyces, 325.
Microsporon furfur, 310, 311.
Microsporon minutissimum, 310, 312.
Microsporon mycoses, human, 311.
Miliaria crystallina, 16.
Miliary tuberculosis, acute general,
277.
Milk sickness, 299.
bacillus of, 299.
symptoms of, 299.
Mirror-sphygmograph of Frank and Pet-
ter, 750.
Mitral facies, 892.
Mitral insufficiency, 893.
Mitral stenosis, 891. •
Mixed breathing, 521.
Monilia, 309.
Monilia Candida Monorden, 319.
characteristics of, 320.
Monocystis rpil helialis, 423.
Montoyella, 3<>o.
Morbil'li, 412.
966
INDEX
Moritz and von Tabora's method of de-
termining venous blood-pres-
sure, 811.
Mosquito, anopheles, as a carrier of mala-
ria, 348.
Mosquitoes, as carriers of dengue fever,
391.
as carriers of yellow fever, 389.
Mountain disease, 456.
Mouse typhoid, bacillus of, 229.
Movements, of the body, diseases due to
alterations of the direction of,
458.
unaccustomed, diseases due to, 458.
Mucedinacae, 322.
Mucor, in lung, 647.
Mucor corymbifer, 308.
Mucor rhizopodiformis, 308.
Mucor septatus, 308.
Mucormycosis, human, 309.
Mucous membranes, 14.
Mucous patches in mouth in secondary
syphilis, 371, 373.
Muenzer's sphygmoturgograph, 797.
Mumps, 442.
definition of, 442.
diagnosis of, 444.
epidemiology of, 442.
etiology of, 442.
sublingual, 443.
symptoms of, 443.
Murmur, Roger's, 896.
Murmurs, cardiopneumatic, 524.
heart, 727.
Mycetoma, 328.
definition of, 328.
Mycetoma fungi, 328.
Mycoderma immite, 317.
Mycoses, 306.
due to sporotrichum and related fungi,
322.
due to streptothrix, 325.
due to yeasts and yeast-like fungi,
312.
human, due to trichophyton tonsurans,
310.
human microsporon, 311.
resembling Schenck's sporotrichosis,
325.
Myocardial insufficiency. See Circulatory
insufficiency.
chronic, course of, 864.
Myocarditis, 877.
acute interstitial, 877.
chronic fibrous, 878.
definition of, 877.
etiology of, 877.
parenchymatous form of, 877.
pathology of, 877..
purulent form of, 877.
rheumatic, 878.
symptoms of, 878.
syphilitic, 878.
tuberculous, 878.
Myofibrosis cordis, 888,
N
Naevi, 16.
Nasal catarrh, chronic, 554.
Nasal cavity, anatomy of, 460.
Nasal hydrorrhea, 560.
Nasal polypi, 558.
Nasal septum, deflections and distortions
of, 559.
diagnosis of, 559.
occurrence of, 559.
symptoms of, 559.
Nasal spurs, 559.
Nasopharynx, palpation of, 465.
Negri bodies, in hydrophobia, 385, 386.
Neisser's gonococcus, 202.
Neisser-Wechsberg phenomenon, 115.
Nephropathic cardiopathy, 900.
Neuroryctes hydrophobiae, 386.
Nicholson's sphygmomanometer, 794.
Night sweats, in chronic pulmonary tuber-
culosis, 619.
Nocardia asteroides, 330.
Nocardoses, 325.
Nodes, in secondary syphilis, 372.
Noguchi's butyric acid test, 82.
Noguchi's luetin test, 177.
Nomotopic stimuli, 697.
Non-exanthematous diseases, 442.
Nose, diagnosis of diseases of, 548.
examination of, 462.
foreign bodies and parasites in, 557.
hemorrhage from, 557.
inflammatory diseases of, 550.
palpation of, 465.
syphilis of, 556.
tuberculosis of, 556.
tumors of, 558.
Obesity, heart of, 899.
Oidiomycoses, 312.
Oidium albicans, 320.
Oidium coccidioide, 317.
Oidium protozonide, 317.
Oliver-Cardarelli's sign, 470.
in aortic aneurism, 915.
Oliver mercurial compressed-air manom-
eter, 795.
Onychia, in secondary syphilis, 372.
Ophthalmia neonatorum, 204.
Ophthalmo-reaction in tuberculosis (Cal-
mette; Wolff -Eisner), 174.
in typhoid fever, 241.
value of, 175.
Opisthotonos, 217.
Opsonins, 107, 109, 118, 171.
immune, tests for, 171.
Oral actinomycosis, 327.
Oriental sore, 342, 344.
Ornithodorus moubata, as a carrier of re-
lapsing fever, 365.
Oroya fever, 382.
Orthodiagraphy, 50, 711, 713,
Orthopercussion, 499.
Qrthopnea, 486,
INDEX
967
Orthotonos, 217.
Oscillomanometer, Widmer's, 797.
Oscillometer, Fedde's, 797.
Pachon's sphygmometric, 795.
Osteomyelitis, acute, 198.
acute and chronic, diagnosis and differ-
ential diagnosis of, 198.
etiology of, 198.
symptoms of, 198.
chronic, 198.
Osteoperiostitis, toxicogenic, in bronchiec-
tasia, 594.
Otitis media, acute, preceding mastoiditis,
572.
Otomycosis, 308.
Ovary, tuberculosis of, 275.
Ovination, 422.
Ovinia, 421.
Ozena, 555.
Pachon's sphygmometric oscillometer, 795.
Pachydermia laryngis, 576.
Pacemaker of the heart, 827.
Pain, abdominal, in caisson disease, 455.
in pleurisy, 654, 656.
on swallowing, in mumps, 443.
Palpation, 24.
Pal's sphygmoscope, 797.
Pan-carditis, 871.
Pandy's test, 83.
Papilloma of the larynx, 584.
Pappataci fever, 405.
Paracentesis abdominis, 71.
in hemopericardium, 886.
in hydropericardium, 886.
Paragonimus westermanii, as a cause of
endemic hemoptysis, 648.
in sputum, 539.
Paraluetic stage of syphilis, 374.
Paralysis, in acute poliomyelitis, 397.
of the adductor muscles, 582.
infantile, 392.
of the internal thyro-arytenoid muscle,
582.
laryngeal, due to lesion of the N. recur-
rens, 581.
of the laryngeal muscles, 580.
of the N. laryngeus superior, 582.
of the N. vagus, 582.
postdiphtheritic, 258.
vasomotor, in acute infections, 866.
