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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 
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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., 
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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 
organs.     Arch.  Rontg.  Ray,  London,  1910-11,  xv,  3-12. 


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- 
buch  der  Biologie,  Pharmakologie  und  Klinik  des  Radiums,  Mesothoriums, 
Thorium  X,  Aktiniums  und  der Emanationen.  Berlin,  1913,  Adler.  349  p. 

Max  (0.)  &  Klee  (P.).  Eine  praktische  Kombination  von  klinischem  Rontgenkabinett  mil 
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- 
more, 1914,  Ivii,  106;  141. 

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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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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solution  of  the  tuberculosis  problem.  New  York,  1909 ,  M  off  at,  Yard  & 
Co.  394  p.  16°. 

Leivandowsky  (F.).  Die  Tuberkulose  der  Haul.  In:  Ergebn.  d.  allgem.  Pathol.  [etc.] 
(Lubarsch  tfc  Oslerlag).  Wiesbaden,  1912,  xri,  Abth.  i,  454-549. 

Martin  (5.).  Remsed  by  W.  C.  Bosanquet.  Tuberculosis.  In:  Syst.  Med.  (AllbuH  A'- 
Rolleston).  8°.  London,  1909,.  U,  pL  1,  258-301. 

Mosny  (E.},  Bernard  (L.)  [et  al.].  Mdkulir*  /w/wx/Y//m's  communes  a  Vhomme  el  an.r 
animaux.  Tuberculose,  scrofulc,  HHHTC,  c/i<irlx>n,  rage,  Ichinox,  actino- 
mycose,  pxillacoxc,  mycoses,  (ftdiomycoee,  (ispcrgillose,  ladrerie,  trichinose, 
ankylostomow .  I'nri*,  1911,  J .  B.  BaiUiere  ^  Jils.  566  p.  8°.  [Nouv. 
traite  de  med.  de  tfierap.,  iv.] 

Petruschky  (/.)•  Die  spezifische  Diagnostik  und  Therapie  der  Tuberkulose.  Ergebn.  d. 
inn.  Med.  u.  Kinderh.,  Berlin,  1912,  i.r,  557-620. 

Ziegler  (O.)  &  Krause  (P.).  Rontgenatlas  der  Tuberkulose.  Beitr.  z.  Klin.  d.  Tuberk. 
(II.  Suppl.  Bd.),  Wurzburg,  1910,  1-15,  61  pi. 


2.     Etiology  (Tubercle  Bacillus;  Disposition) 

Armand-Delille  (P.  A.),  Mayer  (G.  5.)  &  Terroine  (E.  F.).  Le  bacille  tulwrculeux; 
culture  en  milieu  chimiquement  defini,  nutrition  azotee.  J.  physiol.  et 
pathol.  gen.,  Paris,  1913,  xv,  797-811. 

Baldwin  (E.  R.).  Tuberculosis:  history  and  etiology.  In:  Mod.  Med.  (Osier).  8°.  Phil- 
adelphia &  New  York,  2d  ed.,  1914,  287-338. 

Calmette  (A.}.  Role  de  Vheredite  dans  I'infection  tuberculeuse.  Transmission  du  germe 
par  les  generateurs.  Heredo-dystrophies  et  predispositions  specijiques. 
Ztschr.  f.  Tuberk.,  Berlin,  1913,  xxi,  46-52. 

Cornet  (G.)  &  Kossel  (#.)•  Tuberkulose.  Erster  Teil:  Die  Tuberkelbacillen.  ZweiterTeil: 
Tuberkulose.  In:  Handb.  d.  pathogen.  Mikroorg.  (Kolle  &  Wowr- 
mann).  2.  Aufl.  Jena,  1913,  v,  391-548. 

Ehrlich  (P.).  Erinnerungen  aus  der  Zeit  der  dtiologischen  Tuberkuloseforschung  Robert 
Kochs.  Deutsche  med.  Wchnschr.,  Leipzig  u.  Berlin,  1913,  xxxix,  2444- 
2446. 

Glas  (E.)  &  Kraus  (E.}.  Einfluss  der  Schwangerschaft  auf  die  Tuberkulose  des  Kehlkopfes. 
Med.  Klin.,  Berlin,  1909,  v,  963,  1008. 

Harris  (Alfred).  The  etiology,  diagnosis  and  prophylaxis  of  pulmonary  phthisis,  considered 
chiefly  from  the  public  health  point  of  view,  with  an  appendix  on  the  tuber- 
culin treatment  of  the  disease.  Bristol,  1912,  J.  Wright  &  Sons.  126  p. 
1  lab.  8°. 

Keilty  (R.  A.).  Cultivation  of  tubercle  bacillus  directly  from  sputum  by  method  of  Petroff. 
J.  Exper.  M.,  Lancaster,  Pa.,  1915,  xxii,  612-614. 


DISEASES    DUE    TO    BACILLI 


289 


Koch  (Robert).  Die  Aetiologie  der  Tuber culos'e.  Berl.  klin.  Wchnschr.,  1882,  xix,  221- 
230. 

Die  Aetiologie  und  die  Bekdmpfung  der  Tuber culose.    Eingeleitet  von  M. 
Kirchner.    Leipzig,  1912,  J.  A. Barth.     7 4  p.     8°. 

Kossel  (H.).  Die  Tuberkelbacillen.  In:  Handb.  d.  pathogen.  Mikroorgan.  (Kolle  & 
Wassermanri),  2d  ed.,  1913,  v,  391-480. 

Lewis  (P.  A.}  &  Margot  (A.  G.}.  The  function  of  the  spleen  in  the  experimental  infection 
of  albino  mice  with  bacillus  tuberculosis.  J .  Exper.  Med.,  Lancaster,  Pa., 
1915,  xxi,  84-90. 

Lowenstein  (#.)•  Die  Anwendung  des  Tuberkulins  beim  Menschen.  In:  Handb.  d. 
pathogen.  Mikroorg.  (Kolle  &  Wassermann).  2.  Aufl.  Jena,  1913,  v. 
549-659. 

Moss  (W.  L.)  &  Barnes  (F.  M.,  Jr.).  Concerning  the  Much- Holzmann  reaction.  Johns 
Hopkins  Hosp.  Bull.,  Baltimore,  1911,  xxii,  278-282. 

Much  (//.)•  Ueber  die  granulare,  nach  Ziehl  nicht  farbbare  Form  des  Tuberkulosevirus. 
Beitr.  z.  Klin.  d.  Tuberk.,  Wiirzburg,  1907,  viii,  85-89. 

Rosthorn  (A.)  &  Fraenkel  (A.).  Tuberkulose  und  Schwangerschaft.  Deutsche  med. 
Wchnschr.,  Leipzig  u.  Berlin,  1906,  xxxii,  675-678. 

Smith  (T.).  Notes  on  the  biology  of  the  tubercle  bacillus.  J.  M.  Research,  Boston,  1913, 
xxviii,  91-110. 

Wankel  (/.)•  Die  Theobald  Smithsche  Reaktionskurve  als  Hilfsmittel  zur  Differenzierung 
humaner  und  boviner  Tuberkelbacillen.  Deutsche  med.  Wchnschr.,  Leip- 
zig u.  Berlin,  1913,  xxxix,  2461 . 

Wherry  (W.  B.}.  Some  chemical  conditions  influencing  acid-proofness  and  non-acid- 
proofness  in  a  saprophytic  culture  of  B.  tuberculosis.  J.  Infect.  Dis., 
Chicago,  1913,  xiii,  144-154. 

Wolff.  Alkohol  und  Tuberkulose.  Beitr.  z.  Klin.  d.  Tuberk.,  Wiirzburg,  1905-06,  iv, 
239;  391. 


3.     Immunity ;  Anapliylaxis 

Austrian  (C.  JR.)»  The  effect  of  hypersensitiveness  to  a  tuberculo-protein  upon  subsequent 
infection  with  B.  tuberculosis.  Johns  Hopkins  Hosp.  Bull.,  Baltimore, 
1913,  xxiv,  11-25. 