Parameba hominis, 332.
Paranasal sinuses, diagnosis of diseases of,
560.
examination of, 162.
rontgenography of, 466.
transillumination of, 466.
Parasaccharomycoses, 312.
Parasites, animal, 97.
of malaria, 346.
methods of staining, 142.
of pleura, 682.
pneumopathies due to, 645, 647.
vegetable, 97.
Parasitic sycosis, 311.
Parasyphilis, 374.
Paratyphoid bacillus, 229, 248.
Paratyphus abdominalis A, 249.
Paratyphus abdominalis B, 248, 249.
Paravertebral triangle of dullness in pleu-
risy with effusion, 657.
Parendomycoses, 312.
Paresis, general, 374.
juvenile, 376.
Paronychia syphilitica, 372.
Parotid gland, swelling of, in mumps, 443.
Parotitis epidemica, 442.
Paroxysmal fibrillation, 842.
Paroxysmal tachycardia, 836.
Passive congestion, in chronic circulatory
insufficiency, 863.
Pasteuria negrii (Noguchi), 384.
Pasteur's treatment for the prevention of
rabies, 387.
Pasteur's virus, disease due to, 383.
Pectoriloquy, 516.
whispered, 516.
Pectus carinatum, 480.
Pediculus capitis as a carrier of tvphua
fever, 301.
Pediculus vestimenti, as a carrier of re-
lapsing fever, 365.
as a carrier of typhus fever, 301.
Pendulum-rhythm, 720.
Penetrometers, 44.
Penicillium, 308.
Penicillium montayai, 309.
Percussion, 24.
comparative, 509.
deep, 498.
direct, 495, 497.
feeling of resistance on, 504.
indirect, 495, 497.
linear, 505.
over lungs, dullness and flatness on, 510.
pathological tympanitic sounds on,
511.
palpatory, of Ebstein, 706.
principles of, 496.
superficial, 498.
tactile, 504.
threshold-value, 499.
of Ewald-Goldscheider, 706.
topographical, 505.
Percussion-hammer, 495.
Percussion sounds, clang-content of, 502.
intensity and quality of, 500.
fullness of, 501.
loudness of, 501.
metallic, 503.
pathological fullness or emptiness of.
511.
pitch of, 501.
timbre of, 502.
tympanitic, variation in the pitch of,
512.
Percussion-stroke, strength of, 499.
Perforation, in typhoid fever, 235, 239.
Perforative peritonitis in typhoid fever,
239.
968
INDEX
Periarteritis, 910.
Periarteritis nodosa, 912, 920.
definition of, 920.
diagnosis of, 921.
symptoms of, 920.
Pericardial cavity, exploratory puncture
of, 70.
Pericardial friction fremitus, 767.
Pericardial friction sounds, 740.
Pericarditis, 879.
classification and pathology of, 879.
definition of, 879.
diagnosis of, 883.
with effusion, 879.
etiology of, 879.
fibrinous or dry, 879.
hematogenous form of, 879.
lymphogenous form of, 879.
symptoms of, 879.
Pericarditis adhesiva, 880.
Pericardium, adherent, 880.
associated with mediastino-pericardi-
tis, 881.
Broadbent's sign in, 881.
non-inflammatory diseases of, 885.
Periostitis, chronic gummatous, in congen-
ital syphilis, 376.
syphilitic, 374.
Perisporiacea, 308.
Peritoneal cavity, exploratory puncture
of, 71.
Peritonitis, perforative, in typhoid fever,
239.
Pernicious malaria, 350.
Pertussis, 222.
Petechiae, 16.
Peyer's patches, hyperplasia of, 232.
necrosis and sloughing of, 234, 235.
Pfeiffer's experiment, 153.
Phagocytosis, 106.
Pharyngeal tonsil, hypertrophy of, 464.
Pharyngoscopy, 464.
Phlebitis and thrombophlebitis, 921.
Phlebogram, normal, 778.
Phlebograms, 746, 777.
Phlebosclerosis, -923.
Phlebotomus pappatacii, as a carrier of
pappataci fever, 405.
Phlegmasia alba dolens, 921.
Phonoscope of Weiss, 721.
Phthisis, acute, 266.
symptoms of, 266.
acute tuberculous pulmonary, 614.
chronic fibroid, 268.
chronic ulcerative, 266.
anamnesis in, 266.
physical findings in the lungs in, 267.
gold-miner's, 646.
pneumonic form of, 266.
pulmonary, 265, 613.
Phthisis florida, 266, 619.
Phthisis incipiens, 267.
Phthisis renum, 275.
Phycomycetes, 308.
Physical causes, diagnosis of diseases due
to, 445.
Physical methods of diagnosis, 25.
Pick's syndrome, 883.
Pigeon breast, 480.
Pigeon-fancier's disease, 308.
Pigeon-feeders, disease of, 647.
Pigmentation, 15.
Piles, 923.
Pinta, 309.
von Pirquet's cutaneous tuberculin reac-
tion, 173.
Pityriasis rosea, 310.
Pityriasis versicolor, 311.
Placenta, tuberculosis of, 275.
Plague, 225.
definition of, 225.
diagnosis of, 226.
incubation period in, 225.
portals of entry of infection in, 225.
symptoms of, 226.
Plague bacillus, 225.
diseases due to, 225.
Plague bubo, 226.
Plague carbuncle, 226.
Plague pneumonia, 225.
Plague pustule, 226.
Plasmodium immaculatum sive precox,
350.
Plasmodium malariae, 349.
IMasmouium vivax, 349.
Plastic pleurisy, 654.
Pleocytosis, 93.
Plessimeter, 495, 497.
Plessimeter-finger, 497.
Plethysmograms, 747.
Plethysmpgraph, 751.
Pleura, circulatory disturbances involving,
673.
diagnosis of diseases of, 653.
inflammations of, 653.
inflammations of, pathology of, 653.
parasites of, 682.
tumors of, 680.
Pleural cavity, anatomy of, 461.
exploratory puncture of, 67, 68, 69.
gas in, 675.
Pleural friction sounds, 524.
Pleural thickening, 664.
definition of, 664.
etiology of, 665.
exploratory puncture in, 665.
symptoms and signs in, 665.
Pleurae, examination of, 478.
Pleurisy, 653.
diaphragmatic, 660.
dry, 654.
with effusion, 655.
definition of, 655.
diagnosis of, 660.
etiology of, 655.
exploratory puncture in, 660.
symptoms and signs of, 655.
fetid, 664.
interlobar, 660.
mediastinal, 660.
plastic, 654.
with purulent exudate, 661.