Baldwin  (E.  R.).  Allergy  and  re-infection  in  tuberculosis.  Johns  Hopkins  Hosp.  Bull., 
Baltimore,  1913,  xxiv,  220-224. 

Bronfenbrenner  (/.)•  ^  preliminary  communication  on  complement-fixation  test  in  the 
tuberculoses  with  Besredka's  antigen.  Proc.  Soc.  Exper.  Biol.  &  Med., 
New  York,  1914,  xi,  92-93. 

Dudgeon  (L.  S.),  Meek  (W.  O.),  &  Weir  (H.  B.).  A  preliminary  inquiry  as  to  the  value 
of  the  complement-fixation  test  in  tuberculosis.  Lancet,  London,  1913,  i, 
19-21. 

King  horn  (H.  M.}  &  Twichell  (D.  C.).  Further  notes  on  the  serum  diagnosis  of  tubercu- 
losis. Am.  J.  M.  Sc.,  Philadelphia  &  New  York,  1906,  n.  s.,  cxxxii, 
549-554. 

Koch  (R.).  Weitere  Mittheilungen  uber  ein  Heilmittel  gegen  Tuberculose.  Deutsche  med. 
Wchnschr.,  Leipzig  u.  Berlin,  1890,  xvi,  1029-1032. 

Fortsetzung    der    Mittheilungen  uber  ein    Heilmittel   gegen    Tuberculose. 
Deutsche  med.  Wchnschr.,  Leipzig  u.  Berlin,  1891,  xvii,  101-102. 
Weitere    Mittheilung    uber    das   Tuberkulin.     Deutsche   med.    Wchnschr., 
Leipzig  u.  Berlin,  1891,  xvii,  1189-1192. 

Laird  (A.  T.).  Notes  on  complement  fixation  in  tuberculosis.  J.  M.  Research,  Boston,  1912- 
13,  xxvii,  163-175. 


290  DIAGNOSIS    OF    INFECTIOUS    DISEASES 

Lowenstein  (E.).  Tuberkulose-Immunildt.  In:  Handb.  d.  pathogen.  Mikroorg.  (Kolle  & 
Wassermann).  2.  Aufl.  Jena,  1913,  v,  660-702. 

Porter  (A.  E.).  The  precipitin  reaction  in  tuberculosis.  J.  Infect.  Dis.,  Chicago,  1910,  vii, 
87-98. 

Webb  (G.  B.}.  Immunity  in  tuberculosis.  Further  experiments.  J.  Am.  M.  Ass.,  Chi- 
cago, 1914,  Ixiii,  1098-1104. 

Wigharn  (J.  T.).  Upon  the  agglutination  test  in  the  diagnosis  of  tuberculosis.  J.  Hyg., 
Cambridge,  1906,  vi,  212-214. 

4.     Acute  Millar y  Tuberculosis 

Benda  (C.).     Die  akute  Miliartuberculose  vom  dtiologischen  Standpunkt.     In:  Ergebn.  d. 

allg.   Pathol.    (Lubarsch-Osterlag) ,  Wiesbaden,  1898,  J.  F.  Bergmann,   v, 

447-481- 
Cornet  (G.}.     Acute  general  miliary  tuberculosis.     New  York,  1914,  P.B.  Hoeber.    107  p. 

Steinitz  (E.)  &  Rostoki  (O.).  Die  akute  Miliartuberkulose.  In:  Handb.  d.  inn.  Med. 
(Mohr  &  Staehelin),  1911,  i,  856-875. 

5.  Tubercle  Bacilli  in  the  Blood 

Anderson  (J.  F.).  The  presence  of  tubercle  bacilli  in  the  circulating  blood  in  clinical  and 
experimental  tuberculosis.  Washington,  1909,Gov't  Print.  Office.  42  p.  8°. 

Berry  (Jane  L.}.     Tubercle  bacilli  in  the  blood.    J.  Infect.  Dis.,  Chicago,  1914,  xiv,  162-175. 

Klopstock  (F.)  &  Seligmann  (F,.).  Zur  Frage  des  Vorkommens  von  Tuberkelbacillen  im 
strfimendenBhU.  Ztschr.f.  II yg.,  Berlin,  1913,  Ixxvi,  77-96. 

Rist  (E.),  Leon-Kindberg  &  Cain  (A.).  Etude  analomo-pathologique  sur  un  cas  de 
bacillemie  tuberculeuse  massive,  terminate  avec  endocardite  vegetante, 
nephrite  el  anemia  pernicieuse.  Arch.  d.  med.  exper.,  etc.,  Paris,  1913, 
xxv,  106-193. 

6.   Tuberculosis  in  Cliildlwod 

v.  Behring  (F,.).  Ueber  alimenldre  Tuberkuloseinfektionen  im  Sauglingsalter.  Beitr.  z. 
Klin.  d.  Tuberk.,  Wurzburg,  1904,  Hi,  83-100. 

Brown  (P.  K.).  Primary  infection  ivith  tubercle  bacilli,  unth  special  reference  to  the  thoracic 
glands.  Tr.  Ass.  Am.  Physicians,  Philadelphia.,  1913,  xxviii,  408-420. 

Caloe  (J.)  &  Lelievre  (//.)•  Radiography  of  the  vertebral  column  in  profile  in  Pott's  disease. 
Am.  J.  Orthop.  Surg.,  1914,  xi,  193-206. 

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... 


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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 

Austen  (E.  E.}.    Blood-sucking  and  other  flies  known  or  likely  to  be  concerned  in  the  spread 
of  disease.     In:  Syst.  Med.  (Allbutt  &  Rottestori).     8°.    London,  1910.  ii, 
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. 

349  p.,  4  Pi;  8°. 

Castellani  (A.)  &  Chalmers  (A.  J.).  Manual  of  tropical  medicine.  2d  ed.  London, 
1913,  Bailliere,  Tindall  &  Cox.  1779  p.  8°. 

Doflein  (F.).    Lehrbuch  der  Proiozoenkunde.     3d  ed.    Jena,  1911 ,  G.  Fischer.     1043  p. 

Doflein  (F.)  &  Koehler  (O.).  Ueberblick  uber  den  Stamm  der  Protozoen.  In:  Handb.  d. 
pathogen.  Mikroorg.  (Kolle  &  Wassermannfr.  2.Aufl.  Jena.  1913,  vii, 
1-166. 

Jeanselme  (E.}  &  Rist  (E.}.  Precis  de  pathologic  exotique.  Paris,  1909,  Maison  &  Cie. 
821  p.  8°. 

Lambert  (H.  C.}.  A  practical  handbook  of  the  tropical  diseases  of  Asia  and  Africa.  Lon- 
don, 1914,  C.  Griffin  &  Co.,  Ltd.  324  P-  6  pi. 

Le  Dantec  (A.).  Precis  de  pathologic  exotique  (Malades  des  pays  chauds  et  des  pays  froids). 
3d  ed.  2  v.  Paris,  1911,  0.  Doin  etflls.  757  &  1102  pp.  8°. 

Mense  (Carl}.  Handbuch  der  Tropenkrankheiten,  unter  Mitwirkung  von  A.  Baelz,  P. 
Bassett-Smith,  P.  van  Brero  [etc.],  Hrsgb.  von  C.  Mense.  2.  Aufl.  3  Bde.. 
Leipzig,  1913-15,  J.  A.  Barth.  4°- 

Minchin  (E.  A.}.  An  introduction  to  the  study  of  the  protozoa,  with  special  reference  to  the 
parasitic  forms.  London,  1912,  E.  Arnold.  520  p. 

Netter  (A.},  Mosny  (E.)  [et  al.].  Maladies  exotiques.  Paris,  1912,  J.  B.  Balliere  &  fils. 
440  P-  8°.  [Nouv.  traite  de  med.  de  therap.,  vi.] 