INDEX
969
Pleurisy, with purulent exudate, diagnosis
of, 663.
etiology of, 661.
symptoms and signs of, 661.
with putrid exudate, 664.
etiology of, 664.
exploratory puncture in, 664.
symptomatology of, 664.
with serous or serofibrinous effusion,
655.
serofibrinous, as a part of a polysero-
sitis, 660.
with serohemorrhagic effusion, 661.
Pleuritis, 653.
ozenous, 664.
Pleuritis chronica productiva, 664.
Pleuritis exudativa, 655.
Pleuritis purulenta, 661.
Pleuritis serofibrinosa, 655.
Pleuritis serosa, 655.
Pleuritis sicca, 654.
Pleuritis suppurativa, 661.
Pleuropericardial friction, 524.
Pleuropericardial friction sounds, 741.
Pneumobacillus, diseases due to 213, 598.
Pneumococcal septicemia, 202.
Pneumococci, diseases due to, 199.
differentiation of, from streptococci, 200.
pathogenic, 199.
in sputum, 538.
Pneumococcus, 199, 597.
in bronchopneumonia, 608.
Pneumococcus mucosus, 200.
Pneumography, 490.
Pneumonia, apical, 600.
aspiration 608.
asthenic, 601.
caseous, 614, 619.
catarrhal, 607.
central, 601.
chronic ulcerative, 610.
croupous, 202, 597.
double, 601.
embolic, 608, 610.
ether, 608.
fibrinous, 597.
focal, 607.
foreign-body, 608.
genuine lobar, 597.
complications of, 601.
definition of, 597.
diagnosis of, 601.
etiology of, 597.
sequelae of, "601.
special forms of, 600.
symptoms of, 598.
hypostatic, 608.
lobar, 202.
lobular, 607.
massive, 601.
metastatic, 610.
plague, 225.
pleurogenous, 613.
pseudolobar, 608.
tuberculous, in children, 285.
Pneumonia migrans, 600.
Pneumonias, 597.
interstitial, 613.
parenchymatous, 597.
Pneumonic plague, 226.
Pneumonoconioses, 645.
definition of, 645.
disposition to, 646.
symptoms of, 646.
varieties of, 646.
Pneumonomycosis aspergillina, 308.
Pneumopathies, 596, 597.
characterized by alterations of the al-
veolar lumen, 634.
of circulatory origin, 638.
due to foreign bodies and parasites, 645.
neoplastic, 648.
specific inflammatory, 613.
Pneumopericardium, 886.
Pneumothorax, 675.
artificial, 676.
closed, 676.
external, 675.
internal, 675.
open, 675.
valvular, 676.
Poliomyelitis acuta adultorum, 399.
Poliomyelitis, acute, virus of, 392.
acute anterior, 392. See also Heine-
Medin Disease.
rudimentary, of E. Muller, 399.
Polyarthritis, acute rheumatic, 191.
gonococcal, 204.
Polyarthritis meningococcica, 209.
Polyarthritis rheumatica acuta, 191.
Polycythemia, chronic, hypertension in,
807.
Polycythemia hypertonica, 807.
Polygraph of A. G. Gibson, 750.
ink, of James Mackenzie, 747.
Polypi, nasal, 558.
Portal of entry, in small-pox, 424.
in acute poliomyelitis, 396.
of infections, 100.
Portal vein, obstruction of, 17.
Posadasia esseriforme, 317.
Postdiphtheritic paralyses, 258.
Post-typhoid psychosis, 236.
Post-typhoidal elevations of temperature,
241.
Posticus paralysis, 581.
Potassium-iodid-starch method for cata-
lyser action, 176.
Pott's disease of the spine, 272.
Precipitin test, for human blood, 170.
for meningococcal infection, 171.
Precipitins, 109, 119, 170.
bacterioprotein, 120.
protein, 120.
tests for, 170.
Precordial boss or voussure, 702.
Precordial crackling of mediastinal em-
physema, 742.
Precordial movements other than the apex-
beat, 763.
Precordium, wave-like movements of, 763.
Pregnancy and tuberculosis, 278.
970
IKDEX
Preventive inoculation, in typhoid fever,
242.
Profeta's law in congenital syphilis, 375.
Prostate, tuberculosis of, 275.
Protein, anaphylactic test for (Pfeiffer),
179.
Protozoa, diseases due to, 331.
Pseudo-actinomycoses, 329.
Pseudochylous effusion, 674.
Pseudotuberculosis aspergillina, 308, 647.
Psoriasis, syphilitic, 372.
Psychosis, exhaustion, in typhoid fever,
236.
post-typhoid, 236.
Ptomains, 102.
Puerile breathing, 518.
Puerperal sepsis, strep tococcal, 189.
streptococcal, diagnosis of, 189.
Pulex cheopis, as a carrier of plague ba-
cilli, 225.
Pulex irritans, as a carrier of Leishmania
infantum, 344.
Pulex serraticeps, as a carrier of Leish-
mania infantum, 344.
Pulmonary actinomycosis, 327.
Pulmonary anthrax, 214.
Pulmonary artery, diagnosis of aneurisms
of, 916.
pulsations over, 764.
Pulmonary conus, dilated, 895.
Pulmonary embolism, 640.
Pulmonary gangrene, 611.
Pulmonary hemorrhage, 639.
Pulmonary insufficiency, 894, 895.
Pulmonary resonance, limits of, 505.
Pulmonary stenosis, 893, 895.
Pulmonary thrombosis, 640.
Pulmonary sounds, pulsatile, 741.
Pulmonary tuberculosis, 265, 613.
early diagnosis of, in adults, 280.
in children, 283.
Pulsations, in abdomen, 767.
Pulsations, in the back, 767.
epigastric, 767.
hepatic, 768.
Pulse, alternating, 771.
arterial, graphic registration of, 773.
palpation of, 770.
in arteries, 769, 770.
in capillaries, 769.
complete dicrotic, 775.
curves or tracings of, 773.
equality of, 773.
extrasystolic irregularities of, 771.
frequency of, 770.
fullness of, 772.
infradicrotic, 774.
irregular, 771.
monocrotic, 775.
in pneumonia, 599.
quickness or celerity of, 772.
regular, 771.
respiratory irregularities of, 771.
rhythm, 771.
supradicrotic, 775.
tension of, 772.
Pulse, value of, studies of, 769.
venous, 769, 776.
volume of, 771.
Pulse pressure, 791.
Pulse pressure amplitude, 791.
Pulse tracings, in heart block, 852.
in pulsus alternans, 846.
Pulsus alternans, 826, 846.
pulse tracings in, 846.
significance of electrocardiogram in, 847.
Pulsus bigeminus, 830, 846.
Pulsus irregularis respiratorius, 827.
Pulsus paradoxus, in chronic mediastini
tis, 693.
Pulsus trigeminus, 830.
Punctates, appearance of, 78.
bacteriological examination of, 86.
cytodiagnostic examination of, 86.
freezing-point of, 80.
molecular concentration of, 80.
odor of, 78.
physical and chemical examination of,
78.
protein content of, 79.
serological examination of, 86.
specific gravity of, 79.
Purpura variolosa, 427, 432.
Pustule, malignant, 214.
of plague, 226.
Pyocyaneus sepsis, 261.
Pyopneumothorax, 663, 675, 677, 679.
Pyorrhea, amebic, 334.
Q
Quantimeter of Kienbock, 43, 49.
Quantimetry, 47.
Quartan malaria, 349.
Quincke's edema, 19.
R
Rabies, 383.
definition of, 383.
diagnosis of, 385.
immunity in, 383.
incubation period in, 383.
symptoms of, 384.
virus of, 383.
Radial, goose-neck, 906.
Radio-injury, precautions against, 452.
Radiometer of Sabouraud-Noire, 43, 47.
Radiometry, 47.
Radium, diseases due to injuries from, 451.
Rag-picker's disease, 214.
Rales, 522.
in abscess of the lung, 611.
in acute pulmonary tuberculosis, 619.
in bronchopneumonia, 608.
cardiac, 524.
in chronic pulmonary tuberculosis, 617,
618, 619.
crepitant, 522.
dry, 522.
in emphysema, 637.
gurgling, 522.
INDEX
971
Rales, medium sized bubbling, 522.
metallic ringing, 523.
moist, 522.
non-ringing or non-consonating, 523.
in pneumonoconiosis, 646.
ringing, or consonating, 523.
subcrepitant, 522.
Rash, in chicken-pox, 419.
copper-colored, in syphilis, 371.
in German measles, 418.
in measles, 413, 414, 415.
in Rocky Mountain spotted fever, 441.
in scarlet fever, 408.
in small-pox, 425, 427, 429, 431, 432,
433.
in typhus fever, 303.
Rat flea as a carrier of plague bacilli,
225.
Rat sarcoma, 405.
Rauchfuss's triangle, in pleurisy with, ef-
fusion, 657.
Ray-fungus, 326.
von Recklinghausen's method of determin-
ing the minimal arterial blood
pressure, 800.
von Recklinghausen's tonometer, 796.
Rectify ing-switch apparatus, 30, 31, 32.
Recurrens paralysis, complete, 581.
partial, 581.
Relapses in dysentery, 253.
in typhoid fever, 237.
Relapsing fever, 365.
definition of, 365.
diagnosis of, 368.
symptoms of, 365.
mode of infection in, 365.
Renal disease, chronic diffuse, hyperten-
sion in, 806.
Renal tuberculosis, chronic, 275.
Resistance, 105, 106, 107.
feeling of, on percussion, 504.
Respiration, frequency and rhythm of,
483.
Respiratory abdominal reflex of R.
Schmidt, in dry pleurisy, 655.
Respiratory apparatus, diagnosis of dis-
eases of, 460.
Respiratory movements, inspection of, 482.
Respiratory system, diagnosis of diseases
of, 548.
Retro-ovination, 422.
Retro-vaccinia, 422.
Rhagades, in congenital syphilis, 376.
Rheostat, 29.
Rheumatic fever, acute, 191.
etiology of, 191.
definition of, 191.
symptoms of, 193.
Rheumatism, acute articular, 191.
chronic articular, 195.
gonorrheal, 204.
Rhinitis, 550.
acute catarrhal, 550.
complications and sequelae of, 550.
symptoms of, 550.
acute pseudomembranous, 551.
Rhinitis, acute purulent, 551.
acute purulent, complications of, 551.
etiology of, 551.
chronic, 554.
chronic atrophic, 555.
chronic purulent, 554.
protective or hyperplastic, 554.
syphilitic, 376.
Rhinomycosis, 308.
Rhinorrhea, 560.
cerebrospinal, 560.
Rhinoscleroma, 213.
bacillus of, 213.
Rhinoscopy, anterior, 462.
posterior, 464.
Rhizopoda, 97.
pathogenic, diseases due to, 332.
Rhodesian trypanosomiasis, 339.
Rhonchi, 522.
sibilant, 522.
sonorous, 522.
Rice-water stools in Asiatic cholera, 297.
Rickety rosary, 481.
Riggs' disease, 334.
Rigor, 134.
Ringworm, eczematous, 310.
of the hairy scalp and beard, 310.
of the nails, 311.
superficial, 310.
Risus sardonicus, 217.
Rivalta's .test, 80.
Riva Rocci's sphygmomanometer, 792, 794.
Rocky Mountain spotted fever, 441.
definition of, 441.
differential diagnosis of, 441.
etiology of, 441.
symptoms of, 441.
Rb'ntgen apparatus, 27.
Rontgen-cinematography, 29.
Rontgen energy, quantitative measurement
of, 43.
Rontgen-injury of the skin, 452.
of the sex glands, 453.
Rontgenograms, of heart and aorta, 747.
Rontgenography, 27.
in aortic aneurism, 915.
in adherent pericardium, 883.
cinematographic, 63.
of ethmoidal and sphenoidal sinuses,
467.
exposure time in, 58.
of frontal sinuses, 466.
hardness of tubes used in, 58.
instantaneous, value of single-impulse
apparatus in, 29.
of lungs, 543.
of maxillary sinuses, 467.
of mediastinum, 687.
photographic technic in, 52.
in pulmonary tuberculosis, 621.
special clinical applications of, 60.
stereoscopic, 60.
technic of, 57.
use of intensifying screen in, 43.
Rontgenology, qualitative and quantative
measurements in, 44.
972
INDEX
Rontgenoscopy, 27.
in adherent pericardium, 883.
in aortic aneurism, 915.
of chest, in pleurisy with effusion, 659.
horizontal, 55.
of lungs, 542.
in pneumonia, 599.
in pneumothorax, 677.
in pulmonary tuberculosis, 621.
simple, of cardiovascular stripe, 709.
technic of, 53.
use of fluorescent screen in, 43.
vertical, 55.