Neuman  (Rudolf  Otto)  &  Mayer  (Martin).  Atlas  und  Lehrbuch  wichtiger  tierischer 
Parasiten  und  ihrer  Uebertrager,  mil  besonderer  Berucksichtigung  der 
Tropenpatholo'gie.  Munchen,  1914,  J.  F.  Lehmann.  673  p. 

Nuttall  (G.  H.  F.).  Lectures  on  the  Herter  Foundation:  I.  Spirochaetosis.  II.  Trypan- 
osomiasis.  III.  Piroplasmosis.  Johns  Hopkins  Hosp.  Bull.,  Baltimore, 
1913,  xxiv,  33-39,  83-89,  307-316. 

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). 

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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 


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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  "^ 

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01  a 

5  a 

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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 


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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 

Fournier  (A.).  Treatment  of  syphilis  and  prophylaxis  of  syphilis.  English  translation  of 
the  2d  ed.  (revised  and  enlarged),  by  C.  F.  Marshall.  London,  Rebman 
Co.,  1906.  275  p.  8°. 

The  prophylaxis  of  syphilis.  Translation  by  C.  F.  Marshall.  London, 
1906,  Rebman.  219  p.  8°.  Bound  with  Fournier  (A.),  The  treatment 
of  syphilis. 

Hutchinson  (J.).    Syphilis.    In:  Syst.  Med.  (Allbutt  &  Rolleston).    8°.    London,  1909, 
ii,  pt.  1,  843-381. 
Syphilis.     New  and  enlarged  edition.    London,  1909.     12°. 

Keyes,  Jr.  (E.  L.).    Syphilis.     New  York  &  London,  1908,  D.  Appleton  &  Co.    577  p.' 8°. 

Osier  (Sir  William).  Syphilis.  Mod.  Med.  (Osier).  8°.  Philadelphia  &  New  York, 
2d  ed.,  1914,  ii,  144-215. 

Power  (D'Arcy)  &  Murphy  (J.  K.).  System  (A)  of  syphilis  in  six  volumes.  Edited  by 
D'Arcy  Power  and  J.  Keogh  Murphy,  with  an  introduction  by  Jonathan 
Hutchinson.  London,  1908-1910f  H.  Frowde  and  Hodder  &  Stoughton. 

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- 
trand's  "Lehrb.  d.  klin.  Untersuchungsmethoden,"  published 
by  Urban  &  Schwarzenberg,  Berlin.) 


PATHOGENIC    MASTIGOPHOEA,    OR   FLAGELLATA       377 

2.  Etiology ;  Treponema  pallidum 

Fournier  (A.}.    Syphilis  and  marriage.     Transl.  by  R.A.  Morrow.     New  York,  1882.     12°. 

Metchnikoff  (E.)  &  Roux  (E.).     Recherches  experimentales  sur  les  singes  anthropoides. 
Bull.  Acad.  de  med.,  Paris,  1903,  3e  s.,  i,  101-108.     Also:   [Abstr.]  Bull, 
de  I'Inst.  Pasteur,  Paris,  1903,  i,  620. 
Etudes  experimentales  sur  la  syphilis.     Ann.  de  I'Inst.  Pasteur,  Paris, 

1903,  xvii,  809-821. 

Etudes  experimentales  sur  la  syphilis.    Ann.  de  VInst.  Pasteur,  Paris, 

1904,  xviii,  1-6.     Also:  [Abstr.]  Bull,  de  I'Inst.   Pasteur,   Paris,  1904, 
ii,  178. 

Etudes  experimentales  sur  la  syphilis.     Ann.  de  I'Inst.  Pasteur,  Paris, 

1904,  xviii,  657-671.     Also:  [Abstr.]  Bull,  de  I'Inst.  Pasteur,  Paris,  1905, 
Hi,  73. 

Eludes  experimentales  sur  la  syphilis.     Ann.  de  I'Inst.  Pasteur,  Paris, 

1905,  xix,  673-698.     Also:  [Abstr.]  Bull,  de  I'Inst.  Pasteur,  Paris,  1906, 
iv,  116. 

Recherches  microbiologiques  sur  la  syphilis.  Bull.  Acad.  de  med.,  Paris, 
1905,  3e  s.,  liii,  468-476.  Also:  [Abstr].  Bull,  de  I'Inst.  Pasteur,  Paris, 
1905,  Hi,  451. 

Miihlens  (P.).  Treponema  pallidum.  In:  Handb.  d.  pathogen.  Protoz.  (Prowazek), 
Leipzig,  1912,  i,  361-473. 

Neisser  (A.),  Baermann  (G.)  &  Halberstadter  (L.).  Versuche  zur  Uebertragung  der 
Syphilis  auf  Affen.  Deutsche  med.  Wchnschr.,  Leipzig  &  Berlin,  1906, 
xxxii,  1;  49;  97. 

Nichols  (H.  J.).  Observations  on  a  strain  of  Spirochceta  pallida  isolated  from  the  nervous 
system.  J.Exper.  Med.,  Lancaster,  Pa.,  1914,  xix,  362-371. 

Noguchi  (H.}.     A  method  for  the  pure  cultivation  of  pathogenic  treponema  pallidum  (Spiro- 
chceta pallida).     J.  Exper.  M.,  Lancaster,  Pa.,  1911,  xiv,  99-108. 
The  direct  cultivation  of  Treponema  pallidum  pathogenic  for  the  monkey. 
J.  Exper.  M.,  Lancaster,  Pa.,  1912,  xv,  90-100. 

A  method  for  cultivating  Treponema  pallidum  in  fluid  media.  J.  Exper. 
M.,  Lancaster,  Pa.,  1912,  xvi,  211-215. 

Experimental  research  in  syphilis,  with  special  reference  to  Spirochceta 
pallida  (Treponema  pallidum).  J.  Am.  M.  Ass.,  Chicago,  1912,  Iviii, 
1163-1172. 

Schaudinn  (F.)  &  Hoffmann  (E.).  Ueber  Spirochdtenbefunde  im  Lymphdriisensaft 
Syphilitischer.  Arb.  a.  d.  k.  Gsndhtsamte.,  Berlin,  1905,  xxii,  527-534. 
Also:  Deutsche  med.  Wchnschr.,  Leipzig  &  Berlin,  1905,  xxxi,  711-714. 

Schereschewsky  (/.)•  Vereinfachung  des  Verfahrens  zur  Reinzuchtung  der  Syphilisspi- 
rochdten.  Deutsche  med.  Wchnschr.,  Leipzig  u.  Berlin,  1913,  xxxix,  1408. 

Sobernheim  (G.).  Syphilisspirochdte  (Spirochceta  pallida  s.  Treponema  pallidum  Schau- 
dinn). In:  Handb.  d.  pathogen.  Mikroorg.  (Kolle  &  Wassermann). 
2.  Aufl.  Jena,  1913,  vii,  745-834. 

Zinsser  (H.)  &  Hopkins  (J.  G.).  The  viability  of  the  Spirochceta  pallida  in  diffuse  light 
at  room  temperature.  J.  Am.  M.  Ass.,  Chicago,  1914,  Ixii,  1802-1803. 


3.  Reinfection 

Benario  (/.)•  Die  Reinfektionen  bei  Syphilis.  Nach  den  Erfahrungen  der  letzten  Jahre 
dargestellt.  Samml.  zwangl.  Abhandl.  a.  d.  Geb.  d.  Dermat.  [etc.],  Halle 
a.  S.,  1913-1914,  Hi,  1-127. 

Pinard  (M.).  .L'immunite  dans  la  syphilis;  superinfection  et  reinfection  syphilitiques, 
Paris,  1910.  8°. 

Richards  (T.  W.).  Early  reinfection  with  syphilis.  U.  S.  Naval  M.  Bull,  Washington, 
1915,  ix. 

Schleicher  (M.).  Reinfectio  syphilitica  vom  Standpunkte  der  modernen  Syphilisforschung. 
Dermatol.  Ztschr.,  Berlin,  1914,  xxi,  397-428. 


378  DIAGNOSIS    OF    INFECTIOUS    DISEASES 


4.  Clinical 

Adamson  (H.  A.}.  A  clinical  lecture  on  the  skin  eruptions  of  syphilis,  and  their  diagnosis. 
Clin.  J.,  London,  1915,  xliv,  217;  223;  225. 

Audrain  (/.)•    La  syphilis  obscure.     Paris,  1911.     8°. 

Baeslack  (F.  W.).    A  sero-enzyme  diagnosis  of  syphilis.    J.  Am.  M.  Ass.,  Chicago,  1914, 

Ixii,  1002-1004. 
Boas   (Harold).     Die   Wassermann'sche   Reaktion  mil  besonderer  Beriicksichtigung  ihrer 

klinischen  Verwerlbarkeit.    Berlin,  1911,  S.  Karger.     192  p.     8°. 

Billings  (F.).     Visceral  syphilis.    J.  Am.  M.  Ass.,  Chicago,  1911,  Mi,  1653-1656. 

Bruck  (C.).  Immunitdt  bei Syphilis.  In:  Handb.  d.  pathogen.  Mikroorg.  (Kolle  &  Wasser- 
mann).  2.  Aufl.  Jena,  1913,  vii,  1045-1086. 

Brugsch  (T.)  &  Schneider  (E.}.  Syphilis  und  Magensymptome.  Berl.  klin.  Wchnschr., 
1915,  Hi,  601-606. 

Carson-White  (E.  P.)  &  Ludlum  (S.  D.  W.).  Syphilitic  tests  in  latent  and  treated 
syphilis.  J.  Nerv.  &  Ment.  Dis.,  New  York,  1914,  xli,  286-291. 

Cole  (H.  N.}  &  Eng-Kiu  Chiu  (5.).  The  coagulation  test  for  syphilis  as  devised  by  Hirsch- 
feld  and  Klinger.  Arch.  Int.  M.,  Chicago,  1915,  xvi,  880-889. 

Corner  (E.  M.}.  Sepsis  in  the  recognition  and  non-recognition  of  syphilis.  Lancet,  London, 
1914,  ii,  491-492. 

Bowling  (O.).     Hygiene  of  syphilis.    South.  M.  J.,  Nashville,  1913,  vi,  28-35. 

Ehrlich  (Paul}.  Experimental  chemotherapy  of  spirilloses.  New  York,  1911,  Rebman  Co. 
181  p.  5  pi. 

Ellis  (A.  W.  M.)  &  Swift  (H.  F.).  The  cerebrospinal  fluid  in  syphilis.  J.  Exper.  M., 
Lancaster,  Pa.,  1913,  xviii,  162-182. 

Erb  (W.).  Betrachtungen  uber  die  neueste  Gestaltung  des  Begriffs  und  Wesen  des  Metalues. 
Deutsche  Ztschr.f.  Nervenheilk.,  Leipzig,  1913,  I,  55-60. 

Finger  (E.).  The  treatment  of  syphilis.  English  transl.  by  C.  F.  Marshall.  London  &  New 
York.  1906.  8°. 

Gordon  (A.").  Intrathecal  intracranial  injection  of  autoneosalvarsanized  serum  for  syphilitic 
headache.  J.  Am.  M.  Ass.,  Chicago,  1915,  Ixv,  1545-1547. 

Graves  (W.  W.).  Can  rabbits  be  infected  with  syphilis  directly  from  the  bloods  of  general 
paretics?  Observations  on  the  recognition  of  the  virus  in  the  later  periods 
of  the  disease.  J.  Am.  M.  Ass.,  Chicago,  1913,  Ixi,  1504-1509. 

Hazen  (H.  H.}.     The  leucocytes  in  syphilis.    J.  Cutan.  Dis.,  N.  Y.,  1913,  xxxi,  618;  739. 

Hoover  (C.  F.}.  Report  of  cases  of  syphilis  of  the  viscera.  Cleveland  M.  Gaz.,  1899-1900, 
xv,  859-365. 

Hutchinson  (J.}.  The  eruptions  of  syphilis  (syphilodermia) .  In:  Syst.  Med.  (Allbutt  & 
Rolleston).  8°.  London,  1911,  ix,  505-515. 

Jones  (F.  A.).  Visceral  syphilis,  with  special  reference  to  its  early  effects  upon  the  heart  and 
kidneys.  Memphis  M.  Month.,  1912,  xxxii,  221-231. 

Kraus  (H.}.  Fieber  als  einziges  Symptom  latenter  Lues.  Wien.  klin.  Wchnschr.,  1913, 
xxvi,  2030-2033. 

Leschly  (W.)  &  Boas  (H.).  Untersuchungen  uber  eine  Modifikation  der  Herman-Perutz- 
schen  Reaktion.  Ztschr.  f.  Immunitdtsforsch.  Jena,  1913,  Orig.,  xix, 
615-622. 

Lynch  (K.  M.),  Mclnnes  (B.  K.)  &  Mclnnes  (G.  F.).  Concerning  syphilis  in  the 
American  negro.  South.  M.  J.,  Nashville,  viii,  450-456. 

McDonagh  (J.  E.  R.).  Salvarsan  in  syphilis  and  allied  diseases.  London,  1912,  H. 
Frowde.  152  p.  8°. 

Miller  (Florence  W.).  The  advantage  of  the  Noguchi  technique  in  the  diagnosis  of  syphilis. 
Interstate  M.  J.,  St.  Louis,  1913 ,  xx,  145-148, 


PATHOGENIC    MASTIGOPHOKA,    OR   FLAGELLATA      379 

Noguchi  (H.).    A  cutaneous  reaction  in  syphilis.    J.  Exper.  M.,  Lancaster,  Pa.,  1911,  xiv, 

557-568. 

Pusey  (W.  A.).  The  present  situation  in  syphilis.  Am.  J.  M.  Sc.,  Philadelphia  &  New 
York,  1913,  cxlvi,  497-512. 

Sabin  (B.).  Etude  de  la  loi  de  Profeta  par  la  sero-reaction  de  Wassermann.  Ann.  d  malad 
vener.,  Paris,  1913,  viii,  263-281. 

Southard  (E.  E.).  Statistical  notes  on  a  series  of  6,000  Wassermann  tests  for  syphilis  per- 
formed in  the  Harvard  neuropathological  testing  laboratory,  1913.  Boston 
M.  &S.J.,  1914,  clxx,  947-950. 

Stevenard  (Louis).    Le  secret  medical  et  la  syphilis.     Paris,  1905.     122  p.     8°. 

Taylor  (George  G.  Stop  ford)  &  Mackenna  (Robert  William).  The  salvarsan  treat- 
ment of  syphilis  in  private  practice,  with  some  account  of  the  modern  methods 
of  diagnosis.  London  [1914],  W.  Heinemann.  102  p. 

Uhlenhuth  (Paul  [Theodor]).  Experimentelle  Grundlagen  der  Chemotherapie  der  Spiro- 
chdtenkrankheiten,  mit  besonderer  Berucksichtigung  der  Syphilis.  Gesam- 
melte  Abhandlungen.  Berlin  &  Wien,  1911 ,  Urban  &  Schwarzenberg. 
319  p.  4  pi.  4°. 

War  thin  (A.  S.).  The  persistence  of  active  lesions  and  spirochetes  in  the  tissues  of  clinically 
inactive  or  "cured"  syphilis.  Tr.  Ass.  Am.  Physicians,  Philadelphia, 
1914,  xxix,  416-429. 

von  Wassermann  (A.)  &  Lange  (C.).  Serodiagnostik  der  Syphilis  (Wassermann' sche 
Reaktion).  In:  Handb.  d.  pathogen.  Mikroorg.  (Kolle  <fe  Wassermann). 
2.  Aufl.  Jena,  1913,  vii,  951-1044. 