Rontgen rays, apparatus for production of,
27.
biological effects of, 43.
chemical effects of, 43.
clinical application of, 53.
diseases due to injuries from, 451.
divergent, 50.
dosage of, 47.
"erythema dose" of 48.
examination with, 27.
in examination of lungs, pleurae and
diaphragm, 542.
origin, nature and properties of, 40, 41,
42.
parallel, 50.
penetrability of, 42.
projection of, 50.
propagation of, 42.
secondary radiation of, 42.
Rontgen tubes, 34, 35, 36, 37, 39, 44.
Roger's murmur, 896.
Rogers Tycos manometer, 795.
Rose spots in typhoid fever, 234.
Rosenbach's "palpatory puncture," in
pleural thickening, 665.
Roseola syphilitica, 371.
Ross and Jones's test, 82.
Roteln, 417.
Rous, filtrable virus of, 405.
Rubeola, 417.
definition of, 417.
diagnosis of, 418.
etiology of, 417.
prognosis of, 418.
symptoms of, 418.
Rupia syphilitica, 371.
S
Sabouraud-Noire's radiometer, 43.
Saccharomyces non-liquefaciens, 320.
Saccharomycoses, 312.
Saddle-nose, in syphilis, 374, 376.
Sahli's absolute sphygmogram, 809.
Sahli's sphygmobolometry, 817.
Salpingitis, gonococcal, as a cause of ster-
ility, 203.
Salpingitis tuberculosa, 275.
San Joaquin Valley disease, 317.
Sarcoma of the larynx, 583, 585.
of the pleura, 680.
transmissible, 405.
Sarcosporidia, 382.
Scarlatina, 407.
surgical, 409.
Scarlet fever, 407.
abortive, 409.
anginose, 409.
complications and sequelae of, 409.
definition of, 407.
diagnosis of, 410.
etiology and epidemiology of, 407.
fulminant, 409.
hemorrhagic, 409.
prognosis of, 410.
symptoms of, 408.
Scars, 16.
Schaudinn's spirochaeta pallida, 368.
Schenck's disease, 322.
Schick's intracutaneous test in diphtheria,
256.
Schizomycetes, 97.
Schizotrypanum cruzi, 336, 337, 339.
Scleroma bacillus, diseases due to, 213.
Screen, fluorescent, in rontgenoscopy, 43.
intensifying, in rontgenography, 43, 60.
Scrofula, 269.
Scrofulids, 286.
Scrofuloderma, 274.
Sea-sickness, 458.
Seminal vesicles, tuberculosis of, 275.
Sepsis, meningococcal, 209.
otogenous, 189.
pyocyaneus, 261.
streptococcal puerperal, 189.
Septicemia, anthrax, 214.
pneumococcal, 202.
staphylococcal, 197.
streptococcal, 185.
Seropneumothorax, 675, 679.
Serositis, tuberculous, 270.
Serous membranes, tuberculosis of, 270.
Serum disease, 126.
Sex glands, rontgen-injury of, 453.
Sheep-pox, 421.
Shock, surgical, hypotension in, 809.
Siderosis, of lung, 646.
Silvermann's tonograph, 797.
Singer's nodes, 576.
Singer's sphygmomanometer, 796.
Sinus, maxillary, sounding of, 469.
Sinus thrombosis, streptococcal, 189.
Sinuses, ethmoidal and sphenoidal, ront-
genography of, 467.
frontal, rontgenography of, 466.
maxillary, rontgenography of, 467.
paranasal. See Paranasal Sinuses.
Sinusitis, causes of, 563.
ethmoidal, 569.
diagnosis of, 569.
symptoms of, 569.
frontal, 567.
diagnosis of, 569.
symptoms of, 567.
maxillary, 565.
definition of, 565.
differential diagnosis of, 566.
symptoms of, 565.
INDEX
973
Sinusitis, sphenoidal, 570.
diagnosis of, 572.
symptoms of, 570.
Sinusoscopy, 465.
Situs inversus cordis, 897.
Skin, examination of, 14, 20, 44.
rontgen-injury of, 452.
tuberculosis of, 273.
ulcerative miliary tuberculosis of, 274.
Skoda's resonance, in pleurisy with effu-
sion, 657.
in pneumonia, 598.
Skull cavity, exploratory puncture of, 77.
Sleeping sickness, 338.
Small-pox, 421.
black, 427, 432.
complications of, 433.
contagiousness of, 425.
definition of, 421.
diagnosis of, 433.
epidemiology of, 424.
the
eruptive stage of, 428.
etiology of, 423.
the florid stage of, 429.
immunity in, 425.
incubation period in, 425.
mortality from, 425, 431.
occurrence of, 421.
portal of entry of virus of, 424.
susceptibility to, 425.
symptoms of, 425.
Smears, examination of, 140.
Snuffles, in congenital syphilis, 375.
Soft chancre, 254.
bacillus of, 254.
Sore, Bagdad, 344.
tropical, 344
Sphenoidal sinusitis, 570.
Sphygmobolometry, Sahli's, 817.
Sphygmogram, the absolute, 809.
Sphygmograph, 747.
Sphygmography, 773.
Sphygmomanometer of von Basch, 792.
of Bendick, 795.
Bing's 797.
of Cook, 794.
Erlanger's, 796.
mercury, of Taught, 794.
recording, Gibson's, 796.
of Hertz, 795.
of Hill, 794.
of Janeway, 794.
of Nicholson, 794.
of Riva Rocci, 792, 794.
Singer's, 796.
of Staunton, 794.
Sphygmomanometry, 790.
Sphygmoscope, Pal's, 797.
Sphygmosignal, Vaquez's, 797.
Sphygmotonograph, Brugsch's, 797.
Bussenius, 797.
Uskoff's, 796.
Sphygmoturgograph, Muenzer's, 797.
Spine, caries of, 272.
Pott's disease of, 272.
Spirals, Curschmann's, 532.
Spirochaeta carteri, 365.
Spirochaeta duttoni, 365.
Spirochaeta novyi, 365.
Spirochaeta obermeieri, 365.
Spirochaeta pallida, 368.
Spirometry, 488.
Splashing sounds, 742.
Spleen, exploratory puncture of, 77.
in malaria, 354.
Splenomegaly, tropical, 343.
Spondylitis tuberculosa, 272.
Spores, stains for, 145.
Sporotrichum, 322.
properties of, 322.
and related fungi, mycoses due to, 322.