Wollstein  (Martha)  &  Lamar  (R.  V.).  The  presence  of  antagonistic  substances  in  the 
blood  serum  in  early  and  late  syphilis  and  in  paresis  and  tabes.  Arch. 
Int.  Med.,  Chicago,  1908,  i,  314-319. 

Zinsser  (H.).  The  Wassermann  reaction.  In:  Infection  and  resistance  (H.  Zinsser),  New 
York,  1914,  198-211. 

5.   Congenital  Syphilis 

Berkowitz  (S.).  Late  congenital  syphilis;  report  of  an  unusual  type,  with  post-mortem  notes. 
N.  York  M.  J.  [etc.],  1915,  cii,  131-134. 

Fournier  (Alfred).    L'heredite  syphilitique.     Paris,  1891.     8°. 

La  syphilis  hereditaire  tardive.     Paris,  1886.     8°. 

A  propos  de  la  prophylaxie  et  du  traitement  de  Vheredo-syphilis.    Quatre 

fautes  d  ne  pas  commettre.     Paris  [1910],  C.  Delagrave.     136  p.     12°. 

Fournier  (Edmond).    Stigmates  distrophigues  de  Vheredo-syphilis.     Paris,  1898.     8°. 

Recherche  et  diagnostique  de  Vheredo-syphilis  tardive.     Paris,  1907,  Masson 
&  Cie.     416  p.     1  pi.     8°. 

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. 

Rietschel  (H.).  Das  Problem  der  Uebertragung  der  angeborenen  Syphilis.  Ergebn.  d. 
inn.  Med.  u.  Kinderh.,  Berlin,  1913,  xii,  160-195. 

Yerington  (H.  H.)  &  Holsclaw  (F.  M.).  A  consideration  of  tardy  syphilis.  Am.  J. 
Dis.  Child.,  Chicago,  1914,  vii,  32-40. 

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 

Bezold  (F.).  Die  Krankheiten  des  Warzentheiles.  Handb.  d.  Ohrenheilk.  (Schwartze) . 
Leipzig,  1893,  U,  299-351. 

Bishop  (S.  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  und  Folgen  der  Erkrankungen  des  Warzenteils  und  ihre Behand- 
lung.  Samml.  zwangl.  Abhandl.  a.  d.  Geb.  d.  Nasen-,  Mund-  u.  Halskr., 
Halle  a.  S.,  1900,  Hi,  12.  HfL,  1-65. 

Katz  (L.),  Preysing  (//.)  &  Blumenfeld  (F.).  Handbuch  der  speziellen  Chirurgie  des 
Ohres  und  der  oberen  Luftwege.  Wurzburg,  1912. 

Lamacq  &  Dormoy.  Semeiologie  des  ganglions  mastoidiens  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. 

Oppenheirner  (S.).  The  venous  system  of  the  temporal  bone  and  Us  relation  to  the  compli- 
cations of  mastoid  disease.  Tr.  Am.  Laryngol.,  Rhinol.  &  Otol.  Soc.,  1902, 
New  York,  1903,  viii,  295-306. 

Masioid  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.  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. 
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Leipzig,  1910,  c,  204-220. 

Sjoblom  (J.  Ch.).  Experimentelle  Untersuchungen  uber  den  Einfluss  einiger  zentripetaler 
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1915,  cxvii,  397-418. 

Venza  (A.).  Respiratorische  Neurosen  traumatischen  Ursprungs  und  deren  Simulation. 
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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 

1.   General 

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Cloetta  (M.)  &  Anderes  (E.).  Zur  Kenntniss  der  Lungenvasomotoren.  Arch.  f.  exper. 
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Cole  (R.  /.).  Treatment  of  pneumonia  by  means  of  specific  serums.  J.  Am.  M.  Ass., 
Chicago,  1913,  Ixi,  663-666. 

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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., 
Chicago,  1914,  xxvi,  316-321. 

Dreschfeld  (/.)•  On  creeping  pneumonia  (pneumonia  migrans)  and  its  relation  to  epidemic 
pneumonia.  Med.  Chron.,  Manchester,  1885,  ii,  353-364. 

Edgeworth  (F.  H.}.  On  the  cerebral  symptoms  of  lobar  pneumonia  in  children.  Bristol 
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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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Hare  (H.  A.)»  The  ratio  of  blood-pressure  to  pulse-rate  in  croupous  pneumonia  from  a 
diagnostic  and  therapeutic  standpoint.  Therap.  Gaz.  [etc.],  Detroit,  1910, 
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. 
Sc.,  Philadelphia  &  New  York,  1908,  n.  s.  cxxxvi,  645-658. 

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- 
delphia, 1907,  n.  s.,  cxiii,  1-10. 

Parkinson  (/.)•  ^  clinical  trial  of  aethylhydrocuprein  in  pneumonia.  Ztschr.  f.  Chemo- 
therap.  [etc.],  Leipzig,  1913,  ii,  Orig.,  1-10. 

Porter  (W.  T.),  Newburgh  (L.  H.}  &  Newburgh  (/.)•  The  state  of  the  vasomotor  appara- 
tus in  pneumonia.  Am.  J.  Physiol.,  Baltimore,  1914,  xxv,  1-14- 

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" 
et  la  radioscopie.  Ann.  d.  med.  et  chirurg.  infant.,  1913,  xvii,  275-280. 

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- 
field, 1905,  vii,  145-149. 

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- 
caster, Pa.,  1912,  xvi,  693-700. 

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 
lobar  pneumonia  and  the  susceptibility  of  pneumococcus  strains  to  univalent 
antipneumococcus  serum.  J.  Exper.  M.,  Lancaster,  Pa.,  1912,  xvi,  680- 
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. 

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tuberculose  pulmonaire.  Ann.  d.  schweiz.  balneol.  Gesellsch.,  Aarau,  1914, 
Heft  10,  62-65. 

Thomson  (H.  H.).    Consumption  in  general  practice.    London,  1912,  H.  Frowde.    350  p. 

8  . 

Trudeau  (E.  D.).     The  sanitarium  treatment  of  incipient  pulmonary  tuberculosis  and  its 
results.     Tr.  Ass.  Am.  Phys.,  Philadelphia,  1900,  xv,  36-51. 
The  sanitarium  treatment  of  tuberculous  patients,  with  some  interesting 
historical  data.     Am.  Med.,  Burlington,  Vt.  &  New  York,  1915,  n.  s.,  x, 
13-20. 

Trudeau  (E.  £,.)•  The  history  and  work  of  the  Saranac  Laboratory  for  the  study  of  tuber- 
culosis. Johns  Hopkins  Hosp.  Bull.,  Baltimore,  1901,  xii,  271-275. 

Williamson  (A.  M.).  Housing  and  tuberculosis.  Brit.  J.  Tuberculosis.,  London,  1915 1  ix, 
111-125. 


NOTE. — For  other  references,  see  Tuberculosis,  in  Part  IV. 


DISEASES    OF    THE    LUNGS  627 

2.  Etiological;  Experimental 

Bacmeister  (A.).  Wesen  und  Gang  der  tuberkulosen  Infektion  bei  Entstehung  der  mensch- 
lichen  Lungenphthise.  Ergebn.  d.  inn.  Med.  u.  Kinderh.,  Berlin, 
1913,  xii,  515-552. 

Besredka  (A.).  Du  serodiagnostic  de  la  tuberculose  au  moyen  de  I'antigene  a  I'ceuf.  Paris 
med.,  1913-14,  xv,  219-223. 

Ueber  die  Fixationsreaktion  bei  Tuberculose  der  Meerschweinchen,  Kanin- 
chen  und  Menschen.  Ztschr.  f.  Immunitdtsforsch.  u.  exper.  Therap., 
Jena,  1914,  Orig.,  xxi,  77-82. 

Besredka  (A.)  &  Manoukhine  (/.)•  De  la  reaction  de  fixation  chez  les  tuberculeux.  Ann. 
de  I'lnst.  Pasteur,  Paris,  1914,  xxviii,  569-575. 