Sporozoa, 97.
pathogenic, diseases due to 382.
Sporotrichoses, 322.
Sporotrichosis, prognosis of, 324.
symptoms of, 324.
Spotted fever, 300.
Sputum, actinomyces in, 539.
in acute pulmonary tuberculosis, 619.
amount of, 531.
aspergillus in, 539.
bacteria in, 537.
black, 530.
blastomyces in, 539.
bloody, 529.
blue, 530:
cells in, 534.
in chronic pulmonary tuberculosis, 617.
618, 619.
color of, 530.
consistence of, 530.
crystals in, 536.
elastic fibers in, 536.
in emphysema, 637.
Entameba histolytica in, 540.
after perforation of lung by liver ab-
scess, 648.
examination of, 526.
in gangrene of the lung, 612.
heart failure cells in, 530.
hematoidin crystals in, 536.
influenza bacilli in, 538.
lung tissue in, 531.
microscopic study of, 534.
mucopurulent, 529.
mucous, 528.
nummular, 529.
odor of, 530.
Paragonimus westermanii in, 539.
parasites in, 537.
pneumococci in, 538.
in pneumonoconiosis, 646.
protein-content of, 530.
prune-juice, 529.
purulent, 529.
raspberry-jelly-like, in tumors of the
lung, 649.
rusty, 529.
serous, 529.
sources of, 526.
sulphur granules in, 539.
tubercle bacilli in, 538.
974
INDEX
Sputum, varieties of, 528.
white, 530.
yellow, 530.
Sputum fragments, 531.
Stable-fly, as a carrier of acute poliomye-
litis, 394, 395.
Staphylococcal septicemia, 197.
Staphylococci, diseases due to, 197.
portals of entry of, 197.
Staphylococcus, in bronchopneumonia, 608.
Staphylococcus albus, 197.
Staphylococcus aureus, 197.
Staphylococcus citreus, 197.
Staphylolysin, 197.
Stasis-dilatation, of heart, 888.
Status praesens, 7, 10, 22.
Staunton's sphygmomanometer, 794.
Stegomyia calopus fasciata, as a carrier of
yellow fever, 389.
Stenocardiac attacks, 901.
Stethometer, of Burdon-Sanderson, 490.
of Gibson, 490.
Stereoscope, Wheatstone, 61.
Stereoscopic views of lungs, 544.
Stimulins, 107.
Stokes' collar, 685.
Stomatitis epidemica, 404.
Stomoxys calcitrans, as a carrier of acute
poliomyelitis, 394, 395.
as a carrier of leprosy, 293.
Strawberry tongue, in scarlet fever, 408.
Strasburger's method of estimating func-
tional capacity of heart, 815.
Streptococcal angina, 190.
Streptococcal arthritis, chronic, 196.
Streptococcal puerperal sepsis, 189.
Streptococcal septicemia, 185.
Streptococcal sinus thrombosis (otogen-
ous sepsis) , 189.
Streptococci, diseases due to, 183.
Streptococcus, in bronchopneumonia, 608.
Streptococcus mucosus, 183.
Streptococcus putridus, 183.
Streptococcus pyogenes, 183.
Streptococcus viridans, 183.
as the cause of endocarditis lenta, 875.
Streptococcus vulgar is hemolyticus, 183.
Streptothrices, 306.
Streptothrix, 97.
in lung, 647.
mycoses due to, 325.
Streptothrix actinomyces, 326.
Streptothrix foersteri, 325.
Streptothrix freeri, 328.
Streptotrichomycoses, 329.
of the brain, 330.
of the digestive tract, 329.
of the eye, 330.
of the lungs, 329.
of the skin, 329.
Streptotrichosis, of the lung, 633.
Streptotrichoses, 325.
Stridor, 470.
Subarachnoid space, exploratory puncture
of, 72.
Substance sensibilitrice, 115.
Subsultus tendinum in typhoid fever, 234.
Succussion splash, 525.
Hippocratic, 677.
in pneurnopericardium, 886.
Sulphur granules, 326.
in sputum, 539.
Sun-stroke, 445.
Sweat, bloody, from Bacillus prodigiosus,
16.
green, in infections with Bacillus pyo-
cyaneus, 16.
sour, in rheumatic fever, 194.
yellow, in jaundice, 16.
Sweating-sickness, 441.
Sycosis, parasitic, 311.
Syphilid, gummatous, 371.
*macular, 371.
miliary, 371.
papular, 371.
pustular, 371.
ulcerative, 371.
Syphilis, 368.
acquired, 369.
diagnosis of, 374.
symptoms of, 369, 371, 374.
cercbrospinal, 374.
congenital, 375.
symptoms of, 375.
definition of, 369.
lenticular, 371.
of the lung, 632.
paraluetic stage of, 374.
primary, 369.
secondary, 371.
tertiary, 374.
viscera], 374.
Syphilis hereditaria tarda, 376.
Syphilitic aortitis, 910.
Syphilitic laryngitis, 578.
Systolic blood-pressure, 790.
Szillard's ionto-quantimeter, 43, 48.
Tabes, juvenile, 376.
Tabes dorsalis, 374.
Tabes mesenterica, 269.
Tachograph, 751.
Tachograms, 747.
Tachycardia, 720, 770.
paroxysmal, 826, 836.
Tachypnea, 484.
Tactile percussion, 504.
Teeth, Hutchinsonian, in congenital syph-
ilis, 376.
Telangiectases, 16.
Telerontgenography, 51, 711, 716.
Telerontgenoscopy, 51.
Temperature, 14, 131,
measurement of, 132.
normal, 133.
Temperatures, febrile, 134.
Tertian malaria, 349.
Testis, tuberculosis of, 275.
INDEX
975
Tetanus, human, 216.
course of, 217.
definition of, 216.
diagnosis of, 218.
incubation period in, 217.
portals of entry of infection in, 217.
symptoms of, 217.
Tetanus antitoxin, 216.
Tetanus bacillus, 216.
diseases due to, 216.
Tetanus facial is, 217.
Tetanus hydrophobicus, 217.
Tetanus idiopathicus, 217.
Tetanus neonatorum, 217.
Tetanus puerperalis, 217.
Tetanus rheumaticus, 217.
Tetanus toxin, 216.
Tetanus traumaticus, 217.
Thermometry, 132.
Thoracentesis, 69.
Thoracography, 490.
Thoracolysis pericardiaca, 882.
Thorakograph of Fick, 490.
of Levy-Dohrn, 490.
of P. Bert, 490.
Thorax, asymmetry of, 481.
barrel-shaped, 480.
contraction of, 481.
emphysematous, 480.
expansion of, 481.
expiratory type of, 479.
forms of," 479.
inspection of, 479.
inspiratory type of, 480.
mensuration of, 495.
normal, 481.
palpation of, 494.
retraction of, in pleura! thickening, 665.
Thorax paralyticus, 479.
Thread reaction, for agglutinins, 121.
Threshold-value percussion, 499.
Thrills over heart, 766.
Thromboangeitis obliterans, 920.
Thrombo-endocarditis septica, 872.
Thrombo-endocardifis superficialis, 872.
Thrombophlebitis, recurring, 921.
Thrombosis, 919.
pulmonary, 640, 643.
Thrush, 319.
Thrush fungi, diseases due to, 319.
in lung, 647.
Thrush mycosis, 312.
Thyreotoxic cardiopathy, 901.
Thyroiditis parasitaria, 336, 337, 339.
Ticks, as carriers of relapsing fever, 365.
as carriers of Rocky Mountain spotted
fever, 441.
Tonicity of heart muscle, failure of, 870.
Tonograph, Silvermann's, 797.
Tonometer of Giirtner, 792, 794.
von Recklinghausen's, 796.
Tonometry, 790.
Tonsil, pharyngeal, hypertrophy of, 464.
Tonsillitis, as a factor in causing acute
rheumatic fever, 193.
Toxins, 101.
Trachea, anatomy of, 461.
auscultation of, 471.
diagnosis of diseases of, 586.
examination of, 470.
inspection of, 470.
palpation of, 470.
stenosis of, 595.
Tracheal breathing, 519.
Tracheal tug, 470.
in aortic aneurism, 914.
Tracheitis, 585.
Tracheobronchitis, acute catarrhal, 586.
etiology of, 586.
physical signs in, 587.
symptoms of, 586.
Tracheopathies, 586.
Tracheostenosis, 595.
Trachoma of vocal cords, 576.
Transformer, 30.
Transillumination in rontgenoscopy, 55,
57.
Transudates, 80.
Trembles, the, 300.
Treponema pallidum, 368.
stains for, 144.
Treponema pertenue, 379.
Triatoma, 337.
Trichomonas intestinalis, 335.
Trichomonas vaginalis, 335.
Trichomycetes, 97.
Trichophytia profunda, 311.
Trichophytia superficialis, 310.
Trichophytia tonsurans capillatii, 310.
Trichophytia unguium, 31l.
Trichophyton, 308.
Trichophyton tonsurans, 310.
human mycosis due to, 310.
Tricuspid insufficiency, 895.
Tricuspid stenosis, 894.
Trigeminal pulse, 830.
Trismus, 216.
Tropical liver abscess, 333.
Tropical malaria, 350.
Tropical sore, 344.
Tropical splenomegaly, 343.
Trypanosoma gambiense, 336.
Trypanosoma rhodesiense, 336, 337, 339.
Trypanosome fever, 338.
Trypanosomes, 97, 336.
Trypanosomiasis, Brazilian, 339.
definition of, 339.
symptoms of, 339.
mode of infection in, 337.
Rhodesian, 339.
definition of, 339.
occurrence of, 339.
symptoms of, 339.
Trypanosomidae, pathogenic, diseases due
to, 336.
Tsetse flies, as carriers of trypanosomes,
337, 338.
Tubercle, conglomerate, 265.
miliary, 265.
Tubercle bacillus, 263, 614.
in acute pulmonary tuberculosis, 619.
antiformjn method, 86, 114.
976
INDEX
Tubercle bacillus, in chronic pulmonary
tuberculosis, 617, 618, 619.
diseases due to, 263.
paths of, in infection of, in tuberculosis,
264.
pathogenicity of, 264.
portals of entry of, 264.
in sputum, 538.
stains for, 143.
Tuberculids, 286.
Tuberculin, 614.
Tuberculin reaction, cutaneous, (von Pir-
quet) 173.
subcutaneous (Koch), 172.
conjunctiva! (Calmette; Wolff-Eisner ) ,
174.
Tuberculin tests, 172.
Tuberculosis, acute disseminated miliary,
614, 620.
acute general miliary, 277.
definition of, 277.
symptoms of, 277.
acute miliary, in children, 284.
acute pulmonary, 619.
and alcohol, 280.
of bladder, 275.
of the bones, 271.
of the bronchial glands, in children, 285.
after chicken-pox, 420.
chronic pulmonary, 614.
of epididymis, 275.
general miliary, 264.
hematogenous, 264.
of the hip- joint, 270.
differential diagnosis of, 270.
of the joints, 270.
of the lymph glands, 269.
lymphadenoid, diagnosis and differential
diagnosis of, 269.
lymphogenous, 264.
of the kidney, 275.
of the knee-joint, 271.
differential diagnosis of, 271.
simple effusion in, 271.
of the mammary gland, 275.
and marriage, 279.
after measles, 416.
of the meninges, 276.
miliary, differential diagnosis of, 278.
modes of infection in, 615.
of the ovary, 275.
of the placenta, 275.
predisposition to, 616.
and pregnancy, 278.
of prostate, 275.
pulmonary, 265, 613.
causes of death in, 620.
in children, 285.
complications of, 5286.
chronic forms of, physical signs in,
617.
clinical examination in, 617.
complications of, 620.
conditions of disposition to, 616.
definition of, 613.
disseminated forms of, 619.
Tuberculosis, pulmonary, etiology of, 614.
historical note on, 613.
hypotension in, 808.
modes of infection of, 614.
ordinary chronic forms of, 617.
pathology of, 614.
pneumonic form of, 619.
roentgenography in, 621.
rontgenoscopy in, 621.
acute, diagnosis of, 620.
of seminal vesicles, 275.
of the serous membranes, 270.
of the skin, 273.
of testes, 275.
of urogenital system, 275.
of the uterus, 275.
Tuberculous lenses, 533.
Tuberculous laryngitis, 577.
Tuberculous spondylitis, 272.
Tubular breathing, 520.
Tumor albus, 271.
Tumors, of the lung, 648.
Turgograph, Fleischer's, 797.
Tussis convulsiva, 222.
Tympanitic sound, 503.
Tympany, 511, 512.
Typhoid-colon group of bacilli, 229.
Typhoid bacillus, 228.
diseases clue to, 228.
Typhoid-bacillus carriers, 230.