Brown  (L.),  Heise  (F.  H.)  &  Petroff  (S.  A.).  Ueber  das  Vorkommen  von  Tuberkelbazillen 
imBlutevon  Patienten  mil  Lungentuberkulose.  Ztschr.  f.  Tuberk.,  Leipzig, 
1915,  xxiv,  97-101. 

Carrington  (P.  M.).  Interstate  migration  of  tuberculous  persons;  its  bearing  on  the  public 
health,  ivith  reference  to  the  State  of  California.  Pub.  Health  Rep.,  Wash- 
ington, 1915,  xxx,  826-84.1 . 

Courmont  (P.)  &  Delorme.  Causes  d'erreur  et  valeur  de  reaction  de  Moriz-Weiss.  Lyon 
med.,  1914,  cxxiii,  77. 

Davies  (H.  M.).  A  consideration  of  the  influence  of  the  first  costal  cartilage  on  apical  tuber- 
culosis, based  on  a  study  of  402  specimens.  Brit.  J,  Surg.,  1913,  i,  55-69. 

Dunges  (A.}.  Untersuchungen  und  Betrachtungen  zur  Aetiologie  und  Therapie  der  Lungen- 
tuberkulose. Beitr.  z.  Klin.  d.  Tuberk.,  Wurzburg,  1907,  vii,  7-25. 

Evans  (H.  M.),  Bowman  (F.  B.)  &  Winter  nit  z  (M.  C.).  An  experimental  study  of  the 
histogenesis  of  the  miliary  tubercle  in  vitally  stained  rabbits.  J.  Exper.  M., 
Lancaster,  Pa.,  1914,  xix,  282-302.  4  pi- 

Foster  (A.  D.),  Interstate  migration  of  tuberculous  persons;' its  bearing  on  the  public  health, 
with  special  reference  to  the  States  of  North  and  South  Carolina.  Pub. 
Health  Rep.,  Washington,  1915,  xxx,  74-5-774- 

Fowler  (O.  S.}  &  Philpott  (J.  A.).  An  experimental  study  to  determine  the  relation  of 
tubercle  bacilluria  to  pulmonary  tuberculosis.  Colorado  Med.,  Denver, 
1915,  xii,  48-53. 

Garvin  (A.  H.).  The  evidence  of  immunity  in  tuberculosis;  the  development  of  phthisis; 
the  first  infection;  the  second  infection.  Albany  M.  Ann.,  1915,  xxxvi, 
384-391. 

Grulee  (C.  G.)  &  Harms  (F.).  Tuberculosis  as  a  disease  of  the  newborn.  Am.  J.  Dis. 
Child.,  Chicago,  1915,  ix,  322-330. 

Hamburger  (F.).  Was  verdankt  die Lehre  von  der  Tuberkulose  der  experimentellen  Medizin? 
Beitr.  z.  Klin.  d.  Tuberk.,  Wurzburg,  1914,  xxxii,  49-65. 

Hart  (C.).  Die  anatomische  Grundlagen  der  Disposition  der  Lungen  zu  tuberkuloser  Er- 
krankung.  In:  Ergebn.  d.  allgem.  Pathol.  [etc.]  (Lubarsch  &  Ostertag). 
Wiesbaden,  1910,  xiv,  AU.  i,  337-428. 

Betrachtungen  iiber  die  Entstehung  der  tuberkulosen  Lungenspitzen- 
phthise.  Ztschr.  f.  Tuberk.,  Leipzig,  1915,  xxiii,  313-327;  xxiv,  87-96. 

Hekman  (/.)•  A  new  method  of  serological  research  for  the  first  time  applied  to  sufferers 
from  tuberculosis.  Folia  microbiol.,  Delft,  1914,  Hi,  126-140. 

Hinsdale  (Guy).  Atmospheric  air  in  relation  to  tuberculosis.  Washington,  1914,  Smith- 
son.  Inst.  146  p.  93  pi.  8°. 

Holitscher  (A.).  Alkohol  und  Tuberkulose.  Internal.  Monatschr.  z.  Erforsch.  d.  Alko- 
holismus  [etc.],  Basel,  1914,  xxiv,  285-288. 

Jobling  (J.  W.)  &  Petersen  (W.).  Fermenthemmungskorper  der  Tuberkelbazillen.  Ztschr. 
f.  Tuberk.,  Leipzig,  1914,  xxii,  521-526. 

Kaiser  (F.).     Rontgenologische  Studien  iiber  die  Beziehungen  zwischen  Rippenknorpelver- 
knocherung  und  Lungentuberkulose.    Beitr.  z.    Klin.  d.  Tuberk.,   W 
,  1914,  xxxii,  67-93. 


628     DISEASES    OF    THE    RESPIRATORY    APPARATUS 

Landis  (H.  R.  M.)«  The  pottery  industry  and  its  relation  to  tuberculosis.  Am.  J.  Pun 
Health,  New  York,  1914,  iv,  739-753. 

Letulle  (M.)«  Le  role  de  la  cohabitation  dans  la  transmission  de  la  luberculose  humaine 
d'apres  les  experiences  de  M.  Chausse.  Rev.  d'hyg.,  Paris,  1914,  xxxvi, 
799-812. 

Lewis  (P.  A.}  &  Montgomery  (C.  M.}.  Experimental  pulmonary  tuberculosis  in  the 
dog.  The  effect  of  large  amounts  of  tubercle  bacilli  of  bovine  type  intro- 
duced directly  into  the  lungs  by  way  of  the  air  passages.  J.  Exper.  M., 
Lancaster,  1913,  xvii,  527-534. 

Moss  (W.  L.}.  An  attempt  to  immunize  calves  against  tuberculosis  by  feeding  the  milk  of 
vaccinated  cows.  Johns  Hopkins  Hosp.  Bull.,  Baltimore,  1915,  xxvi, 
241-245. 

Park  (W.  H.).  The  transmission  of  tuberculosis  in  childhood.  Arch.  Pediat.,  New  York, 
1915,  Ixxxviii,  337. 

Petroff  (S.  A.).  A  new  and  rapid  method  for  the  isolation  and  cultivation  of  tubercle  bacilli. 
directly  from  the  sputum  and  feces.  J.  Exper.  M.,  Lancaster,  Pa.,  xxi, 
38-42. 

von  Pirquet  (C.).  Bronchogeneous,  placentogeneous,  dermatogeneous  and  entcrogeneous  in- 
fection with  tuberculosis  in  infancy.  J.  State  Mcd.,  London,  1915,  xxiii, 
16-20. 

Radcliffe  (J.  A.  D.).  Mixed  and  secondary  infections  in  pulmonary  tuberculosis.  Ztschr. 
f.  Tuberkul,  Berlin,  1913,  xxi,  24;  258. 

Schultze  (W.  //.)•  Anomalien  des  ersten  Rippenringes  und  Lungentuberkulose  mil  bcson- 
derer  Berucksichtigung  der  Hartschcn  Lehre  von  der  mechanischen  Dis- 
position derLungen  zur  tuberkulosen  Phthise.  Beilr.  z.  Klin.  d.  Tuberkul., 
Wurzburg,  1913,  xxvi,  205-236. 

Smith  (T.)  &  Fabyan  (M.).  The  vaccination  of  cattle  against  tuberculosis.  III.  The 
occasional  persistence  of  the  human  type  of  tubercle  bacillus  in  cattle.  J.  M. 
Research,  Boston,  1915,  xxii,  523-537. 

Sweet  (E.  A.}.  Interstate  migration  of  tuberculous  persons;  its  bearing  on  the  public  health, 
with  special  reference  to  the  Slates  of  Texas  and  New  Mexico.  Pub. 
Health  Rep.,  Washington,  1915,  xxx,  1225-1255.  2  pi. 

Tendeloo  (N.  P.).  Ueber  lymphogen?  Ausbreitung  der  Tuberkulose  beim  Mcnschen.  Wien. 
med.  Wchnschr.,  1915,  Ixv,  321-3*1. 