Typhoid-bacillus excretors, 230.
Typhoid fever, 229.
complications of, 238.
convalescence in, 236.
course of, 232.
definition of, 230.
diagnosis of, 241.
differential diagnosis of, 241.
disposition to, 231.
epidemiology of, 230.
history of, 229.
incubation period in, 232.
mild forms of, 236.
preventive inoculation in, 242.
prophylaxis of, 242.
recrudescences and relapses in, 237.
symptoms of, 232.
typical course of, 232.
variations from typical course of, 236.
Typhoid form of meat- and food-poisoning,
248.
Typhoid hosts, 230, 242.
Typhoid-ophthalmo-reaction, value of, 178.
Typhoid state in pneumonia, 601.
Typhoprotein conjunctival test (Chante-
messe; Austrian), 178.
Typhus abdominalis, 229.
Typhus abortivus, 236.
Typhus ambulatorius, 236.
Typhus exanthematicus, 300.
Typhus fever, 300.
diagnosis of, 304.
definition of, 300.
etiology of, 300.
occurrence of, 300.
prophylaxis of, 302.
INDEX
977
Typhus fever, symptoms of, 303.
Typhus levissimus, 236.
Typhus manchuricus, 249.
U
Ulcer, atheromatous, 905.
Ulcers, 16.
tuberculous, 265.
varicose, 923.
Ulcus molle, 254.
Undulant fever, 212.
definition of, 212.
diagnosis and differential diagnosis of,
212.
incubation period of, 212.
occurrence of, 212.
portals of entry of microorganism of,
212.
prognosis of, 212.
prophylaxis of, 212.
symptoms of;, 212.
Uremic asthma, 486.
Urogenital organs, gonococcal inflamma-
tions of, 203.
Urogenital system, tuberculosis of, 275.
Uskoff's sphygmotonograph, 796.
Utah, 344.
Uterus, tuberculosis of, 275.
Vaccination, 422, 435.
complications of, 439.
dangers of, 439.
definition of, 435.
historical note on, 435.
symptoms following, 436.
technic of, 435.
Vaccination mark, 437.
Vaccine virus, 435.
Vaccinia, 421, 435.
Valve closure, shocks due to, 765.
Valves of heart, frequency of defect m,
888.
insufficiency of, 886.
obstruction of, 886.
regurgitation of, 886.
stenosis of, 886.
Valvular diseases, definition of, 886.
effects of, 887.
etiology of, 886.
of the heart, 886.
recognition of, 889.
relation of age to, 888.
Vaquez's sphygmosignal, 797.
Varicella, 419.
Varicocele, 17.
Varicose ulcers, 923.
Varicose veins, 922.
definition of, 922.
etiology of, 922.
of leg, 17.
symptoms of, 922.
Variola, 421.
Variola confluens, 425, 431.
Variola discreta, 425, 427.
Variola hemorrhagica, 427, 432.
Variola inoculata, 427, 433.
Variola sine eruptione, 425, 432.
Variolation, 422.
Varioloid, 425, 431.
Varix, esophageal, hemorrhage from 923.
as a symptom of cirrhosis of the
liver, 923.
Vein, right jugular, auscultation of, 744.
Veins, diseases of, 921.
pulse in, 769, 776.
of neck, diastolic collapse of, in adher-
ent pericardium, 881.
Vena cava, inferior, obstruction of, 18.
Venous hum, 744.
Venous thrombosis in typhoid fever, 240.
Venous tone, 744.
Vermes, 97.
Verruga peruviana, 381.
definition of, 381.
symptoms of, 381.
Vesicular breathing, 517.
modifications of, in disease, 518.
suppression of, 519.
Vibrio asiaticae, 296.
Vibrio cholerae, 296.
Virulence tests, 149.
Virus, of acute poliomyelitis, 392.
of Ashburn and Craig, 391.
of chicken-pox, 419.
of dengue fever, 391.
of Flexner and Noguchi, diseases due to,
392.
of the Heine-Medin disease, 392.
Pasteur's, disease due to, 383.
of rabies, 383.
of Reed, Carroll and Agramonte, disease
due to, 389.
of yellow fever, 389.
Viruses, filterable, 97.
diseases due to, 382.
ultramicroscopic, diseases due to, 382.
Visceral syphilis, 374.
Vocal cords, trachoma of, 576.
Vocal resonance, 515.
Voice sounds, abnormalities of, 516.
auscultation of, 514.
cavernous, 516.
changes in, 515.
in healthy persons, 515.
normal, 515.
origin of, 514.
W
Walter's penetrometer, 44.
Warmth-stroke, 445.
Washerwoman's itch, 310.
Wasp-waist, in atelectasis, 635.
Wassermann reaction, 87, 156.
clinical value of, 163.
in syphilis, 374.
Water-wheel sound, 742.
in pneumopericardium, 886.
978
IOTDEX
Water-whistle sound, in pneumothorax,
677.
Wehnelt's cryptoradiometer, 45.
Weil's disease, 300.
Weight, 12.
Welch's bacillus, 215.
Wheatstone stereoscope, 61.
White swelling, 271.
Whooping-cough, 222.
complications of, 223.
definition of, 222.
diagnosis of, 223.
essential, 222.
nature of, 222.
sequelae of, 223.
susceptibility of, 222.
symptomatic, 222.
symptoms of, 223.
Widal reaction, 151.
in typhoid fever, 233, 235, 241.
Widmer's oscillomanometer, 797.
Williams' tracheal tone, in pleurisy with
effusion, 658.
Wilson's and Giemsa's stain, 142.
Wolff-Eisner's tuberculin test, 174.
Woolsorter's disease, 214.
Worms, 97.
X-ray burn. See Rontgen-injury.
X-ray examination, in emphysema, 637.
X-ray examination, for tumors of the lung,
649.
in pleural thickening, 665.
X-ray examining room, description of, 33.
X-rays. See Rontgen rays.
Yaws, or frambesia, 379, 557.
definition of, 379.
diagnosis of, 380.
etiology of, 380.
prognosis of, 380.
symptoms of, 380.
Yeast fungi, 97, 306.
Yeast threads, 312.
Yeasts and yeast-like fungi, mycoses due
to, 312.
Yellow fever, 389.
definition of, 389.
diagnosis of, 390.
epidemiology of, 389.
symptoms of, 390.
virus of, 389.
Ziehl-Neelsen's stain, 142.
Zuntz and PleschV method of estimating
the functional capacity of the
heart, 817.
Zymonematoses, 312.
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