Weinberg  (W.}.  Lungenschioindsucht  beider  Ehegatten;  einBeitrag  zur  Lehre  von  der  Tuber- 
kulose in  derEhe.  Beitr.  z.  Klin.  d.  Tuberk.,  Wurzburg,  1906,  v,  365-398. 

Zbinden  (T.}.  Present  day  methods  for  finding  the  tubercle  bacillus.  Ohio  M.  J.,  Columbus, 
1914,  x,  666-669. 

Zueblin  (E.)  &  Proescher  (F.).  Volatile  substances  isolated  from  tubercle  bacilli  cultures 
and  their  effects  on  experimental  tuberculosis.  Am.  Med.,  Burlington,  Vt., 
&  New  York,  1914,  n.  s.,  ix,  578-582. 

3.  Pathological- Anatomical 

Landis  (H.  R.  M.).  The  clinical,  anatomical  and  pathological  comparison  of  tuberculous 
cavities  in  the  lungs.  Am.  J.  M.  Sc.,  Philadelphia  &  New  York,  1906, 
n.  s.,  cxxx.ii  j  554-559. 

Nicol  (/£.)•  Die  Entwicklung  und  Einteilung  der  Lungenphthise.  Pathologisch-anatomische 
und  klinische  Betrachlungen.  Beitr.  z.  Klin.  d.  Tuberk.,  Wurzburg,  1914, 
xxx,  231-321. 

Wollstein  (Martha)  &  Bartlett  (F.  H.).  A  study  of  tuberculous  lesions  in  infants  and 
young  children,  based  on  post-mortem  examinations.  Am.  J .  Dis.  Child., 
Chicago,  1914,  viii,  362-376. 

Woodhead  (G.  S.).  The  incidence  of  tuberculosis  in  childhood;  bovine  tuberculosis  in  re- 
lation to  tuberculosis  in  the  child.  J.  State  Med.,  London,  1914,  xxii,  705- 
714. 


DISEASES    OF    THE    LUNGS  629 

4.  Clinical    . 

Bar  bier  (//".)•  Note  sur  un  cas  de  bronchoalveolite  bacillaire  caseeusa  aigue  chez  un  nourrisson 
de  trois  mois  et  demi.  Bull,  et  mem.  Soc.  med.  d.  hop.  de  Paris,  1915,  3.  s., 
xxxix,  312-314. 

Baumann  (F.  £,.)•  Kritische  Betrachtungen  der  Sympiome  der  Lungentuberkulose,  vor- 
wiegend  der  Friihsymptome.  Beitr.  z.  Klin.  d.  Tuberk.,  Wiirzburg,  1909- 
10,  xiv,  49-78. 

Bissell  (F.  5.)  &  Richards  (E.  T.  F.).  The  early  diagnosis  of  pulmonary  tuberculosis. 
Am.  J.  Roentgenol.,  Detroit,  1914-15,  n.  s.,  ii,  521-525. 

Bonney  {S.  G.).  Functional  nervous  disturbances  in  pulmonary  invalids.  J.  Am.  M.  Ass., 
Chicago,  1898,  xxxi,  1395-1398. 

Bronfenbrenner  (J.}.  The  complement-deviation  test  with  Besredka's  tuberculin  and  the 
occurrence  of  tuberculosis  among  syphilitics  as  diagnosed  by  this  test. 
Arch.  Int.  Med.,  Chicago,  1914,  xiv,  786-803. 

Bronfenbrenner  (/.),  Rockman  (/.)  &  Mitchell  (W.  J.},  Jr.  Comparisons  of  urinary 
and  serum  findings  in  the  diagnosis  of  tuberculosis.  Biochem.  Bull.,  New 
York,  1915,  iv,  80-85. 

Bronfenbrenner  («/.)  &  Schlesinger  (M.  /.)•  On  new  methods  of  serum  diagnosis  of 
tuberculosis.  Nat'l  Ass.  Study  &  Prev.  Tuberc.,  Washington,  1915,  242- 
247. 

Brown  (//.)•  Some  errors  in  the  diagnosis  of  pulmonary  tuberculosis.  Johns  Hopkins 
Hosp.  Bull,  Baltimore,  1914,  xxv,  112-117. 

Diagnostic  theses  in  pulmonary  tuberculosis.     J.  Am.  M.  Ass.,  Chicago, 
1915,  Ixiv,  1977. 

Cullender  (G.  R.}.  Roentgenography  in  pulmonary  tuberculosis.  Interstate  M.  J.,  St. 
Louis,  1915,  xvii,  598-603. 

Cohen  (S.  S.).  When  and  how  to  use  tuberculin  preparations  in  private  practice;  efficacy 
of  administration  by  mouth.  Am.  J.  M.  Sc.,  Philadelphia,  1915,  cxlix, 
81-96. 

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- 
dren. Am.  J.  Dis.  Child.,  Chicago,  1915,  ix,  405-417. 

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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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. 

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Napoli,  1914,  vii,  228,  275. 
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1914,  xv,  359;  375;  406;  4%2. 


DIAGNOSIS   OF   THE   MEDIASTINUM  691 

Cazzaniga  (A.).    Semeiologia  de  tumori  mediastinici;  considerazioni  suite  alterazioni  anato- 

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xv,  744;  759;  775;  788;  808. 
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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 

Adam  (A.).  Nervus  recurrens-Lahmung  bci  Mcdiastinilis.  Arch.  f.  Laryngol.  und  RhinoL, 
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°. 

Giffin  (H.  Z.}.    Luetic  mediastinitis:  a  report  of  five  cases.    Journal-Lancet,  Minneapolis, 

1914,  xxxiv,  183-185. 

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 

Allbutt  (T.  C.).     Cardiac  physics.     Phila.  M.  J,,  1900,  v,  212-222. 

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 
reference  to  accidental  murmurs.  Med.  News,  Philadelphia,  1895,  Ixvii, 
548-550. 

Certain  misconceptions  regarding  cardiac  murmurs  and  their  interpretation. 
Chicago  M.  Recorder,  1896,  xi,  161-167. 

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- 
murs, with  special  reference  to  life  insurance.  J.  Mich.  M.  Soc.,  Grand 
Rapids,  1915,  xiv,  275-282. 

M'Aldowie  (A.  A/.).  Cardiac  bruits  audible  at  a  distance  from  the  chest.  Edinb.  M.  J., 
1892-93,  xxxviii,  619-622. 

Martius  (F.).  The  time  of  heart  murmurs  and  the  significance  of  the  apex-beat.  Internal. 
Clin.,  Philadelphia,  1900,  9.  s.,  iv,  176-183. 

Moore  (N.}.  Cardiac  murmurs  audible  without  touching  the  chest.  St.  Barth.  Hosp.  Rep., 
London,  1890,  xxvi,  165-168. 

Naunyn  (B.).      Ueber  den  Grund,  weshalb  hin  und  wieder  das  systolische  Gerausch  bei  der 
Mitralinsufficienz  am   lautesten  in  der  Gegend  der   Pulmonalklappe  zu 
vernehmen  ist.    Berl.  klin.  Wchnschr.,  1868,  v,  189-190. 
Systolisches  Gerausch  am   Pulmonalostium  bei  Mitralinsufficienz.    Berl. 
klin.  Wchnschr.,  1868,  v. 

Oddo  (C.).  De  la  propagation  lointaine  des  grands  souffles  cardiaques.  Marseille  med., 
1893,  xxx,  601-613. 

Russell  (W.}.  The  differentiation  of  endocardial  murmurs.  Scot.  M.  &  S.  J.,  Edinburgh, 
1898,  Hi,  289-303. 

Sahli  (H.).  Die  Herzgerausche.  In:  Lehrb.  d.  klin.  Untersuchungsmethoden.  5.  Aufl. 
Leipzig  u.  Wien,  1909,  348-377. 

Ueber  diastolische  accidentelle  Herzgerausche.  Cor.-Bl.  f.  Schweiz.  Aerzte, 
Basel,  1895, .xxv,  33-42. 

Sherrington  (C.  5.).  Cardiac  physics.  Syst.  Med.  (Allbutt).  New  York  &  London, 
1898,  v,  464-479. 

Soulier  (//.)•  Souffles  cardiaques  par  lesion  orificielle;  rapport  entre  la  veine  fluide  (Chau- 
veau)  d'une  part,  d'autre  part  leur  siege  (maximum)  et  leur  propagation. 
Lyon  med.,  1899,  xci,  287-291. 

Stengel  (A.).  The  significance  of  systolic  murmurs  over  the  apex  and  base  of  the  heart. 
Cleveland  J.  M..  1898,  Hi,  191-203. 


740     DISEASES    OF    THE    CIKCULATOEY    APPAEATUS 

Thayer  (W.  S.).    On  the  commoner  types  of  functional  cardiac  murmur.     Canadian  Pract. 
&  Rev.,  Toronto,  1910,  xxxv,  481-494. 

Thayer  (W.  S.)  &  MacCallum  (W.  G.)»    Experimental  studies  of  cardiac  murmurs.    Am. 
J.  M.  Sc.,  Philadelphia,  1907,  n.  s.,  cxxxiii,  249-256. 

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 

Barker  (L.  F.).     Paroxysmal  arteriospasm  with  hypertension  in  the  gastric  crises  of  tabes. 
Am.  J.  M.  Sc.,  Philadelphia  &  New  York,  1910,  cxxxix,  631-638. 

Cantieri  (C.)»     Ipertensione  e  coleslerinemia.     Riv.  crit.  di  din.  med.t  Firenze,  1913,  xiv, 
657-667.     Also  in  Wien.  klin.  Wchnschr.,  1913,  xxvi,  1692-1698. 

Dale  (H.  H.)  &  Dixon  (W.  E.}.    The  action  of  pressor  amines  produced  by  putrefaction. 
J.  Physiol.,  London,  1909,  xxxix,  25-44. 


808    DISEASES    OF    THE    CIRCULATORY   APPARATUS 

Jane  way  (T.  C.}.  The  pathologiccl  physiology  of  chronic  arterial  hypertension  and  its 
treatment.  Am.  J.  M.  Sc.,  Philadelphia  &  New  York,  1907,  cxxxiii, 
60-55. 

When  should  the  general  practitioner  measure  the  Uood-pressure?     Albany 
M.  Ann.,  1911,  xxxii,  159-168. 

A  clinical  study  of  hypertensive  cardiovascular  disease.     Arch.  Int.  Med., 
Chicago,  1913,  xii,  755-798. 

A  study  of  the  causes  of  death  in  one  hundred  patients  with  high  blood 
pressure.    J.  Am.  M.  Ass.,  Chicago,  1912,  lix,  2106-2110. 
Nephritic  hypertension:  clinical  and  experimental  studies.     Am.  J.  M. 
Sc.,  Philadelphia  &  New  York,  1913,  cxlv,  625-656. 

Lawrence  (C.  H.).  The  relation  of  hypertension  to  urinary  excretion.  Am.  J.  M.  Sc., 
Philadelphia  &  New  York,  1912,  cxliv,  330-340. 

Lee  (R.  /.)•  Pathologic  findings  in  hypertension.  J.  Am.  M.  Ass.,  Chicago,  1911,  Ivii, 
1179-1184. 

Lichty  (M.  J.)*  Hypertension:  a  report  of  cases  under  prolonged  observation,  and  a  pro- 
test against  some  ideas.  Am.  J.  M.  Sc.,  Philadelphia  &  New  York, 

1914,  cxlvii,  681-392. 

Moritz  CF.).  Anomalien  des  Blutdruckes.  Handb.  d.  allg.  Pathol.  (Krehl  &  Marchand). 
Leipzig,  1913,  ii,  2,  60-67. 

Rlesman  (D.).     Are  we  exaggerating  the  dangers  of  high  arterial  pressure?     Penn.  M.  J ., 
Athens,  1914-15,  xviii,  193-196. 
The  limits  of  safety  in  blood-pressure  changes.     Am.  J.  Obst.,  New  Yor!:, 

1915,  Ixxi,  428-433. 

Roberts  (S.  R.}.     High  pressure  disease.     N.  York  M.  J.  [etc.],  1913,  xcviii,  169-1SO. 

Stoll  (H.  /*.)•  The  role  of  syphilis  in  hypertensive  cardiovascular  disease.  Am.  J.  M.  Sc., 
Philadelphia,  1915,  cl,  178-195. 

Stone  (W.  /.)•  The  differentiation  of  cerebral  and  cardiac  types  of  hypcrartcrial  tension  in 
vascular  disease;  a  clinical  study.  Arch.  Int.  M.,  Chicago,  1915,  xvi,  77  T,- 
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 

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Schlomovitz  (B.  H.),  Eyster  (J.  A.  E.)  &  Meek  (W.  /.)•  Experiments  on  the  origin  and 
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von  Tabor  a  (D.).  Anomalien  der  Schlagfolge  und  Schlagfrequenz  des  Herzens.  Handb.  d. 
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Zahn  (A.).  Experimentelle  Untersuchungen  ueber  Reizbildung  und  Reizleitung  im  Atrio- 
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Zwaardemaker  (H.).  DieEnergetik  der  autochthon  periodischenLebenserscheinungen.  In: 
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3.   General  Clinical 

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8°.  London,  1909,  vi,  493-546. 

Barton  (W.  M.}.  Non-technical  differentiation  of  cardiac  arhythmias.  South.  M.  J.t 
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Da  Costa  (J.  M.).  On  irritable  heart:  a  clinical  study  of  a  form  of  functional  cardiac  dis- 
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Gerhardt  (/>.)•  Die  Unregelmassigkeiten  des  Herzschlags.  Ergebn.  d.  inn.  Med.  u. 
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Gibson  (G.  A.).  The  nervous  affections  of  the  heart.  Edinburgh  &  London,  1904 ,  Y.  J. 
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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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Hoover  (C.  F.).  Functional  diseases  of  the  heart.  Mod.  Med.  (Osier).  8°.  Philadelphia 
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James  (W.  B.).  A  clinical  study  of  some  arrhythmias  of  the  heart.  Am.  J.  M.  Sc.,  Phila- 
delphia &  New  York,  1908,  cxxxvi,  469-483. 

Kulbs  (F.}.  Storungen  der  Schlagfolge  des  Herzens.  Handb.  d.  inn.  Med.  (Mohr  &  Staehe- 
lin),  Berlin,  1914,  ii,  938-958. 

Lewis  (Thomas).  Clinical  disorders  of  the  heart  beat.  2.  ed.  New  York,  1914,  P.  B. 
Hoeber.  116  p. 

Moritz  (F.)  &  von  Tabora  (D.).  Die  allgemeine  Pathologie  des  Herzens  und  derGefasse. 
Handb.  d.  allg.  Pathol.  (Krehl  &  Marchand),  Leipzig,  1913,  ii,  2, 1-129. 

Miiller  (F.).     The  nervous  affections  of  the  heart.    Arch.  Int.  Med.,  Chicago,  1908,  i,  1-22. 
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Weird  (G.  E.  S.).  The  investigation  of  cardiac  irregularity  by  means  of  the  polygraph.  Arch. 
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826     DISEASES    OF    THE    CIECULATOKY   APPARATUS 

Wenckebach   (Karl  Friedrich).     Die  unregelmassige    Herztdtigkeit  und  ihre  klinische 
Bedeutung.    Leipzig  &  Berlin,  1914,  W.  Engelmann.     255  p.     2  pi.     8°. 
Les  irregularities  du  coeur.     Arch.  d.  mal.  du  coeur  [etc.],    Paris,   1908, 
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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CLINICAL   DISORDERS    OF   THE    HEART   BEAT      $39 


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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. 


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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. 

(4) 


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